FAMILY MEDICINE EOR: Cardio 15%, Pulm 12%, GI 11%, EENT 8%, OBGYN 8%, MSK 8%, Neuro
6%, Derm 5%, Endo 5%, Psych 5%, GU 5%, Heme 4%, ID 4%, Urgent Care 4%
CARDIO 15%
CARDIO About
Myocarditis Inflammation of heart muscle due to
myocellular damage  necrosis and
dysfunction  heart failure
MCC: Viral infection
Etiologies:
•Infectious: Enterovirus (MC),
coxsackie B, adenovirus, parovirus,
HHV-6, EBV, HIV, VZV
•Bacterial: Lyme, RMSF, Chagas
•Toxic: diphtheria, scorpion
•Autoimmune: SLE, rheumatic, RA,
•Systemic: Uremia
•Medications: Clozapine,
Methyldopa, ABX, Isonizid,
Cyclophoshamide…
Dilated MC CARDIOMYOPATHY
Cardio-
myopathy Systolic dysfunction, LVEF <40%
 ventricular dilation  dilated,
weak heart *MC in Men
Causes:
Idiopathic (MC)
Viral: Enterovirus, Coxsackie, PB19,
Chagas, HIV, Lyme
Toxic: Alcohol, cocaine,
Doxorubicin
Other: pregnancy, metabolic
Hypertrophic Inherited genetic disorder (autosomal
Cardio- dominant)  mutation of sarcomeres
myopathy •LV or RV hypertrophy *esp septal
Pathophysiology:
•subaortic outflow obstruction 
hypertrophied septum, systolic
anterior motion of MV and papillary
muscle displacement
•diastolic dysfunction: impaired
relatxation and filling
Clinical Presentation
1. Viral prodrome: fever, myalgia,
malaise  HF symptoms
2. Heart Failure:
dyspnea at rest
exercise intolerance
syncope
tachypnea, tachycardia
impaired systolic function (S3/S4)
megacolon
+/- concurrent pericarditis
3. Pericarditis:
fever
chest pain
friction rub
effusion
Heart Failure symptoms
-systolic failure
-left ventricular dilation
-decreased ejection fraction
-arrhythmias
Exam: S3 gallop, laterally displaced
PMI, MR or TR
•Dyspnea (MC complaint)
•Angina, Syncope, Arrythmias
•Sudden cardiac death
Diagnostics
•CXR: cardiomegaly
•EKG: dysrhythmias, sinus tachy
•Labs: (+) cardiac enzymes, ESR
•TTE Echo: ventricular dysfunction
•Endomyocardial biopsy: infiltration
of lymphocytes with myocardial tissue
necrosis
*GOLD STANDARD!
•CXR: cardiomegaly, edema, effusion
•EKG: arrhythmias, tachycardia
•Echo: LV dilation
Murmur:
•Harsh, mid-systolic crescendo-
decrescendo murmur, at 3rd/4th ICS
•Best heard at left sternal border
•louder with valsalva, standing
•quiet w/ squat, supine
•EKG: LVH (V5, V6, aVL)
•Echo: DIAGNOSTIC
assymetrical wall thickeness
systolic anterior motion of mitral valve
Treatment
•supportive symptomatic therapy
•beta blockers
•IVIG
•Treat underlying source
•CHF management: ACEI, diuretics, beta
blockers, Na+ restriction
•Prevention of sudden cardiac arrest
•Avoid volume depletion and extreme
exercise
•Beta-blockers (1st line), Verapamil
(CCB), Disopyramide
-Negative inotropes that increase
ventricular diastolic filling time
•Septal myetomy/alcohol septal ablation
*inject alcohol-kill off part
CARDIO About Clinical Presentation Diagnostics Treatment
Restrictive •Impaired diastolic function with •Right sided HF sx •CXR: enlarged atria •Treat underlying cause if
Cardio- relatively preserved contractility •Pulmonary HTN •EKG: low voltage known
myopathy •Rigidity impairs filling (stiff) •Normal ejection fraction
•Echo: non-dilated ventricles with normal wall
Cause: Amyloidosis (MCC), Exam: Kussmaul sign (JVP increases with thickness  dilation of both atria, diastolic
sarcoidosis, hemochromatosis, inspiration) dysfunction
scleroderma, fibrosis, cancer, chemo

Stress- •Can cause an ACS or STEMI • psycho or physiological stress EKG: ST elevations, (+) enzymes •Recover in a few weeks
Induced •event causing catecholamine surge  Systolic dysfunction of apex Echo/LV angiography: LV apical ballooning •Beta Blockers for one year
(Takotsubo) *MC in postmenopausal women and/or mid segments

CARDIO About Symptoms Management

Sinus Arrhythmia •Cyclic increase in normal heart rate with reflex changes in vagal influence on the normal No treatment required
inspiration and decrease with expiration pacemaker and disappears with breath holding or *not pathologic
increase in heart rate

Sinus Bradycardia Heart rate <60bpm
Rate increases with exercise, atropine
Causes:
•Increased ICP: hemorrhage
•Anterior MI: Inf. wall MI -> RCA supply SA
•OSA: decreased Hr <30bpm in apnea
•Other: hypothermia, hypothyroidism
•Increased vagal influence on the normal pacemaker •1st line-permanent pacemaker
or organic disease of sinus node
- Fear, bearing down, SSS Acute setting: transcutaneous pacing, temporary
transvenous pacing, Atropine (ACLS protocol)
•Severe <45bpm-sinus node pathology
SX:
•weakness, dizziness, confusion, syncope

Sick Sinus Syndrome •Commonly have recurrent supraventricular “When they go into AFIB its really fast then when Symptomatic  Pacemaker (PPM)
arrhythmias and bradycardia “tachy-brady” they go out of afib they go into a really slow sinus
brady”
•MC in elderly •Cause: medications

Sinus Tachycardia •HR >100bpm Symptoms: palpitations, lightheadedness Physiologic: *usually compensatory
•Onset & termination usually GRADUAL *usually related to the cause
Symptomatic: Beta-blocker (Metoprolol), CCB
Causes: MC-exercise, anger/stress •2 types: inappropriate, POTS

CARDIO About Causes Signs and Symptoms Diagnose/Management

Premature ectopic focus in the atria that fires •increased frequency with age Palpitations •Not required most of the time
Atrial before the next sinus node impulse •structural changes •Beta Blockers if significant symptoms
Contractions *diff P wave morphology •precuroseor to afib, aflutter •Class IC antiarrhythmis is second-line

Premature Premature depolarization originates *frequently in normal heart •Palpitations MC complaint Usually no treatment needed
Ventricular from the ventricles •caffeine, stress, alcohol
Contractions - wide QRS complex w/ pause •electrolyte abnormalities EKG: T wave usually opposite QRS, Symptomatic: BB (Metoprolol)
occurring earlier than expected •thyroid QRS is wide 2nd line: Class Ic or III AAD
 Significant burden: cath ablation

CARDIO About Causes Signs and Symptoms Diagnose/Management

AV Block First degree: PR >0.20 with all atrial
impulses conducted, P for every QRS
*AV node
dysfunction Second degree: intermittent blocked
beats, not a P for every QRS
Mobitz type I (Wenckebach) AV block:
AV conduction time (PR) progressively
lengthens with the RR interval
shortening before the blocked beat
*abnormal conduction AV node
Mobitx type II AV block: there are
intermittently non-conducted atrial beats
*block in HIS bundle
•PR prolonged, all the same length
Third degree: complete heart block, in
which no supraventricular impulses are
conducted to the ventricles
•regular P-P intervals and regular R-
R, but are not related to each other
First Degree and Mobitz Type I:
•may occur in normal individuals
with heightened vagal tone
•drug effect
•electrolyte abnormalities
•organic disease: ischemia, infarction,
inflammatory, fibrosis, calcification,
infiltration
Mobitz Type I:
•Causes: inferior wall MI, AV node
blocking agents (BB, CCB, Digoxin),
Lyme, hyperkalemia, surgery
Mobitz Type II:
•Causes: RARE in structural heart
disease; AV node blocking agents,
ablation, surgery
Third degree:
•ORGANIC DISEASE involving the
infranodal conduction system
•transient or permanent
•AV dissociation
•inferior wall MI, AV nodal blocking
agents, endocarditis, myocarditis
First Degree Block:
-diagnosed by EKG alone
Mobitz type I:
-most commonly asymptomatic
-may note palpitations, DOE,
dizziness
Mobitz type II:
irregular rhythm
-may be asympatomatic
-palpitations, DOW, weakness, dizzy
Third-Degree block:
-sx vary; worse w/ exertion
-palpitations, DOE, weakness, near
syncope, syncope, and/or HF
Diagnostic Studies:
•Review medications & HX
*REVIEW FIRST!
•12 lead EKG
•telemetry monitoring (inpt)
•echo to r/o structural disease
•S/S ischemia -> cath
Labs: CBC, CMP, TSH
Management:
•First Degree:
-avoid medications that may prolong PR
interval and slow AV conduction
-asymptomatic: no treatment
-symptomatic: Atropine, Epi
•Mobitz type I:
-avoid meds that slow AV conduction
-symptomatic: Atropine
•Mobitz type II/Third-Degree:
-unstable, usually require pacemaker

CARDIO About Causes Symptoms Management

Atrial Results from an ectopic atrial focus firing at a rate •severe COPD -palpitations •treat underlying conditions
Tachycardia faster than the sinus rate -> becomes pacemaker •structural heart disease -heart racing sensation
•may occur in normal hearts -SOB •CCB (Verapamil) 1st line option
•Onset and termination occur abruptly *not commonly -dizziness *especially if have COPD
•Atrial rate about 100-160bpm •digoxin toxicity -near syncope
•Unifocal or multifocal (3+ different morphologies) •refractory: class IC or III

AV AV node becomes the dominant pacemaker •sinus disease EKG:

Junctional •CAD •regular rhythm
Dysrhythmia Junctional: rate 40-60 •Digoxin •inverted P waves or not seen
s Accelerated: 60-100 •myocarditis •narrow QRS
Junctional tachycardia: >100
CARDIO About Causes Signs & Symptoms//Diagnosis Management
Paroxysmal •Common cause of paroxysmal •MC mechanism for •Awareness of rapid heart beat Acute Management: STABLE PT
Supra- tachycardia paroxysmal supraventricular •Chest pain, SOB 1. Mechanical measures *done by pt
ventricular tachycardia is reentry •Dizziness, syncope •valsalva*
Tachycardia Two common types of reentry: - typically initiated by •Abrupt onset and termination, last •stretching the arms and body, lowering the head
•AVNRT (AV node reentrant a PAC or PVC seconds to several hours or longer between knees*
tachy): one normal and one •coughing, breath holding*
accessory pathway within the node EKG: •cold water
*within the node •rate ~140-240 •carotid sinus massage-> PROVIDER
*Most Common
•Orthodromic (95%): regular, 2. Drug Therapy (IV therapy): “ABCD”
•AVRT (AV reciprocating tachy): narrow complex tachy with no •Adenosine**, CCB (Diltiazem), BB (Metoprolol)
one normal and one accessory discernable P waves •wide complex: Amiodarone
OUTSIDE the node “if you cant tell if the bump is a P
 WPW: accessory path (bundle or a T, then it must be SVT” 3. Cardioversion (shock) *sedate if awake
of kent) preexcites ventricles •FIRST LINE if hemodynamically unstable
 LGL •Antidromic: regular, wide •synchronized electrical cardioversion at 100J
*accessory path outside AV node complex tachy (mimics v-tach)
4. Definitive: ablation
WPW EKG:
W: wave  delta wave (slurred WPW:
QRS upstroke) •Procainamide**, Amiodarone
P: PR interval short •avoid AV blocking agents ABCD (Adenosine, BB,
W: wide QRS CCB, Digoxin)
•DEFINITIVE: Ablation

Prevention: BB & CCB are 1st LINE

CARDIO Phases Risks/Causes/Complications Symptoms Management
Atrial •Multiple irritable atrial foci fire at Risks: Symptoms: Three-Fold:
Fibrillation fast rates •CHF* & HTN* •may be asymptomatic 1. Rate control
•MC chronic arrhythmia •Old age •palpitations, heart racing 2. Rhythm control
•CAD •chest pain, SOB, fatigue, CHF 3. Thromboembolic event prevention (ALL)
Paroxysmal: in and out on own •valvular disease
Physical Exam: Rate Control:
Persistent: >7 days Causes: •irregularly irregular rhythm •CCB (Verapamil, Diltiazem) *NOT in HF!
•alcohol •signs of CHF •Beta Blockers (Metoprolol, Atenolol,
Long Standing Persistent: 1 year •thyroid disease, lung, heart •distal pulses may be difficult Esmolol)
•fhx •Digoxin
Permanent (Chronic): staying in •sleep apnea EKG:
•pericarditis •irregular irregular ~250bpm Rhythm Control: dependent on comorbidities
•no P waves
Complications: HF, thromboemboli •Ashman’s phenomenon
(wide QRS after short R-R)

Rhythm Control Anticoagulation Maintenance/Education

Hemodynamically unstable:
Cardioversion
*most successful within 7 days of
onset  echo prior to make sure there
is no thromboemboli
AF >48 hours: anticoagulation
needed for 3 weeks before
cardioversion, continue for 4 weeks
after cardioversion
CHA2DS2SASc Score
*calculate on EVERY Afib pt
•Score 0: no therapy
•Score 1: consider oral anticoag or
antiplat (ASA 81)
•Score 2: oral anticoagulant
•Valvular (mitral stenosis or
regurg) heart disease: Coumadin
Long-Term:
•Warfarin (INR goal 2-3)
•Dabigatran (Pradaxa): reduce if
CrCl 15-30
•Rivaroxiban (Xarelto): reduce if
CrCl 15-50
•Apixaban (Eliquis: reduce if 2+:
80+, wt </=60kg, Cr 1.5+
Maintenance:
•CBC and BMP q6months
•outpatient ambulatory monitoring
*if on Amiodarone, then make sure they are
getting routine imaging and labs
Patient Education:
•avoid alcohol ANYTIME
•control underlying risk factors
•monitor for signs of bleeding if anticoagulated

•Edoxaban (Savaysa): reduce if

CrCl 15-50

Atrial Causes/Risks/Presentation Treatment

Atrial Flutter •One atrial focus firing at a fast rate Stable: vagal maneuvers Unstable: Higher rate of cure with catheter-based
(~300bpm) •Rate: BB, CCB (Diltiazem, •synchronized cardioversion radiofrequency ablatation
•Presentation, risk factors, causes are cVerapamil) - DEFINITIVE
the same as afib •Anticoagulation: CHADSVASc
CARDIO Definition/ Causes Symptoms Management
Ventricular •Three or more consecutive PVCs Patient may be asymptomatic, Acute sustained VT Long-Term therapy
Tachycardia -nonsustained: less than 30 seconds, especially with nonsustained Unstable: immediate synchronized direct (prevention/recurrence):
-sustained: greater than 30 seconds current cardioversion •ICD
•usual rate is 120-300bpm Majority have symptoms: *unsynchronized if no pulse •BB
•palpitations, heart racing •Amiodarone, Sotalol (class III)
Causes: •near syncope, syncope Stable: •catheter ablation
•ischemic heart disease (MC) •confusion, fatigue •IV Amiodarone likely will convert to sinus
•structural heart defects •chest pain, SOB •IV Lidocaine *MI or still in VT with Amio Non-sustained VT: Beta
•prolonged QT interval •Add IV Magnesium *Torsades Blockers
•electrolyte abnormalities (low Mg, K, Ca) EKG: regular, wide complex

Torsades De •Variant polymorphic ventricular tachy •palpitations EKG: polymorphic ventricular tachycardia IV Magnesium Sulfate
Pointes •dizziness (cyclic alteration of the QRS amplitude) (suppresses early afterdepol)
•Prolonged repolarization and early •fatigue *sinusoidal waveform
afterdepolorization, and triggered activity •dyspnea •discontinue all QT prolongating
•chest pain agents
Causes:
•prolonged QT
•electrolytes (low Mg, K, Ca)
•meds: Class IA, Digoxin, Macrolides,
antipsychotics, antidepressants, antiemetics
Arrhythmias Definition
Ventricular •Leading cause of sudden death •unresponsive, pulseless,syncope IMMEDIATE UNSYNCHORNIZED
Fibrillation •MCC is ischemic heart disease DEFIBRILLATION & CPR

Arrhythmia About Mechanisms Causes/Management

Accelerated Regular wide complex rhythm with a rate Two possible mechanisms: 2. escape rhythm due to suppression of higher No treatment unless UNSTABLE
Idioventricular of 60-120bpm 1. Slow ventricular tachycardia pacemakers resulting from sinoatrial and AV
Rhythm due to increased automaticity block or depressed sinus node

CARDIO About Causes Evaluation Management

Left Bundle •MC in pts with underlying heart Causes: Evaluation: Asymptomatic and isolated LBBB:
Branch Block disease; Can also be seen in -structural heart disease •chest pain/ACS sx -no specific therapy
(LBBB) structurally normal heart -functional LBBB (rate-related) -treat underlying cause (treat like MI)
Diagnostics:
*Left anterior descending artery •echo SX pts with LBBB and low EF: CRT
 •stress test or LHC
Right Bundle Receives blood supply from septal Conduction can be compromised by: Generally asymptomatic Do not require further dx or tx
Branch Block branches of the left anterior •Structural heart disease
(RBBB) descending •Functional factors

Pulseless PEA: organized rhythm seen on a •CPR & epinephrine

Electrical monitor, but patient has no pulse
Activity/ •Check for shockable rhythm every 2
Asystole Asystole: no rhythm minutes

Class I Drug About Drug Side Effects/CI/PK/Caution

Class IA
•decreases conduction velocity
•prolongs repolarization
•prolongs refractory period
•prolongs action potential
•increase excitation threshold
moderate depression of phase 0
WORKS ON FAST SODIUM
Quinidine •Potent anticholinergic properties that affect SA and AV •Increased ventricular rates with afib or aflutter
nodes -> increase SA nodal discharge rate and AV nodal  PROLONG QT INTERVAL -> torsades
conduction  Add BBB, CCB, or Digoxin to prevent
•SE: GI, N/V/D
*don’t use because of QT prolongation, and rhythm issues •PK: CYP3A4 inducer or inhibitor
Procainamide •No anticholinergic property •Prolongs QT -> Increases torsades
•LUPUS (SLE) clinical syndrome *MC
•N/V/D, fever

Disopryamide •Potent anticholinergic and negative inotropic effects •Prolongs QT -> Increases torsades
(Norpace)  Use more for HOCM •Precipitation of CHF
•Dry mouth, urinary retention, constipation, blurred vision

•CI: reduced LV EF (<40%)

Class IB
•decreases conduction velocity
•shortens repolarization
•shortens actions potential
Lidocaine •Selective to ischemic tissue
•Active fast sodium channel in the bundle of HIS, purkinje
*IV form fibers, and ventricular myocardium
 Little effect on non-ischemis tissue, atrial
myocardium, SA node
•best for ventricular dysrhythmias with acute MI
•SE: CNS, dizziness, disorientation, tremor, agitation, seizure,
respiratory arrest
•Caution: liver failure *stop if Lidocaine level is over 4
•PK: hepatic metabolism

*do not effect QRS complex Mexiletine •Similar to lidocaine but oral *not used alone •SE: GI, N/V highly, neurologic effects
*can use in combo with class IA and III drugs for refractory - Dizziness, confusion, ataxia, speech disturbances
*oral form ventricular dysrhythmias

Class IC
•decreases conduction velocity
•NO effect on action potential
Flecainide •Slows conduction velocity in the Purkinje fibers and the AV •SE: rapid VT resistant to resuscitation
(Tambacor) node  Lengthen PR interval and QRS duration
•Used for afib/aflutter - Blurred vision, dizziness, HA, tremor, N/V
•CI: CAD, LV dysfunction, LVH, valvular disease

NORMAL repolarization Propafenone •Slows conduction velocity of purkinje fibers and AV node; •SE: same as Flecainide, metallic taste
LONGER depolarization (Rythmol) mild non-selective BB effect  May lengthen PR interval and QRS
*similar to Flecainide

Class II Drugs
Beta Blockers
-Metoprolol (cardioselevtive)
-Esmolol (IV)
-Atenolol, Carvedilol, Labetlol
Class III
*use these pretty routinely
Block potassium channels and
prolong repolarization, widening
the QRS and prolonging the QT
interval
 Decrease automaticity and
conduction and prolong
refractoriness
 Cant fire neighboring cell
as easily, takes longer
*avoid w/ QT prolongation drugs
 Anti-psychotic drugs
 Anti-fungals
 -Fluoroquinolones
•Used for afib/aflutter
About
Decreased automaticity (lowers resting threshold, takes longer to fire off),
prolong AV conduction, prolong refractoriness
 (-) chonotripic and inotropic effects
*beta blockers A  M are cardio selective, N and lower are NOT
Drugs About
Amiodarone •Possesses characteristics of all 4 classes
(Pacerone) •K+ channel blocks, but also blocks sodium channels,
non-selective BB activity, weak CCB propreties
•Works on all cardiac cells
•Minimal to no negative inotropic effects
*can use in LV dysfunction
MOST
COMMON
DRUG USE!
Sotalol •Has non-selective B-adrenergic blocking properties
(Betapace) •PUT IN HOSPITAL TO START AND MONITOR
 Decrease cardiac contractility
 Prolongs atrial and ventricular refractoriness
Dofetilide •Results in prolonged action potential and an increased
(Tikosyn) QT interval
 Effects atria more than ventricles
•No negative inotropic effects *Safe in LV dyfcuntion
*must have board of pharmacy certification in order
to prescribe because of QT prolongation
Dronedarone •Exhibits AA properties of all 4 classes
(Multaq)  However, does not work as well
“safe cousin of Amiodarone”
*don’t use often & more expensive
•CI: CAD, LV dysfunction, LVH, valvular disease
Indication
Useful in suppressing ventricular dysrhythmias and
supraventricular dysrhythmias
•CI: bradycardia, 2nd 3rd degree AV block
SE/CI/DDI
SE: *cumulative effects after years, not a one-time dose
•metabolite accumulation of IODINE in numerous organs
•Pulmonary Toxicity *pulmonary fibrosis
 Stop immediately if occurs
•Thyroid abnormalities (hypo or hyper) due to iodine
•Ocular complications (corneal and lens) *rarely effects vision
 Photophobia, halos, blurred
•GI: Nausea (acute), vomit, anorexia, abdominal pain *common
•Neurologic toxicities frequently (warn about)
 Tremors, ataxia, peripheral neuropathy, fatigue, insomnia
•Derm: photosensitivity, blue/gray skin IN SUN (warn about)
Monitor:
•CXR and dilated eye exams yearly
•TSH & LFTs every 6 months
•wear sunscreen
DDI: CYP 3A4 inhibitor-Warfarin
*can double serum digoxin concentration
CI: LV dysfunction
SE: QT prolongation; DC if QT >550ms
*most due to BB properties; do NOT combine with other BB
SE: development of torsades
*pt in hospital on telemetry with q12h EKGs for first 3 days
DDI: cimetidine, ketoconazole, megestrol, prochlorperazine, Bactrim,
verapamil
PK: Renal excretion (CI if CrCl <20) *regular BMP for CrCl
CI: symptomatic CHF, permanent AF, hepatic
SE: CHF exacerbation, QT prolongation, bradycardia, hepatotoxicity,
pulmonary toxicity, N/D, pruritis, dyspepsia
 Monitor: BUN/CR, EKG q3mo for 1st 6mo tx

Ibutilide •Similar to sotalol, but no beta-blocking activity SE: torsades (QT prolongation)
(Corvert) •Close to a pure potassium channel blocking agent *monitor on telemetry for several hours following IV infusion
•Only in IV form and indicated for afib/flutter
cardioversionto sinus rhythm CI: LV dysfunction and electrolyte abnormalities (low K & Mg)
 Monitor in ICU

Class IV Drugs About SE/CI/DDI

Calcium Channel Verapamil •Decreases automaticity and AV conduction CI: LV dysfunction; heart failure (due to negative inaotropic)
Blockers Diltiazem •Potent negative inotropic effects
*Non-dihydropuridines SE: peripheral edema, bradycardia, AV blocks

Other Drugs Drugs About

Digoxin •Predominant AA effects on AV node
-inhibits calcium currents in AV node and activated ACH-
mediated K+ currents in the atrium
-slows conduction through the AV node and prolongs AV
refractory period
-mainly used for slowing ventricular rate in afib/aflutter and
termination reentrant arrhythmias involving AV node
EKG changes: PR prolongation and ST segment depression
PK:
•IV or oral; DOSING IN MICROGRAMS
•Tablets incompletely bioavailable
•Slow distribution to effector sides
*requires loading dose of 0.6-1mg over 24 hours then reduce to maintenance dose
•t ½ of 36 hours
•renal elimination (reduce dose in renal insufficiency)

DDI: amiodarone, quinidine, verapamil, diltiazem, itraconazole, propafenone, flecainide

*decrease clearance, decrease digoxin with these meds

Digoxin •Can be precipitated by: S/S: visual disturbances (blurry/tunnel vision), dizziness, weakness, N/V/D, anorexia, any
Toxicity -declining renal function dysrhythmia
-electrolyte abnormalities
-hypoxia or drug interactions Treatment:
•Manage arrhythmias
•Narrow therapeutic index •IV hydration and electrolyte correction
*can check therapeutic levels •Digoxin immune Fab (immunoglobin fragment)-> high affinity for digoxin molecules

Adenosine •Activates potassium channels and by increasing the outward •Used for converting SVT  sinus rhythm *essentially sinus arrest (stop the heart)
potassium current hyperpolarizes the membrane potential (doesn’t let • t ½ short <10 seconds, so sinus arrest does not last long
*SVT anything in to block it), decreasing spontaneous SA nodal
depolarization
 Inhibits automaticity and conduction in the SA/AV nodes 
SLOWS AV NODE SE: chest discomfort, dyspnea, flushing, HA
*doesn’t really work for atrial fibrillation/atrial flutter *causes vasodilation with a stress test

Atropine •Parasympathetic that enhances both sinus nodal automaticity and •Used in emergent setting of symptomatic bradycardia
AV nodal conduction through direct vagus action •Blocks ACH at parasympathetic neuroeffector sites
 Someone that has a vagal response
SE: tachycardia, paradoxical slowing of HR in patients with Mobitz type II AVB and third
 INCREASES HEART RATE degree AVB *never use this drug unless you have a crash cart ready

*Class I and III primarily used for rhythm, class II and IV primarily used for rate control

Goals of dysrhythmia management: prevent sudden death, reduce symptoms, improve QOL, reduce hospitalizations,
- consider costs and risk of therapies, overall patient condition

CARDIO About Clinical Presentation Diagnostics Management

Angina Substernal chest pain usually
Pectoris brought on my exertion
*complication of coronary
artery disease causing SX
Pathophysiology:
•inadequate tissue perfusion due
to decreased blood supply &
increased demand
Classes
•Class I: strenuous activity
•Class II: more prolonged
rigorous activity
•Class III: daily activity
•Class IV: at rest
History:
•Chest pain: poorly localized,
substernal
•Radiation: arm, teeth, jaw
•Duration: Short
(1-5 minutes, <30 minutes)
•Alleviating: rest, NTG
•Aggravating: exertion, anxiety
Other SX: diaphoresis, dyspnea,
fatigue, numbness, nausea
Exam: usually normal
Low Dose ASA Prevention:
•considered for primary
prevention in patients 40-75
who are not at increased
bleeding risk
•NOT for ages >70 for primary
•NOT for anyone with increased
risk of bleeding
ALL: EKG and CXR
EKG: WITHIN 10 MINUTES
•ST elevation •ST depression *classic findings
•+/- T wave inversion, poor R wave progression
Stress Test *most useful non-invasive tool
•exercise stress test: ST depression,
hypotension/HTN, arrhythmias, sx
•myocardial perfusion (exercise, pharm)
-thallim-201 or 00m-technetium sestamibi
-indication: baseline EKG abnormalities
-pharm agents: Adenosine
-CI: asthmatics
•stress echo: assess global and regional wall
motion abnormalities
-Dobutamine  increases O2 demand
•cardiac MRI: dobutamine infusion, assess
perfusion and wall motion abnormalities
Coronary Angiography (GOLD) “Cath”
Revascularization
•PCI: 1 or 2 vessel disease not of L main
•CABG: L main or 3 vessel of EF <40%
Medical Management
•NTG
-increase supply, O2, decreases demand,
-SE: headache, tachyphylaxis, flushing
•Beta-Blockers
-increases blood supply by prolonging coronary
artery filling times
-reduces demand by reducing HR
•CCB (Diltiazem, Verapamil)
-prolongs diastolic filling increasing supply
-decreased contractility reducing demand
•Aspirin: does not work with supply/demand,
but prevents progression of by preventing
platelet aggregation
Outpatient: ASA*, BB*, statin, NTG

CAD/ Causes: Pathophysiology: RV infarction triad: elevated JVP, clear lungs, •PCI (w/n 90 minutes) or TPA (30 minutes)
Acute •MCC: atherosclerosis 1. fatty streak formation: lipid (+) Kussmaul sign •MONA: morphine (if NTG fails to relieve
Coronary (hardening and narrowing of deposits in the WBC *no sx *inferior wall MI may be associated with heart pain), oxygen, NTG, ASA*avoid NTG and
Syndrome the coronary arteries) blocks or bradycardia morphine in posterior and inferior wall MIs
•Coronary artery vasospasm 2. early plaque formation:
•Aortic stenosis/regurg LDL enters endothelium in the STEMI: (+) enzymes, ST elevation >1mm Normal EKG:
•Pulmonary HTN fatty streak and LDL is oxidixed *total occlusion MONA + serial enzymes and EKG
•HTN NEW LBBB IS STEMI EQUIVALENT
•HOCM 3. foam cells: macrophages UA or NSTEMI: MONA, Hepatin, BB
ingest LDL NSTEMI: (+) enzymes, ST depressed •TIMI or HEART assessment
Risks: *subtotal occlusion
•DM (biggest risk!) 4. mature fibrous plaque: STEMI: MONA, Heparin, BB, reperfusion
•smoking •HLD proliferating smooth muscle and Unstable: (-) enzymes, ST depressed •ACEI for long term therapy
•HTN •males connective tissue *subtotal occlusion
 •age (>45 men, >55 women)
•fhx Symptoms:
CP: retrosternal, pain at rest, no
relief with NTG, >30min
Enzymes:
CK/CK-MB: appears in 4-6hr, peak 12-24h
Troponin I: appears 4-8h, peak 12-24h
*false elevations in renal failure, HF, PE, CVA
Location:
Anterior: V1-V4 (LAD), V1-V2 (p LAD)
Lateral: V5-6, I, aVL (Circumflex)
Inferior: II, III, aVF (RCA)
Posterior: ST dep in V1-V2 (RCA, CFX)

Vasospastic Triggers: cold weather, exercise, Chest Pain: •EKG: transient ST elevations, resolves with •1st line: CCB (Diltiazem, Verapamil,
(Variant, cocaine, hyperventilation •rest (midnight, mid-morning) symptom resolution Amlodpine, Nicardipine) nightly
Prinzmetal •not exertional •Angiography: r/o CAD, may rule in •2nd line: NTG
) Angina Risks: female, >50, smoker •not relieved by rest vasospasm esp with Ergonovine AVOID BETA BLOCKERS

CARDIO About Pathophys/Clinical Presentation Diagnostics Treatment

Congestiv Inability of heart to pump enough blood to meet Pathophysiology:
e Heart the demands of the body (MCC: CAD) Increased preload and afterload
Failure and/or reduced contractility
•Acute: began last few days to weeks
*systolic  HTN, MI, papillary muscle tear Compensations
1. increased sympathetic
•Chronic: sx present for months 2. myocyte hypertrophy/remodel
*typically cardiomyopathy or valve disease 3. RAAS activation  fluid
overload, ventricular remodeling
•High: heart can’t meet demands
(supply<demand) Left: Increased pulmonary venous
-thyrotoxicosis, anemia; pagets, wet pressure  fluid backing to lungs
beriberi, AV shunting, decreased CO -SOB
-Rales
•Low: insufficiency forward output (low EF) -Chronic, non-productive cough
with pink frothy sputum
•Systolic: reduced EF (HFrEF) *MC type, S3 *MCC transudative effusions
-MI, dilated cardiomyopathy, myocarditis -increased sympathetic (adrenergic):
-thin ventricles, dilated chamber sweating, dusky/pale skin,
tachycardia, cool
•Diastolic: preserved EF (HFpEF), S4
-normal or increased EF  forced contraction Right:Increased venous pressure 
into a stiff ventricle systemic fluid retention
-HTN, LVH, elderly , constrictive pericarditis, -edema
restrictive cardiomyopathy -JVD
-thick ventricle, small chamber -ascites, HSM, RUQ tenderness
•Left: DOE, PND, orthopnea, fatigue Symptoms:
-MCC CAD, HTN •Chest pain, HTN, Flu-like sx
•Right: JVD, ascities, edema Physical Exam:
-MCC LHF, pulmonary, mitral stenosis General: tachy, diaphoresis
Narrow pulse pressure: <25
Pulsus Alternans: LV HF
Precordial: lateral displaced PMI
Heart Sounds: S3 & S4
GOAL: confirm sx &
cause of HF
Initial Testing
EKG
CXR: kerley B, effusion,
congestion, cardiomegaly,
butterfly pattern
Initial Labs:
•CBC, CMP, coagulation
studies, glucose, lipids
•BNP
(>100 likely, >500 very)
-released by ventricles
•cardiac enzymes
Echo: GOLD
Normal EF: 55-60%
EF <35% high mortality
NYHA Class:
I: normal activity, no sx
II: stairs, mild sx
III: walking, marked
limitation
IV: conversation/rest
Lifestyle modifications:
•Wt loss, sodium <2g/d, fluids <2L/d
•Daily weight monitoring, smoking cessation
CI: No-Dihydro CCB( Diltiazem, Verapamil)
Pharmacotherapy: **loop, ACEI, BB
Loop Diuretics (Furosemide, Torsemide)
MOA: inhibits water transport across loop
SE: hypOkalemia, hypOcalcemia, hypOnatremia
Class I: *reduce mortality
*ACEI (“-pril”)
-reduce preload and afterload
-reduce aldosterone production (RAAS);
vasodilates
-reduces ventricular remodeling
SE: hypotension, hyperkalemia, cough,
angioedema, renal insuffieiency (CrCl <30)
CI: hypotension, pregnant
*Entresto (Sabucitril + Valsartan)
*BB (Carvedilol, Metoprolol, Bisprolol)
-reduce mortality (increase EF, reduce ventricular
size)
SE: dizziness, hypotension
-stop during decompensated HF because EF
reduces initially
-caution: 1st AVB, asthma, bradycardia
*Aldosterone Antagonists (Spironolactone)
-SE: hyperkalemia, gynecomastia
-CI: K+ >5 or GFR <30
*Hydralazine/Nitrate (if black + ACEI/BB)
*safe in pregnancy

CARDIO About
HTN Risks:
OSA, smoking, alcohol, obesity,
metabolic syndrome, NSAIDs,
high sodium in diet (low K+)
Pre-HTN: 120-139/80-89
Stage 1: 140-159/90-99
Sage II: >160/100
*isolated systolic is at
GREATER risk for
cardiovascular disease then
isolated diastolic
Secondary HTN due to an underlying,
HTN identifiable cause
*suspect is refractory to
medication
HTN Hypertensive Urgency
Urgency v. >220/125 WITHOUT end-
Emergency organ damage
Hypertensive Emergency
>220/125 WITH end-organ
damage
Clinical Presentation
Causes:
1. Sympathetic NS & RAAS
2. Pressure/natriuretic
3. Renal/cardio development
4. Increase in Na & Ca levels
Fundoscope:, arterial narrowing
 AV nicking  hemorrhages
and exudates  papilledema
(malignant HTN)
Causes:
Renal: MCC of secondary
Endo: hyperaldosteronism,
pheo, cushings
•Urgency: poorly controlled
•Emergency: identify organ
failure  brain, kidney, heart
Diagnostics
2+ elevated readings on 2+ different
visits >140/90
•UA, BMP, EKG, lipids
Complications:
Cardio: CAD, HF, MI, LVH, dissection,
AAA, PVD
Neuro: TIA, CVA, aneurysm,
encephalopathy
Neph: renal stenosis, CKD
Optic: retinal hemorrhage, retinopathy
Other: coarc, sleep apnea, ETOH, OCPs,
COX-2 inhibitors
•CBC, CMP, UA; EKG, CXR
•CT if neuro sx in emergency
Complications:
•Renal-nephrosclerosis
•Eye-retinopathy, cotton wool
•Vascular-atherosclerosis, aneurysm
•CVA (SPB); S4, heave
MOA: reduces preload and afterload
SE: dizziness, HA, tachyphylaxis
Acute: LMNOP: Lasix, Morphine, O2, Nitrate,
position
Management
•healthy >60yo-150/90
•<60yo, CKD, DM-140/90
•1st line-ACE/ARB
•AA 1st line-CCB/thiazide, HF/MI-BB
Diet: restrict sodium <2.4g/day
“
Hypertensive Urgency: adjust medications
Decrease BP over 24-48h with ORAL agents
-hospital: Clonidine, Captopril, Nifedipine
-oral: labetolol, captopril, NTG, clonidine
Hypertensive Emergency: 1st line: BB, CCB
Nicardipine, Labetalol, Esmolol
-ischemic CVA: keep BP 180-200
-hemorrhagic CVA: <130
-dissection: 100-110
HTN PHARM Mechanism of Action Side Effects CI
ACE Inhibitors Decreases synthesis of AG II/Aldosterone Hypotension CI:
“-pril” Cardio & renoprotective Cough (high bradykinin) Pregnancy
synergestic effect when used with thiazides Renal Insufficiency AKI
Reduce preload & afterload Hyperkalemia
Angioedema (high bradykinin)

ARB Blocks the effects of angiotensin II Hypotension CI

“-sartan” *consider if cant tolerate ACEI or BB Renal Insufficiency Pregnancy
Hyperkalemia
Calcium Channel Dihydropyridines: potent vasodilators HA CI:
Blockers -little or no effect on contractility or conduction Dizziness, lightheaded CHF *especially non-dihydro
Dihydropyridine *commonly used for HTN Flushing AVB
Nifedipine Edema
Amlodipine Non-dihydro: affect cardiac contractility and conduction
Non-dihydro *commonly used in HTN and A-Fib Verapamil: constipation
Verapamil
Diltiazem
Beta Blockers Catecholamine inhibitor Fatigue AVB
“-olol” Blocks adrenergic release of renin Depression Decompensated HF
Impotence Asthma/COPD
Alpha-1 blockers Blocks alpha-1 Syncope
Prazosin (Minipress) Increases HDL and loswers LDL Dizziness
Terazosin (Mytrin) Improves insulin sensitivity headache
Doxazosin (Cardura)
*good for HTN with BPH
Thiazide Diuretics Affect BP by reducing blood volume Hyponatremia
HCTZ Prevents kidney Na and water reabsorption in DISTAL TUBULE Hypokalemia
Chlorthalidone HyPERcalcemia
Metolazone *caution with gout and DM HyPERuricemia
HyPERglycemia

Loop Diuretics Inhibits water transport across loop of Henle Volume depletion Sulfa allergy
Furosemide Increases excretion of water, Na, Cl, K Hypokalemia, natremia, calcemia
Torsemide Hyperglycemia
Bumetanide Metabolic alkalosis
Ototoxicity

K+ Sparing Diuretics Inhibits aldosterone-mediated Na+/H2O absorption Hyperkalemia Renal Failure

 Spironolactone Gynecomastia *spirolnolacton Hyponatremia
Amiloride
Eplerenone

**choices for gout: CCB or Losartan (only ARB that does not cause hyperuricemia)

CARDIO About Clinical Presentation Diagnostics Management

Hyper- Causes:
lipidemia •Hypercholesterolemia:
hypothyroidism, pregnancy,
kidney failure
•Hypertriglyceridemia: DM,
ETOH, obese, steroids, estrogen
Linkage between LIPIDS and
INFLAMMATION
•Xanthomas (fatty growths
underneath skin-joints)
•Xanthelasama (lipid plaques on
eyelids)
Pancreatitis may be seen in
hypertriglycerides
Screening:
Ages 20-79 every 4-6 years
High risk: screening 20-25yo M, 30-35yo F
Low risk: 35yo M, 45yo F
Who to Treat:
1. DM between 40-75 years old
2. 40-75yo with risk 7.5% and higher
3. Age 21+ and LDL 190+
4. Clinical ASCVD
Lifestyle: weight, exercise, dietary changes
Pharmacotherapy:
•LDL: Statin, bile acid sequestrants
•Triglycerides: Fibrates, Niacin
•increase HDL: Niacin, Fibrate
High intensity:
Atorvastatin 40-80 & Rosuvastatin 20-40
•Age 40-75yo with DM
•Clinical CAD
•LDL 190+,
•Age 40-75 10 year risk >7.5%

Goals: LDL <100, Cholesterol <200, HDL >60

HLD PHARM Mechanism of Action Side Effects CI

HMGcoA Reductase Inhibits the rate limiting step in hepatic cholesterol synthesis Myositis/myalgia/rhabdo Best given at bedtime when cholesterol
Inhibitors (Statins) Removes LDL from the blood Hepatitis synthesis is maximal
BEST DRUG TO REDUCE LDL *SE rate increased with tetracyclines

Fibrates Inhibits peripheral lipolysis and reduced hepatic triglyceride Myositis, mylagias CI: hepatobiliary disease or severe renal
Gemfibrozil production (by decreasing hepatic extraction of fatty acids) Hepatitis disease
Fenofibrate Gallstones (blie acide lithogenicity)
BEST DRUG TO REDUCE TRIGLYCERIDES

Niacin (B3) Increased HDL, reduces plasma fibrinogen levels, decreased hepatic Flushing *decrease with ASA before PUD
production of LDL and VLDL Headache, Warm sensation High glucose
Pruritis Hepatotoxicity, N/V/D
Hyperuricemia, Hyperglycemia Dry skin

Bile Acid Binds bile acid in intestine blocking liver reabsorption of bile acids GI: N/V/ bloating, cramping
Sequestrates Hepatitis
Cholestyramine ONLY MEDICATION SAFE IN PREGNANCY Increased TGs
Colestipol *can also be used for pruritis with biliary obstruction
Colesevelam
Ezetimide (Zetia) Inhibits intestinal cholesterol absorption  lowers LDL
*may be used with statins
CARDIO About
Cardiogenic Primary cardiac/myocardial
Shock dysfunction  inadequate perfusion
 low CO and increased systemic
vascular resistance (SVR) &
pulmonary wedge pressure (>15)
Orthostatic Fall in SBP by 20mmHg and/or
Hypotension DBP by 10mmHG
Causes:
•impaired autonomic function
•medications: anti-HTN, diuretics,
narcotics, antipsych, antidep, alcohol
•neuro: parkinsons, DM neuropathy
•hypovolemia
Vasovagal Systemic hypotension associated with
Syncope bradycardia and/or peripheral
vaso/venodilation
MCC of syncope!
CARDIO About
Endocarditis Cause: ORAL (dental, candy, brush)
-others: IVDU, EGD, TURP, cath,
•Localization of the infection is
determined by turbulent blood flow
•Infection of endothelium/valves due
to colonization
•MC bug: S. aureus
•MC on Left side, TV MC in IVDU
Clinical Presentation
Causes:
Cardiac disease: MI, myocarditis,
valve, congenital, arrhythmia
Cerebral hypoperfusion
•dizziness, lightheadedness
•palpitations
•blurred vision
•darkening of visual fields
•syncope
Prodromal: dizziness,
lightheadedness, epigastric pain,
palpitations, blurred vision
Postdromal: syncope
Clinical Presentation
MC:
•fever (90%), chills, night sweats
•MSK pain (back)
•murmurs (80%)
•CHF (2/3 cases)
Peripheral Manifestations:
•petechia *strep or staph
•splinter hemorrhages *strep, staph
•osler nodes *strep *PAIN (finger)
•Janeway *PAINLESS (palms)
•Roth Spots (eyes on funduscopic)
Diagnostics Treatment
•Oxygen
•Vasoconstriction •Isotonic fluids (NOT AGGRESSIVE)
•Hypotension *only shock where large amounts of fluids
•Low CO and increased pulmonary are not given
capillary wedge pressure
Inotropic support: increase contractility
and CO
•Dobutamine, Epinephrine
•blood pressure Conservative:
•tilt table: BP reduction at 60 degrees •increase salt and fluid intake
•labs •gradual position changes
•compression stocking
•discontinue offending meds
Medication
•Fludrocortisone *if fail conservative
Triggers:
•blood
•phobias
•emotiona stress/fear
•trauma
Diagnostics Treatment
3 blood cultures, 1 hour apart Acute Endocarditis: Nafcillin +
EKG, TTE  TEE echo Gentamicin x4-6 weeks
Increased ESR and CRP
Subacute Endocarditis: PCN or
DUKE CRITERIA Ampicillin + Gentamicin
Major criteria
• (+) blood culture (2 are +) Prosthetic valve: Vancomycin +
•endocardial involved on echo (TEE) Gentamicin + Rifampin
•new regurg murmur
Fungal: Amphotericin B
Minor Criteria:
•heart condition or IVDU Prophylaxis: Amoxi 2g 30-60min

•Acute: infection of normal valves
•Subacute: abnormal valve
•IVDU: MRSA, Pseudomonas
•Prosthetic: Staph epidermis
CARDIO About
Pericarditis Inflammation in pericardium
Causes:
•Idiopathic *MC
•Viral (entero, coxsackie, echo)
*MC!
•Systemic: thyroid, lupus, RA
•Neoplasms: lung & breast CA
•Drugs: procainamide, INH,
hydralazine
•Myocardial Injury
•Pericardial Injury
Pericardial •Fluid in pericardial space
Effusion
•MCC: pericarditis
•Others: infection, radiation, cancer,
dialysis, CT disease
Cardiac Effusion causing significant pressure
Tamponade on the heart  restricted filling 
decreased CO
Constrictive Thick, fibrotic and calcified heart
Pericarditis  diastolic dysfunction
 increased venous pressure and
decreased stroke volume
MCC=TB *underdeveloped
MC is radiation, surgery, and viral
Clinical Presentation
•PLEURITIC CHEST PAIN
-worse with inspiration & supine
-sharp pain, persistent
-relieved with sitting up and leaning
forward
-radiate to back, neck, shoulder
•Fever
Auscultation:
pericardial friction rub *washing
-best at end of expiration while
upright and leaning forward
Distant (muffled) heart sounds
BECKS TRIAD:
•JVD
•Muffled heart sounds
•hypotension
Exam: Kussmaul & Pulses paradoxus
>10mmHg decrease in SBP with
inspiration
-increased filling of R heart with
inspiration  decreased L filling
•Dyspnea (MC sx)
•RHF: JVD, edema, N/V, ascites
Kussmaul sign: increased JVD with
inspiration
Murmur: pericardial knock
-high pitched 3rd heart sound due to
sudden cessation of ventricular filling
•fever (>100.4F) -prosthetic heart valves
•vascular and embolic PNA -prior endocarditis
•immunologic phenomena -cyanotic congenital heart disease
•microbiologic evidence -cardiac transplantation
*1 normal, or 2+ abnormal
Interpretation:
•Definitive: 2 major or
1 major + 3 minor, or 5 minor
Diagnostics Treatment
•Viral titers •FIRST LINE-NSAIDS x7-14d
•Cardiac enzymes -Ibuprofen 600-800mg TID or
•Echo: assess complications *nml Indomethacin TID for 1-2 weeks
•CBC, BMP, ESR/CRP -ASA post MI
EKG: diffuse ST segment elevation 2nd line: Colchicine
 pseudonormalization  T wave -use for recurrence
inversion  normal
-smiley face & diffuse Steroids if sx >48h and refractory
-concave V1-V6, PR depressions in
leads with ST elevation
*opposite in AVR
CXR: cardiomegaly Small/no tamponade: observe and
EKG: low QRS voltage treat underlying cause
Echo: increased pericardial fluid
Echo: effusion + diastolic collapse of Pericardiocentesis
cardiac chambers Pericardial window if recurrent
EKG: electric alternans (alternate small
and big QRS complexes)
Echo: thickening of pericardium, Diuretics for sx improvement
CXR: pericardial calcificiation Definitive: pericardiectomy
-if unresponsive to diuretics
Cardiac CT/MRI: thickening
Cardiac Cath: *CONFIRMATORY
“square root sign”
 pericarditis *developed from thickened pericardium

VALVE DISORDERS
•Increase in venous return increases the intensity of ALL murmurs EXCEPT: HOCM and MVP click
“when the MVP with the hypertrophied arms squatted, the sound of the crowd got lower in anticipation”
“when the MVP with the hypertrophied arms stood up, the sound of the crowd got louder”
•Inspiration increases the intensity of right sided murmurs & decreases intensity of left sided
•Radiation: axilla (MR), carotid (AS)

CARDIO General Features Clinical Presentation Diagnostic Studies Management

Aortic Stenosis Congenital v. acquired
-Congenital: bi or quad
-Degenerative: * elderly
•rheumatic fever
•degenerative (Ca2+)
•Risks: HTN, HLD, smoke
Pathophysiology:
thickening & calcification
 narrowing  LVH 
systolic dysfunction,
increased afterload
Most asymptomatic for years
Cardinal SX: angina, syncope, CHF
Murmur:
-Harsh, Mid-systolic at R 2nd ICS
-Crescendo-decrescendo
-louder with leaning forward,
squatting, supine
-decreased with valslava
-Radiates to CAROTIDS
-Thrill, S4 gallop, displaced PMI
Exam: weak, delayed carotid pulse
EKG: may demonstrate LVH
Echo *diagnostic study of choice!
-severe: <1 cm 2 -critical: <0.7 cm 2
•Cardiac Catherization
confirms severe AS and any CAD
•1st line-AV Replacement with Sternotomy
-symptomatic patients, or no sx & severe
•2nd line-Transcutaneous Aortic Valve
Implantation/Replacement (TAVI/R)
-poor candidates for open heart
-multiple comorbidities, high pre-op risk
-higher risk for stroke immediately after
•Balloon Valvuloplasty
-congenital AS; not used for degenerative
*no medical tx-manage symptoms of HF
*avoid nitrates, CCB, BB because patients
are dependent on preload

Chronic Causes: *Asymptomatic  CHF, angina Signs of widened pulse pressure: •Valve Replacement (AVR): those with
Aortic •Aortic leaflets: Water Hammer Pulse: swift upstroke symptomatic severe AR or with LV changes
Regurgitation rheumatic fever, congenital Murmur: and rapid fall of radial pulse accentuated
abnormalities, endocarditis •Early diastolic, radiate to apex with wrist elevation •AR prior to LC dilation greater than 50mm or
•Decrescendo, blowing reduction in EF to less than 50%
•Aortic root: •High pitch, 2nd and 4th L spaces Corrigans pulse: same but carotid
dissection or dilation, •Widened pulse pressure  •Vasodilator therapy-unload the ventricle
Marfan bounding pulses Hills sign: popliteal artery systolic  Arterodilation
•S3&S4 gallop pressure > brachial artery by 60mmHg  Reduce afterload  less pressure to
*LVH due to dilation from •Austin Flint Murmur: mid late (MOST SENSISTIVE) push back into the ventricle
regurg volume diastolic rumble at apex due to
retrograde regurg De Mussets sign: head bobbing w/ beat

Echo*diagnostic of choice
Acute Aortic Causes: •S/S of cardiogenic shock Echo *diagnostic study of choice SURGICAL EMERGENCY
Regurgitation •acute MI •Pale, cool extremities -performed quickly and bedside
•infective endocarditis •Weak, rapid pulse Vasodilator and diuretic if BP is stable
EMERGENCY •trauma rupture of leaflet *LV in unable to accommodate the -Inotropic agents & vasopressors
•aortic root dilation Murmur: increased diastolic volume -> increased
•acute dysfunction of valve •low pitch, early diastolic pressures and pulmonary congestion **Treatment of choice: Urgent AVR

CARDIO General Features Clinical Presentation Diagnostic Studies Management

Mitral Stenosis •2/3 are women
•Don’t develop sx until 20-40 years
following disease ~30-40yo
Causes:
•Rheumatic fever is MCC!
•congenital abnormalities,
connective tissue disorders, left
atrial tumors, aggressive surgical
repair of MR
•Dyspnea, orthopnea
•Atrial fibrillation *enlarged atria
•Blood tinged sputum *pulmonary edema
•mitral facies: ruddy (flushed) cheeks with
facial pallor
Additional findings:
PE, edema, Ortner Syndrome (L recurrent
laryngeal nerve compression due to RAE)
Murmur:
•Diastolic, Low-pitch, rumbling
•Heard at apex in LLD position w/ bel
•Opening snap following S2
EKG: LAE, RVH, A-fib
Echo: *diagnostic of choice
•Rhematic deformitity-doming
(hockey stick)
•Large LA compared to LV
-normal MV area: 4-6cm 2
-critical: <1cm 2
•smoke in left atrium
Cardiac cath: measure CO
Mild to moderate: CONTROL HR
Moderate to Severe (NYHA III-IV):
•Percutaneous balloon valvuloplasty
*not common or definitive treatment
Surgery is definitive treatment with
bioprosthetic or valve replacement

Mitral Valve •1-3% population; MC in women Nonspecific sx (MVP syndrome): DX: Echo •NO TREATMENT if mild prolapse
Prolapse •superior displacement in systole •autonomic dysfunction: atypical CP, *diagnostic study of choice and asymptomatic
anxiety, panic attacks palpitations
Causes: •Beta Blockers in patients with
-connective tissue disorder Murmur: autonomic dysfunction
-Marfans or SLE •Mid-systolic click, usually followed by
-Autosomal dominant late-systolic murmur
-Myxomatous degeneration •Heard at the apex
•Squatting: delays click
•Standing: earlier click
*gallops won’t change with position!

Chronic Abnormalities of mitral leaflets, •fatigue EKG: Reduce Afterload:

Mitral annulus, chordae, papillary muscles •dyspnea on exertion •LA enlargement, LVH, A-fib •vasoduilators (ACEI, hydralazine)
Regurgitation -MVP (MCC!) •peripheral edema •diuretics
-LV dilation, posterior MI Echo: *Diagnostic of choice
-rheumatic fever Murmur: Surgery: annuloplasty *DEFINITIVE
-endocarditis •blowing holosytolic murmur Cardiac Cath: •should be performed before
•heard at apex & radiates to axilla/back •Assess function & filling pressures irreversible myocyte damage and left
•Regurgitating blood flow from LV •mid-systolic click centricular remodeling occur
to LA in systole •best heard in LLD position
•widely split S2 and displaced PMI Monitoring: annual echo
Acute Mitral •LA does not dilate to
Regurgitation accommodate regurg volume -
increase in LA and pulmonary
venous pressure  congestion
EMERGENCY
Causes:
•acute MI, trauma, endocarditis
•tachyarrhythmia w/ chronic MR
•MVP
CARDIO Causes/
Tricuspid *MC in women •Uncommon
Stenosis •Usually associated with AS or MS
Causes
•rheumatic heart disease MCC!
•carcinoid, congenital valve
abnormalities, tumors
•Reduced RA emptying  Increased
venous congestion and reduced RV
CO  fluid overload
Tricuspid •Regurgitating blood flow from RV
Regurgitation to RA
•Secondary to dilation of the RV and
tricuspid annulus due to RV failure
(pulm HTN or L failure)
•Increased RA pressure -> increased
venous congestion & reduced RV
output -> volume overload
CARDIO Causes
Pulmonic CONGENITAL (peds pt)****
Stenosis •Rheumatic disease is RARE
•Noonan, Trisomy 13
•Isolated congenital lesion
fusion of pulmonary leaflets ->
pressure overload -> RVH
Pulmonic •Result of dilation of the PV annulus
Regurgitation secondary to pulm HTN
•usually congenital
Signs of cardiogenic shock
Murmur:
•Soft, low-pitched sound in early systole
*have high index of suspicion
S&S/Physical Exam/Murmur
•Liver congestion
•Varices, Ascites, JVD, LE edema
•Palpable presystolic pulsation with
atrial contraction over liver
*always palpate liver with ascites
Murmur:
•soft, high-pitch, mid-diastolic, L 4th ICS
•Accentuated with inspiration
•Opening snap at left sternal border
•Well tolerated without pulmonary HTN
•As it progresses, may have RV failure:
-fatigue, abd bloat & peripheral edema
Murmur:
•High pitch, pansystolic, tricuspid post
•accentuated with inspiration or leg raise
•Carvallos sign: increased intensity with
inspiration
S/S
Critical at birth:
•Central cyanosis at birth
•otherwise asymptomatic until adolescence
or young adulthood
Moderate-Severe:
•fatigue, dyspnea  RV dysfunction 
RV failure
•Sx due to primary disease and secondary
to RV failure
Diagnostics
•Echo-significant: <1cm 2
•EKG: RA enlargement
•CXR: cardiomegaly from
enlarged R atrium
CXR:
Physical Exam:
•JVD, hepatic congestion and
palpable systolic pulsation
Murmur
Murmur:
•systolic at pulmonic post
•increases with inspiration
•RV lift on palpation of
precordium
•S1 followed by opening click
that’s louder with expiration
Murmur:
•High pitched, blowing
•Heard at 2nd L ICS
SURGICAL EMERGENCY
Urgent valve replacement
Treatment/Management
Diuretics
•Loop diuretics are best
•ascites  ADD aldosterone
antagonists (Spironolactone)
Surgery:
•TV replacement if symptomatic
•Treatment of underlying cause
•Repair TV with annuloplasty
*persistent symptoms
•TV replacement
*pts with underlying primary leaflet
pathologic condition
Management/Treatment
Mild: (pressure <30mmHg)
•asymptomatic and no intervention
Moderate-Severe: (>50mmHg)
•Balloon valvuloplasty or surgical valve
replacement
TREAT PULMONARY HTN!
•PV replacement is rare because its being
 cause by pulmonary HTN, so it will
come back if that is still present
Graham-Steell murmur:
brief decrescendo early diastolic
murmur at LUSB with full
inspiration
•increased w/ squat, inspiration
•decreased with valsalva

CARDIO About/Risks Clinical Presentation Diagnostics/Screening Management

Abdomina •Dilation of the infrarenal aorta Most are asymptomatic! DX: Repair for:
l Aortic is a normal part of aging ~2cm CBC, BMP, PT/INR, PTT -aortic aneurysm larger than 5.5cm
Aneurysm -AAA when >3cm Symptomatic: *more concerning Abdominal US- study of choice -rapid expansion (>0.5cm in 6mo)
(AAA) •UNRUPTURED PAIN *especially if unstable -symptomatic pain & tenderness
Risks: -Mild to severe mid-abdominal
•white male, smoke, age >60 discomfort often radiating to lower back •CT scan w/ IV contrast provide a more >4.5cm: refer to vascular surgery
•Atherosclerosis (MC) -Constant or intermittent reliable assessment of diameter 4-4.5cm: monitor US q6mo
-Exacerbated by gentle pressure -perform when >5cm & surgery 3-4cm: monitor US qyear
Pathophysiology: -Distal embolization is rare -test of choice for THORACIC
Proteolytic degeneration of -pulsatile abdominal mass Beta blockers help reduce shearing
aortic wall, connective tissue, and •Angiography: GOLD forces and decrease expansion
inflammation •RUPTURE PAIN *lethal
-Sudden blood into retroperitoneal space Screening:
Two major groups: -Severe pain, palpable mass, hypotension •One-time screening for:
Fusiform: circumferential -Free rupture into peritoneal cavity is -men 65-75 and have smoked 100
Saccular: outpouching LETHAL *bruising on the back (Flank) cigarettes in a lifetime
*higher risk of rupture
Thoracic Risks: •Most asymptomatic •CXR: widened mediastinum •Repair when 6cm or larger
Aortic •Most due to atherosclerosis *easiest initial tool, do 1st Treatment: endovascular grafting
Aneurysm •Symptoms depend on size and position
•CT disorders: Ehlers-Danlos, -Substernal back or neck pain •CT scan: modality of choice Involvement of proximal aortic arch:
Marfan Syndrome -Hoarseness due to L recurrent laryngeal -open surgery *substantial risk
-aortic regurg due to dilation -may need replacement/repair of AV
•Bicuspid aortic valve -performed by CT surgeon

Aortic •Tear in the innermost part of the
Dissection aorta (intima)
•Locations: Ascending (MC),
descending, aortic arch
*ascending has high mortality
•MC in men over 50
Risks:
•aging, atherosclerosis, HTN
•blunt trauma, Marfans, aortic
S/S: •EKG: LVH Medical control:
•Chest pain: SUDDEN, severe, ripping, •CXR: widened mediastinum *initial *descending with no complications
radiating to back or neck •Multiplanar CT of chest/ abdomen:
•hypertensive immediate diagnostic study BP Control:
•N/V, sweating •CTA, MRA, TEE: GOLD •lower SBP 100-120 & pulse pressure
•syncope, hemiplegia, paralysis of LE •BB first line! (Lebetolol, Esmolol)
•ischemia (MI) Debakey (Stanford) Classes: -can add CCB or Nitroprusside
•unequal blood pressure in both arms •Type I (A): ascending aorta  aortic
-variation >20mmHg b/w R & L arm arch and possibly beyond Pain: Morphine (pain & vasodilation)
•diastolic murmur •Type II (A): confined to ascending
 valve defect, aortic coarctation, •acute new-onset aortic regurg with •Type III (B): descending aorta Surgical: acute proximal or acute distal
preexisting, prego ascending dissection with complications

CARDIO About Clinical Presentation Diagnostics Treatment

PAD Stenosis or occlusion in artery due to
atherosclerosis (MC in LE)
•Coronary artery: angina
•Carotid artery: stroke, TIA
•Renovascular: HTN, renal
•PAD: claudication, limb ischemia
•Distal aorta & proximal iliac: smokers
-buttock, hip, groin pain
-Leriche syndrome: claudication, impotence,
decreased femoral pulses
•Femoral & popliteal: 60+, minorities
-thigh or upper calf
•Tibial artery: Diabetics
-lower calf, ankle, foot
MC in femoral or popliteal artery
•Atypical leg pain
-rest pain means advanced disease
•Intermittent Claudication (MC!)
-aching, pain, tightness in LE
-reproducible
-brought on by EXERCISE
-relieved with rest within 10 min
-sx are distal to lesion
•Functional Impairement
-do not have claudication but have
rest pain or ulceration
•Limb ischemia: ulcer, gangrene
•Pulses: decreased or absent
•decreased capillary refill
•Blood pressure, carotid bruits
•Exam legs and feet
•Skin: COLD, pale, atrophic changes,
thin/shiny hair, hair loss
-ulcers: LATERAL MALLEOLUS
Leg Lift Test: 60 degrees x1min
(+) if feet turn white when lower down
Dependent Rubor: seated to supine,
assess blood flow; longer red  severe
ABI: BEST TOOL (normal 1-1.2)
Abnormal is < 0.90, < 0.50 is severe
-ABI of 0.85 needed to heal ulcer
-use TBI if non-compressible (>1.40)
•Lifestyle: smoking cessation
•Exercise therapy
Pharm: Aspirin or Plavix
•Cilostazol (Pletal)
-supress cAMP degredation
-reversibly inhibits platelete
aggregation
-SE: edema, GI, HA, bleed
-CI: HF
Others:
•ACEI, statin, glycemic control

Arteriography: GOLD STANDARD

Acute Causes: 5 Ps: •MEDICAL EMERGENCY! Immediate revascularization

Arterial •thrombus: stable atheroma with fibrous cap •pallor 1. vascular surgery consult
Occlusion  plaque rupture  acute occlusion •pain/ paresthesias •Doppler: little to now flow 2. begin IV Heparin bolus and
of a Limb (numbness/tingling) •EKG: determine if Afib continuous infusion
•embolus  AFIB MC cause •pulseless •Labs: CBC, PT/INR, PTT
•paralysis (muscles w/ no perfusion) •Echo: done LATER if embolic source is •Once stable: Warfarin for at least
MEDICAL EMERGENCY! •polar (cold) suspected (TEE w/ bubble) 3 months+, goal INR 2-3

Thrombo- NOT ATHEROSCLEROSIS TRIAD: •Aortography: occlusive lesions of TOBACCO CESSATION!

angiitis •Segmental, inflammatory, thrombotic 1. Superficial migratory small/medium vessels with corkscrew
Obliterans processes in small/medium distal arteries thrombophlebitis: large, red, tender collaterals *GOLD -revascularization
(Buerger superficial veins  nodules -amputation frequently required
Disease) •Closely linked to tobacco use •Allen test: abnormal -wound care
•young males <40, smokers 2. Distal ischemia (MC): -assess patency of radial and ulnar -NSAIDS or opioids for pain
claudication, toes to finger ischemia arteries
Pathophysiology: Raynauds: CCB (Nifedipine,
 •Vasodysfunction and microthrombi 3. Raynauds Nicardipine, Amlodipine)

•Presents with distal ischemic rest

pain or ischemic ulceration

Atrial •MC cardiac cancer •Dyspnea Diagnostics: Surgical removal

Myxoma •MC in the left atrium •Weight loss •TEE: pedunculated mass with “ball-
•Syncope *due to mitral stenosis valve” obstruction of the mitral valve
•Can cause an obstruction of the mitral orifice •Flu-like symptoms orifice
mimicking mitral stenosis
Exam: similar to mitral stenosis

CARDIO About Clinical Presentation Diagnostics Treatment

Deep Vein MC in the calf Unilateral swelling of LE (>3cm), tender D-Dimer: highly sensitive but Anticoagulant x3 months-First Line
Thrombosis not specific -LMWH + Warfarin *prego, cancer
(DVT) Pathophysiology: Exam: *negative d-dimer can eliminate -Heparin + Dabigatran (Pradaxa) or
Virchows Triad: •WARM skin & Dusky cyanosis Heparin + Edoxaban (Savaysa)*1st line
1. Venous stasis •Palpable cord, normal pulses Venous duplex US: 1st line -Rivaroxaban (Xarelto) or Apixaban
2. Endothelial damage •Homans sign: calf pain with -noncompressible echogenicity (Eliquis) *1st line
3. Hypercoaguability dorsiflexion (unreliable)
Venography: GOLD Heparin (antithrombin III): PTT
Wells Criteria: Warfarin (Vitamin K antagonist)
Consequences: PE -extrinsic pathway, monitor PT/INR

IVC Filter: recurrent despite anticoag,

anticoagulation is CI, or RV dysfunction

Varicose Veins •Varicose veins develop in LE
•Dilated, tortuous superficial veins
Increased intraluminal pressure 
reverse venous flow
Hallmark: venous reflux & HTN
•Dull, aching heaviness or feeling of
fatigue in legs brought on by periods of
standing, relieved with elevation
•Itching , palpable
•No diagnostic evaluation
•Imaging needed for surgical
intervention-duplex US
•stockings (20-30mmHg), leg elevation
•Surgical:
-sclerotherapy: inject sclerosing agent
-laser therapy: wavelength
-endovenous ablation -vein stripping

CARDIO About Clinical Presentation Diagnostics Treatment

Chronic Venous •Severe manifestation of venous •Burning, aching, heavy leg pain Compression stockings, leg elevation
Insufficiency hypertension -worse with standing/sitting Regular exercise
-better with walking & elevation lipodermato
•Valve leaflets that do not coapt •Edema, hyperpigmentation, Ulcer: UNNA boot, wet to dry dressings
because thickened and scarred or
in a dilated vein so impaired •Venous ulcers: medial malleolus
function atrophic blanche
 legs develop venous •Lipodermatosclerosis
HTN and high -pigmented, swelling, red, “bowling pin”
hydrostatic force
•Atrophie Blanche corona
MCC-prior deep venous -star shaped ivory-white depressed
thrombophlebitis atrophic plaque; red dots within scar Trendelenburg test: elevate one
leg at 90 degrees, occlude great
 •Corona Phlebectatica saphenous vein, have patient
-dilated veins around the ankle stand for 20 sec  slow ankle
fillings suggests competency
Superficial •Inflammation of a vein due to Trousseau’s sign: migratory •CBC: WBC may be elevated 1st line: supportive therapy
Venous clot in the superficial vein thrombophlebitis with malignancy -elevate, warm compression, compression
Thrombophlebiti -great saphenous vein •Venous Doppler US: non- stocking, NSAIDs
s compressible vein with clot
Causes: IV catheter, trauma, Local phlebitis: tender, pain, edema, Septic state:
pregnancy, varicose veins erythema, induration •PCN + Aminoglycoside
•+/- palpable cord •Fever (if septic) •Vanc + Rocephin
•MC pathogen-Staph Aureus
PULM 12%-tobacco
PULM About Presentation Diagnostics Treatment
COPD Progressive irreversible airflow obstruction •cough, dyspnea with exertion Screening: annual screen with Category A (Gold 1-2):
- Loss of elastic recoil of alveoli •excess sputum production CT in adults 55-80yo w/ 30yr SABA or SAMA
- Increased airway resistance pack hx and currently smoke or +/- LABA or LAMA
smoked within past 15yr
Risks Category B:
•SMOKING (>15 pack years) CXR: SABA or SAMA + LABA or LAMA
•secondhand smoke, occupational/environmental •hyperinflation, flat
•alpha-1-antitrypsin deficiency diaphragm Category C:
*only genetic disease linked to COPD in age <40 •increased radiolucency LAMA* (reduce exacerbations)
•narrowed heart shadow + LABA, LABA/ICS
•increased retrosternal space
Category D:
Chronic •Productive cough x3mo for 2 consecutive years •Productive chronic cough Pulmonary Function Tests: LABA/LAMA,
Bronchitis •dyspnea Spirometry *Gold Standard consider triple therapy (Trelegy)
•Chronic airway inflammation  mucus gland •cyanotic, edema, RHF, cor pulm •decreased FVC
*Blue hyperplasia and goblet cell mucus production, •respiratory acidosis •decreased FEV1 > FVC
Bloater airway narrowing, increased airway resistance  •V/Q mismatch (normal in •decreased FEV1/FVC ratio
obstruction *infiltration of neutrophils and CD8 emphysema) •increased TLC (air trapping) Other Therapies:
Pulmonary rehab: Categories B-D
*Increased susceptibility to S. pnuemo and H. flu Exam: rales, rhonchi, wheeze (Outpatient program)

Emphysema •Irreversible enlargement of air spaces distal to •dyspnea with exertion Labs: increased Hgb and Hct and Oxygen therapy:
terminal bronchioles  destruction of alveolar (HALLMARK) hypercapnia due to hypoxia PaO2 ≤55 or pulse ox ≤88%
*Pink Puffer capillaries and wall destruction •pink complexion (C. BRONCHITIS)
•thin, barrel chest, no edema Reduce Mortality:
•loss of elastic recoil in acinus, collapse, and •respiratory alkalosis Pulse Ox: (94-99%) •smoking cessation
increased compliance  trapping & obstruction •pursed lips to prevent airway • >90% mild, <90%-needs O2 •O2 (paO2 ≤55 or 88%, cor pulm)
collapse • <88%–supp O2 by medicare •PNA and Influenza vaccines
Areas:
•centrilobar: proximal acinar-bronchioles Exam: Arterial blood gas Acute Exacerbation (C. Bronchitis)
(MC with smoking) •decreased breath sounds •mild: low O2, nml CO2 •Macrolides (Azithromycin)
•panacinar: diffuse-bronchioles and alveoli •increase A-P diameter (barrel) •mod/severe: low O2, high CO2 •Cephalosporins (Cefuroxime)
(MC with A1AT deficiency) •hyperresonance to percussion •Augmentin
•paraseptal: distal-alveoli only •Fluoroquinalones
 Tidal Volume: volume of air moved into or out of the lungs during quiet breathing
Residual Volume: air in lungs after maximal expiration
Expiratory Reserve Volume: volume of air that can be further exhaled
Inspiratory Reserve Volume: volume of air that can be further inhalaed
Vital Capacity: max volume that can be exhaled following max inspiration
Total Lung Capacity: volume in lungs at max inspiration
Functional Residual Capacity: volume of gas in lungs as normal TV (air which gas
exchange takes place)
Forced Expiratory Volume (FEV1): air exhaled after 1 second forced expiration
Forced Vital Capacity (FVC): volume of air expelled from max inflated lung with
patient breathing as hard and fast as possible
COPD Treatment

- GOLD Guidelines:
o GOLD1: mild  FEV1 80%+
o GOLD 2: moderate  FEV1 50-70%
o GOLD 3: Severe  FEV1 30-49%
o GOLD 4: Very Severe  FEV1 <30%

- Gold Stages
o GOLD A: mMRC 0-1, CAT <10, 0-1 exacerbation
o GOLD B: mMRC 2+, CAT 10+, 0-1 exacerbation
o GOLD C: mMRC 0-1, CAT <10, 2+exacerbation or 1+ hospital
o GOLD D: mMRC 2+, CAT 10+, 2+ exacerbation or 1+ hospital
Class Drugs
SABA Albuterol, Levalbuterol

MOA: interacts with B-2 receptors (peripheral) allowing for dilation of

the smooth muscles in the bronchioles
SE: Tachycardia, Arrhythmias, tremors, CNS stimulation, low K+
-metered dose inhaler: 90mcg two puffs q4-6h prn
-dry powder inhaler: 200mcg, 1 inhalation prn; max 4/day
SAMA Ipratropium

MOA: Central bronchodilator  Inhibits vagal mediated

bronchoconstriction and nasal mucosal secretions
SE: Dry mouth, thirst, Blurred vision, glaucoma, Urinary retention, BPH,
dysphagia
-nasal: 0.03% solution, two sprays per nostril q8-12h
-inhaler:
-metered dose inhaler: 2 puffs q6h -nebulizer: 0.5mg every 6-8h
ICS Pulmicort, Flovent, Azmacort, Qvar, Beclomethasone
MOA: reduces inflammation; SE: thrush

LABA Salmeterol, Formoterol, Arformoterol, Indacaterol, Olodaterol

BBW: asthma-related death as a monotherapy (w/o ICS)

-dry powder: one inhalation BID

LAMA Tiotropium (Spiriva)

-dry powder inhalaer: 1 capsule (18mcg) inhaled daily
-soft-mist inhalaer: two inhalations (5mcg) once daily
Aclindinium (Tudorza)
-dry powder inhalation: one inhalation (400mcg) twice daily
Umeclidinium (Incruse)
-dry powder inhalation: one inhalation (62.5mcg) once daily

LABA-ICS -Budesonide/Formoterol (Sumbicort)

Combo -Fluticasone/Salmeterol (Advair)
-Momentasone/Formeterol (Dulera)
LABA- Tiotropium-Olodaterol (Stiolto Respimat)
LAMA -Soft mist inhaler: 2 inhalations once daily
Combo Umeclidinium-Vilanterol (Anoro Ellipta)
-Dry powder inhaler: 1 inhalation once daily
Glycopyrrolate-Formoterol (Bevespi)
-Metered dose inhaler: 2 inahlations twice daily

Triple Trelegy -dry powder inhaler: 1 inhalation once daily

PULM About Presentation Diagnostics Treatment

Asthma Reversible; airway inflammation &
bronchoconstriction in response to
trigger
Pathophys:
1. airway hyperactivity: IgE binds
to mast cells
2. bronchoconstriction: airway
narrowing due to smooth muscle
contraction, edema, mucus,
•Dyspnea
•Wheezing
•Cough (worse at night)
•Chest tightness
•Fatigue
Physical Exam:
•Prolonged expiration
•Hyperresonance to percussion
•Decreased breath sounds
•Tachycardia, tachypnea
Pulmonary Function Test
Spirometry *GOLD
•low FEV1 & low FEV1/FVC
Bronchoprovocation:
Methacholine challenge (≥ 20 decrease
on FEV1) followed by bronchodilator
challenge (FEV1 increases by 12% and
200ml)
Peak Expiratory Flow (PEFR)
Mild Intermittent:
•SX ≤2d/wk, night awake ≤2x/mo, FEV1 >80%
Mild Persistent:
•SX >2d/wk, night 3-4x/mo, FEV1 >80%
Moderate Persistent:
•SX daily, night awake >1x/wk, FEV1 60-80%
Severe Persistent:
 hypertrophy  air trapping
3. inflammation
Risks: Atopy, FHX, air pollution,
obesity, second hand smoke, males
Atopic Triad: asthma, atopic
dermatitis, allergic rhinitis
Samters Triad: asthma, ASA
allergy, nasal polyps
•Accessory muscles
Severe:
•silent chest (no air movement)
•altered mental status
•pulsus paradoxus
*assesses asthma exacerbation severity •SX throughout day, awake nightly, FEV1 <60%
and response
•Normal is 400-600 Treatment
•discharge criteria is >70% predicted or 1. SABA (all)
>15% initial attempt 2. +ICS
3. +ICS/LABA or med ICS
Culture: curschmann’s spirals, 4. +medium dose ICS/LABA
Charcot-Leyden crystals 5. +high dose ICS/LABA
6. +high dose ICS/LABA or oral
ABG: respiratory alkalosis (due to
tachypnea) Admit if: PEFR <50%, ER within past 3 days, status
asthmaticus

PULM Drugs Side Effects Routes

SABA Albuterol, Levalbuterol SE: Tachycardia, -metered dose: 90mcg two puffs q4-6h
MOA: interacts with B-2 receptors (peripheral) allowing for dilation of the smooth arrhythmias, tremors, low K+ -dry powder inhaler: 200mcg, 1 inhalation
muscles in the bronchioles prn; max 4/day

ICS Pulmicort, Flovent, Azmacort, Qvar, Beclomethasone

MOA: reduces inflammation; SE: thrush

LABA Salmeterol, Formoterol, Arformoterol, Indacaterol, Olodaterol BBW: asthma-related death -dry powder: one inhalation BID
as a monotherapy (w/o ICS)

LABA-ICS -Budesonide/Formoterol (Sumbicort) -Fluticasone/Salmeterol (Advair)

-Momentasone/Formeterol (Dulera)

Mast Cell Cromolyn, Nedocromil SE: throat irritation

MOA: Inhibits mass cell and leukotriene-mediated degranulation

Leukotriene Montelukast (Singulair), Zafrilukast (Accolate), Zileuton (Zyflo) SE: increased LFTs, HA, GI
Modifiers MOA: Blocks leukotriene-mediated neutrophil migration, capillary permeability, mylagias
smooth muscle contraction

Theophylline MOA: bronchodilator that improves respiratory muscle endurance, SE: nervous, tachycardia,
*narrow TI phosphodiesterance inhibitor which inhibits leukotreiene syntheseis and inflammation N/V, anorexia, HA

PULM
Acute •Inflammation of the bronchi •non-productive cough CLINICAL *Reassurance and education
Bronchitis •MC in the winter *HALLMARK •rest and hydration, NSAIDs
•Wheezing CXR: usually normal
MCC: Viral (Adenovirus, parainfluenza, •Rhonchi (clear with cough) AVOID ABX unless indicated!
influenza, coronavirus, coxsackie, •Pharyngitis •Atypicals: Macrolide, FQs
rhinovirus, RSV) •Fatigue/Malaise
Bacterial: S. pneumo, M. cat, H. flu, •Fever (low-grade)
•hemoptysis
Pathophys: infection  inflamed  *acute bronchitis and
 exudate  spasm bronchiectasis are the MCC of
hemoptysis
Two phases:
1. direct inoculation of tracheobronchial
epithelium
2. Hypersensitivity of airway receptors
(persistent 1-3wks)  increased sputum

PULM
Pneumonia •Influenza •Fever, chills, HA, sore throat •NP swab O2, rest, fluids, antipyretics,
(Viral) •adenovirus, parainfluenza, RSV •nonproductive cough •CXR analgesics, IVF
•rhinorrhea, myalgia

Pneumonia •Unicellular, Fungal pneumonia •Fever Labs: Elevated LDH & B-D-glucan •BACTRIM x 21 days
(HIV/Fungal) •dry nonproductive cough •add Prednisone if hypoxic (PaO2
P. jivoreci Transmission: inhalation airborne spread •dyspnea on exertion CXR: diffuse, bilat interstitial infiltrates <70)
•respiratory failure CT scan: ground glass opacitis
Risks: immunocompromised, HIV/AIDS G6PD Deficiency:
(CD4 ≤ 200) Exam: Lavage with fluorescent antibody staining •Atovaquone
•O2 desaturation with ambulation •trophic: wright-giemsa stain •AVOID Dapsome or Primaquine
•cyst: methenamine silver and toluidine blue
stains

Biopsy: DEFINITIVE

Pneumococcal Vaccines
 Pneumovax (PCV) 13: Indications: Administer in patients 6 weeks old – 5 years old; 4 dose series: 2, 4, 6, 12-15 months
 Pneumococcal (PPSV) 23: Indications: ALL adults 65 years and older, younger patients with increased risk of pneumococcal disease
o If given prior to 65 years old, then should be revaccinated at 65 year old unless it was given within 10 years then revaccinate 10 years after vaccines
 No prior vaccines: PCV 13  wait 8 weeks  PPSV 23 If received PPSV 23 in past: PCV 13 on year after PPSY vaccine

PULM
Pneumonia CAP: Typical CXR (PA & Lateral): GOLD CAP Out:
(Bacterial) within 48 hours of hospital or outpatient •productive cough •infiltrates No comorbid/ABX:
-S. pneumo, H. flu, M. pneumo •fever •HAP: new infiltrate •Azithromycin or Clarithromycin
•dyspnea •Doxycycline
HAP/VAP/HCAP: •pleuritic CP CT: if unclear
develops 48hours AFTER •chills (rigors)
Comborbid/ABX:
-Pseudomonas, Klebsillea, S. aureus •tachypnea Labs:
•accessory muscles •hospital: cx, NP, CBC, CMP •Levofloxacin
•Azithroycin + Rocephin
Ventilator: Pseudomonas, Acinetobacter
Typical Exam Admission Criteria:

Aspiration: anaerobes *MC R lower lobe
S. pneumo *gram + diplocci
•commonly see chills and rigors
•MCC of CAP
H. Flu *gram – rods
•extremes of ages
•imunocompromised, pulmonary disease
Klebsiella *gram - rods
•alcoholics
•cavitary lesions on CXR
S. aureus *gram + cocci in clusters
•after viral infection, HAP
•bilateral multilobar infiltrates on CXR
Atypical Bugs:
Pneumonia Mycoplasma (MCC):
•young and healthy (schools, college,
military)
•late summer, early fall
Other bugs:
•Chlamydia pneumonia
•Legionella pneumophila
Legionella •Anaerobic, gram (-) bacteria
Pneumophilia Transmission: contaminated water sources
Risks: immunosuppressed, elderly,
smokers, lung disease
PULM
Tuberculosis Mycobacterium tuberculosis (Mtb)
(Atypical)
Transmission: airborne droplets
Pathophysiology:
Inhalation  alveoli  incorporated into
macrophages  disseminates
•Dullness to percussion PSI: >90=hospital
•Increased TF
• (+) egophony CURB-65 (2+=hospital):
•tachypnea, tachycardia •confusion
•urea (BUN) >19 (>7mmol)
Aspiration PNA •Respiratory rate 30+
•foul smelling sputum (rotten egg) •BP low <90/60
•pulmonary abscess or empyema •age >65
Sputum Colors
rust: S. pneumo (MC)  RLL
green: H, flu, pseudomonas
red currant jelly:
Klebsiella  upper lung
Foul smell/bad taste: anaerobic
Atypical: CXR: reticulonodular pattern
•non-productive cough •diffuse, patchy infiltrates
•low-grade fever
•extrapulmonary symptoms PCR: TEST OF CHOICE
•pharyngitis •cold agglutinins
•URI prodrome
Complications:
Exam: usually normal •SJS, TEN
•cold autoimmune hemolytic
anemia (IgM)
•bullous myringitis
•fever, chills Labs:
•dyspnea •hyponatremia
•GI: diarrhea (watery, non-bloody), •increased LFTs
nausea, vomiting
•Neuro: HA, AMS, confusion DX: PCR, urine antigen
Pulmonary: productive cough, CP, Sputum acid-fast stain
hemoptysis •x3 on 3 consecutive days
Constitutional: night sweats, fever, Quanterferon Gold: blood test,
chills, fatigue, anorexia, weight loss not effected by BCG vaccine
Extra-pulmonary: Mantoux TB skin test
CAP Inpatient:
Non-ICU:
•Levofloxacin or Moxifloxacin
•Rocephin + Azithromycin
ICU:
•Rocephin + Azithromycin
•Rocephin + Levofloxacin
HAP (low risk drug-resistant):
•Levofloxacin, Zosyn, Cefepime
HAP (high): Vancomycin +
1. Cefepime or Ceftazadime
2. Imipenem or Carbapenem
3. Zosyn + Ciprofloxacin
4. Gent or Amikacin
Aspiration:
•ampicillin-sulbactam or Augmentin
Antibiotics
•Macrolides (Azithromycin)
•Doxycycline
Resistant to B-lactams due to LACKING A
CELL WALL
Antibiotics
•Macrolides (Azithromycin)
•Respiratory Fluoroquinalones (Levofloxacin,
Moxifloxacin, Gemifloxacin)
RIPE x2 months (6 months total)
•Rifampin: orange fluids, low platelets
•Izoniazid: hepatitis, neuropathy
*prevent neuropathy w/ Pyridoxine (B6)
•Pyrazinamide: hepatitis, hyperuricemia
*caution with gout and liver
•Ethambutol: optic neuritis (E=eye),
 •vertebral (Potts Disease) (+) 5mm+ peripheral neuropathy
Risks: close contact, immigrants, crowded •cervical lymph nodes (scrofula) •HIV/immunosuppressed *substitution is Streptomycin
conditions, healthcare, immunosupressed •pericarditis •(+) CXR (aminoglycoside)
•adrenal gland and GU •close contact
Types of TB (+) 10mm+ then Rifampin and Isoniazid for 4 months
Primary TB: *CONTAGIOUS Latent TB Criteria: •high risk populations: IVDU,
•initial infection, contagious NEED ALL 3 homeless, age <5yo, immigrant,
•(+) PPD *2-4wk after infection recent travel Latent:
Chronic (latent): *NOT CONTAGIOUS •no symptoms (+) 15mm+ everyone •Isoniazid + Pyridoxine (B6)
•caseating granuloma formation (central •no imaging findings •Rifampin x 4 months
necrosis, acidic, low O2  hard for Mtb) CXR: apical cavities *not contagious in latent period
-reactivation: apical, upper lobes *no sx, (+) PPD, (-) CXR
Secondary (reactivate): *CONTAGIOUS -primary: middle/lower lobe
•reactivation of latent TB -miliary: millet seeds
•apex of upper lobes *increased O2

PULM About Presentation Diagnostics Treatment

Hypoventilatio •involuntary cessation of breathing during sleep •snoring, interrupted sleep Polysomnography (sleep study) •weight loss
n Syndrome Risks: obesity, age, males •daytime sleepiness, fatigue, -15 or more events/hour •avoid alcohol and sedatives
(sleep apnea) •wake up with breath holding, •sleep position
Types: gasping, choking •Alternative: home sleep apnea
Central: reduced CNS respiratory drive •HTN, CAD, DM, mood testing (HSAT) Mild/moderate: CPAP
Obstructive: physical airway obstruction
Exam: Labs: polycythemia Severe: CPAP, surgery
1. pharyngeal wall collapse repetitively •large neck circumference
2. failure of upper airway dilator muscle •crowded oropharynx
3. sleep-related obstruction and breath cessation •micrognathia

PULM About Clinical Presentation Diagnostics Treatment

Carcinoid •Neuroendocrine tumor
Tumor •slow growth, low mets
MC sites: GI tract, lungs
•Asymptomatic (25-40%), wheezing, cough,
recurrent PNA, hemoptysis, SIADH, Cushings
Carcinoid syndrome: diarrhea due to serotonin
•Increased bradykinin and histamine  flushing,
tachycardia, bronchoconstriction, acidosis
Bronchoscope: pink-purple tumor •Ocreotide may reduce SX
*well vascularized, central
Definitive management: surgery
•Secrete serotonin, ACTH, ADH,
melanocyte stimulating hormone MC complication: bleeding
•Biopsy is DEFINITIVE

Solitary Nodule: <3cm Increased Risk of Malignancy *large >2cm CXR: initial test Low (<5%): watch
Pulmonary Mass: >3cm •spiculated, irregular border CT Chest: IMAGE OF CHOICE
 Nodule
Causes: infectious
granuloma (mycobacteria
and fungi)
Risks: Thymomas (MC)
•asymmetric calcification • >40yo, smoker
Decreased Risk: *small <1cm
•well circumcised, smooth borders
•dense diffuse calcifications “popcorn”
• <30yo, non-smoker
Screening: annual low dose CT
55-80 years old with no sx AND
30 year pack history who currently smoke
or quite within 15 years
*stop after 15 years of quitting
Intermediate (5-60%): biopsy
•bronchoscopy if central
•transthoracic needle aspiration if
peripheral
High (>60%): resect with biopsy

Bronchogenic MCC cause of cancer SCLC: fast growing, starts in bronchi (central)
Carcinoma related deaths in US •paraneoplastic syndromes: SVC syndrome,
SIADH (hyponatremia), Cushing, Lambert-Eaton
Risks: cigarettes, asbestosis •lambert-eaton (weakness improves WITH use)
•histology: sheets of small dark blue cells with
Two Types: rosette formation
•NSCLC: adenocarcinoma,
large cell, squamous cell
*MC type is Adenocarcinoma (MC!!): slow, peripheral
adenocarcinoma •lepidic pattern: rare, low-grade subtype with
voluminous sputum and interstitial lung pattern on
•SCLC CXR
•histology: gland formation, mucin production
Squamous: central (bronchial)
•CCCP: central, cavitation, hypercalcemia,
pancoast-shoulder pain, horners, hand atrophy
•histology: keratinization, desmosome
Large: rapid, periphery, aggressive
Superior Vena Cava (SVC) Syndrome: NSCLC: Surgical Resection
•partial of complete obstruction of flow treatment of choice
•SX: face or neck swelling, facial
plethora, headache, dilated neck veins SCLC: Chemo treatment of choice
•CXR: right hilar mass, CT: better
SVC Syndrome: supportive
Lambert-Eaton Syndrome:
•antibodies against presynaptic voltage Lambert-Eaton:
gated Ca+ channels prevent Ach release Pyridostigmine
•SX: proximal muscle weakness, treat underlying
improved with repetitive use, ED, dry
mouth, orthostasis, Pancoast Tumor:
•DX: voltage gated Ca antibody assay •chemo  resection
Superior Sulcus (Pancoast) Tumor:
•tumor in superior sulcus (apex)
compression lower brachial plexus
•SX: shoulder/arm pain,
weakness/atrophy of hand, ulnar
neuropathy, horners (ipsilateral ptosis,
miosis, anhidrosis)
•DX: CXR  MRI  biopsy

Mesothelioma Tumor in the pleura (MC), Pleural: CXR: unilateral pleural thickening, Chemo and resection
peritoneum, tunica •pleuritic CP, dyspnea bloody pleural effusions
vaginalis, or pericardium •fever, night sweats, weight loss Non-surgical: chemo or radiation
•hemoptysis Pleural Biopsy: closed or VATS

GI 11%
GI Types Five Groups Associated Sx Invasive v. Noninvasive Treatment
Acute *more than 90% 1) Travelers diarrhea (Giardia) N/V Noninvasive 1. Fluid Repletion: oral* or IV
Diarrhea diarrhea due to •S. aureus, B. cerus *small bowel •sports drinks, broth, IV saline
infectious agent 2) Consumers of certain foods *begins 1-6h after *enterotoxins, no cell •fluids with glucose, Na, K, Cl
Acute •Chicken-salmonela, campylobacter, shigella •Noro & rotavirus destruction or invasion
<4wks Most acquired by: •Undercooked hamburger-E. coli *begins 24-48h •watery, volume diarrhea 2. Diet-BRAT
Fecal-oral transmission •Fried rice or reheated-Bacillus cereus after •nausea/vomiting •bowel rest (no fiber, milk, alc, caff)
Persistent Ingestion of food/water •Mayo or creams-Staph or Salmonella •no blood, WBC, mucus
2-4wks Disturbances of flora by •Eggs-Salmonella Volume depletion 3. Anti-Motility Agents
 antibiotics  C. diff •Undercooked food or soft cheese-Listeria •Non-inflammatory Invasive: DO NOT GIVE •Indications: patients <65 with
•Vibrio cholera ANTIMOTILITY DRUG mod/severe volume depletion
When to admit: 3) Immunodeficient *large bowel •CI: INVASIVE diarrhea (bloody,
Severe dehydration Immunocomp. *cytokines cause mucosal high fever, systemic toxicity)
organ failure 4) Daycare-shigella, giardia, rotavirus, hep •CMV invasion and damage
altered mental status •Protozoans •vomiting 4. Anti-Emetics: Ondansetron,
hemolytic-uremic syn. 5) institutionalized •fever Promethazine, Metolopramide
(AKI, *MC nosocomial infection •fecal blood, WBC, mucus
thrombocytopenia, ABX-Cipro, Levo; Doxy, Bactrim
hemolytic anemia)

GI About Associated Sx Diagnostics Treatment

Giardia Lamblia •protozoan parasite associated with sporadic or •frothy, greasy, foul-smell diarrhea •antigen assay •rehydration
*Protozoan epidemic diarrheal illness *due to steatorrhea
•no blood or pus Stool: ABX: Metronidazole, Tinidazole,
Sources: contaminated water from streams/wells •abdominal cramps, bloating •trophozoites, cysts Albendazole, Quinacrine
(Beaver’s fever, backpackers diarrhea)

Diarrhea Drugs MOA CI Adverse Effects

Loperamide (Imodium)
Diphenoxylate (Lomotil)
Schedule V; 1st line
Bismuth
Pepto-Bismol, Maalox, Kaopectate
Ocreotide (Sandostatin)
Antispasmodics/ Anticholinergics
Hyoscyamine (Levisin)
Dicyclomine (Bentyl)
Phenobarbital, Atropine, Scopalamine
•Inhibits peristalsis and gut transit
•Opioid receptor agonists (mu receptor gut)
•Reduces secretions, antimicrobial
*can be used in dysentery (fever, bloody)
Inhibits intestinal fluid secretion and stimulates
intestinal absorption*chronic secretory diarrhea
•Relaxes intestinal smooth muscle, inhibits
spasms and contraction
•anticholingeric  inhibits Ach
*diarrhea associated with IBS (Bentyl)
*can use for bladder spasms (Levsin)
•Bloody or C. diff diarrhea; Pts <2yo
•Loperamide: Acute dysentery or
colitis  toxic megacolon
•Children with viral illness
Caution: DM, thyoid, pancreas, kidney,
liver, arrhythmia
•Toxic megacolon
•Inflammatory bowel disease
•Constipation, abd cramp, dizzy, CNS
•Serious: paralytic ileus, toxic megacolon
•Black stool, black tongue
•Constipation, Tinnitus
•Cholelthiasis/cholecystitis/biliary tract
disease
•Edema, Constipation
•Ileus, delirium, nervous, palpitations,
constipation, xerostomia, mydriasis

GI
Acute Causes:
Pancreatiti •gallstone (MC)
s •heavy alcohol
•medications: thiazides, protease
inhibitors, Exenatide, valproic acid,
estrogens, didanosine
Pathophysiology:
•Edema/obstruction at ampulla of Vater
•acinar cell injury  premature or over
activation of enzymes  self-digestion
•Epigastric pain that radiates into the back •Serum amylase & lipase (BEST) Assessment of Severity:
*because retroperitoneal •CBC: leukocytosis Ransons “LAAWG”
-sudden, steady •CMP: high glucose, ALP, LFT, 3+ indicates severe course
-worse w/ activity & supine TG, bilirubin •LDH >350
-improve w/ leaning forward •hypocalcemia: necrotic fat binds •AST >250
•N/V, fever to calcium lowering the levels •Age >55
•Weakness, sweating, anxiety •WBC >16,000
X-ray: •Glucose >200
PE: *can dehydrate quickly •Sentinel loop (localized ileus)
•Epigastric tenderness •colon cut off (abrupt collapse of Treatment:
•Distended abdomen colon near the pancreas) **Supportive:
•Absent BS if with ileus •IVF high volume (LR)
•Tachycardia, hypotension CT: diagnostic study of choice •NPO
•Cullens (periumbilical) & Grey Turners •pain (Demerol)
(flank) ecchymosis Criteria: 2/3
•acute persistent, severe pain ABX: broad spectrum if severe
•elevated of lipase or amylase 3x *not routine
•characteristic imaging finsings

Chronic Chronic inflammation causing •Chronic, steady/intermittent epigastric pain Labs: amylase and lipase normal Oral pancreatic enzyme
Pancreatiti parenchymal destruction  loss of *often radiates to back replacements
s exocrine function, sometimes endocrine •Anorexia, weight loss, N/V, constipation X-ray: calcifications in pancreas
Endoscope US: honeycomb •alcohol abstinence
Causes: Pancreatic insufficiency •low fat diet
•Alcoholism –MC! exocrine: malabsorption & steatorrhea CT (best): pancreatic enlargement, •vitamin supplementation
•Idiopathic endocrine: glucose high or low pseduocysts, calcifications
•hypocalcemia, HLD
•islet cell tumors TRIAD: calcifications, steatorrhea, DM Pancreatic Function: fecal elastase
•familial, traumatic, iatrogenic *MOST SENSITIVE & SPECIFIC

Pancreatic Cystic collection of tissue, fluid, and •Abdominal pain •Study of choice: CT Scan Persists >4-6 weeks
Pseudocyst necrotic debris surrounding the pancreas •Abdominal mass •Ultrasound -percutaneous drainage
-surgical decompression
Associated with: *NO true epithelial lining in the capsule Complications: (pancreaticogastrostomy)
•acute or chronic pancreatitis •Peritonitis, infection -drain into stomach or bowel
•trauma to chest

GI Etiology/Pathophysiology Clinical Presentation Labs/Diagnostics Treatment

Carcinoma •75% adenocarcinoma (ductal) •painless jaundice *classic Labs: Surgical resection if localized disease:
of Pancreas •70% in pancreatic head •weight loss, anorexia, fatigue •Amylase/lipase nml to high •Whipple Procedure *head or duodenal
*poor prognosis with body and •Vague epigastric and back pain •Glycosuria, Hyperglycemia *radical pancreaticoduodenal resection
tail •pruritis (bile salts) •Elevated LFTs if CBD obstruction -precede w/ biliary stenting if CBD block
-often followed with chemotherapy
Risks: Exam: Tumor marker: CA 19-9 *staging laparoscopy performed prior
•Advanced age (>55) •Courvoiser’s sign: enlarged, *metastasis in nodes-will not do
•tobacco use palpable gallbladder, nontender Diagnostics:
•heavy alcohol use •1st line-CT w/ FNA biopsy Distal Pancreatectomy
•obese, chronic pancreatitis, DM •Endoscopic U/S, ERCP •Resection of tumor in body and tail
•fhx, males Non-resectable: ERCP w/ biliary stent if
Staging: TNM symptoms of obstruction, chemo, palliative

GI About/Causes Clinical Presentation Diagnostics Treatment

Alcoholic Liver •Excessive alcohol intake •Fatty liver:
Disease •Men >2drink/day *>5% fatty deposits
•Women >1drink/day -aymptomatic, reversible
*risk increases if consumed -hepatomegaly
daily for 10yrs
*risk most in men •Alcoholic Hepatitis:
-symptomatic, reversible
-fatigue, nausea, anorexia,
Risk of cirrhosis increases if recurrent infections
other associated liver -bouts of jaundice
disease present or obesity
•Cirrhosis:
-symptomatic, NOT reversible
-end stage liver failure
-ascites, abd pain,
-splenomegaly, fever
•Fatty liver: *usually incidental
-mild AST/ALT elevations
-anemia
•Alcoholic Hepatitis:
-Greater AST/ALT elevation
-AST not > 300
-AST >ALT is greater 2:1
-ALP elevations
-Elevated total bilirubin
-Leukopenia, thrombocytopenia
Alcoholic Cirrhosis:
-Elevated total bilirubin >10
-Hypoalbuminemia
-Prolonged PT/PTT
-Anemia
-Last disease -> electrolytes,
elevated BUN/CR
Imaging: CT scan
Definitive Dx: liver biopsy
Abstinence from Alcohol-most important!
-especially if fatty liver or alcoholic hepatitis
•nutritional support
•folic acid, zinc, thiamine supplementation
Pharmacotherapy:
•Methylprednisolone x1 months
*alcoholic hepatitis
*see improvement in bilirubin in ~7days
•Pentoxifylline 400mg TIX x1 month
*severe alcoholic hepatitis, especially if with
hepatorenal syndrome or hepatic
encephalopathy (elevated ammonia)
Prognosis:
•Fatty liver: good IF stop drinking
•Alcoholic Hepatitis:
-unfavorable if: prolonged PT/PTT
-bilirubin >10, hepatic encephalopathy,
azotemia (renal)
Cirrhosis: poor prognosis

Non-Alcoholic NAFL: benign, no fibrosis
Steatohepatitis NASH: inflammation and
(NASH) fibrosis *cirrhosis potential
Causes:
•Obesity, DM, metabolic
•TGs, HLD
•Medications-steroids
•Cushings, PCOS, Genetics
•Asymptomatic or mild, vague •Mildly elevated AST/ALT
symptoms -AST/ALT ratio <1
•RUQ discomfort *differentiate from alcoholic
•Hepatomegaly steatohepatitis
•Signs of chronic liver disease
uncommon •CT scan (do this 1st!)
•Definitive DX: liver biopsy
microvesicular fatty deposits
•Lifestyle modifications: weight loss, exercise,
dietary fat restriction, glucose control
•Hepatic vaccines
•Medications:
vitamin E, thiazolidinediones (Actos, Avandia) and
Metformin, Pentoxifylline, wt loss agents

GI About/Causes Clinical Presentation Diagnostics Treatment/Prevention

Hepatitis Acute viral infection of liver
A •Spiking fever
Incubation: ~30 days
*seen in feces 2wks prior
Route: Fecal-oral route
•Crowding, poor sanitation
•Contaminated food
•International Travel
Acute •Double stranded DNA
Hepatitis •Inner core protein and outer
B surface coat
Incubation: 12-14 weeks
Transmission: percutaneous,
sex, parenternal, perinatal
Causes:
•Bloodborne, Sexual
•Mother  baby
Risk populations:
•IVDU, inmates, healthcare
Hepatitis Incubation: 6 weeks
C *signifies HCV as causes of hepatitis
Transmission:
•Parenternal (blood), sex
-MCC: IVDU
Risk populations: IV drugs,
inmates, healthcare workers
Hepatitis Pathophysiology:
D •Hep D uses BHsAg as its
envelope protein
Hep B co-
infection Transmission: blood
Hepatitis •RNA virus, Waterborne
E •Asia, M. East, N. Africa
Transmission: fecal-oral
•blood, mother to child
Spread: swine, pet, orangs
•Most are asymptomatic
•Malaise, N/V, anorexia, abd pain
•Aversion to smoking (no craving)
Exam:
•RUQ abdominal pain, jaundice
•Mild hepatomegaly, liver tenderness
•Asymptomatic
•Distaste for smoking
Sub-clinical: constitutional (malaise,
myalgia, fatigue, URI, N/V, abd pain)
Icteric: jaundice (30%)
Fulminant: acute hepatic failure
(encephalopathy, jaundice, coag)
Exam:
•Mild RUQ pain and hepatomegaly
•no sx  Fatigue, nausea, RUQ pain
Exam:
•Jaundice wax and wane
•dark urine, clay colored stools
Complications:Hep C, Non-Hodgkins,
DM, glomerulonephritis, pulmonary
fibrosis, thyroiditis
•asymptomatic
•fatigue, myalgia, malaise
•RUQ pain, jaundice
•dark urine, clay colored stools
•malaise, anorexia, N/V, abd pain
Extrahepatic: “PANT”
Pancreatitis, Arthritis, Neuro (Guillan-
Barre), Thrombrocytopenia
Exam: jaundice, hepatomegaly
•Hep A Antibody
-Anti-HAV IgM peak in first week *active
-IgG rises for months  years.
-past exposure: (+) IgG, (-) IgM
Labs: High ALT, AST, bilirubin
Blood smear: Atypical large lymphocytes
Window: (+) anti-HBc IgM
Acute: (+) HBsAg, (+) anti-HBc IgM
Chronic: (+) HBsAg, (+) anti-HBc IgG
Immunization: (+) anti-HBs, rest negative
Recovery:
(+) anti-HBs, (-) HBsAG, (+) anti-Hbc IgG
•HBsAG (surface antigen)-infective! *1st marker
(+) means acute or chronic
•Anti-HBs (surface antibody)-recovery or vaccine
(+): vaccine (rest -) or recovery (will have + IgG)
•Anti-HBC (antibody to core antigen)-IgM or IgG
•BEeAG (envelope antigen)-rapid replication
•HBV DNA: best way to test viral replication
•Elevated LFTs, bilirubin, ALP, PT
HCV antibodies (Anti-HCV)=INFECTION!
•HCV RNA: indicates current infection
-CONFIRMATORY (most sensitive)
•ALT/AST rise and decline
•anti-HDV
Confirmation: immunochemical staining of liver
biopsies for HDAg or RT-PCR assay of HDV RNA
Labs: elevated LFTs and bilirubin
•IgM anti-HEV in serum
Treatment: self-resolving
•Symptomatic  rest & fluids
Post-Exposure Prophylaxis: *2 wk
•healthy 1-40years old: vaccine
•healthy >40yo: vaccine +/- Ig
•immunocompromised or liver:
vaccine + immunoglobulin (Ig)
•Recovery ~3-6 months
•Rest, increase fluids, nutrition
•Avoid activity, alcohol, hepatotoxic
•Hep B Immunoglobulin *within 7d
Persistant/Severe Symptoms:
•Entecavir, Tenofovir
Cleared Infection:
•Two consecutive tests 4wks apart
Vaccine: *CI if bakers yeast allergy
Infant: birth, 1-2mo, 6-18mo
Adult: 3 doses 0, 1, 6 months
Treatment: *all equal efficacy
•Ledipasvir-Sofosbuvir
•Direct Acting Antiviral (DAA)
•Interferon
Response to therapy determined by
PCR-RNA load at 12-24 weeks
•no FDA approved treatments
•Interferon alpha
Prevention: Hep B vaccination
•Self-limited
•Oral Ribavirin x3 months
•Recombinant vaccines
*highest mortality due to fulminant
hepatitis in pregnancy
GI About/Causes Clinical Presentation Diagnostics Treatment
Autoimmune Idiopathic chronic inflammation of •Insidious onset  sudden •AST/ ALT >3x nml (ALT >1000) Prednisone
Hepatitis liver due to circulating antibodies •Vague abdominal pain, nasuea •Elevated total bilirubin -improves sx and inflammation
•Spider Nevi & Hepatomegaly •Positive ANA -Adding Azathioprine lowers steroid dose
•MC in young women •pANCA, anti-SLA (antibodies)
•Usually follows virus Extrahepatic: arthritis, failed therapy  liver transplant
thyroiditis, associated Definitive dx: LIVER BIOPSY *can progress to cirrhosis
autoimmune conditions
Complications: cirrhosis, pericarditis,
myocarditis, glomerulonephritis, uveitis

Drug/Toxin Causes: “Herbals” •Elevated ALT >AST •Can progress to liver failure
Induced Acetaminophen *alcohol •Hepatomegaly
Hepatitis Isoniazid *Rifampin •Jaundice •Stop offending agent
ABX-Tetracyclines •Fatigue, N/V •May require transplant if liver failure
develops
Fulminant Acute hepatic failure in patients •Encephalopathy: vomiting, •combination of symptoms Supportive:
Hepatitis with hepatitis coma, AMS, asterixis (flapping •IVF
tremor of hand) Labs: •electrolyte repletion
Causes: •hypoglycemia •Mannical (ICP elevation)
•Acetaminophen toxicity •Coagulopathy: increased •increased ammonia •blood products or cryo
•viral hepatitis, autoimmine PT/INR/PTT
•Reye syndrome (NSAIDS) Definitive: liver transplant
•GI: hepatomegaly, jaundice

•Reye: rash, vomiting, liver

damage, encephalopathy, dilated
pupils, multi-organ failure

GI About/Causes Clinical Presentation Diagnostics Treatment

Cirrhosis Irreversible liver fibrosis with S/S: Insidious onset •AST/ALT & ALP elevated •No cure w/o liver transplant
“liver failure” nodular regeneration  replaces •Weakness, fatigue, sleep changes •Bilirubin elevated •Treat complications!
functional hepatocytes w/ nodules •N/V, abdominal pain, ascites •Hypoalbuminemia
•Anemia •Avoid alcohol & liver toxic medications
Pathophysiology: •Portal HTN: esophageal varices, •WBC fluctuations •Strict dietary management: protein, low carb and
•nodules cause increased portal splenomegaly •Thrombocytopenia sodium; reduce protein if encephalopathy
pressure •Skin: spider angioma, palmar •Prolonged PT/PTT •Nutritional supplements
erythema, telangiectasias, caput •Vaccinations: HBV, HAV, flu, pneumococcal
Causes: medusa Diagnostics:
•Alcoholic hepatitis •Menstrual abn, ED, gynecomastia •US: assess size and ascites Pruritis: Cholestyramine
•Chronic hepatitis C (MCC) •Vitamin & nutrient deficiencies: •CT: assess liver nodules Encephalopathy: Lactulose, Rifamxin
•NASH anemia, glossitis, cheilosis •Biopsy: definitive DX Ascites: Spironolocatone, Furosemide
•Drug toxicity •EGD: varices *cirrhosis
•Autoimmune hepatitis Encephalopathy: confusion, Staging: Child-Pugh Classification-total bilirubin,
•Hemochromatosis lethargy, asterixis albumin, PT INR, ascites, encephalopathy
•Genetic, metabolic *elevated ammonia levels Class A: 5-6 points
Class B: 7-9 points
Class C: 10+ points
Cirrhosis Complications
Ascites/Edema •Sodium restriction •Transjugular Intrahepatic Portosystemic Shunt (TIPS)
•Diuretics (Spironolocatone, Furosemide) -primary indication for variceal bleeding
•Paracentesis -shunts blood out of portal system -> reduces portal HTN ->
-if unresponsive to diuretics, can’t tolerate diuretics, resp sx decreased occurrence of ascites
-can use with albumin to move fluid
Problems: bleeding, shunt occlusion, hepatic encephalopathy

Spontaneous Bacterial Peritonitis •Infection of asitic fluid without perforation of the bowel •TX: Cefotaxmine or Ceftriaxone
*MCC- E. Coli •SX: fever, chills, abdominal pain, diarrhea, fluid wave
•DX: paracentesis and culture (cell count 250 +) •Prophylaxis: Bactrim of oral fluoroquinolone

Hepatorenal Syndrome •Azotemia in the absence of intrinsic renal disease Labs: increase BUN/Cr, hyponatremia, oliguria

Occurs in 10% of patients with •Two types: •TX:

advanced cirrhosis and ascites -type I: sudden doubling of Cr >2.5 Stop diuretics & Increase blood flow to kidneys
-type II: slowly progressive IV albumin, Dialysis; TIPS, Liver transplant

Hepatic Encephalopathy •Stages: mild confusion -> drowsiness, stupor, coma TX:
•Causes: CNS drugs, TIPS •reduce protein intake
•lactulose (breaks down ammonia and neutralizes it)
•DX: clinical (elevated ammonia w/ sx), no imaging •ABX (Rifaximin, Metronidazole) lower ammonia producing bacteria

Anemia and Coagulopathy •Iron deficiency: ferrous sulfate •Transfusion if due to severe blood loss from bleeding varices
•Vitamin K for severe coagulopathies w/ FFP
•Folate deficiency: folic acid *most common in alcoholics •Oral thrombocytopoetin (maybe for thrombocytopenia)

Esophageal Varices •DX: EGD *all cirrhosis patients should undergo a EGD •Procedures: banding, sclerotherapy, balloon tamponade
50% patients with cirrhosis *balloon tamponade has complications, only do if others don’t work
•TX: IV fluids, PRBCs, FFP, Ocretotide, EGD when stable, ABX
•Prevention: band ligationg AND BB (Propranolol), TIPS, transplant

GI
Irritable •Idiopathic, with NO organic cause •abdominal pain with altered •Diagnosis of exclusion 1st line: lifestyle and diet changes
Bowel defecation/bowel habits •low fat, high fiber
Syndrome Onset: late teens, early 20s *MC in women •pain relieved with defecation Rome IV Criteria: •unprocessed food diet
(IBS) Recurrent crampy, abdominal •avoid sorbitol or fructose
Pathophysiology: ALARM SX: pain 1d/wk for 3 MONTHS •avoid gas producing (beans, veggies)
•abnormal motility: chemical imbalance in •GI bleeding, anemia AND 2/3: •sleep, smoking cessation, exercise
intestine (serotonin & Ach) •anorexia, weight loss -relieved with defecation!
•visceral hypersensitivity •fever -Change in stool frequency Diarrhea:
•psychosocial and altered CNS •nocturnal sx -change in stool form •Loperamide
•family history of GI cancer •Dicyclomine (anticholinergic)
•IBD or celiac •Eluxadolin, Rifamixin
•diarrhea  dehydration
•severe constipation or impaction Constipation:
•prokinetics: fiber, psyllium
•polyethylene glycol can be added
GI
Acute Inflammation/irritation of mucosa •MC asymptomatic H. pylori: urea breath test, stool H. pylori: triple therapy
Gastritis •Epigastric pain
Gastropathy: mucosal injury without •N/V EGD with biopsy NSAID:
evidence of inflammation •anorexia *MOST ACCURATE •PPI (Omeprazole)
•biopsy CONFIRMS MOA:block H+/K+ ATP-ase of
Erosive: NSAIDs, alcohol, stress parietal cells, reducing acids
Non-erosive: H. pylori (MCC), systemic SE: B12 deficiency
•Misoprostol, Sucralfate

Peptic Ulcer MCC OF UGI BLEED •Epigastric Pain (dyspepsia) worse at night Upper Endoscopy with Biopsy: 1. Triple Therapy x10-14d
Disease *HALMARK SIGN GOLD STANDARD CAP: Clarithromycin,
Two Types: •Dull, aching, “hunger” Amoxicillin, PPI
•Duodenal (MC)-H. Pylori •Food relief (duodenum) *returns in 2-4h H. Pylori tests:
•Gastric-NSAIDS •Food worsens (gastric) •endoscopy with biopsy (GOLD) 2. Quadruple Therapy x10-14d
•urea breath test; stool (HpSA) PPI + Bismuth (pepto) +
Pathophysiology: increased aggressive, •Nausea, anorexia •antibodies Tetracycline + Metronidazole
decreased protective *erosion >0.5cm •GI bleed (melena, coffee ground emesis)
*may be asymp until bleed Complications: H.Pylori Negative:
Causes: Bleeding, perforation, •PPI: Omeprazole
•H. pylori infection *MC in duodenum Physical Exam: tenderness over epigastric obstruction, malignancy •H2 Blocker: Ranitidine
•NSAIDS *MC in stomach MOA: reducing acid/pepsin
•Zollinger-Ellison syndrome SE: B12 deficiency, high LFTs
•ETOH, smoking, stress, cancer, male, old
Refractory: parietal vagotomy
Gastric Adenocarcinoma MCC worldwide Asymptomatic until advanced Iron deficiency anemia Early local: edoscopic resection
Adeno- Other: lymphoma (4%) •Dyspepsia, vague epigastric pain
carcinoma •weight loss, persistent abdominal pain Diagnostic: EGD & biopsy Surgical resection: gastrectomy
Risks: *risk reduced with chronic NSAID •Anorexia, wt loss, early satiety
•H. pylori •Chemotherapy and/or radiation
•high salt or nitrate foods PE: *palpable mass (20%) •Palliative measures
•low fruits and vegetable diets •left supraclavicular lymph (virchows)
•Non-Hodgkin lymphoma (MC site of •umbilical node (sister mary joseph)
extranodal NHL) •rigid rectal shift (Blumer shelf)
•ovarian mets (Krukenburg tumor)
•L axillary node (Irish sign)
GI
GERD •Reflux of gastric contents into the
esophagus due to incompetent lower
esophageal sphincter
•Transient relaxation of lower esophageal
sphincter (LES)
Barretts Esophageal squamous epithelium
Esophagus replaced by metastatic columnar cells
from the cardia of the stomach
Esophageal Squamous cell:
Cancer •MC type worldwide
•MC in mid-upper 1/3 esophagus
•risk: smoking, alcohol
•people: African Americans
Adenocarcinoma:
•MC type in US; MC in distal/junction
•risk: GERD, Barretts, smoke, high BMI
•people: Caucasian males, younger
Esophagitis Causes:
•GERD (MCC)
•Infectious: Candida, CMV, HSV
•Eosinophilic: allergic reaction
•Pill-induced: bisphosphonates, BB,
CCB, NSAIDs
•Caustic (corrosive): acidic or basic
Pill- Esophagitis due to prolonged pill contact
Induced
Esophagitis Meds: bisphosphonates, BB, CCB,
NSAIDs, KCl, iron, vitamin C
Hiatal Protrusion of the abdominal cavity
Hernia through the esophageal hiatus of the
diaphragm
•Type I: sliding hernia (MC)
•Type II: rolling hernia  fundus
protrudes, GE junction remain in location
•Heartburn (pyrosis) HALLMARK
~30-60min after meals
•Reflux of sour/bitter contents (regurg)
•Dysphagia (1/3)
•Asthma, cough, laryngitis, chest pain
ALARM: dysphagia, odynophagia,
weight loss, bleeding
•Progressive dysphagia: solid to fluids
•Odynophagia
•weigt loss, anorexia
•Tracheo-esophageal fistula
•horners syndrome
•Chest or back pain (mediastinal
estension)
3 Classics:
•odynophagia (HALLMARK)
•dysphagia
•retrosternal chest pain
Candida: linear yellow-white plaques
CMV: large superficial shallow ulcers
HSV: small, deep ulcers
•odynophagia
•dysphagia
•asymptomatic, incidental findings
Possible:
•epigastric or substernal pain
•postprandial fullness
•retching of nausea
•clinical diagonsis
•24hr pH monitoring
GOLD TO CONFIRM
Upper endoscopy: 1st line if
persistent or complication
Complications:
•Esophagitis, Stricture
•Adenocarcinoma
•Barrett’s Esopagus 
squamous to columnar
Upper endoscopy with
biopsy
Upper endoscopy w/ biopsy:
STUDY OF CHOICE
Early lesions:
•superficial plaques
•nodules, ulcerations
Late lesions: strictures, ulcer
Endoscopic US: Staging
Upper endoscopy
Endoscopy: small, well-
defined ulcers
Chest x-ray
1st: lifestyle modifications
•elevate head
•avoid lying down x3hr
•avoid acidic food and alcohol
•smoking cessation
•weight loss
< 2 episodes/ week
•H2 receptor agonists (Ranitidine) prn
2+ episodes per week: PPI (Omeprazol)
Barrets, no dysplasia: PPIs, rescope q3-5yrs
Low-grade: PPI, rescope 6-12 months
High-grade dysplasia: Ablation
Curable: surgery and chemo
Incurable: chemo, palliative
Treat the underlying
Candidal: Fluconazole, Voriconazole,
Caspofungin
CMV: Gangciclovir, Valgangciclovir,
Foscarnet
HSV: Acyclovir, Foscarnet
•Take pills with at least 4 ounces of water
•avoid recumbency at least 30-60min after
•Type I: same at GERD  PPI, weight loss
•Type II: surgical repair
Disease About Clinical Manifestation Physical Exam Diagnosis and Treatment
Colon Polyps •Fleshly lesions protruding into intestinal lumen usually asymptomatic Diagnostics: •remove
(Adenomatous) •Growth arises due to DNA changes in the lining •Colonoscopy with polypectomy that
of the colon *cause 95% adenocarcinomas Adenomatous Polyps: is sent to pathology Screening: 50-75 YEARS OLD
MC NEOPLASTIC Colonoscopy (BEST)
Pseudopolyps: due to inflammatory bowel disease •Tubular adenoma (MC) Risk factor for high grade dysplasia: •10 years if average risk or 1st
(UC, Crohn) *not cancerous -nonpedunculated *high-grade dysplasia/CA degree relative 60+
•Tubulovillous •polyps >1cm •q5 years if 1st degree relative <60
Hyperplastic: low risk for malignancy •Villous •villous histology
*MC non-neoplastic polyp -highest risk of cancer •number of polyps FOBT
-most likely sessile •flat polyps •yearly at age 50 if avg risk
Hamartomatous •yearly at 50 if 1st degree relative
•Juvenile Larger Polyp SX
•Junvenile polyposis syndrome: autosomal •bleeding Flexible Sigmoidoscopy every 5
dominant  increased risk of colorectal and •change in bowel habits years + FOBT every 3 years
gastric cancer •obstruction
•Peutz-Jeghers: STK11 mutation, mucocutaneous •abdominal discomfort Prevention: Diet, weight loss
hyperpigmentation (lipis, oral, hands)

Colon Cancer *3rd MC cancer among men and women •iron deficiency anemia Lynch Screening: Colonoscopy q1-2 Staging and Management: TNM
*2nd leading cause of CA death •rectal bleeding years at age 20-25 system
•Adenomatous (MC) •abdominal pain *tumor, node, metastasis
•change in bowel habits Familial Screening: Sigmoidoscopy
Genetics: yearly at age 10-12 years old Treatment: *good prognosis if
•Familial adenomatous polyposis MCC OF LARGE caught early
•Turcot Syndrome BOWEL OBSTRUCTION Labs: •Surgical resection  post-op
•Lynch Syndrome: autosomal dominant, due to IN ADULTS •iron deficiency anemia chemo
loss of DNA function •CEA tumor marker (not for •Chemotherapy/radiation
-Type I R side, Type II increased risk Proximal (R side) screening-not specific) -stage II-III (node/tissue
of endometrial, ovary, SI, brain, skin •chronic occult bleed involvement)
•Peutz-Jehgers: risk of breast & pancreatic CA •diarrhea Diagnostics: -stage IV (metastatic ds)
•barium enema: apple core lesion
Risk factors: Distal colon •Colonoscopy: DEFINITIVE
•>50yo, African Americans •Obstruction *CT/MRI used for staging
•family history of colon cancer •changes in stool diameter
•diet (red meat, fat, low fiber) •Hematochezia
•smoking, alcohol •Urgency/tenesmus (rectal)
•obesity •Strep bovis endocarditis
•IBD (UC >Crohns)

Protective: activity, NSAIDS

Familial •Inherited mutation (APC gene) Soft tissue tumors in skin Diagnosis confirmed with genetic Prophylactic colectomy
Adenomatous •Development of 100s and adenomatous polyps and osteomas testing recommended!
Polyposis *stomach and duodenum
GI
Inflammatory Ulcerative Colitis and Crohns Extra-Intestinal Manifestations CROHNS DISEASE CROHNS DISEASE
Bowel *Crohns disease or UC Labs: (+) ASCA (anti-saccharomyces *NOT curative!
Disease (IBD) Risks: •MSK pain, arthritis, ankylosing cerevisiae antibodies) •Diet
•Ashkenazi jews, white spondylitis, osteoporosis •Stop smoking
•age 15-35 onset •erthema nodosum, pyoderma Initial Test: upper GI series (barium study) •Symptomatic medications
•males (UC), females (crohns) gangrenosum •String Sign (barium through narrow area)
•genetics •conjunctivitis, anterior uveitis/iritis Limited Ileocolonic:
•smoking (Crohns), may be (ocular pain, HA, blurred vision) Endoscopy: segmental skip areas, 1st line:
protective in UC •fatty liver, primary sclerosing cobblestoning, apthous ulcers, strictures •oral mesalamine (5-ASA)
•western style diet cholangitis •Glucocorticoids
•infections •B12 and Iron deficiency (Crohns!!) GOLD=Colonoscopy w/ biopsy
•meds: NSAID, OCP, hormones  skip lesions with cobblestone Ileal and proximal colon:
appearance, noncaseating granulomas •glucocorticoids
Crohns •Autoimmune inflammatory disease Ileocolitis (MC)
Disease •Crampy RLQ abdominal pain Complications:
•Transmural inflammation and skip •Diarrhea (intermittent, non-bloody) •fistuals, fissures
lesion that affects any part of GI tract •weight loss, fatigue & fever •perianal disease
*MC-terminal ileum and cecum •abscesses
Jejunoileitis:
•malabsorption (iron & B12 deficiency),
•steatorrhea
•nutritional & electrolyte deficiencies
ULCERATIVE COLITIS ULCERATIVE COLITIS
Colitis and perianal: diarrhea, abscess, Labs: high ESR/CRP, anemia, (+) P-ANCA *CURATIVE
fistula, fissure, obstruction
Upper GI Series: “stovepipe” sign due to Mild-Moderate Distal:
extra-intestinal manifestation: loss of hausta •topical 5-ASA, can add oral
•arthralgia, arthritis, iritis, uveitis
•apthous ulcers Gold Standard-COLONOSCOPY Mild-Moderate Pancolitis
•skin: Pyoderma gangrenosum  crypt abscess, basal plasmacytosis, •topical + oral ASA, steroids
erythema nodosum uniform inflammation, ulceration, polyps *same for severe but high
-CI IN ACUTE COLITIS dose

Ulcerative •Relapsing and remitting episodes of •Crampy lower LLQ abdominal pain Fulminant:
Colitis inflammation, spreads proximally •BLOODY diarrhea, pus/mucus •steroids + fluids + ABX
*mucosal layer of colon ONLY, •Fecal urgency and tenesmus
*can mimic rectum is always involved •tenesmus
diverticulitis *smoking decreases risk for UC
Complications:
mild: <4 BMs/day •Severe bleed
moderate: >4 BM/day •fulminant colitis (>10BMs/day)
Severe: 6 BM/d + •toxic megacolon, perf

GI What is it Causes Symptoms Treatment

Constipation •infrequent bowel •motor disorders (CA, DM, hypothyroid) straining See below
movements <2x/wk •drugs (Verapamil, opioids) •hard stool
 •Hirschsprung distease •feeling of incomplete evacuation

IBD Pharmacotherapy Indication MOA Side Effects/Adverse Events/ BBW Notes

Aminosalicylates Induction and maintenance Inhibits prostaglandin •N/V, HA, hypersensitivity *must exert effect directly to
(5-ASA) therapy of UC and CD production, producing anti- •CI: sulfa or ASA allergy colon
Sulfasalazine** inflammatory effects
Mesalamine
Corticosteroids Most effective to induce *Can use Budesonide (Entrocort)
(Prednisone remission in severe flare for maint. crohns disease for ~3mo
40-60mg daily) *acute flare -> CD and UC
Immunomodulators/ •Steroid dependent CD and UC Leukopenia, thrompoenia, anemia
Immunosuppressants Remission maintenance in mild- Infection, N/V/D
Azathioprine (Imuran) severe disease Malaise, arthralgia
6-Meracaptopurine Adverse: lymphoma, severe
(Pruinethol) (6-MP)
BBW mutagenic potential, rapid growth, CA

Immunomodulators/ Methotrexate: Cyclosporine: Cyclosprine SE: *must put on folic acid if taking
Immunosuppressants •Mild-moderate active C and •Severe UC/CD refractory to •Multiple serious adverse effects to Methotrexate
Methotrexate maintenance *NOT IN CD steroids
Cycosporine
Antitumor Necrosis TREATMENT OF CHOICE for Inhibits TNF (which •Fever, rigors, N/V, myalgia, urticarial,
Factor Antibodies someone with crohns disease promotes inflammation) hypotension
Infliximab (Remicade) and a fistula
Adalimumab (Humira) •Mod-severe active CD and UC BBW severe infection/sepsis, malignancy
Certolizumab (Cimzia) maintenance

GI
Acute GI bleed •Ligament of Treitz is
defining location
seperating UGI from LGI
bleed
Medications:
•NSAIDS, anticoags,
antiplatelets,
•Iron (melena)
•Beets (hematochezia)
Social:
•Alcohol  gastris, liver
hx similar sx: 60% UGI
from same lesions
Hematesmesis: bleed proximal to ligament •type and crossmatch Upper GI Bleed
-coffee-ground: mild, frank blood: severe •CBC ALL GET ENDOSCOPY
-normocytic: acute
Hemathochezia: maroon/bright red  LGI -microcytic: chronic Stable: consult GI/surgery
•CMP: high BUN: CR >30-UGI Unstable: IVF, PRBC: FFP (4:1)
Melena: black, tarry stool (altered hgb from •PT/INR: endoscopy can not be
digestive enzymes )  UGI performed until INR <2.5 Lower GI
•consult GI/general surgery
signs of significant bleeding: hypotension, •EKG & cardiac enzymes •consider endoscopy to r/o UGI
tachycardia, low pulse pressure, tachypnea •discuss colonoscopy v angiography
•sign of shock: cool, pale, low cap refill NG Tube (suspected UGI)
•visual inspection of gastric content Others:
•hyperactive BS: UGI bleed  MOST SENSITIVE PPI: acid suppression
•tenderness: inflame/infectious •Pantoprazole 80mg IV bolus
•non-tender: vascular •indicated for bleeding from PUD
•ascites/hepatosplenomegaly: liver Somatostatin analong
Rectal exam: if LGI suspected  guaiac test •Ocreotide 50mcg bolus
•use for variceal bleeding
Constipation Drugs MOA CI Adverse Effects
Fiber/Bulk Forming Laxatives •Fiber promotes intestinal motility by increasing “bulk” of stool •GI obstruction •GI obstruction
Metamucil Citrucil, •Draws water into stool (retains water) •Abdominal
FiberCon Benefiber *problem if not drinking water with fiber then can cause constipation cramps/distention
•Flatulence
Stool Softeners/Surfactants •Emollient that covers stool and softens it •Do NOT use for
Ducosate (Colace) •Allows it to pass through colon easier SEVERE
Mineral Oil don’t typically see mineral oil because can interfere with absorption

Osmotic Laxatives •Increases secretion of water into the intestine •Abdominal bloating/cramps
Milk of Magnesia •Softens stool and promotes defecation •Flatulence
Miralax •Usually works within 24h *not immediate relief •Diarrhea
Enulose *use for opioid induced and chronic constipation

Bowel Cleansers •Osmotic laxatice

Polyethylene glycol (GoLYTELY) •More rapid, COMPLETE bowel cleanse
Magensium citrate
Sodium phosphate (Fleets) *used prior to colonoscopy, bowel surgeries

Stimulant Laxatives •Stimulate fluid secretion and colonic contraction -> “irritants” •NOT for long term use •N/V/D, abdominal cramps
Bisacodyl (Ducolax) •Irritate intestinal wall, causing fluid accumulations and increased contractions •Electrolyte abnormalities
Senna (Senekot) of intestines -> increases motility *can become dependent
Cascara *works within 6-12 hours; can use about 3-4x per week “rescue” agent

Enemas •Commonly used as adjunct to bowel cleanse (osmotic laxative) prior to

Tap water surgical procedures/colonoscopy
Sodium Phosphate (Fleets)
Mineral Oil (ok to use here) *common in hospital setting
GI
Anal Fissure •Linear tears/ulcerations around anus
*MC posterior midline
•Due to trauma to anal canal during
defecation  constipation/hard, straining
Causes: low fiber, large & hard stools,
constipation, anal trauma
Perianal ½ perianal abscesses are caused by fistulas
Abscess and MC in posterior rectal wall
Fistula Bugs: S. aureus, E.coli, Bacteroids, Strep
Abscess: infection of anal ducts or glands
Fistula: open tract b/w two epithelium areas
Diverticulosis/ Infection/inflammation of diverticuli
Diverticulitis
Diverticula: outpouching due to herniation of
the mucosa into the colon wall
*MC in RIGHT colon
Diverticulitis: perforation of a diverticulum
leading to inflammation & necrosis
*MC in SIGMOID colon
Risks: low fiber, constipation, obesity
Hemorrhoids •Engorged rectal & hemorrhoidal veins
•Proximal (above) the dentate line
Causes: constipation, low fiber, straining,
pregnancy, obesity, cirrhosis (increased
venous pressure)
Complications:
•Thrombosed external hemorrhoids *painful
•sitz bath, topical ointments, clot evacuation
•Tearing pain with defecation
•Bleeding
*small amount with bright red
blood (streaking on TP)
Abscess:
•anorectal swelling
•rectal pain wrose with sitting,
coughing, defacation
•worse with sitting, cough, poo
Fistula: anal discharge and pain
Diverticulosis:
•asymptomatic
**Diverticulosis is the MCC of
lower GI bleed
Diverticulitis
•Acute LLQ abdominal pain
•Fever, N/V, bowel changes
Physical exam:
•LLQ tenderness, palpable mass
Internal (superior vein, proximal)
*less pain
•Intermittent bleeding
•Prolapse
•mucoid discharge
External (inferior vein, distal)
•perianal pain and bleeding
•possible tender, palpable mass
Inspection
•longitudinal tear in anoderm
-extends proximally than the
dentate line
•skin tags seen as chronic
Clinical rectal exam
Fistula DX: US/CT
Labs:
•Diverticulitis: leukocytosis
Imaging:
•Diverticulosis: colonoscopy
•Diverticulitis: CT Abd/pelvis
***BEST TEST
Complications: peroration, bleed,
abscess, stricture. fistula,
obstruction
PE: inspect, DRE
•anoscopic evaluation
Staging:
•I: confined in anal canal, no
prolapse
•II: prolapse with straining
•III: require manual reduction
•IV: always out, irreducible
>80% resolve spontaneously
•1st line: toileting, Sitz bath, Fiber
Chronic fissures:
•Topical NTG, Botulinum injection
•Surgery- sphincterotomy
Perianal Abscess:
•I & D  WASH (warm water,
cleansing, analgesics, sitz baths, high
fiber diet)
•Antibiotics; sitz baths, high fiber
Fistula treatment: Fistulectomy
Diverticulosis:
•bleeding will stop spontaneously
•high fiber diet
Diverticulitis: Clear liquid
•Augmentin 875mg BID x7-10d
•Metronidazole + Ciprofloxacin or
Levofloxacin x7-10d
•Metronidazole + Bactrim
Admit: complication, high risk
Conservation
•proper toileting, high fiber, sitz bath
•topical analgesics (lidocaine)
•Preparation H, Anusol, Proctofoam
Surgical
•band ligation (MC)
•sclerotherapy
•infrared coagulation•
•hemorrhoidectomy (stage IV ext.)
GI
Cholelithiasis Gallstones in the biliary tract Asymptomatic •Ultrasound Symptomatic (Biliary Colic):
WITHOUT inflammation *procedure of choice •Laparoscopic cholecystectomy
Symptomatic (biliary colic)
Gallstone form from: •RUQ pain (hallmark) •CT No surgery:
•Ratio of cholesterol too high -follow fatty meals Ursodeoxycholic acid
•Ratio of bilirubin too high -may radiate to back and
•Gallbladder not emptying bile right shoulder blade! Complications:
choledocholithiasis, acute
Types: Cholesterol gallstones (MC!) *don’t typically see N/V, fever, chills cholangitis, acute cholecystitis
Risks: 5 F: fat, female, fertile, fair, forty with biliary colic

Choledocolithiasi Choledocolithiasis: gallstones in Choledocolithiasis Choledocolithiasis •IV fluids, pain control, NPO
s and Cholangitis common bile duct (CBD); symptomatic •Intermittent RUQ pain, prolonged Labs: elevated LFTs, ALP, GGT •ERCP w/ stone extraction &
-passes are “uncomplicated” •Jaundice sphincterotomy
-typically symptomatic •Intermittent N/V Cholangitis
PE: normal Labs: •ABX with acute cholangitis
Cholangitis: gallstone lodged and •Leukocytosis -mild-moderate: Cipro + Flagyl
obstruction in CBD  infection Cholangitis •high alk phos, GGT, bilirubin -severe: Zosyn (Pip/Tazo) + Flagyl
-Bacterial infection or hepatic injury •Charcot Triad
*when become a problem -RUQ pain, Fever, jaundice Diagnostics: Complications:
•Reynolds Pentad: •US/CT (FIRST!) •liver damage
Bugs: E. coli, Klebsiella, Enterobacter, -Charcot + low BP/shock •septic shock with acute
B. fragilis + mental status changes •ERCP-diagnostic test of choice cholangitis
PE: RUQ pain & hepatomegaly GOLD STANDARD

Cholecystitis Inflammation and infection of the •RUQ Pain Labs: Management: NPO, IVF, ABX
gallbladder due to obstruction of the -steady, sharp pain, continuous •Leukocytosis •Ceftriaxone +/- Metronidazole
cystic duct by gallstones -precipitated by meal •increased bilirubin, ALP, LFTS •IV Morphine or Demerol for pain
•N/V & Fever •Lap cholecystectomy in 24-72hr
Bugs: E. coli (MC), Klebsiella, •precipitated by fatty or large meals Imaging:
Enterococci •Ultrasound-1st line Complications:
Exam: -thick gallbladder, sludge, stones •Gangrene
Chronic: • (+) Murphy Sign •Chronic Cholecystitis
•fibrosis and thickening due to chronic • (+) Boas: referred pain to R shoulder •HIDA scan: MOST ACCURATE
inflammatory cell infiltration  irritation of the phrenic nerve (+): no visualization of gallbladder

Acute Acalculous •Necroinflammatory disease of the •fever Labs: leukocytosis Supportive Care
Cholecystitis gallbladder NOT due to gallstones •jaundice •IV fluids
•sepsis Ultrasound: INTIAL TEST •Bowel rest
Pathophysiology: •vague abdominal discomfort •distended gallbladder •Pain control
•gallbladder stasis and ischemia  •without calcifications •Correct electrolytes
inflammation reaction  concentration •Broad spectrum ABX
of bile salts, distention, perforation CT: if dx uncertain after US
HIDA: is uncertain after CT
Risks: hospitalization, critically ill
EENT 8%

EENT About Presentation Diagnostics Treatment

Bacterial Bugs: •purulent discharge •clinical diagnosis Mild-moderate: Topical Sulfonamide
Conjunctivitis •S. aureus (Adults) •lid crusting •culture and gram stain for discharge •Polytrim (Polymyxin B, Trimethoprim)
•S. pneumoniae “eye stuck shut” •Erythromycin ointment
•H flu •conjunctival erythema •fluorescein stain for keratits or corneal
•M. cat •NO visual changes abrasions Contacts: Topical Vigamox, Oflaxacin, Cipro
•Psuedomonas
•Gonococcal (Day 2-5) Gonococcal:
•Chlamydial (Day 5-7) Infection: IM or IV Ceftriaxone
Prophylaxis: Erythromycin ointment 0.5%
Transmission: direct contact *prophylaxis not sufficient for chlamydia

Chlamydial: 1g Azithromycin ORAL

Viral Bugs: Adenovirus •Copious WATERY discharge Slit-lamp: punctate staining •Supportive
Conjunctivitis •foreign body sensation
Transmission: direct contact •erythema, itching, bilateral •COLD compress to reduce discomfort
*SWIMMING POOL •artificial tears
Exam: preauricular LAD •antihistamine (Olopatadine) for itch, redness

Allergic •Atopic asthma •itching, tearing, redness Mild-moderate: topical antihistamines

Conjunctivitis •atopic dermatitis
•allergic rhinitis
Pathophysiology:
•mast cell degranulation and
release of histamine
•pruritis (HALLMARK) •Olopatadine
•stringy discharge •Pheniramine-Naphazoline
•Ketotifen (OTC), Patanol, Bepotastine
Exam: •topical NSAIDs: Ketorolac
•COBBLESTONE papillae
•watery, mucoid discharge Severe: *don’t use if h/o or suspected HSV
•chemosis (conjunctival rednes) •topical corticosteroids-Lotepredenol

Opthalmia •neonatal conjunctival Chemical: due to silver nitrate Clinical diagnosis Chemical: artificial tears
Neonatorum infection during delivery
(Neonatal Gonococcal: Gonococcal:
Conjunctivits) •Day 1: chemical •purulent conjunctivitis with Prevention: •IM or IV Ceftraixone
•Day 2-5: Gonococcal exudate and sewlling of lids •prophylaxis: topical Erythromycin •topical Erythromycin prophylaxis
•Day 5-7: Chlamydia *not effective in preventing Chlamydia
Chlamydia: discharge Chlamydia: ORAL Erythromycin

Disease Clinical Presentation Treatment

Papilledem •optic disc (nerve) swelling due to
a elevated intracranial pressure
Causes:
•idiopathic intracranial hypertension
•space-occupying lesions
•increased CSF
•headache Fundoscope: •Acetazolamide  decreased CSF
•nausea •swollen disc & blurry margins production & aqueous humor
•vomiting •flame-shaped hemorrhage
•refer to ophthalmology
1. MRI or CT first to r/o mass •treat underlying disease
2. lumbar puncture
*DO NOT PERFORM LP
 •cerebral edema

Disease Bugs/Causes Symptoms Treatment

Pterygium •slow growing thickening of bulbar conjunctiva •Fleshy, elevated triangular growing fibrovascular •Artificial tears
mass medially (nasal side) of cornea •NSAIDS or corticosteroid
Risks: wind, sun (UV), sand, and dust exposure •surgery is severe vision impairment

Disease About Clinical Presentation Diagnostics Treatment

Hyphema Causes: trauma, spontaneous pain, photophobia, blurred vision; GOAL: prevent further hemorrhage
N/V-possible IOP •keep supine with head slightly elevated
•hard eye shields
•NO NSAIDS

Disease Bugs/Causes Symptoms Treatment

Bacterial •Inflammation or •ocular pain Slit-lamp: * REFERRAL TO OPHTHALMOLOGIST
Keratitis ulceration of cornea •photophobia •increased fluorescein uptake
(Corneal •eye redness ABX: Topical Fluoroquinolone:
Ulcer) Risks: •vision changes Diagnose: •Oflaxacin 0.3%
•contact lens wear •ocular discharge (hypopyon) and tearing •scrap ulcer for gram stain and •Cipro 0.5%
•dry ocular (Bells Palsy) •difficulty keeping eye open culture •Moxifloxacin
•topical steroids or *DO NOT PATCH
immunosuprresion Exam:
•ciliary injection (limbal flush)
Bugs: •hazy cornea (corneal opacification and
•S. aureus, Streptococci ulceration)
•Pseudomonas (contacts)

Disease Clinical Presentation Treatment

Central Retinal •Retinal artery thrombus or emboli •sudden, painless, monocular Fundoscope: •supine
Artery Occlusion MC 50-80 years old loss of vision • pale, retina •ocular massage
•loss of visual fields • “Cherry-red spot” macula •high concentration of oxygen 100%
Risks: atherosclerosis •amaurosis fugax •afferent pupillary defect (RAPD) •IV acetazolamide or mannitol
•loss of partial visual field •boxcar appearance of retinal vessels •vasodilator
Causes:
•emboli from carotid artery Labs: Giant Cell Arteritis:
•cardiogenic emboli •sed rate and CRP (r/o giant cell) •high dose corticosteroids
•vasculitis

Central Retinal Thrombus in central retinal vein  fluid •first noticed upon awakening Fundoscope: CONSULTATION
Vein Occlusion back up in retina •retinal hemorrhage (blood and •no definitive treatment
•sudden, painless, monocular thunder appearance)
Risks: loss of vision •retinal venous dilation and tortuosity
•HTN, DM, smoking, glaucoma •optic disc swelling
•hypercoaguable states
•multple myeloma
Disease About
Ectropion Eyelid and lashes are turned outward (everted)
due to relaxation of the orbicularis oculi muscle
Risks: elderly, congenital, infectious, CN VII
Entropion Eyelid and lashes are turned inward due to
relaxation of the orbicularis oculi muscle
Risks: elderly, orbicularis oculi spasms
Dacryoadenitis Inflammation of infection within the lacrimal
gland; temporal aspect of upper eyelid
Causes: Sjogrens, mumps (viral), bacterial
Dacryocystitis Inflammation of the lacrimal sac/duct due to
obstruction of nasolacrimal duct
*inner corner of eye near nose
bugs: S. aureus/epidermis, GABHS, pseudomonas
Anterior Inflammation of eyelid, skin, base of lashes
Blepharitis Risks: downs, atopic derm, rosacea, seb derm
Types:
•infectious (ulcerative): S. aureus or S, epidermis
•seborrheic
Posterior Inflammation of the Meibomian glands
Blepharitis •MC type of blepharirits
Bacterial: staphylococci
Hordeolum (Stye) •Localized abscess of eyelid margin
Bugs: Staph aureus
Risks: Seb derm, rosacea
External: infection of eyelash follicle or external
sebaceous gland (glan of Mall/Zeis)
Internal: inflammation/infection of Meibomian
Symptoms
•Irritation, Ocular dryness, tearing
•sagging eyelid, increased sensitivity
•Corneal abrasion from eyelashes
•Ulcerations, erythema, tearing, sensitivity
•Swelling, pain, redness at lacrimal gland
Acute:
•infection: pain, swelling, tenderness, redness
•warmth to medial canthal (nasal side) of lower lid
•purulent material possibly; tearing
Chronic: tearing and discharge
•red-rimmed, burning, erythema of lid
•scales or granulations seen in lashes
•lid margins are hyperemic with telangiectasia
(improper drainage)
•inflamed meibomian glands
•tears may be frothy or greasy
External: localized, red, swollen, tender warm pustule
Internal: meibomian gland abscess
*can progress into cellulitis
Treatment
•Lubricating eye drops and moisture shields
•Surgical correction
•Lubricating eye drops and moisture shields
•Surgical correction
Bacterial: ABX +/- I&D
Viral: supportive care
Acute: ABX: Clindamycin, Vancomycin,
Ceftriaxone and warm compress
Chronic:
•surgery (Dacryocystorhinostomy)
•WARM compress, eyelid scrubbing, lid
washing with baby shampoo, artificial tears
Severe/refractory: topical ABX (Azithromycin,
Erythromycin, Bacitracin solution or ointment)
Inflammation of conjunctiva and cornea:
•long term ABX: Tetracycline 250mg,
Doxycycline 100mg, Minocycline 50-100mg
• corticosteroids: Prednisolone 0.125%
•WARM compression (1st line)
ABX: Topical Bacitracin or Erythromycin
•I&D if no resolution in 48h
Disease About
Macular MCC permanent legal
Degeneration blindness and vision loss
Two types:
•Dry (atrophic): MC,
progressive over decades
•Wet (neovascular/exudative):
more aggressive  months
Clinical Presentation Diagnostics Treatment
•bilateral, progressive, CENTRAL Fundoscope REFER
vision loss (detailed & color) Dry: Drusen bodies  small, round, Dry:
•central scrotomas yellow-white spots on outer retina •zinc and antioxidant vitamins (C & E)
•metamorphopsia •amsler grid at home
(straight lines are bent) Wet (neovascular):
•micropsia new, abnormal vessels Wet:
•intravirtreal VEGF inhibitors:
Bevacizumab *decrease new vessels

Retinal Separation of the retina from •photopsia (lights)  floaters Fundoscope: EMERGENCY
Detachment underlying retinal pigment •”curtain coming down” •detached tissue “flapping” in the •keep supine
epithelium vitreous humor •head turned TOWARD side of
•UNILATERAL PERIPHERAL loss detachment
Risks: myopia, cataract surgery, •no ocular pain or redness (+) Shafers sign: clumping of brown- *do not use miotic drops
old age, trauma colored pigment vitreious cells in the
anterior vitereous humor “dust”

Diabetic MCC of new, permanent Non-proliferative: Proliferative Nonproliferative

Retinopathy vision loss in 20-74 years old •microaneurysms •neovascularization  vitreous •strict glucose control
•cotton wool spots (soft exudates) hemorrhage •laster
3 Types: •hard exudates: yellow dots with sharp
•nonproliferative margins often circinate (lipids) Maculopathy: Proliferative: VGEF inhibitors
•proliferative •flame-shaped hemorrhages (nerve) •macular edema or exudates
•maculopathy •blurred or decreased central vision *ANNUAL EYE EXAM IN DM

Hypertensive •damage to retinal blood vessels Mild: Moderate: SEVERE IS AN EMERGENCY

Retinopathy from longstanding high BP •narrowing •hemorrhages (flame or dot)
•AV nicking (venous compression at •cotton wool spots
the arterial-venous junction) •hard exudates

Severe: ALL + papilledema

EENT Presentation Diagnostics Treatment

Corneal •Eye discomfort Check visual acuity first! Antibiotic Drops:
Abrasion •Tearing, red Non-contact: Erythromycin, Bactrim, Sulfacetamide
•Foreign Body sensation Dx: Fluorescein Stain Contacts: Ciprofloxacin or Ofloxacin (Pseudomonas)
•Photophobia, HA •”ice rink”/inear abrasion seen
•+/- ciliary flush *make sure to evert the lid to •NSAID eye drop-Diclofenac
•+/- changes in vision •Topical anesthetic prior to stain •Tetanus prophylaxis
Proparacain, Tetracain •Follow up if symptomatic in 24-48hr
Disease Causes Clinical Presentation Examination Treatment
Narrow (Closed) •increase in intraocular pressure  •SUDDEN severe, unilateral PAIN Fundoscope: TRUE OPHTHALMOLGIC
Angle Glaucoma damaging optic nerve •loss of PERIPHERAL vision cupping of optic disk EMERGENCY
(“tunnel vision” •prevent or reversal
EMERGENCY Risks: •halos around lights Tonometry: increased IOP •control intraocular pressure
*MC FORM •previous narrow angle or large lens •headache, N/ *recheck 30-60m
•age >60 Gonioscopy:
•females & Asians Signs: GOLD STANDARD •PO or IV Acetazolamide
•conjunctival redness •Timolol 0.5% (topical BB)
Pathophysiology: •corneal edema or cloudiness •Apraclonidine 1% (alpha-2 agonist)
•decreased drainage of aqueous humor via “red, steamy cornea” •Pilocarpine (miotic, cholinergic)
trabecular meshwork and canal of Schlemm •shallow anterior chamber Screening: •Prednisolone Acetate 1%
•mid-dilated pupil (4-6mm) that •40yo+ no risk: q 3-5yrs
Precipitants: poorly, or doesn’t, react to light •40yo+ risks: q 1-2yrs Definitive: Iridotomy (laser or surgical)
Mydriasis (dilation)-dim lights, •60yo+: every 1-2 weeks
anticholingerics, sympathomemetics Exam Order:
•visual acuity & visual field test
Primary: Lens far forward + rests against •pupil evaluation
iris  angle closes •intraocular pressure
•slit lamp exam of anterior segment
Secondary: Anterior angle occluded by •undilated fundus exam
PUSH of ciliary body or PULL of iris

Open (Chronic) •Angle between the cornea and iris is open •initially asymptomatic Cupping of optic disk Pharm:
Angle Glaucoma which leads to degeneration and blockage •painless •Prostaglandins-Latanoprost
of trabecular meshwork Diagnosis: Tonometry •Timilol, Apraclonidine, Pilocarpine
•Increased IOP (>40mmHg) IOP >40=emergent •Carbonic Anhydrase Inhibitors
Risks: •gradual peripheral visual field loss IOP 30-40=urgent (24h) Acetazolamide
•African Americans, age >40, fhx, DM leading to central vision loss IOP 25-29= w/n 1 week
IOP 23-24=repeat/refer Surgery-Laser Peripheral Iridotomy

Glaucoma Drug s MOA SE CI

Prostaglandinds Selective agonist of prostaglandin receptor; increase the outflow of •Bonchospam •raynauds
1st LINE *expensive aqueous humor -> dropping IOP •irritation, increase lashes, change in pigment •asthma •COPD

Beta-Blockers Reduce IOP by interfering with cyclic adenosine monophosphate •bradycardia, hypotension •bronchoscpasm •raynauds
(cAMP) which is used to produce aqueous humor •burning, stinging on application •asthma •COPD

Alpha-2 Adrenergic Causes iris to dilate (mydriasis) causing decreased congestion in the •allergic conjunctivitis •MOAIs •tricyclics
Agonists vessels of conjunctiva -> decreased IOP by reducing production of •hyperemia •CNS depressants, alcohol,
aqueous humor •ocular pruritis BB, cardiac glycosides,
hypertensives
Cholinergic •pupil constriction -> contracts trabecular meshwork -> opens schlemm’s •cramping, diarrhea, watery mouth, sweat
Agonists canal -> increase outflow of aqueous humor -> decreases IOP •fixed, small pupils; visual

Carbonic Slows the action of the enzyme carbonic anhydrase -> decreased •allergy to sulfa
Anhydrase production of aqueous humor
Inhibitors
EENT Causes S/S Diagnostics Treatment
Otitis Externa Inflammation of external •Itching, purulent discharge •clinical Protect ear from moisture + remove
“Diffuse- auditory canal •conductive hearing loss debri/cerumen + topical ABX
Swimmers Ear” •fullness/pressure otoscopy:
Causes: •Severe pain * w/ pulling tragus •edema of external auditory ABX:
Psuedomonas •water, moisture *rise in pH canal •Ofloxacin, Cipro-dexamethasone
Staph epi •trauma (Q-tips) Exam: •Cortisporin Otic Solution
Staph aureus •Pain with palpation (Neomycin, Poly B, Hydrocortisone)
Bugs: •Swollen, red canal *DO NOT USE IF TM PERFORATION
•Pseudomonas (MC!) •Moist debris in canal *AMINOGLYCOSIDE OTOTOXIC!
•Staph epidermis, Staph aureus •TM difficult to visualize •Ear wick

Chronic Otitis Invasive infection of external ear •Severe, deep seated otalgia (pain) out Otoscopy: •Aggressive glycemic control
Externa- canal and skull base (temporal of proportion to exam •Granulation tissue at bony
Malignant/ bone, soft tissue, and cartilage) •Purulent otorrhea, FOUL SMELL cartilaginous junction of ear ABX: IV 6-8wks
Necrotizing canal *hallmark of spreading •IV Ciprofloxacin
Bug: Pseudomonas Complications: •Piperacillin
Psuedomonas •spread to skull base  osteomyelitis CT or MRI: confirm •Cefepime
Risks: •immunocompromised •CN palsies or spread to meninges
•Elderly DM (MC!) biopsy: MOST ACCRATE

Disease Causes Clinical Findings Diagnosis Treatment

Acute Otitis •infection of the middle ear Serous: no infection, just fluid bulging, erythema, +/- fever Effusion but NO inflammation:
Media •usually occurs with viral URI  block AND *serous otitis media
Eustachian tube  negative pressure  Acute: Middle ear effusion •observation
allowing bacteria and viruses to colonize •Ear pain (MC complaint) •Tylenol or Ibuprofen
•Fever, irritability, HA, anorexia, Pneumatic Otoscope:
Risks: N/V/D MOST SENSITIVE Effusion and inflammation:
•children (short, narrow, horizontal ET) •infants pulling at ears •loss of mobility TX FOR 10 DAYS
•day care •Bulging of TM •Amoxicillin-1st LINE!
•pacifier or bottle use, not being breast fed A=normal •Omnicef, Ceftin
•second hand smoke TM EXAM: C.O.M.P.L.E.T.E.S. B=effusion, AOM •Zithromax (not for H. flu)
Color, other conditions, mobility C=Eustachian tube dysfunction •Augmentin (if recent abx)
Bacteria: (decreased), position, lighting, entire D=tubes, perforation •Cephalosporin (if recent abx)
•S. Pneumo surface, translucence, external
•M. cat auditory canal and auricle, seal PCN allergy: Azithromycin
•H. flu
•Group A Strep Exam: Severe: myringotomy + tubes
•bulging and erythematous TM
Virus: RSV, picornaviru), coronavirus, •middle ear effusion Referral for tubes:
influenza, adenovirus •loss of landmarks •3+ AOM within 6mo
•decreased mobility with otoscope •4+ infections within 1yr
Chornic: •unresponsive to ABX
•recurrent or persistan infection WITH TM Chronic:
 perforation for 6 WEEKS •perforated TM Chronic: debride + ABX
•bug: Pseudomonas •recurrent purulent otorrhea •topical ABX (Ofloxacin)

Disease Causes Clinical Findings Diagnosis Treatment

Cholesteatoma •Abnormal keratinized collection of
desquamated squamous epithelium in the
middle ear  possible bony erosion of mastoid
Causes:
•Complication of AOM
•Prolonged Eustachian tube dysfunction
(chronic negative pressure)
•painless otorrhea 
yellow/brown with a strong odor
•vertigo, tinnitus, dizziness
•ear drainage >2 weeks despite tx
•hearing loss (conductive)
Otoscope Refer for surgery for excision
•WHITE MASS behind TM and ossicle reconstruction
•focal granulation, cellular debri

TM Perforation •rupture of the tympanic membrane •acute ear pain Otoscope: •spontaneous healing
•conductive hearing loss •perforated TM
Causes: •sudden pain relief with bloody *do NOT perform pneumatic ABX: Topical Ofloxacin
•penetrating or noise trauma (pars tensa) otorrhea
•otitis media •tinnitus and vertigo *NO AMINOGLYCOSIDES

Disease Causes Clinical Findings Diagnosis Treatment

Acoustic •Benign tumor of schwann •Unilateral sensorineural hearing loss Audiometry: unilateral sensorineural •surgery or focused radiation
Neuroma cells (myelin forming cells) *acoustic neuroma until proven otherwise hearing loss
(Vestibular •Tinnitus, vertigo, ataxia “Example: woke up this
Schwannoma) •arises in cerebellopontine •Dizziness and balance problems Diagnostics: MRI (BEST) morning and could not hear
angle  CN VIII, VII, V •Facial numbness (CN V) or paresis (CN VII) anything from one side”

Labryinthitis/ Vestibular neuronitis:
Vestibular inflammation of vestibular
Inflammation division of CN VIII
Labryinthitis: inflammation of
vestibular and cochlear
portion of CN VIII
•Sudden, persistent, continuous vertigo •Clinical DX •Corticosteroids: 1ST LINE
•N/V; Gait sways toward affected side •May need MRI/CT brain to r/o
•Horizontal nystagmus-beats AWAY central etiology Symptomatic
•Meclizine (antihistamine)
Labrynithisis ONLY: •Head impulse test normal in •Benzodiazepines (Diazepam)
•above + unilateral hearing loss and tinnitus central lesion etiology •Ondansetron (Zofran) for N/V

Causes: idiopathic, viral

BPPV MCC of peripheral vertigo
Benign Paroxysmal
Positional Vertigo Causes:
•displaced otolith particles
(calcium crystals) within the
semicircular canals of inner
ear (canalithiasis)
*MC is posterior canal
•Recurrent, brief episodes of vertigo <1minute Dix-Hallpike Maneuver Reposition Otiliths
•occurs w/n seconds of changing head position *otilith movement  fatigable •Epley Maneuver
•possible N/V
•posterior canal: upward, rotary •Decondition Exercises:
NOT WITH: tinnitus, hearing loss, or ataxia *clockwise •Brandt-Daroff
•anterior canal: downward, rotary •Sermont Maneuver
*counterclockwise
•horizontal Canal: towards floor)

Disease About Clinical Presentation Treatment

Nasal Polyps Causes: •Pale, edematous, boggy mucosally covered masses •Topical nasal steroid for 1-3 months
•Allergic rhinitis (MCC) •Chronic nasal obstruction and decreased smell *surgery is medication unsuccessful
•cystic fibrosis *avoid aspirin in asthma pt
Disease Etiology/Pathogenesis Presentation Evaluation/Diagnosis Treatment
Meniere’s •idiopathic distention of CLASSIC 4 SX: Audiometry: Lifestyle: 1st line
Disease endolymphatic compartment of •Episodic vertigo (min-hours) hearing loss during acute attacks •avoid salt, caffeine, alcohol, choclalte
(Idiopathic the inner ear due to excess •Sensorineural hearing impairment
Endolymphatic fluid (endolymph) *usually unilateral Caloric Testing: Medication: 2nd line
Hydrops) •Tinnitus (low tone & “blowing”) Reduced or absent nystagmus on •antihistamines: Meclizine
Syndrome: unidentifiable cause •Ear fullness affected side •Diazepam
Disease: idiopathic •Promethazine
•Episodic N/V with vertigo •Brain Imaging if central lesion •anticholinergics: Scopalamine
*women 20-40yo •Hearing improves between attack •diuretics: HCTZ
•Chronic, progressive, remitting
Refractory: surgical decompression,
labyrinthectomy, intraaural Gentamicin

EENT About Clinical Presentation Treatment

Epistaxis Posterior:
•sphenopalentine artery
branches, Woodruff’s plexus
Posterior Risks:
•HTN, old, nasal neoplasm
Anterior: Kesselbachs MC
Anterior Causes:
•nasal trauma, FB, rhinitis
•low humidity, hot env.
•alcohol, cocaine
Anterior: Anterior: Posterior:
•bleeding site •Pressure for 5-15 min (1st LINE) seated, lean forward •ENT consult
visualized +/- topical vasoconstrictors (Oxymetazoline, lidocaine •Packing
with epinephrine, 4% cocain) •Oxygen
Posterior •2nd line: electrocautery or silver nitrate •Narcotic analgesic
•anterior not visualized •3rd line: nasal packing •Ligation, Endovascular embolization
•bleeding from both •Balloon catheter (MC)
nares ABX: Augmentin or Cephalexin (Keflex)
•blood into pharynx After control:
*Follow up in 48-72 hours •Avoid vigorous exercise, spicy foods, trauma
•Lubrication w/ pretolatum or Bacitracin oint
•Increase home humidity

Disease Clinical Findings/Causes/Bugs Diagnosis Treatment

Acute Acute inflammation of mucosa of larynx •Hoarseness (hallmark) •clinical diagnosis supportive care: hydration, vocal rest,
Laryngitis •aphonia humidification, warm saline gargles
Noninfectious causes: •dry, scratchy throat Referral: •ENT follow-up
Vocal strain/cyst, singing, polyp, reflux •Laryngitis (hoarseness) lasting >2
•Exudative Tonsillopharyngitis weeks with NO URI sx or in a patient Bacterial: PCN or Erythromycin
Bugs: with fever and anterior cervical that uses tobacco or alcohol
•Virus: rhinovirus, influenza, parainfluenza, LAN-strong bacterial *risk for laryngeal cancer Polyp: surgery
adenovirus, coxsackievirus, coronavirus, RSV •Significant edema
•Bacterial: M. cat, M. pneumo GERD: PPI, ENT referral
•Candidiasis: immunosuppressed
Disease Transmission/Causes
Acute Bacterial Bugs:
Rhinosinusitis •Viral (MC!)
(rhinovirus, influenza,
parainfluenza)
•bacterial
(S. pneumo, M. cat, H. flu)
Causes:
•viral URI
•dental infections
•NG tubes
•smoking, allergies
•cystic fibrosis
Acute: 1-4 weeks
Subacute: 4-12 weeks
Chronic: >12 weeks
Clinical Presentation/Physical Exam Diagnostics Treatment
Signs/Symptoms: •clinical diagnosis ABX: if sx >10-14 days
•nasal congestion and obstruction •No risks: Augmentin 875/125mg BID
•purulent nasal discharge Imaging: *clavuanate improved H. flu coverage
•facial pain/pressure worse with leaning forward CT is study of choice if •Risks: Augmentin 2g/125mg BID
for bending over needed
•fever, cough, hyposomnia or ansomnia, ear PEN ALLERGY:
pressure and fullness, HA, halitosis (bad breath) Definitive: Biopsy •Doxy 100 BID or 200 QD
•Levofloxacin 500mg po qd
Clinical Findings: •Moxifloxacin 400mg po qd
•Maxillary-cheek or upper teeth (MC!)
•Ethmoid-between eyes or retro orbital Complications:
•Frontal-above eyebrow •Orbital cellulitis-Naficillin and Rocephin
•Sphenoid-upper half or retro orbital w/ radiation •Frontal Subperiostela abscess (Potts Puffy
to occiput (back of head) Tumor)-IV ABX
•Intracranial complications

Invasive Fungal Bugs: •Rhinocerebral mucormycosis-black eschar on Biopsy: •Surgical debridement + IV Amphotericin B
Sinusitis •Aspergillus middle turbinate, palate, or face •non-septate broad
(Mucormycosis) •Mucor, Rhizopus, Asidia •Spreads to orbit and cavernous sinus hyphae with irregular Mycetoma: surgery +/- antifungal
•Cunninghamella •acute sinusitis symptoms right angle branching

Risks: Mycetoma (fungal ball):

•DM (DKA) •Long-standing unilateral symptoms,
•immunocompromised •pacification of single sinus

Chronic Bugs: •same symptoms as acute bacterial rhinosinusitis •CT scan •Refer to ENT
Bacterial •S. aureus but for > 12 weeks •ABX-culture guided
Sinusitis •Aspergillus Biopsy: •Intranasal corticosteroids (Flonase)
•Mucormycosis TEST OF CHOICE •Nasal saline irrigation
EENT About Clinical Presentation Diagnostics Treatment
Upper Respiratory Bugs: Rhinovirus SX peak day 2-3, last 10-14 days •clinical •Self-limiting
Tract Infection •nasal saline
(URI) Transmission: Clinical Features: Complications: •oral decongestants (Psuedofed)
“Common Cold” •Hand contact-2h •clear, watery rhinorrhea; nasal congestion •Secondary bacterial •nasal decongestants *few days only
“Viral rhinosinusitis” •Droplet transmission •ears, eyes, noe, throat may ne involved infections:
•Contaminated fomites rhinosinusitis, OM,
(surfaces) * hours Physical Exam: pneumonia
•Nasal mucosal swelling and discharge
•Pharyngeal erythema, Conjunctival injection

Allergic Rhinitis •IgE mediated •Episodic rhinorrhea, sneezing, nasal itching •clinical •1st line-Antihistamine (allegra) and nasal
•Nasal obstruction, post nasal drip, cough•Pruritus •eosinophils in nasal glucocorticoid (Fluticasone, Mometasone)
Allergen exposure of conjunctiva, nasal mucosa, oropharynx secretions, serum IgE
•seasonal elevated Montelukast *prophylaxis before allergy season
•perennial (chronic) Exam: •skin testing •MOA: Inflammatory mediators produced by
•Allergic shiners (dark circle under eyes  edema) leukcytes that are accompanied by production of
Atopic •Allergic salute and crease (rub nose upward) histamines and prostaglandins
•fhx AND •Accentuated lines of the eyes (Dennie-Morgan) SE: dreams, insomnia, anxiey, depression, SI
personal hx •Allergic face: high arched palate, mouth breath,
dental malocclusion •1st Gen antihistamine: Benadryl, Hydroxyzine,
•Nasal mucosa pale, bluish hue and boggy Chlorephenirmaine, Bropheniramine
•Conjunctiva congested and edematous •2nd Gen: Zyrtec, Claritin
•Pharynx cobblestoning •2nd gen metabolite: Allegra *best
•Nasal polyps •Nasal antihistamine: Azelastine, Olopatadine

Disease Clinical Findings/Causes/Bugs Diagnosis Treatment

Acute VIRUS is the MCC: Respiratory Virus •clinical •supportive
Pharyngitis Adenovirus, Rhinovirus, •sore throat, pain •rapid strep to r/o bacterial
Enterovirus, EBV, RSV, •Coryzal sx, Fever (RARE) HSV: Acyclovir, Valcyclovir
Influenza, HZV •NO adenopathy or exud

EBV: white, purple exudate

HSV: vesicles, shallow ulcer

Acute •GABHS
Bacteirla •Rare in children <3 years old
Pahryngitis
(Strep throat) Complications: 2-3 weeks
•Rhematic fever-antibodies
•Peritonsillar abscess
•Poststreptococcal
glomerulonephritis
•Fever, sore throat
•Malaise, N/V
•Tender anterior cervical
lymphadenopathy
•Pharynx, soft palate, tonsil
erythematous and edematous
Scarlantiniform rash-scarlet
fever sandpaper rash from
Centor criteria: FIRST LINE: Pen VK QID
•Fever •Pen G Benzathine-IM
•Cervical LAN (anterior) •Amoxicillin (good alternative)
•Lack of cough •Cephalexin
•Pharyngotonsillar exudate
PCN Allergy:, Azithromycin,
4/4=strong suggestion *just treat Clindamycin, Cephalosporins
3/4 =intermediate 1=unlikely
*ask if recent ABX in 3 MONTHS
 exotoxins of GABHS Labs: Antistreptolysin O (ASO)

Tests: Rapid strep for GABHS *intial

•Throat culture *DEFINITIVE
Disease Clinical Findings Diagnosis Treatment
Peritonsillar •abscess between palentine tonsil and •Severe sore throat-unilateral Labs: CBC, CMP, blood & throat cx •Airway, hospital admission
Abscess (Quinsy) pharyngeal muscle •Fever Trismus, Drooling, •Consult ENT
•MC in adolescents & young adults odynophagia Imaging: •Needle aspiration or I&D
“quinsy abscess” *MC deep neck infection in children and •Neck swelling and pain Differentiates from other deep neck
adolescents •Muffled voice “hot potato” space infections ABX: IV Unasyn or Clinda
•Referred ear pain, Fatigue, •CT w/ IV contrast Add Vanc if no response promptly
Bugs: *often polymicrobial irritable, decreased oral intake •Lateral neck x-rays
•Strep pyogenes (Group A) *not epiglotiss or Retro abscess •Switch to 14d of oral:
•Staph aureus Exam: Augmentin or Clindamycin
•Respiratory anaerobes •swollen, fluctuant tonsil
•Uvula deviation to opposite

Retropharyngeal •deep neck space infection posterior to •Neck swelling/mass, pain lateral neck x-ray: increased •Airway first
Abscess pharyngeal wall •torticollis (wont move neck) prevertebral space >50% width
•MC in children 2-4 years old •Spiking fever ABX: IVAmpicillin-Sulbactam
*complication of •Odynophagia, Dysphagia CT neck with contrast: BEST (Unasyn) or Clindamycin
peritonsillar Bugs: *often polymicrobial •ring enhancing lesion
abscess •Strep pyogenes (Group A) Exam: •surgical incision and drainage if
•Staph aureus •midline or unilat posterior large and mature
•Respiratory anaerobes pharyngeal wall edema
•anterior cervical LAD

Disease About Clinical Findings Diagnosis Treatment

Sialolithiasis •stones within the salivary gland
(Salivary Gland •MC in Whartons duct (submandibular
Stones) gland) & Stensens duct (parotid gland)
Risks: decreased salivation (dehydrated,
anticholinergics, diuretics)
•sudden onset of salivary gland
pain and swelling with eating or in
anticipation of eating
clinical Conservative: Sialagogues 1st line
*increase salivary flow
•tart hard candies, lemon drops
•increase fluids, gland massage
Surgery: sialoendoscopy, laser,
sialodenectomy

Acute Bacterial •bacterial infection of the parotid or •very firm and tender gland swelling CT scan ABX: Dicloxacillin or Naficillin,
Sialadenitis submandibular glands •purulent discharge if massaged Clindamycin + sialogogues
(Suppurative •dysphagia
Sialadenitis) Bugs: S. aureus (MC), S. pneumo, •trismus (reduced opening of jaw)
S. virdians, H. flu, Bacteroides •fever, chills

Risks: obstruction (stone), dehydration,

chronic illness

Apthous Ulcers •maybe association w/ HHV-6 •small, painful round/oval shallow ulcer Clinical •topical oral glucocorticoids:
(Canker Sore, (yellow, white or grey with central exudate) Clobetasol gel, Dexamethasone elixir,
 Ulcerative Risks: •erythematous halo Triamcinolone
Stomatitis) •IBD (Crohns)
•HIV, celiac disease, lupus MC on buccal and labial mucosa •topical nalgesics: 2% viscous
•methotrexate, neutropenia lidocaine

OBGYN 8%

Cystocele: posterior bladder herniating into anterior vagina

Enterocele: puch of Douglas-small bowel herniating into upper vagina
Rectocele: sigmoid colon or rectum herniating into posterior distal vagina

Breast CA About Presentation Diagnostics Treatment

Pagets •Eczematoid eruption •pain, itching, burning •Full-thickness biopsy of lesion •MASTECTOMY
Disease and ulceration •erosion, ulceration •Insitu: no lymph biopsy
•may see bloody nipple discharge •Invasive: biopsy lymph •May try excision of nipple,
•Arises from NIPPLE •retracted nipple areola, local mass
can spread to areola
•palpable mass: 50% (9% invasive cancer)

•no palpable mass: noninvasive cancer or ductal carcinoma

Inflamamtory •Aggressive but rare •Diffuse, brawny edema of skin with erysipeloid border •Suspected mastitis does not rapidly •Chemo  surgery and
Carcinoma •blocked dermal lymphatics by tumor emboli response (1-2wk to ABX  biopsy radiation
•“Peau d orange” (orange peel) skin
•usually NO palpable mass

Medication and Usage MOA Side Effects DDI

SERM •Tamoxifen (Nolvadex)
•Raloxifene (Evista)
•Toremifene (Fareston)
•Used for treatment of breast CA and
chemoprevention of breast CA in
some high-risk women
•binds to estrogen receptors
•block estrogen activity in some
•tamoxifen - blocks in breasts;
mimics in uterus, bone
•toremifene - blocks in breasts;
mimics in uterus, bone
•raloxifene - blocks in breasts,
uterus; mimics in bone
Common •Not for use with other hormone-
hot flashes, nausea, muscle aches and modulating anti-CA therapy
cramps, hair thinning, headache,
paresthesias •SSRIs, cimetidine can reduce efficacy
Benefits: improve bone & lpids •Avoid with QT-prolonging agents
Risks: thrombosis, fatty liver,
endometrial cancer, false thyroid

Aromatase •anastrazole (Arimidex)
Inhibitors •exemestane (Aromasin)
•letrozole (Femara) *induce ovulation
•Used for treatment of breast CA
•May be used alone, in combination
with GnRH blockers, or
before/following SERMs
•inhibit aromatase (enzyme that
blocks conversion of testosterone
to estrogen)
Common:
hot flashes, GI upset, muscle
weakness, joint pain, headache,
worsened ischemic heart disease
Risks:
•Hypercholesterolemia
•Insomnia, impaired cognition,
fatigue, mood changes, Thinning hair
•Caution when using with, or do not use
with, other hormone-modulating anti-CA
therapy
•May increase serum concentration of
methadone or L-methadone
•Do not use with estrogen or
immunomodulating drugs

CI: pregnancy
Fulvestrant •used for metastatic breast cancer
(Faslodex) •attaches to and causes destruction of
estrogen receptors
•does not mimic effects of estrogen
Breast CA About
Breast CA •MCC of non-skin cancer
in women
•2nd MCC cancer death in
women (after lung CA)
Risks:
•personal history
•(+) FHX:
-1st degree relative: 2x risk
-2nd degree relative: 3x risk
•Genes: BRCA1 & BRCA 2
-BRCA 1: higher risk
-BRCA 2: lower risk
•Nulliparity
•First full-term pregnancy
>30
•Early menarche (before 12)
•Late menopause (after 50)
•increasing age
•Postmenopasual HRT
•Hx uterine CA
•GnRH agonists/antagonists
Clinical Presentation
*most arise from intermediate ducts and are
invasive
Types:
•infiltrative ductal carcinoma (MC)
-lymphatic metastases
•infiltrative lobular carcinoma
•pagest disease
•inflammatory
Clinical Presentation
•painless breast mass *>5cm suspicious
•hard, fixed, irregular margins, nonmibile
•upper outer quadrant
*due to more tissue in that area
Exam:
•skin changes: erythema, discoloration,
ulceration, skin retraction (Coopers
ligament), bloody discharge
•Palpation of regional lymph nodes: axillary,
pectoral, supraclavicular, infraclavicular,
subscapular, epitrochlear and lateral chain
•axillary lymphadenopathy
•mets: bone, lungs, liver, brain
•Used to reduce release of GnRH and
FSH/LH
Diagnostics
Mammography: women >40
*can detect cancer as early as 2 years
•microcalcifications & speculated
•Most diagnosed after abnormal test
Ultrasound: women <40
MRI: rapid uptake of contrast
Biopsy:
•FNA: removes the least amount of tissue,
but will not allow for receptor testing
•Core Biopsy: takes more tissue, but
allows for receptor testing
•Open Biopsy: MOST ACCURATE
Genetic Testing
•considered for members of high risk fhx
•genetic counseling needed before and after
Screening:
Mammogram every 1-2yrs women 50-69
•ACS:
CBE q3yrs 20-39, mammo + CBE age 40
•ACOG:
CBE + mammo q1-2yr 40-50, yearly 50+
•USPSTF:
mammo +/- CBE q1-2 yrs, age 50-74
Management
Hormone Receptor Sites
•ER (+) tumor: slightly lower
liklihood of early recurrence
•Er (-): mets to liver, lung, brain
*higher chance of recurrence
(+) ER:
•Anastrozole (postmenopausal)
•Tamoxifen (premenopausal)
*prevention in high risk family history
•Trastuzuma (anti-HER2)
Radiation: usually done after
lumpectomy or mastectomy
Surgery:
Radical mastectomy:
•removal of breast, pectoral muscles,
axillary lymph nodes
Modified radial mastectomy:
•removal of breast and underlying
pectoralis major fascia
Breast Conservation: excise tumor
with negative margins, lymph biopsy
•stage I & II and some III
Follow-Up:
•Close follow-up needed due to high
risk of recurrences
•exam Q 4 mo x 2 yrs, then Q 6 mo x
3 yrs, then yearly
•Mammogram 6 mo after radiation
then becomes yearly
OBGYN About
Fibrocystic •MCC cyclic breast pain in
breast reproductive age women
Chnges •MC age 30-50 years
(Glandular *once cyclic change stops then you
Hyperplasia) wont see this anymore
(stop after menopause unless HRT
Pathophysiology:
•hormonal imbalance that may
produce asymptomatic breast lumps
•estrogen considered factor
•possible increase if drink alcohol
•caffeine can worsen pain
Fibro- •Common, benign solid tumor
adenoma •focal abnormality of breast lobule
•Usually in young women (within
20 yrs of puberty)
•more frequent and earlier age of
onset in black women
Pathophysiology:
•suspected possible hormonal link
•increased in size during pregnany
and with estrogen therapy
•decrease in size after menopause
OBGYN About
Cervical Types:
Cancer •squamous cell (MC!)
•adenocarcinoma
•clear cell (linked with DES)
Spread:
•paracervical nodes (MC)
•parametrial, obturator,
hypogastric, external iliac, sacral
Risks:
Clinical Presentation
•Mass with pain or tenderness
•pain secondary to proliferation of
normal glandular tissue
*can increase and decrease size
•usually present or worse
during premenstrual phase (prior to
menstruation)
Exam:
•multiple, nodular, mobile, smooth
round lumps in both brests
•estrogen stimulates ducts,
progesterone stimulates stroma
•Round, firm, discrete, mobile, non-
tender mass
•may enlarge with pregnancy
•does not change throughout cycle
Clinical Presentation
•asymptomatic in early stages
•post-coital bleeding or spotting
•irregular, heavy vaginal bleeding or watery
discharge
•weakness, weight loss, anemia, pelic pain
*late symtoms
Exam: cervical discharge or ulceration
•early: cervix normal
Diagnostics Treatment
•US or mammogram •reassurance of benign findings
*no mammogram if •avoidance of trauma, well-fitting, supportive bra
<30yo •abstaining from caffeine, coffe, chocolate
•OCPs can reduce symptoms
FNA:
•straw colored or •CAM: evening primrose oil, vit E 400U
green fluid •OTC analgesics: Tyneol, Ibuprofen
(no blood) •severe pain: Danazol, Tamoxifen
•Refractory: surgery
Prognosis: exacerbation may occur until menopause
•clinical •May be confused with Phyllodes tumor: a
fibroepithelial tumor that clinically resemble
US: solid, well- fibroadenomas and has a small chance of malignancy
circumcised,  surgical excision
avascular mass
Unclear diagnosis or rapid growth: surgery
Core Biopsy: •excision with margin of normal tissue
DEFINITIVE
Asymptomatic: monitor, core needle biopsy to confirm
OR repeat US and breast exam in 3-6 months
Diagnostics Management
•colposcopy with biopsy Carcinoma in situ (stage 0)
•excision (LEEP, cold knife)
CIS or pap abnormal: conization •ablation (cryotherapy, laser)
•total abdominal hysterectomy +
bilateral salpingo-oophorectomy
Stage 1A: total hysterectomy or radical
Stage 1A2, 1B, IIA:
•radiaction with brachytherapy
•radical hysterectomy with bilateral
 •HPV (16, 18, 31,33)
•early sexual activity, STIs
•lots of sexual partners
•smoking, DES expsore
•cervical intraepithelial neoplasia
•immunosuppression
OBGYN Risks
Cervical Risk Factors:
Dysplasia/ Sexual Activity Factors:
Cancer •multiple sexual partners
•early onset of sexual activity
•high-risk sexual partner
Infection Factors:
•HPV infection (BIG ONE!)
•History of sexually transmitted
infection
•Immunosuppression (HIV)
Others:
•multiparity
•long term OCP use
Pap Smears
•21-29yo: every 3 years
•30+: HPV + pap q5y or pap only q3y
•30+/+HPV: pap&HPV 1yr or genotype
•>65: stop if no hx dysplasia or CA, 3 (-)
paps or 2 (-) pap + HPV in a row in last
10 years
•late: enlarged, irregular, firm
Cervix
Endophytic: barrel-shaped
Exophytic: friable, bleeding, cauliflower
HPV
HPV & Cervical Dysplasia:
•HPV present in >80% of all CIN
•HPV 16: 50-70% HPV 18: 7-20%
*cigarettes have a synergistic effect
with HPV  cancer
High Risk: 16, 18, 31, 33, 35, 39, 45,
51, 52, 56, 58, 59, 68
•High-risk HPV test performed after
abnormal Pap
•Most + do NOT develop CIN or CA
Vaccines: Gardasil 9
(6, 11, 16, 18, 31, 33, 45, 52, 58)
•female: age 11-26, male: age 11-21
•<15yo: 2 doses, 6 months apart
•>15yo: 0, 2, 6 months
*min interval b/w 1st and 2nd 4
weeks, b/w 2nd and 3rd is 12 weeks
Atypical Screening
3 options:
1. repeat serial cytology: every 6
months until 2 consecutives normal
-second abnormal  colposcopy
2. High-risk HPV: colposcopy if +
3. Immediate referral to colposcopy
Before repeat, treat the underlying:
•hormones if atrophic vaginitis
•antimicrobials for infections
LSIL, HSIL, ASC-H, AGC 
Colposcopy
Locally advanced (IIB, III, IIVA):
•radiation + chemo
Advanced: radiacation, chemo
Dysplasia
CIN I: mild cervical dysplasia
•LOWER 1/3 of epithelial lining
CIN II: moderate cervical dysplasia
•LOWER 2/3 of epithelial lining
CIN III: severe cervical dysplasia
•over 2/3 of epithelial lining; FULL
thickness
ALWAYS treat CIN II and III except:
•pregnant woman (wait till postpartum)
•CIN II in adolescents (high chance of
spontaneous regression)
Colposcopy
Illuminated low-power magnification
-3-5% aqueous acetic acid solution
-directed biopsies of abnormal areas
-curette or brush of endocervical canal
Indications:
•abnormal cytology or HPV test
•clinically abnormal cervix
•unexplained intermenstrual or
postcoital bleed
•vulvar or vaginal neoplasia
•history of in utero DES exposure
pelvic lymphadenectomy
Cancerous
Bethesda System
Atypical Squamous Cell (ASC-US/H)
•undetermined significance, cannot
exclude high grade lesion
Low-Grade Squamous
Intraepithelial Lesion (LGSIL/LSIL)
 corresponds to CIN-1
High-Grade Squamous
Intraepithelial Lesion (HGSIL/HSIL)
 corresponds to CIN II and III
 excision (LEEP) or ablation
Atypical Glandular Cells (AGC)
Glandular cells: normal components of
the endocervix  secrete mucus
Atypical: dont match normal glandular
cells but are not definitely cancer
After Colposcopy
CIN I: expectant
•high chance of regression
•2 paps every 2 months or…
Pap + HPV at 6 months
•repeat if abnormal cytology or HPV+
•if all normal, then routine screening
Surgery:
•CIN II/III
•Invasive Cancer
•Otherwise abnormal or unsatisfactory
colposcopy
 Natural Methods
Contraceptive Coitus Interruptus (pull out):
Methods •withdrawal of penis before ejaculation
(Natural)
Post-coital Douche:
•water, vinegar, commercial product
•theory: flush semen out of vagina
Lactation Amenorrhea:
•suckling  reduced GnRH, LH, FSH
•anovulatory menses for 1st 6mo if
exclusively breastfeeding (not 100%)
*not effective if supplemental feeding
•need amenorrhea to be effective
•recommended to use contraceptive
starting 3 months after delivery
Periodic Abstinence
Periodic Abstinence:
•avoid sex during time when ovum
and sperm could meet
*2-3d before  2-3d after
•methods: calendar, temperature,
combined temperature/calendar,
cervical mucus (billings),
symptothermal method
most effective determinant: LH
•possible increased incidence of
congenital anomalies among
children resulting from unplanned
pregnancies
Calendar Method:
•ovulation after recording
menstrual pattern for several mo
•ovulation normally 14d before
1st day of next menstrual period
•fertile interval: min 2d before
ovulation to min 2 day after
•regular menstrual cycle
•MC method of period
abstinence and least reliable
Ex. Cycle Beads
•white: stop having sex
•brown: ok to have sex
•red bead: period
Combined Temp/Calendar
•well-motivate & compliant
•failure rates 5/100
Temperature Method
•more efficacious than calendar method
•records basal body temp
•take in AM before activity
•slight drop in temp 24-36h after ovulation,
temp rises 0.3-0.4C and stays there
•third day after onset of elevated
temperature-end of fertile period
Cervical Mucus Method “Billings”
•observing changes in cervical mucus
•several days before to just after ovulation
becomes thin and watery
•rest of menstrual cycle: thick & opaque
Symptothermal Method (most effective)
•combines cervical mucus and temp
•uses symptoms before ovulation
•bloating, tenderness, increased libido,
spotting, nausea, headache, mittelschmerz

Long-Acting About/MOA Benefits Side Effects

Depot •150mg 17-acetoxy-6-methyl progesterone IM q3mo Benefits: Major side effect: decreased bone density
Medroxyprogesterone •Take up to 10 months to return to baseline fertility •lower risk of ectopic pregnancy •osteoporosis, calcium loss
Acetate •lower risk of endometrial cancer •can cause irregular menses
“Depo Shot” MOA: Thick mucus & thin endometrium •lower risk of sickle cell crises •prolonged menstrual flow and spotting for
•may improve endometriosis first 6 months
Perfect: 0.3 pregnancies/100, Typical: 3 preg/100 women •dose not increase risk of vascular disease •often amenorrheic later in course

Implants •Single-rod implant; etonogestreol, progesterone •No major complications SE: irregular menses, weight gain
“Implanon” •Efficacious for up to 3 years; Very high efficacy
“Nexplanon”
Vaginal Ring •Flexible ring 5cm diameter and 4mm thick Failure rate: 0.65/100 women •SE similar to COCs
“Nuvaring” •less breakthrough bleeding and spotting
Combo: ethyinyl estradiol and etonogestrel
•works3 weeks/month •vaginal discomfort, leukorrhea, vaginitis,
•maintains efficacy even if removed for up to 3 hours coital problesm
•designed to be left in place during intercourse
Transdermal Patch Combo: norelgestromin and ethinlyl estradiol daily •Higher failure rate for women >198lbs •CI, SE, risks same as COCs
“OrthoEvra” •New patch wkly x 3 weeks followed by patch-free wk
“Xulane” •Attempt to reattach if comes off •slightly more breast symptoms and
Sites: buttocks, lower abdomen, upper out arm, uppter •Detached <24 hours: continue as usual dysmenorrhea (painful cramps)
torso (except breast) •Detached >24 hours: new patch, backup
contraception x1 week

About Combo New Formulation Combo

Oral OCPS: oral contraceptive pills Estrogen: ethanyl estradiol (MC),
Contraceptives mestradiol, estradiol valerate
COCs: combo oral contraceptives
estrogen & progestin Progestin: norethindrone,
levonorgesterel, desogestrel, gestodene,
POPs: progestrin-only norgestimate
•Highly effective when taken as •3rd gen (Desogesterol, norgestimate)
directed and 4th gen (Drispirenone)
-good for hirsutism & acne
-bad because thromboembolism
•Less hormones  less SE
•Monophasic: same dose of
hormones daily
•Multiphasic: different doses of
hormones during cycle
*most now trying to mimic hormone
levels in cycle
•21 days of active hormone,
followed by 7 days of placebo
•84 active pills, 7 days placebo
•365 active pills
•withdrawal bleed 2-5 days after
stopping active pills
 progesterone drops

Oral Administration
Combo Oral Ideal: begin COC 1st day of cycle
Contraceptive
Traditional: begin Sunday following
onset of menses
Quickstart: begin any day of cycle
*may see more breakthrough bleeding if
not at ideal time
•Encourage regular routine of taking
pills same time daily
Missed pills:
•Single missed dose, high-dose
monophasic: conception unlikely
•Multiple missed or missed dose of
lower-dose pills: double next dose &
add barrier contraceptive for 7d
MOA & DDI
MOA:
•Suppress ovulation & implantation
•act on LH a&nd FSH  no follicular
•works on midcycle LH surge
DDI:
•Increase/Decrease effectiveness of
medication
-analgesics: Tylenol, opioid
-Other: warfarin, lamotrigine,
benzos, corticosteroids,
theophylline, metoprolol
•Reduced OCP efficacy
-ABX, anticonvulsants, sedatives
Benefits & Disadvantages
Advantages:
•improves dysmenorrhea, abnormal
uterine bleeding, acne, hirsutism
•Reduced cancer risk (ovarian and
endometrial) *decreases turnover
•MSK: improves bone mass, protects
against osteoporosis
Disadvantages/Side Effects:
•hypercoaguability: MI, CVA
•cervical dysplasia/CA, breast CA
•gallstones and gall stasis
•increased fluid retention
•increased TG
•diabetes mellitus
•nausea, dizzy, weight gain, decreaed
libido, abnormal menses
SE & Caution
CI:
•pregnancy
•undiagnosed vaginal bleeding
•migraine with aura
•women at increased risk of
cardiovascular sequelae
*uncontrolled DM, HTN, lupus
•cigarette smoker over 35yo
•current or prior breast cancer
•active liver disease
Caution:
•may cause/worsen HTN or HA
•may impair quality/quantity of
breast milk

•Any missed pill + coitus in past 5d:

consider emergency contraception

Progestin •Norethindrone (pill) •thickens cervical mucus Benefits: CI:

Only •thins endometrium, suppress ovulation •safe in women who cant take estrogen •unexplained bleeding
•Small quantity of progestin alone •safe during lactation •breast cancer
  does not suppress ovulation
•Take at the same time every day
Emergency About
Emergency •Preventive contraception after
Contraception unprotected intercourse or failure to use
a contraceptive method properly
3 methods: *ideal within 72 hours
•Yupze method
•Levonorgestrel (Plan B)
•Copper IUD (most effective)
•Will not prevent contraception later in
cycle
IUDs Administration/MOA
Copper IUD •Lifespan ~10 years
“ParaGard”
MOA: spermicidal, interfere with ovum
development or fertilization, cause inflammation
of endometrium
Failure: 0.6% per year, typical 0.8% per year
Levonorgesterl •LNG-20 Intrauterine device 52mg
IUD “Mirena” •lifespan ~5 years
MOA: thins endometrium, thickens cervical
mucus, decreased tubal motility
•Irregular menses 1st 3-4 months
•after: significant decrease in menstrual flow,
dysmenorrhea tends to improve
Failure: 0.1% per year, 0.7% after 5 years
Ideal candidates: smokers >35, HTN,
migraines, breast feed, sickle cell, lupus
Yupze
•COCs with Levonorgestrl
•100ug ethinyl estradiol and 500-600ug
levonorgestrel
•2 doses, 12 hours apart
•1st dose within 72h of intercourse
*can do with your birth control
MOA: inhibits or delays ovulation
SE: nausea & vomit
•pre-medicate with antiemetic
Side Effects
Risks/SE:
•PID, ectopic pregnancy
•spontaneous abortion
•uterine perforation
•expulsion
Minor SE: menstrual irregular,
cramp, vaginitis
Risks/SE:
•ectopic pregnancy
•PID
•spontaneous abortion
•uterine perforation
•expulsion
Minor SE:
•irregular menses, HA
•acne, mastalgia
•reduces risk of endometrial cancer •hepatic neoplasms
•pregnancy
Disadvantage: •active liver disease
•must take SAME TIME daily
•higher incidence of irregular bleeding
•higher overall pregnancy rate
Plan B Copper IUD
•2 doses of 750us 12 hours apart •may inhibit implantation or
1st dose-recommended within 72hrs of interfere with sperm function
intercourse •insert up to 7 days from time of
intercourse
•may be effective as long as 5 days *good for patient that missed
after intercourse their 72 hours window
*can leave in after and use as a
•single dose of 1500ug may be as contraceptive method
effective as 2 dose
•most effective method of
emergency contraception
Contraindications
Contraindications:
•intrauterine contents: pregnancy or suspected pregnancy,
previously displaced, distorted uterine cavity (fibroids)
•infections: PID, postpartum or postabortal endometriosis or septic
abortion, mucopurlent cervicitis
•uterine or cervical cner: genital bleeding
•wilson disease
•Liletta: similar but approved for 3 years
•Skyla: lower dose (13.5mg), smaller device size, smaller tube size
for insertion  good for small uterus, low expulsion rate
-duration: 3yrs, NOT approved for heavy flow, dysmenorrhea
•Kyleena: lower dose (19.5mg), last ~5 years, smaller size
-not approved to treat heavy menses or dysmenorrhea
Contraindications: Acute PID unless there has been a subsewuent
intrauterine pregnancy, beast cancer, acute liver disease
 Barrier/Physical
Spermicides •active ingredient: nonoxynol-9 or octoxynol-9
•physical barrier and chemical spermicidal
Sponges •Nonoxynol-9-impregnated polyurethane disc
-inserted up to 24 hours prior ot intercourse
-must remain in place for 6 hours after coitus
Male condoms •Cover for the penis during coitus
-prevents deposition of semen in vagina
-MC used mechanical contraceptive
Female condom •Thin polyurethane with 2 flexible rings
-one ring: depth of vagina
-one ring: near the introitus
Diaphragm and •Circular rubber dome supported by a metal spring
Spermicide
•MUST USE WITH SPERMICIDE-cervical side
-ineffective without spermicide
•Mechanical barrier between vagina and cervix
Cervical Cap •Small, cuplike diaphragm placed over cervix
-held in place by suction
-must fit tightly over cervix
-may be used with spermicide
Elective Abortion
Medical:
- Mifepristone (Mifiprex)  Misoprostol (Cytotec) 24-48h after *safe up to 10 WEEKS
o Mifeprostone: progesterone receptor antagonist (dilation and softening of cervix, placental separation)
o Misoprostol: prostaglandin E1 analog (uterine contractions)
- Methotrexate  Misoprostol 3-7days later *safe up to 7 WEEKS
•Must be placed high in vagina, in contact
with cervix, short before intercourse
•max duration: 1 hour, avoid douching for
at least 6 hours
•Efficacy unchanged by frequency of sex
•More convenient but less effective than
diaphgram or condom
•Latex-may be polyurethane or lamb ceca
•lambs cecum not impermeable to most
organisms
•should be recommended for ALL couples
Advantages:
•under control of female partner
•some protection against STDs
•Position so that the cervix, vaginal fornices,
and anterior vaginal wall are partitioned
from the ramined of vagina and penis
•place up to 6 hours before intercourse
•leave in place 6-24 hours after
•Similar efficacy to diaphragm
•leave in place for 8-48 hours after sex
•confirm placement over cervix after each
sexual act
•High pregnancy rate due to inconsistent use
-do NOT protect from STDs
-can cause local inflammation
Advantages:
•highly effective, inexpensive, protect againt STIs, may
have spermicides
Failure: imperfections, errors, semen escape
Disadvantages
•relatively expensive
•overall bulky
•Trial and error to find correct size
-too small: ineffective, too large: uncomfortable
-weight changes can change size needed
SE: vaginal irritation, increased UTIs
-some protection against STIs
Disadvantages:
•difficult to fit cap properly
•may use for 1-2 days, but foul discharge usually
develops after 1 days
 o Methotrexate: folate antagonist
Intra-Amniotic: induced abortion after 1st trimester
Surgical: can be done up to 24 weeks
- Dilation and Currettage (D&C): includes usage of curette or suction *4-12 weeks gestation
- Dilation and evacuation (D&E): >12 weeks
Post-Abortion: rhoGAM to all RH (-) pts; avoid intercourse, tmapons, douches, intra-vaginal products for 2 weeks
- 2+ procedures can increase risk of mid-pregnancy loss
Menopaus Definitions
e
Menopaus •Cessation of menses for >1 years due
e to loss of ovarian function  low E & P
Risks:
•smoking (advanced age by 2 years)
•reproductive tract disease
•GU infections or tumor
•chemo, readiation, surgical procedures
•ovary blood supply, endocrine, genetic
Stages:
Climacteric: phase when woman passes
from reproductive to nonreproductive
“climacteric sx or complaints”
Menopausal Transition: climacteric
phase before menopause when
menstrual cycle is irregular
(“perimenopause”)
•lasts about 1-3 years
Menopause: final menstrual cycle
•Avg age: 51, premature: ≤40
Postmenopausal: after menopause
•most women live ½ life here
Menopaus About/Clinical Presentation
e
Hormone/HPO Axis Change
•loss of oocytes as ovaries age due to
ovulation and atresia
-7 million at 20 weeks
-1-2 million at birth
-300.000-500,000 by puberty
-400-500 ovulated
•as ovaries lose oocytes, levels of
inhibin slowly decrease
(less inhibin  increase FSH)
*inhibin inhibits FSH
•Oocytes responsive to gonadotropins
disappear from the ovary over time
-remaining oocytes: less
responsive to FSH and LH
-irregular follicle response to
gonadotropins  irregular
length of follicular phase 
irregular menstrual cycles
Artificial Menopause
•permanent cessation of function due to
surgical removal of ovaries or radiation
Treatment
Hormones
ANDROGRENS
•less production of androstenidone
(primary androgen in women)
•decreased levels of testosterone
*less sex hormone-binding globulin
 more active floating around
ESTROGEN: *draw estradiol
level
•reduced endogenous estrogen
•greatest decrease in estradiol
*primarily secreted from adrenal
•estrone levels fall, but not as much
*estrone is predominant estrogen
after menopause
PROGESTERONE
•after menopause, no functional
follicles  no CL  low P
•adrenal glands produce remaining
•NO clinical use in diagnosis
GONADOTROPINS *BEST
•FSH and LH RISE (FSH >LH)
•measure FSH, LH, estradiol to help
diagnose menopause
*can measure FSH & LH with
estradiol (FSH and LH increase
because no negative feedback from
estrogen and progesterone)
Clinical Presentation
Menstrual: irregular, short/long
Somatic: HA, dizzy, palpitations, breast
pain/enlargement, joint pain
Psych/Cognitive: sleep, depression,
irritable, mood swings, memory
Sex: vaginal dryness, low libido
*vaginal atrophy due to low E
vasomotor: hot flashes, sweats
Other: incontinence, dry/itchy skin, hair
loss, hirsutism, wt gain, decreased bone
density, decreased breast size
Reproductive Changes:
•vagina: thin, atrophy, flat ruggae
•cervix: atrophy, small, less mucous
•uterus: atrophy, shrink
•oviducts: decrease in size
•ovaries: atrophy, smaller, less
hormones, no ovulation
•support: loss of tone, relaxation
Urinary: estrogen maintain epithelium of
bladder and urethra  atrophy
•atrophic cystitis: UTI sx
•lose urethral tone(urethral caruncle)
Atrophic Atrophic epithelium with flattened rugae
Vaginitis
•loss of lactobacillus which converts glucose to lactic
acid  increase in vaginal pH to 5-7
S/S:
•vaginal burning, soreness
•dyspareunia
•dryness or thin water or serious discharge
-early: diffuse or patchy red, +/- petechiae, flat ruggae
-late: smooth, shiny, pale
-friable: bleeding w/ minimal traum
-GU: urgency, frequency, dysuria, incontinence
DX: clinical *may do vaginal cytology to assist
About/Clinical Presentation
Hot MC AND CHARACTERISTIC SX
Flashes •alterations in cutaneous vasodilations, perspirations,
reductions in core temp, high HR
•heat or burning in face, neck, chest, back
- HA pressure  flush  sweat
•palpitations, weak, fatigue, faint, vertigo
duration: seconds-10min (avg 4 min)
frequency: 1-2/hr to 1-2x/wk
Initial Treatment:
•FIRST LINE: vaginal moisturizer
*improve symptoms but not atrophy
-Replens, vagisil, K-Y Liquibeads
-Lubricants with sexual activity
Water-based (Astroglide, K-Y),
Silicone-based (Pjur), Oil (Elegenace)
*caution with oil due to condom break
Mod/Severe: Topical Vaginal Estrogen
*even okay if she has a uterus
•restored pH and microflora, increased
vaginal secretions, thickened epithelium,
diminished overactive bladder, fewer UTIs
•systemically absorbed
Treatment (HOMRONAL)
Mainstay: ESTROGENS *transdermal 1st
-block sx and physiologic changes
-E/P combo: if can take E
-increase breast CA risk with P added
•Progestin alone: women cant take E
•Tibolone: synthetic steroid with E, P, A
•Bioidentical hormones: $$$$
-custom-made hormone
•SERM + Estrogen
Other options:
•Prasterone (vaginal DHEA): 6.5mg suppository
-converts androstenedione and T  estrone and estradiol
•Ospemifene (Osphena): SERM (mimics E) 60mg daily
-MC SE: hot flashes, mild endometrial thickening
•Testosterone: 1-2% cream is estrogen is CI
•Pelvic PT: refractory cases
•laser, vitamin, probiotics *mixed data about all of these
Overall: VAGINAL preferred over systemic
-cream: conjugated estrogen or estradiol
-rings: estradiol 7.5mcg releasing x3mo
-tablet: estradiol 4mcg, 10mcg
Treatment (Non-hormonal)
•SSRI/SNRI: *1st line who cant/don’t want HRT
-cautions with SSRI & Tamoxifen (esp Paroxetine)
-increased risk of breast CA or death
•Black Cohosh or Phytoestrogens
-can stimulate breast and uterine tissue
•Gabapentin: SE: sedation
•Clonidine: more effective than placebo (vasodilation)
•Weight loss, acupuncture, mind/body, vitamin E

Benefits Risks Main Treatment Other Options

HRT Known:
•reduced SX (vasomotor, GU)
*vaginal estrogen is as efficaious as
oral or transderm for GU symptoms
•reduced risk of osteoporosis:
improves density, reduce fracture
*benefit from E
Possible
•improved skin collagen & thickness
•reduced UTI
•reduced falls
•reduced cataracts, osteoarthritis, DM
•reduced colon CA (combo therapy)
•reduced CHD (cholesterol clearance)
Lipids
lipids: lower LDL, higher HDL
but can increase TG
•endometrial CA: hyperplasia within 1yr
-unopposed E  proliferation, hyperplasia,
neoplasia; give Progesterone to decrease
•breast CA: only in COMBO (due to P)
-risks: early menarche, late menopause
•thromboembolic: 2x w/ combo, 33% E only
-lower chance with transdermal
•stroke: increased risk in E only and combo
-lower incidence with transdermal v oral
•gallbladder disease: greater risk with E-only
Other Effects *menstrual cycle symptoms
•other: edema, bloat, mastodynia & breast
enlargement, PMS, HA, lots cervical mucus
CI:
1st line: transdermal (decrease SE)
•0.625mg PO conjugated estrogen
•increase dose at 1 month intervals
•must add PROGESTIN if patient
has an intact uterus (no E alone)
-medoxyprogesterone acetate(MPA)
-micronized P: lower risk of breast
cancer and CHD
Regimens:
NOT REC. for >3-4yr
Regimen One: *older method
•Estrogen on days 1-25
•progesterone days 14-25
•withhold both day 26-end of month
•light, painless period each month
Regimen Two: *most common
Other Forms:
•Progesterone only: *better than SNRI
depot MPA IM or po norethindrone
-more effective than SNRI
•Tissue Selective Estrogen Complex
SERM (Duavee or BZA/BE) + Estrogen
-agonist bone; antagonist endometrium
-neutral on breast
-lower risk breast & endometrial CA
SE: VTE, liver disease
•PO Estrogen + Levonorgestrel IUD
-avoid systemic effects of P but prevent
endometrial hyperplasisa and cancer
•SSRI: Citalopram, Escitalopram
-Paroxetine: caution with Tamoxifen
•SNRI: Venlafaxine, Desvenlafaxine
 •breast & E-dependent CA *endometrial,
undiagnosed abdominal vaginal bleeding
•thromboembolism, liver, hypersensivity
•pregnancy
Caution: gallbladder, cholestatic jaundice,
high TG, hypothyroid, flui with cardiac/renal,
hypocalcemia, endometriosis, hepatic
hemangioma
•daily E & P together w/o stop
•initial bleeding or spotting
•eventually: atrophic endometrium
Only use HRT for vaginal
atrophy and hot flashes
SE: insomnia
•Anticonvulsant: Gabapentin,
•Clonidine: helpful with comorbid HTN
and menospausal s/s
CAM: black cohosh, isflavones, Vit E,
exercise, weight loss, relaxation

OBGYN About Causes Diagnostics Treatment

Dysfunctional •abnormal menstrual bleeding and Abnormal bleeding with relatively normal •beta-hCG Acute Hemorrhage:
Uterine bleeding due to underlying causes physical exam •CBC: H/H •IV high dose estrogen
Bleeding (Premarin)
Anovulatory: ovaries produce estrogen •mass or enlarged irregular uterus: Endometrial Biopsy: •observation, COCs
but no ovulation *no corpus luteum leiomyoma •rule out cancer in all women >35 wih •refractory: IUD
•unopposed estrogen leads to obesity, HTN, or DM with •definitive: hysterectomy
endomertrial growth & shedding •symmetrically enlarged uterus: postmenopausal bleeding
adenomyosis, endometrial cancer Postmenopausal:
•exogenous hormones
•atrophy: lubricants

Dysmenorrhe •painful menstruation that affects
a normal activities
Primary: due to increased
prostaglandins
Secondary: due to pelvis or uterus
pathology (endometriosis, PID,
adenomyosis, leiomyomas)
•recurrent, crampy midline lower abdominal Supportive:
pain or pelvic pain 1-2 days before or at •heat compress
onset of menses •vitamin B, E
•diminished over 12-72 hours
NSAIDs/COCs:
•first line medical manage
Laparoscopy: unresponsive to
3 cycles of initial therapy

OBGYN About Work-Up Care and Disposition

Spontaneous Threatened: *only one potentially viable Pelvic Exam hemodynamically unstable: Complete Abortion:
Abortion •products of conception intact •caution in patients beyond 20 -emergent consult •may be discharged home if stable and
•cervical os closed weeks because risk of placentia -fluid and blood vaginal bleeding is decreasing or absent
Pregnancy previa -Rhogam if RH (-) •pelvic rest
that ends <20 Inevitable: •close follow up with OB
WEEKS •products of conception intact Labs: Types •Rhogam if indicated
gestation •bleding, cramps, os dialted •CBC Threatened Abortion:
•blood typing and crossmatch •pelvic rest Setpic abortion
Incomplete: •Rh factor •may be discharge home with •obtain CBC, blood and uterin cx, LFTs,
•some products expelled •B-hcg close follow up with OB BMP, PT/PTT
 •bleeding, cramping, os dilated •Urinalysis •return to ED if significant pain, •OB/GYN consult and asmiddion
fever, vaginal bleeding, passage •Ampicilling/Sulbactam
Complete: Ultrasound of tissue •Clindamycin + Gent
•products of conception expelled transabdominal or transvaginal
•cervical os closed •may confirm fetal death by Inevitable: Incomplete/Missed:
noting evidence of fetus with no •surgical evacuation (D&C) •surgical evacuation (D&C)
Missed: fetal death <20 wks, brownish heartbeat or movement •Misoprostol •Misoprostol
discharge, no fetal tissue is passed •expectant management •expectant management
•US should sac with no heart beat

Septic Abortion MCC incomplete

evacuation
•some products of conception retained
•cervical os closed; cervical tenderness
•brown, foul discharge; fever, chills

OBGYN About Clinical Presentation Diagnostics Treatment

PID and •MC serious infection occurring Clinical Features Labs: empiric treatment for PID:
Tubo- in reproductive-aged women •lower abdominal pain •pregnancy test *r/o ectopic •sexually active women or other women at risk for
Ovarian •occurs when infection ascends •vaginal discharge & bleed, dyspareunia, •wet prep, swab for G/C STDS if they have pelvic pain + no other cause
Abscess from the lower genital tract urinary discomfort, fever, N/V •CBC, ESR, CRP for illness, plus ONE:
•peritoneal symptoms or minimal sx •pelvic US -cervical motion, uterine, or adnexal tenderness
•MCC: Neisseria gonorrhea, •RUQ pain with jaundice
Chlamydia trachomatis (MC)  Fitz-Hugh Curtis Admission criteria Inpatient Treatment options
•failure to respond to outpt tx •Cefotetan or Cefoxitin + Doxy
Risks: pelvic exam: •pregnancy and adolescents •Clindamycin + Gentamicin
•multiple partners, STDs •uterine, adnexal tenderness and/or *adolescents risky because Alternative: Augmentin + Doxycycline
•sexual abuse cervical motion tenderness transformation zone on cervix
•IUD “Chanelier sign” •toxic Oral and Outpaitent Regiments
•douching •cant tolerate oral •Ceftriaxone + Doxy +/- Flagyl
•substance abuse •cant exclude other dx •Cefoxitin + Doxy +/- Flagyl
•adolescents •3rd gen ceph + Doxy +/- Flagyl

OBGYN About Clinical Presentation Diagnostic Treatment

Candidal Bug: Candida albicans
Vulvovaginitis
Risks: DM, HIV, obese, prego,
ABX, steroids, OCPs
•intense vulvar pruritus
•thick, white cottage cheese discharge
•minimal odor
•vulvar erythema, edema
•burning sensation after peeing
•Vaginal pH: elevated 4-5
•saline prep: 1 drop discharge: 1 NS
-branching filaments,pseudohyphage
•KOH: 1 drop 10% KOH
-dissolves epithelial cells & debris
•Culture: GOLD STANDARD
Pharm: 1-3d topical, 1d Fluconazole
•topical or oral antifungals
•boric acid or gentian violet
Complicated:
•4+ episodes/yr, severe symptoms, non-
albicans, uncontrolled DM, HIV,
steroid, pregnancy
-2 doses of fluconazole

Bacterial •overgrowth of abnormal flora •copious, thin, homogenous, gray-white •pH: elevated 5.5-7 (ELEVATED) •Metronidazole (Flagyl) x7d
Vaginosis •decreased lactobacillus vaginal discharge •Clindamycin (Cleocin) x3-7d
*NOT STI •itching, burning, dyspareunia •saline prep: “Clue Cells” •Tinidazoel (Tindamax) x3-7d
 Bug: Gardnerella vaginilis *worse after unprotected sex •KOH: (+) “whiff test” fishy odor
•“fishy” smell, enhanced after KOH prep Prevention: probiotics, acid douche

Exam: no mucosal inflammation

Trichomonal •unicellular flagellate protozoan
Vaginitis
•MC non-viral STD in US
•perinatal complications,
increased HIV transmission
•profuse extremely frothy, greenish, at
times foul-smelling vaginal discharge
•erythema, petechial: strawberry cervix
•pH: elevated 5-5.5 (ELEVATED)
•saline prep: motile trichomonads
•nucleic acid: 45 minutes
•pap smears, culture
•Metronidazole or Tinidazole x1dose
-or Metronidazole 500mg BID x7d
Resistant: Tinidazole 500 TID x 7d
•treat partner & screen for other STIs

Gonorrheal •MC infects glands of cervix, •80-85% of women asymptomatic •nuclei probe or culture of discharge •single IM Ceftriaxone 250mg
urethra, vulva, perineum, anus •copious mucopurulent discharge possible -gram (-) diplococci •Chlamydia TX: Azithromcyin 1g

Chlamydial •may see mucopurulent cervicitis, •culture, immunoassay, nucleic acid •Azithromcyin 1g po once
dysuria, and/or postcoital bleed •can be found on pap smear •Doxycyline 100mg po DIB x 7 days
•treat partner

OBGYN About MOA SE/DDI

Vaginal •less systemic risk; rapid relief •inhibit enzyme for membrane synthesis SE: burn, itch, swell, rash, discharge
Antifungal •weaken latex (caution) •Nystatin: increase permeability of wall
DDI: rarely Warfarin
Oral •higher systemic risk •inhibits enzyme for cell membrane synthesis SE: GI, abd pain, dizzy, HA, drowsy, allergy
Antifungal •delayed relief
(Fluconazole) •can NOT use in 1st T prego DDI: erythro, clopidogrel, warfarin, theophylline, sulfonylureas,
thiazides, rifampin, cimetidine *avoid with hepatotoxic drugs

Nitromidazole bind to and deactivates enzymes SE: dizziness, HA, false lab results •alcohol (3d), Disfulfiram (2 wks), anticaogulatns, phenytoin,
-GU: dark colored urine, irritation lithium
-GI: pain, upset, dry mouth, glossitis, altered taste
-Rare: neurotoxic, anaphylaxis, SS

Clindamycin Binds to ribosomes blocking protein SE: C. diff, local irritation, abd pain, GI, latered tast •macrolides, neuromuscular drugs, antiperistaltis drugs
synthesis Rare: blood dyscrasis, hepatotoxic, anaphylaxis

Gravida: number of times a woman have been pregnant

Parity: Number of pregnancies that led to a birth either at or after 20 weeks
- T (term)  number born at 37 weeks or older
- P (preterm)  born after 20 weeks but before 37 weeks
- A (abortion)  all pregnancy losses prior to 20 weeks
- L (living)  infant who lives beyond 30 days

Nulligravida: woman who currently is not pregnant and never has been pregnant
Primigravida: woman who currently is pregnant and has never been pregnant before
Multigravida: woman who currently is pregnant and who has been pregnant before
Nullipara: woman who has never completed a pregnancy beyond 20 weeks
Primipara: woman who has delivered a fetus or fetuses born alive or dead with an estimate length of gestation of >20weeks
Multipara: woman who completed 2+ pregnancies to 20 weeks gestation or mo
Fundal Height: 12 weeks (above pubic symphysis), 16 weeks (midway between pubis & umbilicus), 20 weeks (umbilicus), 38 weeks (2-3cm below xiphoid
Pregnancy Signs/Symptoms
Pregnancy Amenorrhea
•cessation of menses in a health
•not reliable until 10d + after
menses
•can have “implantation bleeding”
for blastocyst
Vaginal/Cervical Changes
•Chadwick: mucosa appears dark
bluish red & congested
•Goodells sign: cervical softening
•cervical mucus: thick due to P
•uterine change:
•Haegers sign: isthmus soften (6-8)
•Ladin sign: uterus softens (6wk)
Estimate Date of Delivery
Breast Changes
•tenderness & paresthesia
•increase in breast & nipple
•thick yellowish fluid 
colostrum
•areola becomes deeply pigmented
Skin Changes ~16th wk
•increased pigmentation, linea
nigra
•pruritic papules  steroids
•chloasma  “mask”
•striae (stretch marks)
Fetal Movement 16-20 weeks
•Primigravida ~20wk
•Multigravida ~16-18wk
Heart Tones: 10-12 weeks
Prenatal Visit
Diagnostic Tests
Beta human chorionic gonadotropin (B-hCG) Transvaginal US
•produced by syncytiotrophoblasts gestational sac: small anechoic
•blood and urine about 8-9d after ovulation fluid within endometrial cavity
•prevents involution of corpus lutem  first evidence ~4-5wk
•rare false (-): MCC is herephilic antibodies yolk sac: bright echogenic ring
*urine would be negative with anechoic center
•false (+) causes: exogenous hCG, renal failure  confirms location ~5-
with failed hCG clearance, pituitary hCG, tumors 6wk
*home pregnancy tests require value of 12.3 to fetal pole/embryo: ~6wk
detect 95% pregnancies  use 1st urination crown rump length: used up to
12wk to predict the due date,
accurate within 4d
Lab Tests RhoGam
 •Naegele’s Rule
-LMP + 7days – 3 months
-assumes pregnancy begun
2wk before ovulation
•Ultrasound
 1st trimester crown rump
is MOST ACCURATE
History
•obstetrical hx: pregnancies,
complications, infertility
•menstrual: interval between
menses, contraceptives
•fhx, shx, medical hx
Physical Exam
•uterine size *bimanual
-small orange ~6wk
-large orange ~8wk
-grapefruit ~12wk
•cervical dilation, length,
consistency *bimanual
•pelvic architecture *bimanual
First Visit MOA: suppresses immune
•CBC: WBC, Hgb, Hct, Plt response of Rh negative
*monitor anemia & thrombocytopenia individuals to Rh (+) RBCs
Blood type and Rh Factor: if Rh (-) mother and Rh Dose: 0.3mg eradicates 15ml of
(+) fetus then receive RhoGam ~28thwk *RhD fetal RBC
•antibody screening
Should be given
rubella serology: infection in 1st semester can -bleeding or trauma prior to 28wk
cause abortion, malformations -postpartum if infant Rh (+)
-invasive diagnostic prenatal test
•pap smear
•gonococcal & chlamydia, syphilis, HIV, hepatitis Keihauer-Betke
•urinalysis •tests amount of fetal RBC in
•urine culture & sensitivity maternal circulation

Counseling
Prenatal Vitamin
•400 micrograms of folic acid
*4mg if hx neural tube defect
Employment
•work until labor
Weight Gain
•Maternal weight gain is correlated
with infant weight
*obese women who gain <15lb have
the lowest complication rate
*25-35lbs, underweight: 28-40lbs,
obese: gain around 12-20lbs
Obesity associated risks:
•gestational HTN, DM, preeclampsia
•macrosomia
•C-section
Diet: additional 100-300kcal/day
- 60-80g protein/day
Seafood
•avoid fish and shellfish contain mercury
•High risk: shark, sword, mackerel, tile fish
•no more than 6oz of white tuna
Lead
Risk factors:
-recent immigrant
-living near lead source
-using lead glazed pottery
-eating nonfood substances
-using imported cosmetics
-remodeling home with lead
-consuming lead water
-living w/ someone with elevated lead
Seat Belt
three point restraints with lap belt under
abdomen and across upper thigh
Air Travel
can fly up to 36wk, ambulate hourly and
wear TED hose
Dental: no CI including x-rays
Coitus (intercourse): not harmful
Caffeine: >5c can increase abortion,
<200mg (10oz) not associated with issues
Exercise
•do not limit; engage in moderately intense
activity for 30min+/day; *don’t lift >25lb
•avoid: high risk falling or trauma & scuba
Smoking: person to person counsel
•ask, advise, assess, assist, arrange
Alcohol: MC in white; NO ALCOHOL
Illicit Drugs: less likely to obtain prenatal care
Breastfeeding
•exclusive BF preferred until 6mo
•human milk contains protective
immunological substances  IgA and GF
•protects against rotavirus, decreased atopic
dermatitis and resp infections
CI: street drugs, uncontrolled alcohol,
galactosemia, HIV, TB, medications, breast
cancer treatment, active herpes on breast
Routine Care
•Every 4 weeks until 28 weeks
•Every 2 weeks until 36 weeks
•Every week unil delivery
Prenatal Surveillance
At each return visit:
•US fetal growth (dating & anatomy)
•maternal BP/weight
•U/A, protein, glucose
•S/S: leak, contractions, N/V, bleed
Common Complaints
Nausea/Vomiting “morning sickness”
•common in 1st trimester until 16th wk
TX: small meals, BRAT diet, ginger,
vitamin B6 + Doxylamine, Zofran
•Hyperemesis gravidum: vomiting severe that
dehydration, electrolyte, and acid-base
disturbances and starvation ketosis
•hypokalemic, hypochloremic metabolic
alkalosis
Back Pain *low back pain
•increased with gestational age
•Reduce By: squatting rather then bending,
avoid high heels, use a pillow back support,
belly band, PT, Tylenol prn
Hemorrhoids
•increase in pelvic venous pressure, rectal
vein varicositis occur
•pain and swelling occur
TX: topical applied anestheics, warm soaks,
stool softeners
Varicosities
•femoral venous pressure in pregnant woman
increased 8  24mmHg at term
•cosmetic blemished to severe discomfort
TX: rest with leg elevation, elastic stocking
Heartburn *very common
•GERD in lower esophagus due to upward
displacement & compression of stomach
TX: antacids, H2 blockers, PPIs
Pica: craving for strange food  iron def.
Sleeping & Fatigue:
•efficiency declines with gestational age,
increase need
TX: Benadryl, daytime naps
Leukorrhea: increase discharge

Prental Prenatal Diagnosis Down Syndrome & Trisomy

Prenatal Chromosomal Abnormalities:
Diagnosis •Risk of fetal trisomy increased with
maternal age, especially after age
35
•Women with fhx or personal history
of aneuploidy should be referred to
genetic counseling
First Trimester Screening 11-14 weeks
•nuchal translucency: max thickness of the
subcutaneous translucent area b/w the skin
and soft tissue of spine at the back of neck,
>3.5 is abnormal  targeted sonography,
chorionic villous sampling, aminocentesis
•Biochemical screening: beta-hCG, PAPP-
A  1 hour glucola testing
•Downs: elevated hCG & low PAPP-A
•Trisomy 13 & 18: both low
•ultrasound: heart tones around 10-12week
•Chorionic Villous Sampling: 10-13
weeks women with increased chromosomal
abnormalities, prior child with
chromosomal abnormalities, materal age
>35, abnormal 1st or 2nd T maternal
screening tests, abnormal nuchal
Second Trimester: 13-27 weeks
Triple test
•hCG, AFP, & unconjugated estriol
•down syndrome:
low AFP & estriol, high hCG
•trisomy 18: all decreased
•spina bifida: high AFP
Quad Screen
•above + inhibin
•Downs: elevated inhibin
Gestational Diabetes: week 24-48
Aminocentesis: same as chorionic
Combine First & Second Trimester
•enhance aneuploidy detection rates
•combines results from both trimesters
•highest detection of down syndrome
•results after both completed
Third Trimester:
•Gestational Diabetes: 24-28 weeks
•antibody screen in Rh (-): 28wk
*give RHOgam if negative
•CBC repeat: ~28wk, monitor anemia
•UDS repeat if + initial: 28 week
•GBS: vaginal/anal culture 36-37wk
 IV PCN G at labor
*alternative: Clindaycin

Neural Tube Defects
Birth defects of brain:
•anencephaly
*failure to close neural tube that
becomes cerebrum
•spina bifida
*incompetent closure of embryonic
neural tubule  vertebrae
•cephalocele
•rare spinal fusion abnormalities
•elevated AFP in maternal and
fetal serum and amniotic fluid
•AFP synthesized by fetal yolk sac
MSK 8%
MSK About
Ankle MC lateral ligament: anterior
Sprain talofibular and calcaneofibular
•results from inversion (rolling ankle)
Medial liagments: deltoid injuries
result in eversion injury
Achilles •inflammation of Achilles tendon
Tendinitis •MC in people >30yo
Risks: run, jump, speed change i
Cause: overuse
Achilles •5-7cm proximal to insertion of
Rupture tendon on the calcaneous
translucency, prior pregnancy losses
Risk Factors:
•family history, MTHFR mutation
•aneuploidy, diabetes, hyperthermia
•medications *seizure medications
Screening: mom serum AFP b/w 15-20 wk
AFP can be affected by:
•multifetal gestation
•pilonidal cyst
•chorioangioma of placenta
•placental abruption, preeclampsia
•oligohydramnios, FGR
Presentation
•pain, swelling, bruising
•report a pop
•pain with varus stress and
anterior drawer
•pain/stiffness 2-6cm above the
posterior calcaneus *burning pain
•pain relieved with rest
•sudden, severe sharp calf pain
-“gunshot wound” “direct hit”
Types of Spina Bifida:
•myelomeningocele (MC):
meninges and spinal cord herniate
through gap in vertebrae
•occulta: no herniation; overlying
skin may be normal or hair;
dimling or birth mark
•meningocele: only meninges
herniate through gap
Diagnostics
•anterior drawer test
•squeeze test: squeeze tib/fib midcalf
 (+) pain
•dorsiflex and external rotation
X-Ray: Ottawa Rules  Ankle
•pain along lateral malleolus
•pain along medial malleolus
•inability to walk >4 steps
•clinical
•Thompson: absensce of plantarflex
Non-Stress Testing:
Baseline fetal HR 120-160bpm
Reactive: 2+ accelerations at rate 15+
bpm from baseline for at 15 seconds
Nonreactive: no fetal HR accelerations
or <15bpm lasting <15 seconds
•sleeping, immature, compromised
•TX: vibratory stimulation, contraction
stress testing
Contraction Stress Testing:
Negative: no late decelerations
Positive: repetive late decelerations
 hospitalize for fetal monitoring
Treatment
•initially: NSAIDs, RICE, protect ankle,
brace if need
•2nd phase: when pt can bear weight
without increase pain or swelling (~2-
4wk), use braces, start exercises
•3rd phase: ~4-6weeks, functional
conditioning and strength, wean off brace
•RICE, MICE, NSAIDs
•heel pads
•exercise programs
•steroids (last resort)
•Initial: RICE, non-wt bearing, urgent
ortho referral
 •quick, stop and go sports like tennis
or basketball (kobe!)
Mechanism: mechanical overload
from eccentric contraction of
gastrocsoleus complex
•swelling of lower calf •calf squeeze test
•difficult bearing weight -if foot moves  incomplete rupture Nonsurgical: short leg plantarflex cast
•palpable defect -does NOT move foot  full rupture or functional brace with heel lift
•MRI evaluates severity Surgical: reconnects tendon,

Risks: Fluoroquinalones, steroids

Plantar •Inflammation and tears of plantar
Fasciitis fascia due to overuse
•common cause of heel pain (medial
tuberosity at calcaneous)
risks: obese, old, female flat feet
•heel pain worse when initiating
walking (most severe in 1st step in
morning or after long activity)
•resolve with walk but worsens
towards end of day
•relieved by sitting
Exam:
•tenderness with pressure over plantar
medial calcaneal tuberosity and fascia
-dorsiflex toes & palpate
NON-SURGICAL
•OTC orthotic heel pad & home
stretching
•avoid barefoot, flat shoes, activities
•ice and NSAIDs
Persistent steroid injection, non-
removable cast, night splint, surgery if
no relief 6-12mo

MSK About Clinical Manifestation Diagnostics Management

Costochondriti •acute inflammation of the costal •pleuritic chest pain (worse with inspiration) Usually all normal •NSAIDs
s cartilages or costochondral junctions •worsened by inspiration, cough, movement

Causes: idiopathic, posttraumatic Exam:

•reproducible point chest wall tenderness
•MC in 3rd, 4th, 5th ICS •absence of palpable edema

Knee About Presentation Exam and Diagnostics Treatment

ACL Tear •MC knee ligament injury
•MC in female athletes
Mechanism:
•noncontact pivoting
•deceleration, change position
•hyperextension, internal rotation
•sudden pain and giving away of the knee •Lachman *MOST SENSITIVE •rest, ice, crutches, PT, compression
•audible “pop” and swelling •anterior drawer *wrost •possible aspiration for effusions
•knee buckling and inability to bear weight •pivot shift test
•possible hemarthrosis Definitive
•segond FX is pathologic for ACL tear x-ray: AP, lateral, tunnel views •ACL reconstruction is best for
young, active pts
Unhappy (O’Donoghue) Triad: MRI: best for confirm •older or less activity  PT
•ACL + MCL + medial meniscus

PCL Tear •strongest ligament in the knee
Mechanism:
•dashboard: anterior force to
proximal tibia with knee flex
•direct blow/fall on flexed knee
•posterior knee pain •posterior drawer •isolated PCL treated nonsurgically
•anterior bruising *most sensitive -rest, ice, ROM exercsies
•effusion
x-ray: AP and lateral surgical reconstruction: fail above
*ACL may rupture first then PCL MRI: confirm

Collateral •outside the joint and stabilize the •minor ambulatory issues (most play on) Varus and valgus stress Grade I (sprain) and II (incomplete)
Ligament Tear knee against valgus (abduction) •localized swelling, stiffness •LCL: varus stress •conserative: PT, RICE, NSAIDs
(MCL and LCL) and varus (adduction) stresses •tenderness along MCL or LCL *medial trauma •early ROM and quad strengthening
•ecchymosis and effusion in 24h •MCL: valgus stress
 *lateral trauma Grades III (complete): +/- surgery

Meniscal Tears •fibrocartilaginous pads that
function as shock absorbers
Mechanism:
•degenerative or acute
•axial loading and rotation
•swelling, stiffness after activities •tender to medial/lateral joint •RICE, NSAIDs
•locking, catching, popping •postive McMurrays test
•patients can ambulate and play sports Surgery: traumatic tears in younger
•pain on medial/lateral side w/ twist or squat x-ray: AP/lateral, sunrise patients, older patients who do not
respond to conservative
MRI: BEST

Hand About Presentation Diagnostics Treatment

Ganglia of •cystic structure arises from capsule of
the Wrist joint or a tendon synovial sheath
and Hand •MC soft-tissue tumor of hand
•Age 15 to 40 years is MC
Common locations
•dorsum or volar radial of the wrist
•base of the finger
•pain, tenderness, especially with •PA, lateral and oblique xray should be Wrist ganglion:
movement obtained to rule out bony pathology •Typical: reassurance
•atypical: excision and biopsy
Physical Exam •Surgery if significant sx or bothered
•smooth, round or multilobulated
structure Finger ganglion: rupture & massage
•A prominent ganglion will
transilluminate

About Signs and Symptoms/PE Tests and Stages Diagnostics and Treatment
Rotator Cuff 4 muscles: SITS •dull ache deep in shoulder Testing: DX:
•supraspinatus *origates here •difficult sleeping on affected shoulder •suprasinpatus: “empty can test” 90% spec •xray
•inraspinatus •difficult reaching overhead, behind back, -seated, elevated UE to 30-45 degree in •MRI: better
•teres minor and even doing normal ADLs plane of scapula with internal rotation thumb
•subscapularis • “catching” or “grating/grinding” down, resist elevation: (+) pain Treatment:
•conservative tx 1st line
Risks: PE: •infraspinatous:“external rotate & lag” -rest, ice, PT, steroids
•repetitive motions *esp •ROM: active motion limited -maintain position of maximal rotation
overhead •atrophy of infraspinatus if chronic (+) is when lag or angular drop •surgery: arthroscopic, open,
•increase risk with age •cant raise the arm (only shrug) if large tendon transfer, shoulder
•tears due to direct injury •cant hold arm in elevated position •subscapularis: Gerbers test/Lift Off replacement
place their hand behind their back, with the
palm facing out  lift hand away

Labrum Tear •soft tissue that connect glenoid •grinding/catching Impinement Tests:
and humeral head •unstable sensation •Hawkins: anterior pain with int. rotation
•limited ROM •Neer test “like empty can but lift arm
•SLAP tear: superior labrum, above their head”
anterior and posterior •Drop arm: pain with slowly lowering arm
Olecranon •Olecranon Bursa is superficially •Swelling “goose egg” of the posterior •clinical Olecranon Bursitis:
Bursitis located on extensor side of elbow olecranon bursa •avoid further trauma-padding,
“student’s/bake •ROM limited depending on degree •aspiration *septic bursitis or gout
r elbow” Causes: •Possible small tender lump (recur) -WBC <500 (noninfectious) Septic: aspiration & ABX
•Trauma (fall) WBC >2000 (infectious) •Dicloxacillin, Clindamycin
•Inflammation (RA, Gout) Infection, red, tender, warm, painful
•Infection (Septic Bursitis) Admit: persistent or severe

Bicep Tendonitis: Tendonitis: •X-rays to r/o other pathology Tendonitis:

Tendinopathy/ •sports, overhead motion or •pain in anterior shoulder over bicipital •US may be more helpful •NO NSAIDs & streoids
Tendonitis v. lifting groove •MRI to r/o rotator cuff tears •ice, rest, tapping, PT/OT
Bicep Tedon •pain worse with shoulder flexion, •surgery if no improvement
Rupture Rupture: forearn supination, elbow flexion
•fall on outstretched hand Rupture:
•oversuse, heavy lifting, shoulder Rupture: sudden pain in upper arm / •Partial: nonsurgical
tears elbow  “pop” •Complete rupture: surgery
*involves proximal long head •trouble rotating arm palm down or up
• “Popeye” muscle

MSK About Clinical Manifestation Diagnostics Management

Lumbar • MC occur L4-5 or L5-S1
Herniated
Disk Causes: lift & twist *increases pressure
•Develop over time as weaker
posterolateral portion of annulus fibrosis
develops fissures that permit the
protrusion of other disk components
•radicular back pain (UNILATERAL)
•possible radiation down leg with
paresthesia or numbness along dermatome
•Exacerbated by sitting, walking,
standing, coughing, sneezing
Exam: (+) SLR, crossover, limited ROM
Xray: age-appropriate changes Acute: NSAIDs
-avoid prolonged standing,
MRI: CONFIRMS DX sitting, walking
sx > 4 weeks, significant neuro
deficit, or if planned surgery 2nd line: steroid injections
ALP: Surgery: laminectomy &
L4: anterior thigh, weak ankle discectomy if not resolved in 6wk
dorsiflex, decreased knee jerk
L5: lateral thigh, weak big toe
extension, normal reflexes
S1: posterior leg, weak plantar
flexion, decreased ankle jerk

Vertebral Mechanism: jumping/falling from height •localized back pain with focal midline x-ray: loss of vertebral height •surgery consults
Compression tenderness at fracture level •NSAIDS, bracing
Fracture Risks: elderly (osteoporosis), •surgery: kyloplasty *severe
“burst FX” malignancy, children playing
Cauda •Distal end of spinal cord terminates at
Equina the L1-L2 level and below that is a
Syndrome bundle of nerve roots  cauda equina
“Horses
Tail” •neuromuscular and urogenital sx
resulting from compression of multiple
nerve roots below conus medullairs
Causes:
•lumbar disc degeneration
•spinal trauma, herniated risk, neoplasms,
infection, spina bifida, iatrogenic
•Low back pain  Unilateral or bilateral •MRI: STUDY OF CHOICE •Neurologic emergency
sciatica •alternative: CT w/ myelography •Requires surgical
• “Saddle & perineal decompression within 12-24h
hypoesthesia/anesthesia”: decreased -imm. consult w/ surgery
sensation of butt, perineum, inner thigh Labs:
•Bowel and bladder dysfunction •CBC, glucose, BMP, BUN/Cr •NSAIDs and steroids
-urinary retention, bowel incontinence •ESR: elevated •Infection: ABX
-decreased anal sphincter tone •LP to r/o infection & •Neoplasms: Chemo/Radiation
•Reduced or absent LE reflexes inflammation
Physical Exam:
•localized low back TTP
•decreased sensory and motor function
•saddle anesthesia to pin prick, vibration
•DRE: poor anal sphincter tone

Lumbar •narrowing of the spinal canal with •back pain, numbness, paresthesia MRI: TEST OF CHOICE •pain control
Spinal impingement of the nerve roots •worse with extension: standing, walking •corticosteroid infection
Stenosis •relieved with flexion: sitting, leaning
Causes: degenerative, sponylolysis forward, walking uphill, cycling

Spinal Cord •external compression of the spinal cord •SUDDDEN focal neuro deficits •MRI EMERGENCY
Compression Cause: malignancy, infection •hyerreflexia below level •steroid & surgical decompression

MSK About Clinical Manifestation Diagnostics Management

Lumbosacral •strain or tear of paraspinal muscle •back pain and muscle spasms activity related •clinical •NSAIDs
Sprain or •does NOT radiate, NO neuro sx •resume activites if preffered
Strain •MCC of low back pain Exam: decreased ROM, tenderness over muscles •brief bed rest (2 days)

Spondylolysis •pars interaticularis defect due to
filaure of fusion or stress fracture
•MC at L5-S1
Mechanism: hyperextension
•asymptomatic Lateral x-ray: radiolucent defect •observation
•lowback pain with activity in the pars •PT, activity restriction
Oblique x-ray: “scotty dog”,
pars interarticularis break o

Spondylo- •forward slipping of vertebrae •asymptomatic x-ray: forward slipping of •PT, activity restriction
listehsis •bilateral fracture of pars interarticularis •low back pain, possible nerve compression vertebrae •severe needs surgery

Spinal •puss-filled collection *posterior MC TRIAD MRI with gadolinium: BEST •aspiration, drainage, ABX
Epidural •fever •ring enhancing lesion
Abscess Bug: S. aureus (MC), E. coli, Strep, TB •spinal pain: focal and severe ABX: Vanc + Ceftriaxone or
•neurologic deficits: radiculopathy, myelopathy Labs: Cefotaxime
Risks: old, IVDU, immunodeficiency, •high ESR and CRP
steroid, recent spine surgery, epidural •possibel high WBC
 About Causes Clinical Presentation/Diagnostics Complications/Treatment
Fibromyalgia •MC in women Chronic fatigue and aching 3+ months 11/18 trigger pointa needed for Multidisciplinary approach
•Absence of objective findings •involves entire body but bony diagnosis •patient education & CBT
and lab results prominences and around neck, shoulders,
low back, and hips ACR Criteria: Pharm:
Chronic disorder: •h/o chronic widespread pain 3+ mo •Amitriptyline, Fluoxetine, Duloxetine,
•Widespread pain, tenderness •Depression, sleep disorders, fatigue •exhibit 11/18 tender points Milnacipran, Chlorpromazine,
and stiffness of muscles, Cyclobenzaprine, Pregabalin, Gabapentin
associated with CT structures

Seronegative About Clinical Presentation Diagnostics Treatment

Reactive •“Reiter’s Syndrome”
Arthritis
*seronegative •Usually precipitated by a GI or
a GU infection (STD)
-GI: Shigella, Salmonella,
Yersinia, Campylobacter
-STD: Chlamydia, Ureaplasma
•MC in men
TRIAD: arthritis + ocular (conjunctivitis, uveitis) + Synovial fluid: negative, inflammatory NSAIDs – 1st line
genital (urethritis, balanitis, cervicitis) Methotrexate – 2nd line
X-ray: permanent or progressive joint TNF Inhibitors – 3rd line
•Asymmetric  MC in knees, ankles (weight-bearing) disease in the SI and peripherl joints
•Fever, weight loss Can treat STD at the time
and may reduce risks of
•Mucocutaneous lesions: balanitis, stomatitis developing
(inflammation of mucous membranes-mouth and lips)
•keratoderma blennorrhagicum: rash on palms/soles

•Associated with HLA-B27 •extra-articular: urethritis, conjunctivitis, uveitis,

mucocutaneous lesions

Disease About Clinical Presentation

Systemic •Inflammatory autoimmune disorder
Lupus characterized by autoantibodies to
Erythematosu nuclear antigens (ANA)
s (SLE)
•Strong familiar connection/genetic
component  mother/daughter
-Associated with HLA markers
•Suspect in patients having a
multisystem disease & a (+) ANA
Risks:
•young females *before menopause
•african ameriacns, Hispanic, native
americans
•sun exposure
•estrogen (OCPs)
TRIAD: joint pain + fever + malar
“butterfly” rash
General:
•fever, anorexia, malaise, wt loss
•raynaud phenomenon. (20%)
Skin/cutaneous:
•“butterfly” (malar) rash
•panniculitis (lupus profundus), fingertrip
lesions, periungual erythema, splinter
hemorrhages
•cutaneous LE lesions *sun exposed
•alopecia
Discoid Lesions:
•annular red scaly patches
•localized or widespread
•affects cheeks, nose, ears
Lupus profudunfs *face is MC area
•firm, deep nodules resulting in
dented scars (lipodystrophy) as fat
cells are destroyed
Ocular:
•conjunctivitis, photophobia,
transient or permanent monocular
blindness and blurring of vision
Lung:
•pleurisy, pleural effusion,
bronchopneumonia, pneumonitis
•restrictive lung disease
•alveolar hemorrhage
Cardiac
•pericardium  pericarditis
•HF from myocarditis and HTN
•arrhythmias
GI: mesenteric vasculitis

Neuro: CNS, psychosis, seizure

 •severe depression and psychosis
with steroids

Renal: glomerulonephritis,
interstitial nephritis

Diagnostics
• (+) ANA
• (+) antibodies to double-stranded
DNA and to Sm
•depressed complement C3 and C4
Drugs: “CHIMMP-Q”
•Hydralazine, Procainamide,
Isoniazid, Chloropromazine,
Methyldopa, Minoclycline, Quinidine
Diagnostics Criteria: Need 4/11
“SOAP BRAIN MD”
S-serositis
O-oral ulcers
A-arthritis
P-photosensitivity
B-blood disorders
R-renal involvement
A-antinuclear antibodies
I-immunologic phenomena
N-neurologic disorder
M-malar rash
D-discoid rash
Management
•Refer rheumatology
Skin: topical corticosteroids
Joint: NSAIDs and rest
Rash/joint: anti-malarial
(hydroxycholorquine)
*mainstay for treatment
Complications/flare-ups:
•Prednisone 40-60mg po daily
Resistance:
•Cyclophasphamide
•Mucophenolate mofetil
(CellCept)
•Azathioprine (Imuran)
•Belimumab (Benlysta)

Arthritis About Clinical Features Labs

Rheumatoid •Chronic, systemic Systemic: fever, fatigue, wt loss, anorexia Rheumatoid Nodules 20% •Anti-CCP antibodies & RF 70-80%
Arthritis inflammatory disease •occur over bony prominence •Anti-CCP MOST SPECIFIC
(RA) Joint Symptoms: •lungs, sclerae, other tissues •RF: can occur in other disease
•MC in women •Synovitis of multiple joints-BOGGY •correlate with RF in serum *best initial test
•peak 40-50yo F, 60-80 M •Symmetrical swelling of multiple joints •Elevated ESR & CRP
with tenderness and pain
Causes: genetics (HLA) *differentiates from OA Joint fluid analysis: CONFIRMATORY
-monoarticular disease of inflammatory nature of arthritis
Pathophysiology: -stiffness for >30min-1 hour in morning
•formation of hyperplastic Imaging: X-Ray
synovial tissue (pannus) •MC in PIP joints fingers, MCP joints, •radiographs may be normal in 1st 6mo
which erodes cartilage, wrists, knees, ankles, MTP joints Ocular •earliest changes in hands or feet
bone, ligaments, tendons •spared DIP •dryness of the eyes, mouth, and other •later changes of uniform (symettric)
mucous membranes joint space narrowing and erosions
Felty Syndrome: Complications:
RA + splenomegaly + - ulnar deviation Other Manifestations: Treatment: DMARDs + NSAIDS
neutropenia - swan neck deformity •ILD: cough & dyspnea •DMARDS: MTX, Leflunomide
- boutonniere deformity •pericarditis and pleural disease
Caplan Syndrome: •small vessel vasculitis Corticosteroids: Prednisone 5-10mg qd
RA + pneumoconiosis + *hemorrhage in nail fold or finger pulps •Low dose help with inflammation and
pulmonary nodules slow the rate of articular erosion

RA Pharm About Side Effects

DMARDs MOA: folate antagonist •teratogenic  pregnancy test, mandatory contraception
Methotrexate *GIVE FOLIC ACID SUPP. •pantocytopenia  ORDER CBC
Leflunomide •7.5mg PO once weekly •hepatotoxicity w/ fibrosis & cirrhosis (monitor CBC & LFTs q12wk)
Hydroxychlooquin •Max dose 20-25mg/week •lung: interstitial pneumonitis
e •MC: gastric irritation, stomatitis
1ST LINE
Sulfasalazaine •0.5g po BID, increase by 0.5g each week until symptoms improve, max 3g •neutropenia, thrombocytopenia, hemolysis with G6PD deficiency
2nd LINE
CI: ASA allergy
Monitor: CBC q2-4wk for 3 mo, then every 3 mo

TNF Inhibitors MOA: TNF (a pro-inflammatory cytokine) inhibitor •reactivation of tuberculosis, hepatitis B, hepatitis C
Entercept *added to Methotrexate *greater efficacy in combo
Infliximab CI: multiple sclerosis
Adalimumab Methotrexate + TNF Inhibitor
“-mab”

Arthritis About Clinical Manifestation Diagnostics Treatment

Gouty •Metabolic disease  abnormal
Arthritis amounts of urates in the body
*monoarticular
Triggers: purine-rich foods (alcohol,
liver, seafood, yeast)
Meds: thiazide and loop diuretics,
ACEI, Pyrazinamide, Ethambutol, ASA
Two types: *MC in men >30yo
1. Primary: heritable, affects genes that
regulate urate in the kidney
•Sudden onset and usually nocturnal
MC in MTP joint of big toe “podagra”
also common in feet, knee, ankle
•Pain intensifies  swollen joint, tender,
red, warm, possible fever
•Characteristic lesion=tophus: nodular
deposit of monosodium urate crystals
Labs:
•serial serum uric acid
•joint fluid analysis w/ aspiration:
*SENSITIVE
 sodium urate crystals;
needle-like and (-) birefringent
Imaging:
•Early: normal
•Late: “rat bite”-punched-out erosions
with overhanging rim of cortical bone
Acute Attack: *treat arthritis
-NSAIDS (Naproxen 500 or
Indomethacin 25-50mg)
-Colchicine
-Corticosteroids
Between Attacks:
*minimize urate deposition
•diet: avoid alcohol, foods with
high purine; drink lots of water
•avoid hyperuremic meds
• Allopurinol, Uloric 1st line

2. Secondary: acquired by
hyperuricemia *obese, alcohol, chemo

Pseudogout •calcium pyrophosphate deposition
(CPPD) in fibrocartilage and hyaline
cartilage  crystal-induced arthritis
Risks:
•hemochromotonosis
•hyperparathyroidism, hypomagnesium
•Acute, recurrent arthritis involving large
joints
*MC in knees and wrists. MCP joints
X-Ray: linear calcifications of the •Acute: NSAIDS
cartilage (chondrocalcinosis)
•Prophylaxis: Colchicine
Joint fluid: (+) birefringent
rhomboid-shaped crystals

Pharm Mechanism of Action/Indication Side Effects/CI/Dosing

Colchicine •Mechanism is unknown •GI effects: diarrhea, nausea, cramping, abdominal pain, vomiting
- possibly interferes with inflammasome complex present in
neutrophils and monocytes preventing activation of IL-1B •Dose: Load 1.2mg followed by dose of 0.6mg 1 hour later *only take three pills

Xanthine Oxidase •Lowers plasma uric acid level by blocking the final enzymatic steps •Allopurinol SE: hypersensitivity in first few months (rash  TEN)
Inhibitors in production of uric acid
Allopurinol, Uloric Goal uric acid: 6mg/dL •Allopurinol Dose: 100mg/d orally and titrated up every 2-5 weeks; max 800mg
Arthritis About
Osteoarthritis •MC joint disease
(OA) •MC in weight bearing joints
•Loss of articular cartilage and
hount degeneration
Risks:
•obesity *knees and hips
•participation in contact sports
•frequent bending & carrying
•increasing age
Pathogenesis:
degeneration of cartilage and
hypertrophy of bone in
articular margins
 altered mechanics
Clinical Features/Diagnostic Treatment
•Insidious onset, damage over years Labs:
•SX Pain  physical findings  loss of •does NOT cause elevated ESR
function • (+) gram stain and cx
•Pain with motion of joint •synovial fluid non-
•worse with activity or weight bearing; inflammatory:
Relieved with rest -yellow, transparent
•Reduced range of motion, crepitus -high viscosity
•NO systemic manifestation -WBC <2000, PMNs <25%
-no crystals
Exam:
•hard, bony joint, decreased ROM, crepitus Imaging: x-rays
•Bony enlargements of DIP (Heberden *STUDY OF CHOICE
nodes) and PIP (Bouchard nodes) -asymmetric joint narrow
-marginal osteophytes
-subchondral bone sclerosis
-bone cysts
Lifestyle:
•Regular exercise program
*walking, aerobics
•Weight loss
•assistive devices
Pharm:
•Acetaminophen 3-4g/day 1st LINE!
(2 extra strength tab 3-4x/day)
*caution  liver dx, heavy alcohol use
•NSAIDS: Voltaren gel (topical), Meloxicam
*caution with GI bleed and renal
insufficiency
Injections:
•Hyaluronic Acid: injections into the joint to
increase viscosity of synovial fluid
•Intraarticular corticosteroids
Surgery
•total hip and knee replacements
Osteoporosis About
Osteoporosis •Disease of low bone strength
•Inadequate bone mass & quality
*mineral and matrix
•Leads to microarchitecture
deterioration
-increased fragility
-increased risk of fracture
-deformity, pain, loss of
independence, premature death
Pathogenesis:
•Accelerated bone loss during the
perimenopausal period (mid-50s
to 60s in women and 70s in men)
Causes:
•Genetic & environmental factors
•Hormone deficiencies, nutrition,
decreased physical activity,
comorbidity, drug effects
Types
Primary
•usually due to increasing age ad
decreased gonadal function
•menopause; inadequate Ca, sedentary,
tobacco and alcohol
Type I: (Postmenopausal)
•MC in women
•estrogen & testosterone def.
•vertebral compression fracture or
fractures of the distal radius
Type II: (Senile)
•2x more in women, >70yo
•altered calcium metabolism and
intrinsic issues with bone forming
•hip pelvic fracture
Secondary
•results from CHRONIC condition
•MC in males & long-term steroids
•hyperthyroidism, hyperparathyroidism,
multiple myeloma, osteomalacia,
osteogeneis imperfecta
•Heparin, Phenytoin, Lithium,
Levothyroxine
Clinical Findings
• “Dowager hump” suggests multiple
vertebral fracture & decreased volume
•upper or mid-thoracic pain associated
with activity, aggravated by long sitting
or standing, relieved with rest
•spine compression-loss of vertebral ht
Bone Fractures:
•pathologic fracture, back pain, deformity
*VERTEBRAE MC
Physical Exam:
•lid lag: hyperthyroidism
•moon face, buffalo hump: cushings
•cachexia: cancer, eating disorder
•pelvic exams
•fx late findings: vertebrae, forearm,
femoral neck, proximal humerus
X-ray: radiolucency, cortical thinning,
occult fractures
Labs: *rule out or find secondary
•CBC, CMP, testosterone, proloactin,
PTH, calcium, vitamin D, urine
electrophoresis, TSH, T4
Diagnostics
DEXA-GOLD STANDARD
•ALL females >65 years old
•hyperparathyroidism, bone loss
disease, medication cause bone loss
•postmenopausal with 1+ risks
•osteopenia: T-score -1.0 to -2.5
•osteoporosis: T score <-2.5
•T score: compares to young
•Z score: compared to peers
Diet and Exercise:
•Maximize bone formation during
youth with proper diet and exercise
(peak reach 25-28yo)
•adequate calcium and D intake
•regular weight bearing exercise
•avoid tobacco & alcohol
Vitamin D: 800-1200/d
•enhances muscle function and
absorption of calcium
•higher is deficient (2000-4000)
•Vit D2 50,000 IU once weekly
Pharm: Bisphosphonates: 1st line

Medications MOA and Indications Names, Route, Dose CI, SE, Other
Estrogen •Adequate levels are the single most important Estradiol patch: 0.05mg/week topical •CI: hx breast cancer, estrogen-dependent neoplasia,
therapy Conjugated estrogens: 0.0625-1.25mg/d orally abnormal bleeding, thromboembolic

Calcitonin •Hormone directly inhibits osteoclastic bone Treatment until pain is controlled, then taper •Decreases further bone loss at vertebral and femoral
resorption *alternative for estrogen following resolution for 4-6 weeks sites in patients with osteoporosis
-provides analgesic effect Nasal: 200 IU/d instanasally
-good for ACUTE osteoporatic fracture Injectable: 50-100IU/d subcutaneous or IM •SE: nasal-congestion, rhinitis; inject-GI effects

Bisphosphanates •Anti-resportive agents
1ST LINE •Prevent bone loss associated with estrogen
deficiency, steroids, and immobilization
•Bind permanently to mineralized bone
surfaces and inhibit osteoclast activity
Alendronate (Fosamax) *1st line
-75mg po/wk; cheap & tolerated
Risedronate (Actonel)-35mg weekly, 150mg/mo
Ibandronate (Boniva)-2.5mg daily, 150mg/mo
$$$ Soledronic Acid (Reclast)-IV-5mg IV q12mo
•Foods and liquids can reduce absorption
-Give with water 30min before the first meal
-don’t lie down for 30min-less esophagus irritate
•SE: osteonecorisis of jaw
 SERM • Agonist-antagonist on estrogen receptor Ralocifen •SE: vaginitis and hot flashes
-agonist on bone
-antagonist on breast & endometrium •DC 72 h before surgery  thromboembolic
-inhibits trabecular and vertebral bone loss •Causes decreased LDL, no HDL effect
NEURO 6%
Disease Causes Clinical Findings
Vertigo False sense of motions Peripheral: BPPV: episodc vertigo, no hearing loss
•hortizontal nystagmus (beats AWAY from affected side)
2 types: •fatigable Menieres: episodic vertio, hearing loss
•peripheral: labyrinth or vestibular nerve •sudden onset of tinnitus and hearing loss can occur
-BPPV Vestibular neuritis: continueous vertigo, no hearing loss
-MEnieres Central
-Vestibular Neurotis •vertical nystagmus Labyrinthitis: continuous vertgo, hearing loss
-Labyrinthitis •nonfatigable (continuous)
-Cholesteatoma •gait issues
•positive CNS signs
•central : brainstem or cerebellar
-migraine, MS, tumor

NEURO
Parkinson’s •Uncommon under age 40, increase after
Disease age 60
•MC in men
•Reduced Risk: caffeine, coffee, ibuprofen,
statins, cigarette smoking, moderate alcohol
•Increased Risk: age, fhx,
herbicide/pesticide exposure
Pathophysiology:
Degeneration of the dopamine-producing
neurons in the pars compacta of the
substantia nigra and locus coeruleus in
brainstem Dopamine/Ach imbalance
•Lewy bodies within neurons
•resting tremor, rigidity, bradykinesia
Tremor
•resting tremor of distal muscles; “pill
roll”
•less with voluntary movement
•spreads unilaterally up the body
Rigidity
•unilat  spread up then contralateral
• “cogwheel” rigiditiy & lead pipe
Bradykinesia 80% of patients
•generalized slow movement
•starts distally: fingers  loss of arm
swing  feet and legs (shuffling)
Clinical features from hx
& PE
Must have bradykinesia
with either rigidity
and/or tremor
•Aim: blocking the effect of Ach or
administration of Levodopa
•1st line: Levodopa & Carbidopa
•Dopamine Agonist: <65 and mild sx
-Bromocriptine (Cycloset)
-Pramipexole (Mirapex)
-Ropinirole (Requip)
-Amantadine
•Anticholinergic-Benztropine
-young patient w/ tremor as primary sx
•COMT Inhibitors
-Talcapine, Entacapone
-extend life of Levodopa; adjunct tx

NEURO About Cardiac/Other Neuro Diagnostics and Treatment

Syncope Cardiac: carotid sinus,
aortic stenosis, HOCM
Neurologic: basilary artery,
subclavian steal syndrome
Other: orthostatic,
Carotid sinus: slow SA and AV node due
to pressure on carotids (turtleneck)
Aortic Stenosis: low CO due to stenosis
HOCM: murmur increases with valsalva
Basilary Artery: vertigo, visual
dysfunction, perioral numbness, ataxia
Subclavian Steal: Stenosis of subclavian
artery proximal to the vertebral artery 
sx with left arm exertion  angina, finger
ulceration
Diagnostics:
•Head CT: focal neuro, hx SAH
•Position of patient at time of syncope
-lying: seizure, cardiac arrhythmias
-standing: orthostatic, vasovagal
Orthostatic vital signs: SBP drop >20
 vasovagal Vasovagal: decrease in arterial pressure or SBP <90 or pulse increase >30bpm
and HR mediated by parsympathetic tone Orthostatic: rapid change from lying to
sitting or sitting to standing Treatment: varies on cause

NEURO About Clinical Presentation Diagnostics Treatment

Epidural •middle meningeal artery •LOC, HA, N/V, focal sx, CN III palsy •CT of brain: convex (lens) bleed •high ICP: Mannitol
Hematoma •MCC: temporal FX •LUCID INTERVAL  coma -does NOT cross suture lines

Subdural •cortical bridging veins •varies, may have focal neuro sx •CT of brain: concave (cresecent) •evacuate with massive 5mm+ midline
Hematoma •MC in elderly -DOES cross suture lines shift
•MCC: blunt trauma

Subarachnoi •berry (saccular) arterial •”thunderclap” sudden HA •CT of brain •supportive tx: bed rest, elevate head
d aneurysm of AVM •sudden, severe, worst HA of life •LP: CT (-)  xanthrochromia, high CSF •lower BP: IV Labetalol if SBP >160
Hemorrhage •MCC: rupture, AVM •meningeal symptoms, no focal neuro

Intracerebral •intraparenchymal •HA, N/V •CT: intraparenchymal bleed •supportive treatment: +/- Mannitol
Hemorrhage •MCC: HTN, AVM, trauma •DO NOT PERFORM LP (herniation) •gradual BP reduction

NEURO
Delerium •Acute alteration in LOC with change in •sleep-wake cycle disrupted-daytime •Goal: find underlying cause
cognition or perception somnolenece and agitation
“sundowining” at night Acute Agitation
•disturbance in attention (ability to direct, focus, •Haloperidol (Haldol)
sustain or shift attention) and awareness extrapyramidal & QT prolonging
(orientation), develops over hours to days •Lorazepam (Ativan)
*respiratory depression

Alzheimers •MCC form of dementia •short-term memory loss MRI: cortex atrophy TX: ACH inhibitors: Donepezil,
Dementia Risks: age, genetics, family history  long-term memory loss Rivastimine, Galantamine
•cognitive deficites Histology: •alternative: NMDA antagonist:
Pathophysiology: •amyloid-beta protein Memantine
•amyloid hypothesis: amyloid-beta protein deposition
deposition (senile plaques)
•tau hypothesis: meurofibrillary tangles
•cholinergic hypothesis: ACH deficiency 
memory, language, visuospatial loss

Vascular •disease due to ischemia & multiple infarction •SUDDEN decline in functions with a MRI: white matter •strict blood pressure control
Dementia stepwise progression lesions, infarcts
Risks: HTN, DM, CVA, atrial fib

FrontoTempora •localized brain degeneration of the frontotemporal •changes in social behavior, Histology: picks bodies:
l Dementia lobes personality, language round or oval aggreagate
(Picks Disease) •socialy inappropriate behavior of tau protein
•hyperorality (binge eat, change in food
prefernces)
Diffuse Lewy •progressive dementia characterized by the diffuse
Body Disease presence of lewy bodies
*parkinsons is localized, not diffuse
NEURO
CVA A sudden onset of neurologic deficit
resulting from a loss of blood flow
to a part of the brain
*cell death and irreparable damage
to brain tissue w/n 5min
Types:
Ischemia: thrombotic, emboli
*MCC is atrial fibrillation
Hemorrhagic: intracerebral (HTN),
subarachnoid (aneurysm, AVM)
Lacunar •small vessel disease of the
Infarction penetrating branches of the cerebral
arteries in the pons & basal ganglia
Risks: HTN, DM
Transient •transient episode of neurologic
Ischemic dysfunction caused by cerebral
Attack (TIA) acute infarction (blood supply
temporarily blocked  lack of O2
-embolic, thrombotic, or lacunar
-most resolve within 1-2 hours
*body immediately breaks it down
and so symptoms are short
•visual hallucinations
•parkinsonism
•autonomic dysfunction
•hemi/mono/quadriparesis
•hemisensory deficit
•visual loss; one or both eyes, diplopia
•dysarthria, facial droop, ataxia, vertigo
•aphasia (Brocas or Wernickes)
•decrease in LOC
Exam:
•ABCs and vitals
•Skin: petechial, janeway, osler, livedo
reticularis, purpura
•HEENT: trauma, funcoscope, mouth
•Cardio: rhythm, M/R/G, bruit
•Respiratory: breath sounds
•Neuro: CNs, NIHSS scale
0: no sx, 1-4: minor, 5-15: mod
16-20: mod-severe, 21+ severe
Pure Motor (MC): hemiparesis or
hemiplegia in absence of sensory/cortical
signs (aphasia, agnosia, apraxia)
Ataxic Hemiparesis: ipsilateral weakness
and clumsiness legs >arm
Sensory: numb face, arm, leg on onse side
•Assessing severity of symptoms (look for
persistent neurologic deficits)
•Neurologic deficits <24 hours
*most last a few minutes with complete
resolution in 1 hour
Cortical lewy bodies
•Oxygen Saturation
•Finger stick blood glucose
•CT brain w/o contrast
-GOAL: w/n 25min of arrival
Other Immediate Studies:
•CBC, BMP, PT/PTT, troponin
•EKG/cardiac monitoring
Additional Work-Up:
•CTA, MRA, MRI
•carotid duplpex •Echo
Additional Labs: *based on pt
•toxicology, blood alcohol, LP,
ABG, hCG, CXR, EEG, UA/Cx
Sensorimotor: weakness & numb
of face, arm, leg on onse side
Dysarthria “clumsy hand”:
dysarthria, facial weakness,
dyaphgia, clumsy hand
1. Order US of carotids (CAD)
2. EKG, Echo (emboli)
3. MRA/CTA (vessel disease)
ABCD2 Score: 3+ admitted
•Age 60+
•BP >140 or >90
•clinical SX
•duration: >10 min (+1), >60 (+2)
•diabetes
•Keep NPO  IVF
•elevate head 30 degrees, supine
•Hypoglycemia: dextrose
•Blood pressure: Labetolol
•Cerebral edema: Mannitol
•Seizure: Lorazepam
Ischemic: SBP < 185 + DBP < 110
•TPA (Altepase): maintain BP
<180/105 for 24 hours after
*within 3 HOURS
*do not treat BP if not elgible for TPA,
only if BP >220/120
•CI: BP >185/110, recent bleed,
bleeding disorder, recent trauma
•>3-4.5 hours: ASA
Intracerebral : lower BP w/n 1hr to 140
•ASA
•Control risk factors
Pharm:
•Plavix, ASA, Agrenox *antiplatelet
•Control BP, Statin
•TPA if neuro deficit potentially
disabling
Carotid •Most severe within 2cm of the •Symptoms due to reduced blood flow Imaging: Asymptomatic: antiplatelet agents
Artery bifurcation of the common carotid and/or superimposed thrombus formation 1. Carotid Duplex US Symptomatic: endarectomy or stenting
Stenosis artery 2. Order MRA or CTA to see true
Physical Exam: stenosis of the vessels Stenosis 60-99%: vascular surgery for
•HX of stroke-like sx or benign •carotid bruit or palpable sclerosis 3. Cerebral angiography carotid endarcectomy
*GOLD* but not used b/c invasive • <60 and >99 then do nothing

NEURO About Types Symptoms and Diagnostics Treatment

Seizure Episode of abnormal neurologic
Disorder function cause by inappropriate
electrical discharge of neurons
Seizure: One-time event
Disorder (Epilepsy): Multiple
•DX requires at least 2
“unprovoked” seizures
Non-Epileptic Seizure
•Triggered (“provoked”) by a
disorder, event, or other
condition within 7 days
Status Epilepticus:
•seizure activity for 5+ minutes
or 2+ seizures without
regaining consciousness
Refractory: persists despite IV
of 2 antiepileptics
Risk Factors:
•age (MC child, adults >60)
•brain infections, tumor, injury
•family history
•inadequate O2 supply to brain
•cerebral edema, dementia
•vascular disease
•prescription drugs
Type I: Focal (Partial) Seizures-ONE AREA
-simple: no LOC; discongitive: LOC
Type II: Generalized-ALL AREAS, no aura
1. Absence (Petit Mal) Seizures (CHILD!)
•staring  normal when seizure ends
2. Myoclonic Seizures *no LOC
•sudden brief jerks/twitches
(+) sx =contractions, (-) sx=relaxations
3. Atonic (Astatic) Seizure “Drop”
•slumping or nodding >1 second
4. Tonic: muscles (arms, legs, back) tighten
5. Clonic Seizures: convulsive movements 
rhythmic, jerking, muscle movements
6. Tonic-Clonic (Grand-Mal)
•LOC, shaking, body stiffening, bladder/bowel
1. PRE-ICTAL/Aura *simple
Frontal: wave sensation, smell
Parietal: numb or tingling, taste
Occipital: visual
Temporal: déjà vu, hearing
2. ICTAL *during seizure
3. POST-ICTAL: body relaxes
•Todd’s paralysis: transient focal
deficit after a simple or complex focal
zeisure
Diagnostics: HISTORY IMPORTANT
Labs:
•HX: glucose, drug levels, Hcg
•NO HX: “ + BMP, Mg, toxicology
•CT scan of head without contrast
•MRI *progressive or new in pt >20yo
•LP
EEG: *BEST TEST
•electrodes  sense & record activity
•prep: wash hair, no caffeine, take med
Emergency Room:
•turn on side, 2 IV large bore access
•Lorazepam x2 DOSES
•Diazepam, Midazolam
•2nd line: Fosphenytoin, Phenytoin
*phenytoin incompatible with benzos
AED Drugs: * after 2+ unprovoked
-Benzos, Barbituates, Clonazepam,
Gaba, Phenobarbital, Valproic Acid,
***Phenytoin, Carbamazepine
AED SE:
•drowsiness, dizziness, diplopia,
imbalance, N/V, teratogenic
•gingival hyperplasia (Phenytoin)
AED Monitoring:
•CBC, CMP, albumin, depression
Discontinuing AED:
•after at least 2-year seizure free
•slow rates of AED taper (6 months)

NEURO About Clinical Presentation Management

Bells Palsy •CN VII (Facial nerve) palsy •ipsilateral hyperacusis (ear pain)
•lower motor neuron disorder •hemifacial weakness and paralysis
*unable to life affected eyebrow, loss of nasolabial
Causes: idiopathic, HSV infection fold, drooping of corner of mouth
•taste disturbance (anterior 2/3)
Risks: DM, prego (3rd T), URI, dental nerve block ONLY AFFECTS THE FACE
•no treatment needed
•supportive: artificial tears
•Prednisone w/n 72 hours reduces time to recover
Severe: Acyclovir + Prednisone
NEURO
Tension HA Trigger: •Band-like/vise-like or tight in quality Clinical diagnosis •NO TRIPTANS
•STRESS •Pericranial tenderness, poor concentration •Analgesics (NSAIDs, Tylenol)
•depression •gradual onset •Ketoralac + Metoclopramide +
•anxiety •Bilateral, generalized, non-pulsatile Diphenhydramine IV
•NO FOCAL/NEURO COMPLAINTS
•relaxation

Cluster HA •activation of cells in ipsilateral •Minutes  hours, severe, unilateral, temporal •Typically occur at night & •100% O2 via non-rebreather
hypothalamus, triggering trigeminal HA in grouped attacks over a period of time awaken patient •Sumatriptan (Imitrex)
autonomic vascular system •recurring attacks daily and remitting x4 weeks •Dihydroergotamine (DHE)
*MC middle aged men (30-40yo) •average time between attacks is 6mo-2 years •Clinical Diagnosis -CI: HTN, IHD, PAD, prego

•Trigger: alcohol, vasodilators IPSITALERAL SYMPTOMS: Preventative:

•ptosis, miosis, lacrimation, conjunctival •lithium, verapamil, Topamax,
injection, rhinorrhea, congestion, horners Valprate, prednisone. Ergotamine

Migraine HA Neuronal dysfunction in the
trigeminal system vasoactive
neuropeptides such as calcitonin gene-
related peptide leading to neurogenic
inflammation, sensitization, and HA
•3x more common in women
•90% have a family history
•MC type is WITHOUT an aura
Triggers:
stress, menstruation, visual stimuli,
weather, nitrates, fasting, wine, sleep
disturbances, aspartame
Classic migraine attack typically has 4 phases: Criteria without aura:
1. Prodrome (24-48h prior to HA) A. 5 attacks + B-D
•euphoria, depression, irritability, cravings, B. HA last 4-72h
constipation, stiffness, and yawning C. has 2/4 following:
-unilateral
2. Aura (75% don’t have) -pulsating
•attributed to cortical spreading depression -moderate or severe
•transient neurologic sx -aggravated by activity
*MC visual; sensory, verbal, motor D. 1+ of following:
-nausea, vomiting, or both
3. Headache -photophobia or phonophobia
•unilateral, throbbing, or pulsatile
•anorexia, N/V, photophobia, phophobia, Imaging:
cognitive treatment, cutaneous allodynia (touch •CT of the head if abnormal
hurts), blurry vision, hyperalgesia, blurry vision neuro exam, severe HA of
sudden onset,
4. Postdrome-drained, exhausted, euphoria immunocompromised
•NSAIDS (FIRST!)
•Triptans (FIRST LINE)
-CI: prego, CAD, no control HTN
•Ergotamines
•Antiemetics (Zofran!)
ER:
•ketoralac 30mg + Metoclopramide
10mg + Diphenhydramine 25mg IV
*sx treatment: rest in quiet, dark
room until sx subside, cold cloth
Prophylaxis indication:
•Topiramate, valproic acid
•Propranolol (BB), CCB, TCA
Intracranial Syndrome of increased ICP w/o a •Fever, Night sweats DX: MRI •Repetitive LPs/CSF volume
Tumor space occupying lesion •throbbing headache *worse with straining removal until target pressure of 10-
“Pseudotumo •excessive CSF, defective absorption, •transient visual obstructions Lumbar puncture 20cm H2)  1ml CSF lowers
r Cerebri” venous sinus pressure •photopsia  flashing lights •high opening pressure >250 pressure by 1cm H2O
•Immunocompromised/ malignancy hx •CSF is normal
•HA that are typically worse w/ Combo: Oral acetazolamide,
awakening or lying down Exam: papilledema, visual field, CN VI palsy, Furosemide, Steroid, Topiramate
•May awaken person at night high ICP
•New onset HA age >40 New dx: admission
Previous dx: discuss with neuro
Risks:
•obese women of childbearing age
•vitamin A toxicity

Disease Mechanism of Action Drugs CI/BBW Caution Education

Triptans •Agonistics effect on serotonin of
meningeal arteries (5-HT1B) and
trigeminal nerve (5-HT1D)
•inhibit proinflammatory
neuropeptide release
•Sumatriptan (Imirex) *ER
-SC, onset 10-15minutes
•Zolmitriptan (Zomig)
-nasal spray *pt for home
•Treximet (Imitrex+Naproxen)
*tablet
Rest are oral; end in “-triptan”
CI:
•CAD, PVD, IHD
•stroke or risks (HTN, DM,
HLD, TIA, obese)
•prinzmetal angina
•ergot compound meds
•medications for HTN
•SSRIs or SNRIs
•don’t use within 72h of
Ketoconazole
Pregnancy Cat C
•may breastfeed 12h after
dose, but discard milk
within the 12h span
•pain at site & tingling 30min
•don’t use if MOA w/n 14d
•wait 2 hours after taking one
before taking another
•will only tx HA once it has
begun (not prophylaxis)
•do not use <18yo or >65yo
•may impair think/reactions
*driving caution

Ergotamine •Agonist, binding to several
different receptors, producing
*cant give peripheral vasoconstriction and
right away decreased blood flow
•However, may be a vasodilator
in large amounts
•Similar to Epi & serotonin
Preventative •Alteration of central
neurotransmission
*continue for months if helps
•Cafergot (Ergotamine w/
caffeine)
•Migergot with caffeine
•Dihydroergotamine (DHE)
•botox
•acupuncture
BBW: peripheral ischemia
with CYP3A4 inhibitors and
marcolides
CI: PVD, CAD, HTN, renal
impairment, hepatic, sepsis,
pregnancy (cat X),
breastfeeding
•Topiramate (Toapamx)
•Valproic Acid (Depakote)
•Propranaol
•Elderly
•Cardiac disease risk
•Valvular heart disease
•CCB
•Candesartion
•Guanfacine (Intuniv)
SE:
HTN, coronary vasospasms,
peripheral ischemia,
dependency, HA exacerbatib,
valvulopathy, N/V, abd pain, leg
weaknes, myalgia, numbness, int
claudication, photosensitivity
•TCA (Amitriptyline)
•Venlafaxine *EVIL!
•Riboflavin

NEURO
Essential •MC adult onset movement disorder •Rapid action/kinetic tremor bilaterally Clinical Diagnosis •1st line-Propranolol (
Tremor •autosomal dominant -trouble writing, eating, fine motor skills
•Primidone + Propranolol if no response
Defined by: •tremor worse w/ intentional movement *refer if 1st line options don’t work
•enhanced by emotional stress •NO tremor at rest
•decreased with ETOH •2nd-Alprazolam, Topiramate, Gabapentin
•fhx common (dominant) •3rd line-Deep brain stimulation, botox
•no other abnormal findings

NEURO About Clinical Presentation Diagnostics Management

 Concussion •mild TBI  AMS
•may result after blunt force or
acceleration/deceleration injury
Anterior Cebebral Artery:
•Contralatl arm/leg weak (LE >UE) & sensory, contralat homonymous heminaopsia
•Urinary incontinence, personality changes
Posterior Cebebral Artery: (Vs)
•Vomiting, visual changes, vertigo
DERM 5%-dyshydrosis, karposi sarcoma, paronychia, pilonidal disaese
DERM About
Hidradenitis •suppurative disease of the
Suppurativa apocrine gland bearing skin areas
sites: axillae, inguinocrural and
anogenital regions; scalp (rarely)
Risks: obese, females, smoking
•history of acne
•family history
•mechanical frition
Epidermal •encapsulared subepidermal
(Pilar, nodules filled with fibrous and
Sebaceous) keratinous tissue/material
Cyst
Lipoma •benign collection of adipocytes
inside thin fibrous capsule
•MC soft tissue tumor
MC location: trunk, UE
Acanthosis •Common benign disorder of the
Nigricans skin characterized by velvety
hyperpigmented plaques
•typically located in flexural and
intertriginous regions
•Stimulation of insulin-like
growth factor receptors and
tyrosine kinase
•headache, dizziness, brief amnesia CT of Head W/O Contrast: •cognitive and physical rest
•confusion: blank expression, blunted affect •study of choice •resume strenuous activity when
•delayed responses & emotional changes resolution of symptoms & memory
MRI: sx lasting >7-14d recovery
Increased ICP: vomit, HA, increasing
disorientation, changing LOC
•Contralateral motor and sensory, ipsilater CN deficits
Middle Cerebral (MC!): MCA is Most Common Artery
•Contralateral sensory and motor (face and arm > LE)
•Gaze preference toward side of leasion
•Left hemisphere: Aphasia (brocas-expressive, wernickers-sensory), math, agraphia
•Right hemisphere: neglect of other side, flat affect, impaire judegement and impulsivity
Clinical Presentation Diagnosis Treatment
•deep, inflammatory nodules •clinical diagnosis •dietary changes, smoking cessation, local skin
•draining tracts, open comedones care, eliminate irritatints, reduce skin friction
•fibrotic hypertrophic scars Complications
•sinus tracts lead to dermal contractures •secondary infections Mild: topical Clindamycin +/- intralesional
and ropelike elevation of the skin •fistulas Triamcinolone
•inflammatory reactions
Systemic: Tetracycline, Clindamycin +
Rifampin
Deep, recurrent: punch debridement
Painful abscess: I&D
•skin colored freely mobile, compressible •clinical •complete surgical excision of cyst wall intact
cyst or nodule-visible central punctum
•possibel foul, smelling yellowish cheese- histology: stratified squamous
like discharge epithelium
•soft, painless, slow growth, easily mobile •Not painful: leave alone
•subcutaneous nodules
•1-10 cm in size •Painful/growing: remove
Types •Symmetric, dark brown Lifestyle:
•Obesity hyperpigmented plaques with •dietary changes, control blood sugar
*MC with DM, insulin resistance, BMI a velvety, verrucous
metabolic syndrome, PCOS •topical retinoids and/or vitamin D analods
•Typical in neck folds and •refer to GI for endoscopy if cancer
•Malignancy: gastric carcinoma axilla
•Drug Induce: Niacin Diagnostics:
•Skin biopsy diagnostic
Syndromic: Type A and Type B *rarely needed

•MC in African Americans
•A: hyperandrogenism, insulin resistant, •A1C or fasting insulin and
acanthosis, acromegaly glucose
•B: autoimmune (lupus) & DM •plasms T and
dehydroepiandrosterone sulfate
test in women with signs of
hyperandrogensim  r/o
PCOS

DERM About Clinical Presentation Diagnostics Treatment

Pemphigus •Autoimmune disorder of mucous
Vulgaris membrances and skin
•type II hypersensitivity reaction  IgG
against desmoglein (component of
desmosome)  acantholysis (separation)
Risks:
•patients 30-40yo, middle eastern
•meds: Penicillamine, Captopril,
Cephalopsorins, Phenobarbital
MC areas:
•scalp, face, chest, axillae, groin, umbilicus
1. painful erosion/ulceration of
mucous membrane (intraoral)
2. painful, flaccid skin bullae
*easily rupture & bleed
•spares palms and soles
Exam:
•(+) Nikolsky: superficial
detachment of skin under
pressure/trauma
Skin Biopsy:
•intraepithelial splitting with
acantholysis
Direct Immunofluorescence:
•IgG throughout epidermis
•basal keratinocytes
ELISA: anti-desmoglein or
anti-epithelial autoantibodies
•Prednisone 2-3mg/kg + local wound care
*continue steroids until cessation of new blister
formation and disappearance of (+) Nikolsky
Wound Care: wet compression, routine bathing,
anticipate infection
•Concomitant Immunosuppresive
-1st line: Azathioprine or MEthotrexate
Complications: fluid, electrolytes, secondary
bacterial, osteoporosis

Bullous •MC bullous autoimmune disease
Pemphigoi •Interaction of autoantibody with BP
d antigen  BPAG1 and BPAG2
•Type II reaction: IgG autoantibodies
against hemidesmosome and basement
membrane  subepidermal blistering
Risks: elderly
Prodrome: pruritis, urticaria
Classic cutaneous lesion
•large, tense, firm-top bullae
•serous or hemorrhagic fluid
•painful erosions after rupture
Exam: (-) nikolsky
BIOPSY (Gold Standard) Mild (<20% BSA): Topical Steroids (high)
•linear IgG and C3 along
dermal-epidermal junction Severe: systemic steroids (Prednisone)
•subepidermal blister and
eosinophilia •may couple with Azathipoprine 150mg/day
*same complications as pemphigus vulagris
ELISA: BPAg 180 & 230
*highly sensitive & specific

•MC sites: axilla, medial thigh, groin,

abdomen, ventral forearm, lower legs

About/Causes Clinical Presentation Types/DDX/DX Treatment

Lichen •Acute or chronic •6 PS: purple, polygonal, planar, pruritic, Primarily clinical diagnosis •topical steroids under occlusion
Planus inflammatory dermatosis papules, plaques with fine scales -Triamcinolone
involving skin and or mucous DX: punch biopsy & immunofluorescence (cotton gloves, cotton socks, wraps)
membranes •Papules, flat top-polygonal, oval, annular •saw-tooth lymphocyte infiltrate at the
•white lines (Whickham striae) dermal epidermal junction 2nd line: intralesions steroids, topical
Causes •dark phototype: hyperpigmented tretinoin, UV lihgght
 •idiopathic MC
*cell mediated Location: volar wrists, lumbar region, shins, Mouth: Cyclosporine & Tacrolimus
•drugs scalp, glans penis, mouth solution mouthwash
•metals (gold and mercury)
•infection (hepatitis C) Koebners phenomenon:
•new lesions at site of trauma

Lichen Skin thickening in patients •repetitive rub & scratching “itch-scratch” clinical •Avoid scratching
Simplex with atopic dermatitis •scaly, well-demarcated, rough •topical corticosteroids
Chronicus hyperkeratitic plaques with exaggerated (Triamcinolone)
skin lines

About Clinical Presentation Diagnostics Treatment

Seborrheic •MC benign tumor
Keratosis •MC on chest abd back
Risks: genetics, age, fair skin,
sun exposed
Pathophysioloy: benign
proliferation of keratinocytes
•MC associated malignancy is
adenocarcinoma of GI tract
•“stuck-on” appearing papules and
plaques with well-defined borders
•well-demarcated
•velvety, warty lesions “postage stamp”
•skin-colored, pink, light brown, yellow-
brown, and brownish-black to black
lichenoid keratosis: inflamed SK  pink
shiny papule or plaque, appears like BCC
Dermatosis papulosa nigra: papular SK
(dark brown 1-3 mm papules) on the face of
individuals with darker skin phototypes
Usually a clinical diagnosis •No treatment needed
•best appreciated with side-lighting •Can treat for cosmetic or
symptoms
Dermatoscope:
•ridges, fissures with comedone like •Cryosurgery 1st line
openings  cerefriform pattern *may cause dyspigmentation
•looped, hairpin vessels •Curettage & cautery
•Chemical peels
Biopsy: well-demarcated proliferation of •Laser therapy
keratinocytes with small keratin-filled cysts
•Multiple eruptive SKs with a
visceral cancer is sign of Leser-
Trélat

Actinic •Neoplastic condition of
Keratosis precancerous epithelial lesions
on sun-exposed areas
“Solar
Keratosis” •MC pre-malignant skin
condition *can lead to SCC
MC Areas:
•ears (face), scalp, eyelid, neck,
upper chest, forearm, hand, shins
•dry, rough macules or papules
•“sandpaper” rough feel (feel before see)
•transparent, yellow scaling
•Easily palpated “gritty” scales
Pigmented:
similar to nonpigmented AK with the
addition of moth-eaten or sharp borders
and gray dots/granules
Actinic cheilitis: lower lip
*white scaly flat papules or confluent plaque
DDX: SCC (lips and ears MC) •Avoid sun exposure
•SPF 30+ when in sun
CLINICAL DIAGNOSIS
Treatment:
Punch/shave biopsy: atypical epidermal Lesion-Targeted
keratinocytes, hyperchromatic pleomorphic •cryosurgery liquid nitrogen
nuclei from basal layer •curettage and electrosurgery
•shave excision/biopsy
•biopsy if: >1cm, indurated, ulcerated, rapid
growth, fail to respond to therapy Field Therapies *multiple
•5-FU 0.5% cream BID x3-4wk
Dermoscopy: White-yellow surface scale, •Imiquimob cream 5%
erythema revealing a pseudo-network around
hair follicles, linear-wavy vessels

About Clinical Presentation Diagnostic Treatment

Common •benign overgrowth of skin cells •asymptomatic without •dermatoscopy •none if diagnosis is confirmed
Melanocytic change -will not appreciate
Nevi Types: •symmetric neoplastic changes Indications for excision:
•congenital (CMN): develop defect in melanoblasts •sharp borders •locations: scalp, anogenital, mucosa
  increased risk of melanoma development if large •uniform color •rapid change
•irregular borders
•Acquired (MN): develops early in childhood •erosions
 often regresses by age 6 •persistent itching, pain, bleeding
Dysplastic •pigmented lesion from proliferation of atypical •asympatomatic •clinical diagnosis & •observe with dermoscopy +/- digital
Melanocytic melanocytes •irregular shape confirmed w/ histopathology
Nevi (DN) •MC onset in late childhood-early adulthood •sharp and ill-defined •surgical excision w/ biopsy-r/o melanoma
•precursor to superficial spreading melanoma (SSM) bordered Education: -indications: changing, cant observe
-one lesions increase risk by 2x •varigated color •monthly self-exams
-10+ lesions increase risk by 12x •maculopapular •sun protection •routine exams q3-12mo
•family member skin checks -3 if fhx of DN or melanoma, 6-12 if
sporadic DN

About Clinical Presentation Diagnostic Treatment

SCC •Malignancy of cutaneous
epithelial cells
(keratinocytes) on sun-
exposed areas
•Greater risk of mets on the lip
and oral mucosa
MC Areas & people:
•face and dorsal hands
•MC skin cancer in AA
Risks:
•sun exposure, fair skin
•fhx skin cancer, increased age
•scarring processes
•radiation, immunosuppression
•HPV, tattoos, piercing, burn
Differentiated:
•Hard, firm papule, plaque, nodule with a
thick adherent keratotic scale
•Erythematous, yellow, skin colored
•LAN with mets
Undifferentiated: *large, irregular border
•soft, fleshy, erosive papule/nodule
•papillomatous, cauliflower, bleeds easy
•found on less sun exposed areas
Squamous in situ (SCCIS): BOWENS
•confined to epidermis
•more frequent & aggressive in
immunosuppres
•organ transplant and HIV/AIDS
Tumor Subtypes:
•bowen diseae (SCCIS)
•acantholytic, adenoid, psuedoglandular
•well v poorly differentiated
Biopsy BEST TEST
•atypical keratinocytes & malignant cells,
pleomorphic and hyperchromatic SCC
with variable nuclear size
•loss of full-thick epidermal maturation
•excision w/ margins (3-5mm) & Mohs
*TREATMENT OF CHOICE
-6mm margin in high risk
Non-surgical Candidates
Superficial: electrodessication, curettage
(x3) with margins of 3-4mm, radiation
Others: Imuquimob, 5-FU, IF-alpha,
electrochemotherapy, Intralesional
-CAN NOT USE PICATO

Kaposi •vascular cancer •macular, popular, nodular plaque-like Biopsy: angiogenesis, inflammation and •HAART therapy
Sarcoma •associated with HHV-8 brown, pink, red, or violaceous lesions proliferation (whorls of spindle-shaped
cells with leukocytic infiltration) •chemotherapy, radiation
Risks: immunosuppressed

About Types Clinical Presentation Diagnostics and Treatment

Melanoma •aggressive malignancy of Superficial spreading melanoma (MC) Classifications: 3 ways:
melanocytes •asymmetric macule with variegated •de novo melanoma (70%): new •Clark
•MC cancer in young women pigmentation & notched/ragged borders pigmented papule, plaque or nodule •TNM (tumor, node mets)
between 25-29yo •MC trunk in men and LE in women •precursor melanoma (30%): develop •Breslow (>0.76mm)
from precursor (DN or CMN)
Sites:skin, mucous, nail, eye Nodular melanoma (2nd MC) Clark level
RAPID GROWTH 2 phases of growth: •Level I: in situ (within the epidermis)
Associations: •dark brown to bluish-black nodule •radial (thin): remains in epidermis •Level II: invades the papillary dermis
•genetics •ulcerate or bleed •vertical: extends to dermis/vessels •Level III: reaches reticular dermis
•exposure to UVA/UVB in •MC on trunk, head, and neck •Level IV: invades the reticular dermis
light skin types ABCDS: •Level V: invades the subcutaneous fat

Risk Factors:
•age, light skin, fhx, UV
• > 25 nevi, atypical nevi
•immunosuppression
MC Sites of Mets
•skin/subcutaneous
•lymph, lung, liver, brain
Lentigo maligna melanoma
SLOW GROWTH
•asymmetric brown/black macule or patch
with color variegation & irregular borders
•dermal induration or nodularity
Acral lentiginous melanoma
SLOW GROWTH
•Asymmetric brown/black macule with
variegated pigment and irregular borders
•MC on palms, soles, or nail apparatus
•asymmetric
•borders irregular Treatment:
•change in color Surgical excision (treatment of choice)
•diameter large (>6mm) •In situ: margins at least 0.5cm
•evolution •tumor <1mm: margins of 1cm
•tumor 1-2mm: margins 1-2cm
Best test: •tumor 2+: margins 2cm
•full-thickness wide excisional biopsy
•shave biopsy discouraged Skin Exams:
•age 18+ should have yearly skin exams
•BCC and SCC: skin exam every 6 mo
•melanoma: skin exam every 3 months

About Clinical Presentation Diagnostics Treatment

Basal Cell •MC SKIN CANCER Nodular (MC!) Superficial Multicentric •Good prognosis w/ tx
Carcinoma •neoplasm of basal keratinocytes •translucent “pearly” papule/nodule *can rub alcohol pad over it •likely recurrence in 5 years
•well defined borders (rolled-edge) •thin plaque/patch, pink/red
(BCC) MC locations: •smooth, firm, telangiectasias •+/- scaling Education:
•head and neck •Avoid sun exposure
•upper chest and back •Followed by dermatology
•upper extremities •watch for suspicious lesion
•SPF30+
Risks: •protective clothing
•light skin phototype Ulcerating
•sun exposure •translucent-pearly, smooth, firm, Pigmented Treatment:
•radiation telangiectasia with a central ulcer •firm papule/nodule +/- umbilications •MOHS SURGERY
•advanced age •+/- elevated border (rodent ulcer) •smooth pearly surface •electrodisection
•immunosuppression •generally pigmented or stippled globules •surgical excision
•personal hx •Vismodegib (Erivedge) or
Sonidegib (Odomzo)
Hereditary conditions associated: MOA: hedgehog pathway inhibitors
•albinism Dose: once daily
•xeroderma pigmentosum Sclerosing
•nevoid basal cell carcinoma •plaque, scar like lesion
•rasmussen syndrome •pink/white in color, telangiectasia
•rombo syndrome •ill-defined borders Diagnosis:
•bazex-dupre-christol syndrome
•punch or shave biopsy
•darier disease
•nests and cords of basaloid keratinocytes
with peripheral palisading and a central
arrangement

DERM About Clinical Presentation Risks/Diagnostics Diagnostics/Management

Impetigo •highly contagious, superficial
vesiculopustular skin infection
•MC in children
Risks: poor hygiene, poverty,
Bullous: *exfoliative toxin A (-) nikolsky •warm water soaks 15-20min then •topical
•vesicles  large bullae with rupture Bactroban TID x10d
•”varnish-like crusts” DX: gram stain & cx
•fever, diarrhea Widespread infection:
Complications: •Cephalexin, Dicloxacillin, Erythromycin
 crowding, warm/humid weather,
skin trauma
Bugs: S. aureus, GABHS
Molluscum Molluscipoxviru (Poxviridae)
Contagiosum •Benign viral infections
•Skin-skin: bathing, sexual
•HIGHLY contagious
•MC in young children
DERM About
Atopic •Defetive skin barrier susceptible to
Dermatitis drying  rash, pruritis, inflammation
(Eczema) •Impaired barrier function leads to
increased water loss and infection
•IgE mediated
•MC in persons with darker skin
ATOPIC TRIAD: atopic dermatitis,
allergic rhinitis, asthma
Locations: face, scalp, torso, popliteal
folds, antecubital
•MC in FLEXOR creases
Environmental triggers: heat, humidity,
detergent, soaps, abrasive clothing,
chemicals, smoke, stress
Acute •Recurrent pruritis vesicular rash
Palmoplantar affecting the palms and/or soles
(Dyshidrotic)
Eczema Triggers: sweat, stress, warmth, metals
Contact •Inflammation of the dermis and
Dermatitis epidermis from direct contact w/ irritant
or allergy
Irritant: MC form  ONE exposure
•chemical, alcohols, creams
•diapers
Allergic: delayed type IV; 24-48h
•nickle MCC
•poison ivy, oak, sumac
Non-bullous: MOST COMMON FORM
•papules, pustules, vesicles with weeping
 “honey colored, gold crust”
•usually at site of superficial skin trauma
•scattered, discrete lesions  satellite
•Small, smooth, dome shaped papule with
umbilicated center
•Pink/pearly/flesh color
•Grouped or linear
•Palms and soles are spared
Clinical Manifestation
•HALLMARK: pruritis
•scaly erythematous, ill-
defined blisters, papules,
pustules
•”itch that rashes”
•lichenification in chronic
Nummular:
•Round or coin-shaped
erythematous scaly plaques
•sharply defined
•Minute fissures, round
erosions, crusts located within
•Papules/vesicles  plaques
Location: dorsum of hands,
feet, extensors (elbow, knees)
•puriritic “tapioca-like” small
tense vesicles
•palms, soles, fingers
•desquamation later
Acute: erythema, vesicles,
bullae
•prutitis, stinging, burning
Chronic: scaling,
lichenification, fissures, cracks
Toxicodendron:
•caused by poison ivy /oak
•cellulitis
•acute Prevent: BPO wash, check family members,
glomerulonephritis ethanol or Isopropyl gel for hands
Histology: •Self-limiting  NO TREATMENT
•Henderson-Paterson *6mo-2 years! DON’T PICK
bodies (keratinocytes
with eosinophilic •cryotherapy/curettage (cause scarring),
inclusion bodies) •Podofilox 0.5%
•salicylic acid (compound W)
Diagnostics Diagnostics and Management
•not necessary, clinical dx •avoid triggers: hot water, stress, infection,
irritants, sweating, env alelrgies
•can do IgE
•Skin biopsy can help & culture 1st line: topical corticosteroids
•Triamcinolone (medium potency)
•Desonide (low potency-FACE)
•SE: atrophy, hypopigmentation, striae
•alternative: Tacrolimus, Pimecrolimus
*no atrophy
Itching: antihistamines
•Benadryl, Hydroxazine, Allegra, Zyrtec
Cleansers/Emollients: twice daily
•CeraVe, Cetaphil, Vanicream
•clinical diagnosis •Topical corticosteroid ointments:
Triamcinolone (medium potency)
•cold compress, burrows solution
•clinical diagnosis •identification and avoidance of irritants
•patch testing *allergy referral
1st line: topical corticocteroids
*oral if severe or extensive reactions
Review medications: OTX, RX, homeopathic,
hot water, humidifier, Antihistamine
(Hydroxyzine or Benadryl), animals
 •detergents, cleaners, acids, water

Perioral •MC in young women •erythematous grouped •eliminate topical corticosteroids and irritations
Dermatitis papulopustules
Risks: •spares vermillion border Topical: Pimecrolimus, Metronidazole,
•history topical corticosteoirds Erythromycin
•fluoride toothpaste

About Clinical Presentation Treatment

Psoriasis •immune-mediated
multisystemic disease
•inflammatory disorder causing
hyperproliferation of
keratinocytes in the epidermis
Pathophysiology:
•keratin hyperplasia &
proliferating cells in the stratum
basale & stratum spinosum
•T-cell proliferation of the
epidermis  over production of
epidermal cells & turnover
Risks:
•MC 20-30yo, 50-60yo
•Usually family history &
stressor
Progression:
1. Normal
2. psoriatic skin without active lesion
•slight dilation, increase mast cell; thick
3. developing lesion
•capillary dilation, mast cells, T-cells,
macrophage; increased thickness
4. fully developed lesion
Chronic/Plaque (MC): raised, well-
demarcated, pink-red plaques or papules
with thick silvery white scales
*MC on extensor surfaces
Auspitz sign: punctate bleeding with
removal of plaque or scale
Koebner’s phenomenon: new isomorphic
lesions at the sites of trauma
Nail involvement: pitting nails, yellow-brown
under nail (oil spot-pathognomic)
Pustular Psoraisis
•increase in PMN leukocytes
•caused by corticosteroid withdrawal
•erythematous patches or thin plaques
 studded with numerous pinhead-
sized sterile pustules
Generalized “von zumbusch”
•pusutles coalesce into “lakes” of pus
• (+) Nikolsky sign in generalized
•life threatening
•relapses & remission occur over yrs
Eruptive/Guttate
•lots of salmon-pink small teardrop
papules with fine scales
•spontaneous remission
•follows strep pharyngitis
•most often evolves into chronic
Inverse:
•erytheamtosu (lacks scale)
Mild-Moderate:
•topical corticosteroid (Clobetasol)
•Vitamin D analogs (Calcipotriene)
-apply ointment to wet skin, cover with
plastic wrap and leave overnight
-re-apply steroid to lesion in AM and
leave uncovered
Moderate/Severe
•phototherapy, UVB, PUVA
Severe:
•systemic: Cyclosporine, Retinoids,
biologics, MTX
Scalp: Tar shampoo  steroid lotion
Palmoplantar Pustolosis: PUVA soak
Inverse/Genital: short topical steroid
Nails: PUVA, oral retinoid, MTX or
cyclosporine

Vitamin D MOA Indication and Application SE/CI Vehicle

Calcipotreine •binds to vitamin D receptors and Indication: psoriasis SE: burn, itching, irritation, •solution, ointment
(Dovonex, regulated cell growth photosensitive, high Ca+ cream, foam
Calcitrene) -inhibits proliferation of keratinocytes Directions: thin layer to rea BID  avoid apply to •Solution best for
-inhibits proinflammatory cytokines <40% body surface area-max 100g/wk CI: hypersensitivity scalp
0.005%
Calcitriol •binds to vitamin D receptors and
regulates cell growth
0.0003% -inhibits proliferation of keratinocytes
ointment -inhibits proinflammatory cytokines
DERM Risks
Adverse Drug •medication induced changes in
Reactions the skin and mucous membrances
•most are self-limited
About
Exanthematou MC drug reaction; Type IV
s Drug
Eruption •5-14 days after drug initiation
•1-2 days if previously sensitized
Causes: Penicillin, Bactrim,
NSAIDs, Allopurinol
Angioedema •self-limited, locazlied
subcutaneous swelling resulting
from extravasation of fluid
Types:
•mast-cell: allergic
•bradykinin: ACEI, hereditary
Fixed Drug Eruption
Other Types •Solitary erythematous
patch/plaque that will recur at
same site if re-exposure
Lesion:
•sharply marginated macule
•erythema; dusky-red color
•edematous & bullous  erode
Indication: psoriasis
Directions: apply thin layer to affected area BID
20g/wk max
Risks
•foods
•animal/insect bites
•drugs
•environmental
•exercise induced
•infections
Presentation
•morbilloform or maculopapular
•macules/papules after drug
inititation
•bright red macules and
papules  plaques
Mast cell: other allergic sx
•urticaria, flushing, pruritis
•bronchospams, stridor
Bradykinin: NO allergic sx
Management *remove agent
•non-eroded: steroid ointment
•eroded: topical ABX
(Bactroban or Mupiciron)
•SX: antihistamines for pruritis
liquid compound for oral lesions
SE: hypercalcemia, photosensitivity
CI: none
Immediate V Delayed Types
Immediate: <1hr of last dose •Type I: IgE mediated-urticarial,
•urticaria, angioedema, anaphylaxis angioedema *immediate
•Type II: cytotoxic, antibody-
Delayed: occurring after 1 hour, usually mediated (drugs)
before 6 hours, occasionally weeks-months •Type III: immune antibody-antigen
•exanthematous eruptions v. fixed drug comples (serum sickness)
eruptions v. systemic reactions •Type IV: delayed (cell mediated)
Ex. erythema multiforme
Information Treatment
•High: PCN, carbamazepine, allopurinol, gold •withdrawal of offending agent
•Medium: sulfonamides, NSAIDS, isoniazid, Symptomatic treatment:
chloramphenicol, erythromycin, streptomycin •antihistamine (H1): Benadryl
•Low: barbituates, BZDs, phenothiazines, Severe: oral steroids
tetracyclines
•affect mucosal tissues of face, lips, tongnue, •airway protection
larynx, hands, feet, genitalia
Mast-Cell:
•epinephrine, steroids, antihistamine
Bradykinin:
•Ecallantide, Icatibant
Pustular Drug Eruption
•An acute febrile eruption Labs: leukocytosis
Clinical Findings: Course/Prognosis:
•sterile pustules on an erythematous base, •pustules resolve over 2 weeks then
often start in the intertriginous fold and/or face desquamation for 2 weeks
•fever
DERM About Clinical Presentation Diagnostics Treatment
Urticaria •edema of superficial layers of the skin due •circumscribed hives or wheals Clinical diagnosis Acute Urticaria
to histamine-related increase in vascular •blanchable, raised, erythematous areas on •ED evaluation, can be life-threat
permeability skin or mucous membrances •Triple Regimen: H1(initial)+ H2+steroid
•Type I IgE mediated •intense pruritis
•transient hives (disappear in 24h) H1: Diphenhydramine, Hydroxyzine,
Pathogenesis •+/- dermatographism Chlorpheniramine
•mast cells and basophils release vasoactive H2: Ranitidine
substances  extravasation of fluid Acute: <6 weeks (infection, allergy)
Chronic Urticaria
Triggers: food, meds, head, cold, stress, Chronic: recurrent and >6 weeks (physical, •antihistamines (Allegra, Claritin)
insect bites, environment, infection autoimmune, idiopathic) •refer to dermatology

About Clinical Presentation Diagnostics Treatment

Melasma •Acquired light or dark brown •mask-like hypermelanotic Tests •Tri-Luma (1st line)
pigmentation due to increased symmetrical macules •Woods lamp à unchanged -Fluocinolone 0.01%
melanin •MC on malar and frontal areas of the •Histology: increased melanin -Hydroquinone 4%
•MC on the face face -Tretinoin 0.05%
•MC in females & hot climates
Counseling
Risks: •Avoidance of sun
•Increased estrogen (prego, OCPs) •Sunscreen >30spf q80m
•Genetics *Titanium dioxide and zinc oxide
•Amount of sun exposure •Remove estrogen exposure
•Medications (diphenylhydantoin)

Vitiligo •depigmenting disorder
characterized by a patchy absence
of melanocytes
•destruction or discontinued function
of the melanocyte
•½ of all cases begins b/w 10-30yo
3 Theories
•Autoimmune : Selected
melanocytes are destroyed by certain
lymphocytes
•Neurogenic : Interaction of
melanocytes & nerve cells
•individual “chalk” white macules
with sharp margins
•loss of color to mucosal membranes,
retina or hair overlying areas of
depigmented skin
•Painless and without pruritus
•Often seen first in sun-exposed
•new macules in areas of recent trauma
(Koebner phenomenon)
Generalized (MC): symmetrical
•”lip-tip” pattern (outh, fingers, toes,
nipples, genitalia)
Segmental: one side/part of body
Wood’s lamp: fluorescence
Skin biopsy: normal skin with
lack of melanocytes
•TSH, T4, fasting glucose,
ANA, CBC ACTH stimulation
if autoimmune
Course and Management: No cure
•possible spontaneous repigmentation
•SPF >30 recommended
Repigmentation
•Topical Glucocorticoids
*Intermittent high potency steroid, D/C if no
response in 2 months
•Topical Photochemotherapy: 8-MOP + UVA
•Systemic Photochemotherapy: 8-MOP + UVA
*tx x1yr with poor results for “lip-tip”
•Narrow-band UVB: TOC child >6 years old

•Self-destruction : Melanocytes Localized: 1-3 macules in single sight Depigmentation

destroyed by toxic substances •bleaching of normal pigmented skin
Vitiligo Universalis: confluence •hydroquinone 20% (MEH) cream

DERM About Stages Treatment

Pressure •Breakdown of the skin and underlying I: III: •reduce/eliminate underlying risk factors
Injury tissue resulting from unrelieved soft tissue
pressure between bony prominence and
external surface
Risks: elderly, immobile, incontinent,
aging skin
Location: sacrum/hip, bony prominences
Pathophysiology:
•pressure impairs oxygen and nutrient
delivery & waste removal
•superficial, nonblanchable •full thickness of the skin •optimize nutrition
•redness, intact skin •possible subcutaneous layer •redistribute pressure every 2hr
•pain control
II: IV: deep, beyond fascia,
•epidermal damage muscle, tendon, bone Local wound care
•extending into dermis (blister or Stage I: cover with film for protection
abrasion)
Granulation: scar tissue Stage II: dressing with moist environement
Unstageable: Eschar: dry, dark scab of skin •transparant film or hydrocolloid dressing
•tissue loss obscured by slough or eschar Slough: moist, thick, stringy,
•do not remove a stable eschar Epibole: rolled wound edge Stage III/IV: debridement

DERM About Clinical Presentation Diagnostics Treatment

Verrucae •cutaneous warts Common & Plantar: Clinical Most resolve within 2 years
•HPV: 1, 2, 27, 57 •firm, hyperkeratotic papules 5-10mm •Biopsy can to r/o SCC •Cryotherapy q4wk  debride surface
*MC IN KIDS •red-brown punctations •Electrosurgery
3 types: (thrombosed capillaries) Histology:
•verruca vulgaris (common) •koilocytotic squamous cells Topical: salicyclic acid
•verruca plantaris (plantar) Flat Warts: sharply defined with hyperplastic •desquamation of hyperkeratotic skin
•verruca plana (flat warts) •numerous, flesh-color papules 1-5mm hyperkeratotis •soak  file  apply

Condyloma •HPV 6, 11; Others: 16, 18, 31, 22
Acuminatum •MC in sexually active YA
“Genital warts” Transmission: invasion of the basal
cells of epidermis by microabrasion
•active lesions NOT required for
transmission
Risks: sex, partner with HPV, STIs
Pathogenesis:
•Low risk: one partner,
immunocompetent, regular protection
•High risk: IVDU, multiple partners,
immunocompromised
•usually asymptomatic
•painless papules  soft, fleshy
cauliflower-like lesions
•skin colored/pink/red/tan/brown
Types:small popular
•cauli-flower-floret
•keratotic warts
•flat topped papules/plaques
Laryngeal: HPV 6 and 11
•MC on vocal cords, age <5 or >20
•risk of SCC, squamous cell in situ
CLINICAL
•dermoscopy (HALLMARK)
•shave biopsy if refractory
Acetic Acid:
•whitening of lesion
Histology: koilocytotic
squamous cells with
hyperplastic hyperketatosis
•Imiquimod, podofilox, tricloracetic acid
•cryotherapy q2-4wk x3mo
•electrosurgery
•surgical removal (best if >1cm)
•laser: recurrent or resistant
•curetage (pairing)
Prevent: pap smear, Garadasil 9, condoms
< 15 years old: 2 doses 6 months apart
> 15 years old: 3 doses (0, 2, 6 month)

PHARM MOA Application SE/CI Education

Imiquimob 5% •Induces immune systems response Apply small amount at night 3x/week and rub until gone •SE: localized reaction •Avoid sexual contact during
Not in SCC to recognize and destroy lesions -wash off in morning with mild soap (6-10h) -If too severe, can take a application times
holiday then resume

Podofilox •Prevents cell division and causes •apply q12h for 3 days then off 4 days, then repeat MC: mild-severe irritation •Apply initial tx in office to
tissue necrosis •apply to normal skin between lesions; avoid open wounds MC systemic SE: HA educate on proper application
•wash medication off after 1-4 hours •Avoid sexual activity
•tx area <10cm AND total volume <0.5ml/d CI: pregnancy

Tricholoracetic •Burns, cauterizes, erodes •Apply Vaseline around lesion to create barrier then apply VERY EFFECTIVE
Acid medication to area with cotton top applicator x6-10weeks

5-FU •Blocks DNA synthesis: apoptosis •BID to affected region x2-4wk •localized skin reaction Education: success is parallel
and selective cell death -Alt: daily for face & anterior scalp only burn, itch, erythema, to compliance
•D/C once erythema, erosion, crusting, and necrosis have erosion, crusting, ulceration
occurred •F/U in 2 weeks

Ingenol 1. disrupt cell membrane & •0.015% gel: face/scalp once daily x3days •Localized skin irritation; AK ONLY
Mebutate DNAcell necrosis •0.05% gel: trunk/extremities, apply nightly x2d erosions
(Picato) 2. Neutrophil-mediated cytotoxic •Plant derivative
•Caution: risk of SCC?
Diclofenac •COX-2/prostglandin inhibit •3% Gel-Apply to treatment area BID x60-90d •Localized skin reaction

DERM About Clinical Presentation Diagnostics Treatment

Pediculosis Bug: Pediculous humanus capitis •Maculae cerulae or pruritis stains on •demonstration of lice or nits •Primetherin 5% (off-label)
Capitis •Live 30 days on the host and <1 day skin of occipital scalp and nape of neck on hair visually or under •Spinosad (>4yo)
“Head lice” off the host microscope •Malathion 0.5% lotion
•Occipital and cervical LAN •Ivermectin-formulated lotion
Transmission: person •Pyodermas in the scalp Nits: white, oval-shaped egg •Oral Invermectin (off label)
•Louse, Nits, hair casts capsules *seen on woods lamp
Risks: girls > boys •Manual nit removal with comb
•less risk: African american Hispanics lice: oblong structure attached
•MC in warmer months to hair Eyelid: Petrolatum BID to margin for at
least 8 days

Pediculosis Bug: Pediculus humanus corporis •Extremely pruritic, rash concentrated •clinical 1st line: hygiene improvement
Corporis where clothing is
“body lice” •live in/lay eggs on clothing Tests: examine clothing *MC •wash all clothes and linins
•2-4mm, wingless, blood-sucking Maculae cerulean: blue grey macules at seams •iron seams to destroy lice
arthropods are pathognomonic for lice •shake clothes over paper & •Permethrin 5% cream if heavy infestation
examine
Risks: poor hygiene, poverty, “vagabond disease” •woods lamp: fluoresce
homelessness •chronic (parasitic melanoderma) yellow-green
•thickened and darkened skin after a •confirms w/ finding live
Transmission: usually sex long period of bites and rubbing louse or nit
•examine pubic and head lice

Pediculosis •Highly contagious •Live on hair between pubic and perianal •finding louse or nit •CDC-sexual partners w/n 1mo notified
Pubis Bug: Phtirus pubis regions, eyelashes, eyebrows, and face •nits: brown & full(nymph) •wash, clean all clothes and linens
“pubic lice translucent and flat (cast) •Permethrin 1% or Pyrethrins
or crabs” Transmit: person-person •Extreme pruritus (MAIN) due to
•usually sexual saliva or anticoagulant during feed

Scabies Bugs: Sarcoptes scabiei
Pathophysiology:
•female mites burrow into the stratum
corneium of the epidermis to lay eggs,
•Itching is worse at night, especially
after just getting into bed
•Typically, 10-20 mites
Exam:
•clinical diagnosis
Skin scraping: mites, eggs,
feces
•Treat infected & close contacts, repeat
treatment in one week
•1st line-Permethrin 5% or Rid: use about
8-14hr prior to shower
 feed, and defecate  reaction
Risks: children, sex, poor hygiene,
long-term care facilities, overcrowding
Transmission: person to person
•multiple, small erythematous papules
•linear burrows
*PATHOGNOMONIC
 MC in intertriginous zones, web
spaces
•usually spares face and neck
•red, itchy papules or nodules on
scrotum, glans, body folds
Dermoscopy: darker, V-
shaped structure  “jetliner
with its trail”
•Oral Ivermectin 200ug/kg PO single dose
•Last Resort-Lindane
-CI: teratogenic, breastfeeding, <2yo
-SE: seizures *do not use after shower
*avoid in crusted due to CNS toxicity
Patient Education:
•symptoms should improve within 3d,
pruritus can persist for 4 weeks after tx
•put all clothing & linens in bag x72hr

DERM
Tinea Capitis •MC in children & African Americans Endothrix: occurs within hair shaft Clinical diagnosis PO Antifungal:
•MCC Trichophyton Black Dot: broken hair near scalp  swelling •Oral Griseofulvin
•diffuse & poorly circumcised KOH: MC initial test *monitor CBC, Cr,, LFTs
Non-inflammatory: -T, tonsurans, T. violaceum •fungal element insure or •Terbenafine (Lamasil)
•scaling, prutitis, alopecia, adenopathy surrounding base of hair •Itraconazole, Fluconazole
Kerion: inflammatory mass & loose hair
Inflammatory: pain, tenderness, alopecia •boggy, purulent, inflamed nodules & plaque Woods lamp: microsporum Antifungal shampoo:
•painful, drain pus; hair falls out when pull *T. tonsurans does not •Ketoconazole
-T. verrucosum, T. mentagrophytes fluoresce
Prevention:
Favus: “honeycomb” thick/yellow crust Culture: DEFINITIVE -wash furniture, clothes, linens
•avoid pillow cases, head to head
Ecothrix: occurs outside hair shaft •disinfect combs
“grey scaly patch”  scaly

Tinea Cruris •MC in inguinal folds  thighs •Large scaling, well demarcated dull Clinical diagnosis •Topical Ketoconazole,
“Jock Itch” T. rubrum red/tan/brown plaques, sharply demarcated Clotrimazole, Butenafine
with a raised border KOH: MC initial test •oral Griseofulvin or Terbenafine
Risks: males, copious sweating, •segmented hyphae •put on socks before pants
immunocompromised •PRURITIS •avoid tight fitted clothing
Culture: DEFINITIVE •use cotton underwear

Tinea •Fungal/dermatophyte infection involving •Asymptomatic KOH: segmented hyphae •Topical Clotrimazole,
Corporis anywhere on the body •Pruritis, well-defined plaques or patches Ketoconazole (use first)
(Ring Worm) •T. rubrum with central clearing Culture: DEFINITIVE •Oral Terbinafine, Itraconazole

Tine Pedis •MC dermatophyte infection Interdigital (MC): pruritis, erythematous Clinical diagnosis Topical Antifungal x2-4 weeks
(Athletes foot) T. rubrum, T. interdigitale erosions or scales between the toes •Ketoconazole and Econazole
•MC 20-50yo *MC between 4th and 5th KOH: skin scrapping
•segmented hyphae Oral Antifungal: *if topical fail
Risks: hot, humid climate; occlusive Hyperkeratotic: soles, lateral & medial •Terbinafine (Lamisil)
footwear, hyperhidrosis surfaces, with “moccasin” distribution Culture: DEFINTIVE •Fluconazole, Itraconazole

Vesiculobullous/Inflammatory: pruritic Prevention: BPO, antifungal

vesicur or bullous eruption, medial foot powder, shower shoes
Tinea *NOT caused by dermatophytes
Versicolor •Overgrowth of Malassezia furfur
Risks: climate, sweating, immunodef.
products, steroid use, oily skin
•hyper or hypopigmented, well-demarcated KOH: hyphae & budding •Selenium sulfide
round or oval macules with fine scaling •Zinc Pyrithione
Woods lamp: yellow-green •Sodium Sulfacetamide
•MC on trunk and proximal extremities fluorescence •Itraconazole or Fluconazole if
widespread or failed topical

Cutaneous •Superficial fungal of intertriginous skin
Candidiasis •MC neonates and age > 65
•Candida Albicans *NOT TINEA
Risks: warm, moist environment,
immunocompromised (DM), obese
Areas: genitocrural, gluteal, interdigital, Clinical diagnosis Mild-Mod: topical antifungal
inframammary, axilla, pannus •Ketoconazole, Clotrimazole
KOH: skin scrapping
•Pruritic, tender, painful •budding yeast +/- Severe: oral-Fluconazole
•Erythematous, “beefy red” plaques and pseudohyphae Prevent: keep dry (powder-
erythematous satellite lesions Zasorb AF)

DERM Cause/Incubation/Tran Contagious Presentation Diagnostics/Treatment

Hand Foot and •Incubation: 3-7d •very contagious in •oral painful, red, ulcers surrounded by red halo lesions on •supportive
Mouth •Tranmission: person, secrete first week tongue, gums, palate, buccal mucosa, palms, feet, and butt •MC complication: dehydration
Coxsackie Virus •MC in summer/autumn •contagious until
blisters disappear

Herpangina Coxsackie Virus A •sudden onset high fever •Supportive treatment

•MC in child 3-10 years old •stomatitis: small, yellow-white papulovesicular lesions on •Complication: aspect meningitis, GB
•MC in summer, early fall posterior pharynx that ulcerate

Herpes Simplex •HSV-1 •active lesions very •grouped vesicles on erythematous base •supportive, lasts about 7-14 days
(HSV-1) contagious •ulcers, perioral area, lips; LAN; stinging/burning

Varicella Incubation: 10-21d •can spread 1-2 days •itchy, fluid filled; rash  papule  vesicle  crust •varicella vaccine (12-15mo, 4-6yr)
Varicella Zoster Transmission: respiratory before rash and until •dew drop on a rose petal •Acyclovir
all have scabbed

Rubeola Children <5; Paromyxovirus 8 days total: 4d with •Koplik spots-white/blue papules with red base on mucosa •MMR vaccine (12-15mo, 4-6yr)
(Measles) (1st) incubation: 7-14d; airborne rash, 4d w/o rash (no •Red blotchy: face  arm  trunk  leg •MC complication: OM, diarrhea
Rubeolla Virus school x4d after rash) •high fever, cough, coryza, conjunctivitis •PNA MCC measles-related death

Mumps Incubation: 12-15d •5 days isolation after •swollen parotid glands •MMR vaccine, supportive care
transmission: airborne, saliva swelling •fever, HA, myalgia, anorexia •Complication: orchitis, encephalitis

Rubella (3rd) Transmission: airborne, •10d before rash  •postauricular and occipital LAN •Complication: rubella syndrome
contact, pregnancy 1-2 weeks after gone •fine pink rash face  trunk  arms  legs (deaf, cataracts, heart defects), arthritis

5ths: Erythema •Parovirus B19; child 5-7yo •most contagious •prodrome: fever, HA, rhinitis •can suppress RBC aplastic crisis
Infectiosum Incubation: 1-2 weeks BEFORE rash •fiery-red facial erythema “slapped cheek”  lacy, •supportive, IVIG if
reticular on extremities immunosuppressed

Roseola 6ths •Children 6mo-3yr •high fever 3-5d  rash (rosey pink nonpruritic •supportive
(HHV 6 and 7) Incubation: 5-15 days; maculopapular rash) •MC complication: seizures
Transmission: airborne
 About Symptoms Causes, Risks, Complic. Treatment
Onycho- •Fungus of the nail, MC on toes •thick, opaque, discolored •Fungal culture + rapid •topical antifungal: Ciclopirox or Efinaconazole
mycosis •lifting of the nail from bed test (KOH or PAS)
Cause: *culture by clip/scrap •oral antifgunals: Terbinafine (Lamisil)
•Trichophyton (T. rubrum MC) •must rule out melanoma -6 weeks for fingers, 12 weeks for toes
•Epidermophyton *longitudinal melanichia  Periodic Acid Schiff (PAS): -monitor CBC and LFT at baseline and monthly
biopsy •MOST SENSITIVE -risks: hepatotoxic, pantocytopenia, agranulocytosis
Risks:
•tinea pedis, psoriasis home remedy: 50/50 apple cider vinegar and water
•fhx, old age, climat 10min soaks x6months
•poor health, trauma, immunosupress
•fitness, communal bathing, footwear

DERM About Clinical Presentation Risks/Diagnostics Diagnostics/Management

Erysipelas •Acute superficial infection
(dermis & dermal lymph vessel)
•MC in young children & adults
Bugs: GABHS (MC!), S. aureus
Cellulitis •dermis and subcutanoues tissue
•MC in middle age adults
Causes:
•S. aureus), GABHS
•Cat/dog: Pasturella multocida
•Freshwater: Aeromonas
•Salt water: V. vulnificus
Prodrome: fever, chills, anorexia, malaise •clinical diagnosis •MRSA: IV Vancomycin, Daptomycin
General: +/- sepsis -Oral: Clindamycin, Bactrim, Doxycycline
Labs: CBC, CMP, ESR,
Lesion: painful, tender, hot blood cx, US or MRI •MSSA: IV Cefazolin, Clindamycin, Nafcillin
-bright red, raised, swollen, indurated plaque -Oral: Cephalexin, Nafcillin, Clindamycin
with SHARP borders
Prodrome: fever, chills, anorexia, malaise Complications: •Dog/cat: Augmentin *Altnerative:
General: +/- sepsis •abscess formation Doxycycline
•bacteremia, endocarditis •Human bite: Augmentin
Lesion: painful, tender, hot •osteomyelitis •Fresh water: Ciprofloxacin
-bright red, raised, swollen, indurated plaque •metastatic infection •Salt water: Doxycycline
with INDISTINCT borders •sepsis, toxic shock
syndrome

About Clinical Presentation Diagnostics Presentation

Alopecia •T-cell mediated autoimmune disorder
Areata •associated with other autoimmune
•MC in children <25yo
•Usually family history
Causes:
•definicieny in vitamins
•high and low temperature
•disease of digestive system, endocrine
•hormonal changes, genetic
•hairstyles
Pathophysiology:
•Damage to hair follicle in anagen stage
•tranform to catagen & telogen
•NO SCARRING
•Smooth, discrete, circular patches of
complete hair loss
•gradual over weeks to months
•oval, round defined border
Nails: pitting, fissure, trachyonychia
Areas: scalp, beard, eyebrow, extremities
Exam:
•Black dots: no scaring
•Dermoscope: hair breaks before surface
•Exclamation hairs: blunt distal end and
taper proximally near scalp
•appear when browkne hair (black dots)
are pushed out of follicle
Subtypes:
•Alopecia areata: solitary or multiple
•AA totalis: total loss of terminal scalp
•AA universalis: total loss of all
terminal body and scalp hair
•Ophiasis: bandlike pattern of hair loss
over peripheral of scalp
•Nails: fine pitting (hammers brass) of
dorsal nail plate
Diagnosis: clinical
•punch biopsy is DEFINITIVE-
peribulbar lymphocytic inflammatory
infiltrates
•Spontaneous remission, can reoccur
Pharm
Local: intralesional steroids
Extensive: Topical corticosteroids
(Triamcinolone) with Minoxidil
Others:
•ILK (intra-lesional kenalog)
•Minoxidil 5% (best if combo)
•Anthralin: safe in kids
Androgeneti •genetically predetermine progressive
c Alopecia loss of terminal hairs
•Male and Female pattern baldness
Pathophysiology:
•dihydrotestosterone (DHT) key
angrogen
•activation of androgen receptor
shortens the anagen  tellagen phase
•Men: after puberty, 20s-40s
•Women: MC after 50
Men:
•bitemporal thinning of frontal scalp then
involves the vertex
Women:hair between frontal and vertex
Clinical diagnosis
Labs: DHT, T, DHEA, Prolactin
Dermatoscope: miniaturized hair and
brown perihilar casts
Biopsy: telogen & atrophic follicles
Trichogram: increased telogen hairs
Hormones: T, DHEA, Prolactin
Topical:
•Minoxidil/Rogain 2%, %5 BID
MOA: widens blood vessels to allow
oxygen and nutrients
*hair loss first before regrowth
Oral:
•Finasteride 1mg po daily (2nd line)
*MEN ONLY , inhibits T & DHT
•Spironolactone 50-100mg QD
MOA: blocks action of DHT
CI: breast cancer; SE: K+ levels

•Hair transplant, hair piece/wig

Recurrent: antiviral qd
BILAT & SYMMETRICAL Exam: (-) Nikolsky Complications:
•infection, fluid/electrolyte

About Clinical Presentation Diagnostics Treatment

Rosacea •Chronic, inflammatory
•hyperreactivity of capillaries
•MC in lighter skin & females
Triggers:
•hot or cold weather, sun
•hot drink, spicy, caffeine, alcohol
•hot baths
•medication: hrmones, Niacin
•emotions
•exercise
DERM About
Folliculitis •Infection of hair follicle
Bugs: S. aureus, step, gram (-),
fungi, pseudomonas
Predisposing factors:
•shave hairy areas, hair occlusion
•hot tub *Pseudomonas
•topical CS, systemic ABX
•diabetes, immunocompromised
DERM About
Brown •MC in southwest & Midwest
Recluse •Loxosceles reclusa: violin pattern
Bite on anterior cephalothorax
Pathophysiology:
•venom is cytotoxic and hemolytic
 local sx, necrosis
Black •Latrodectus Hesperus
Widow •red hourglass shape on underside
Bite of belly
Pathophysiology: neurotoxin
•acne-like rash (papulopustules), centrofacial erythema, •Clinical diagnosis Lifestyle:
flushing, telangiectasias, skin coaorsening •Definitive is biopsy •avoid triggers
•burning and stinging, red eyes •camouflage w/ green/yellow-tint makeup
•cleaners, moisturizer , daily sunscreen
Exam: NO comedomes
•rhinophyma: red, enlarged nose Telangiectasia/Erythema: Brimonidine
•gnathophyma: chin Rosacea Fulminans: Prenisolone
•metophyma: forehead
•blepharophyma: eyelids Mild/Moderate:
•otophyma: ear •Topical Metronidazole (1st line)
•15% azelaic acid gel
Types: •Ivermectin cream
•erythematotelangiectatic (MC): persistent erythema of •Sodium sulfacetamide with 5% sulfur
central face, telangiectasia, sting •Brimonidine gel (Mirvasa)
•papulopustular: papules, pustules, edema
•phymatous: enlarged cobblestones, nose Moderate-Severe:
•ocular rosacea: blepharitis, conjunctivitis, hyrpemia •Oral Tetracycline antibiotics *1st line
•Metronidazole, Azithro, Isotretinoin
Clinical Presentation Diagnostics/Management Management
•singular or clusters of perifollicular papules •clinical Mild (few): warm compress, soap
•surrounding erythema on hair bearing skin •Topical Bactroban
•Non-tender or slightly tender, pruritis •gram stain, C/S •Clindamycin, Erythromycin, BPO
•KOH if fungal
•Hot tub: Pseudomas (trunk) *KOH dissolves the skin so you see Severe/Refractory:
•Viral: herpetic and molluscum the actual fungus •oral Cephalexin or Dicloxacillin
•Fundal: candida, malassezia
•Other: syphilis MRSA: Doxycycline, Bactrim
Clinical Presentation Diagnosis Treatment
•lack severe symptoms: possible fever, chills, N/V •clinical •local wound care & pain control (NSAIDs)
• “red, white and blue”
GOLD: wound care
1. Local: burning, erythema at bite  blanching of area spider •clean with soap and water
(vasoconstriction) collection & •cold packs
2. erythematous “red halo” for 24-72 hr indentificatio •elevated or neutral position
3. hemorrhagic bulla  eschar formation  DIC n
Latrodectism: pain at bite  systemic and neurologic “ Mild: wond care and pain control
symptoms in 30min-2 hours
Moderate/Severe:
•muscle pain, spasms, rigidity •muscle relaxants (Benzos, Methocarbamol)
•blanched, circular patch with surrounding red perimeter
and central punctum (target) •antivenom reserved to pts not responsive to above
 About
Acne •Inflammatory skin condition
Vulgaris involving pilosebaceous units
•Women > men b/c hormones
•Begins around puberty due to
androgens stimulation
pilosebaceous unit changing
keratinzation at follicular orifice
•MC on face, back, upperchest
Pathogenesis:
1. increased sebum (oil)
2. Follicular hyperkeratinzation
3. proliferation of the bacterium
Propionibacterium acnes
4. inflammation
Clinical Presentation
•open comedones (blackheads): incomplete
•closed comedones (whiteheads): complete
Inflammatory: papules and pustules
nodules and cysts: >5mm can cause scarring,
including pitted or hypertrophic scar
Causes/Location
•COMEDONES MUST BE
PRESENT!
•Definitive-skin biopsy
•Itchy back, shoulder, scalp  scrap
for potassium hydroxide (KOH) for
Pityrosporum folliculitis  fungal
shampoo
Clinical Presentation
•Acne often resolves after teen years
•nodulocystic acne will require more
aggressive treatment
•acne requires consistent, regular care over
months
Mild: topical retinoids, BPO, topical
antibiotics (Clindamycin, Erythromycin)
Moderate: + oral ABX (Doxycyline)
Severe: oral Isotretinoin

Class Drugs Indication/About MOA SE/CI

Topical Tretinoin, Tazarotene •1st line for comedonal & inflam decreases cohesion and increases turnover Side effect: dryness, photosensitivity
Retinoids Adapalene Gel •every 3rd night  nightly of epidermal cells *speed up exofiliation CI: pregnancy

Benzoyl •Start with lowest concentration •no baceterial resistance  Release free- SE: skin irritation, bleaching of hair/clothing
Peroxide (2.5%) than increase as tolerable radical oxygen oxidized protein
(BPO)
 Topical Clindamycin (BID, foam qd) •Mild-moderate inflammatory acne •reduces number of P. acne in SE: skin irritation
Antibiotics Erythromycin (BID) (papulopustular) pilosebaceous unit
* use with BPO
Oral ABX Doxycyline or minocycline Moderate acne with inflammatory •Inhibits P, acnea SE: upset stomach, photosensitivitiy, lupus
*add 100mg BID papules or deeper-seated lesions •Quickers results than topicals

Tetracyclines *1st line •Anti-inflammatory and ABX CI: pregnancy and young children
SE: photosensitivity, teeth staining in children

Macrolides Erythro &Azithromycin *1st Increased resistance Pregnancy category B

Bactrim *2nd line •Severe acne unresponsive to SE: SJS, TEN; CI: Avoid in pregnancy
others
Oral Isotretinoin •Severe resistance nodular/cystic •Decrease in P. acnes SE: dryness of skin and mucous membranes,
Retinoids (Claracis or Acutane) •Inhibition of sebaceous gland headaches, suicide & depression, teratogenic
*monotherapy •2 contraceptives *can decrease athletic performance •increased TG and cholesterol
*after FAILED oral •2(-) pregnancy tests & monthly
test •no blood donation Labs: CBC, LFT, lipids monthly CI: tetracycline; pregnancy  birth defects

ENDO 5%
ADRENAL GLAND: GFR-ACE (out to in): Glomerulosa-Aldosteron, Fasiculata-Cortisol, Reticularis-Androgens (E/T)
Hypothalamus (CRH)  Anterior Pituitary Gland (ACTH)  Adrenal Gland

Disease Causes/Types Presentation/Labs & Testing Work-Up Treatment/Management

Primary Bilateral idiopathic TRIAD: HTN + HYPOKALEMIA + BMP: High NA+ and bicarb,low K+ Unilateral Adrenal Adenoma “ Conn”
Hyper- adrenal hyperplasia METABOLIC ALKALOSIS •surgical excision + Spironolocation
aldosteronism *increased urinary hydrogen excretion Plasma Renin & Aldosterone
Primary: *in the morning in seated position Bilateral Adrenal Hyperplasia (MC)
•Renin-independent •Refractory hypertension (young age •aldosterone:renin ratio (ARR):>20:1 •Medical management
•idiopathic(MC) w/o risk factors) *high aldosterone, low plasma renin •Low Na+ diet
•conn syndrome •K+ spare diuretics:
“unilateral adenoma” Hypokalemia: CT Scan-Adrenal Spironolactone or Eplerenone
•proximal muscle weakness <4-Conn, >4- carcinoma •HTN: ACEI, CCB, ARB
Secondary: •polyuria, constipation •thickening-hyperplasia
•increased renin  •decreased DTR •negative CT  adrenal vein sampling Adrenal Carcinoma: Oncology referral
increased aldosterone •hypomag
in RAAS Adrenal Vein Sampling Referrals: Endo, Cardio
*perform if negative CT scan
•assess aldosterone in blood Monitor: HTN and electrolytes

Confirmatory:
•sodium loading test (oral preferred)
-high urine aldosterone >12  primary
*If no oral, then IV over 4 hours while
seated, >10 is confirmatory
Pheo- Catecholamine Triad: Plasma Free Metanephrines Management: resection of tumor after 1-2
chromocytom secreting adrenal episodic palpitations, HA, diaphoresis •sit 15min; elevated  assess urine weeks of hypertensive therapy
a tumor  NE and E •Anxiety, pallor, syncope, tachycardia
*Adrenal •Paroxysms <1hr 24h Urine Metanephrine and Creatinine Awaiting Surgery: Maintain BP < 160/90
Gland Rule of 10s: • (+) if >2.2mcg/mg of creatinine •Alpha-Adrenergic Blockers:
•10% bilateral *triad + HTN is HIGHLY suggestive Cardura, Minipress, Hytrin
•10% extra-adrenal Imaging: CT/MRI with contrast
•10% malignant Diet-high salt and water intake

Adrenal Nonfunctional (MC) Nonfunctional: Asymptomatic •Detailed HP Surgery referral

Adenoma/ Benign, does NOT •Labs based upon suspected adrenal
Carcinoma secrete steroids Functional: *related to cellular zone affected
involvement
LOW ACTH Functional: •Glomerulosa-hyperaldosteronism •Fine Needle Aspiration
•Benign >1cm •Fasiculata-cushings *only to r/o metastasis in patient with
•Secrete steroids ind. •Reticularis-hyperandrogenism known malignancy
ACTH/ RAAS •Medulla-pheochromocytoma *must r/o Pheochromocytoma

ENDO
Addison’s Autoimmune disease *glucocorticoid & mineralcorticoid deficiency •CBC: Eosinophilia, lymphocytosis Chronic: Oral glucocorticoids
Disease of adrenal gland •CMP: -Hydrocortisone 15-30mg daily
(Primary •skin and mucosal hyperpigmentation low Na, & glucose; high K+, BUN/Cr 2/3 in morning, 1/3 later
Adrenocortical ↓ cortisol •Anorexia, weight loss, fatigue, low stamina •Culture: Blood, sputum, urine
Insuffciency) ↓ aldosterone •dizzy, hypoglycemia, weakness, fever, lymphoid •Plasma Cortisol and ACTH @ 8am •Glucocorticoid Stress therapy
hyperplasia, N/V/D *ACTH elevated in primary, decreased -Increase dose by 50% with stressors,
HIGH ACTH •orthostatic hypotension (dehydration) in secondary surgery, or illness
*Adrenal •Serum DHEA (<1000)
Gland Adrenal Crisis: Chronic: •Plasma Renin @ 8am •Mineralocorticoid: Fludrocortisone 0.05
MCC: abrupt •vitiligo (10%)  ACTH binds to melanocyte •ACTH Stimulation (Cosyntropin) *can be added only in primary
withdrawal of •Changes in hair *loss CYP11+17, gain CYP21 *(+) if low or absent rise in serum
steroids •Generalized pain cortisol (<18) after ACTH Acute Adrenal Crisis
•Psychiatric: anxiety, irritable •Hydrocortisone: Loading IV  IV q6h
Causes: •Neurologic: gait, coma Adrenal Crisis: for 24h  oral when tolerate oral food
•autoimmune (MC) Low Na and glucose, high K+ •Fludricortisone, IVF (normal saline)
•infection (TB, HIV) Acute: Sudden “Adrenal Crisis” •Broad ABX, tx electrolytes/glucose
-MC symptom: Shock  low BP and volume
Education: medical alert bracelet

Acute Adrenal •Sudden worsening •Hypovolemic Shock (MC!) BMP •IVF: normal saline (D5NS if
Insufficiency of adrenal •Hypotension, Hypovolemia •hypoglycemia hypoglycemia)
“Addisonian insufficiency due to •Abdominal pain, N/V •hyponatermia
Crisis” “stressful” event •Fever, Weakness, lethargy, confusion •hyperkalemia •IV HIGH dose Hydrocortisone

*normal response is Triggers: abrupt steroid withdrawal, surgery, Confirm: cortisol and aldosterone •Reversal of electrolytes
a 3x increase trauma, volume loss, hypothermia, MI, fever, •Fludricortisone
 sepsis, hypoglycemia

Cushing’s ↑ cortisol •Fatigue, reduced physical endurance CBC: leukocytosis, low eosinophils Cushing SYNDROME Management
Disease HIGH ACTH •Central obesity with protuberant abdomen, CMP: elevated glucose, hypokalemia •hydrocortisone=DOC
plethoric “moon face”, supraclavicular fat
pads, “buffalo hump” Dexamethasone suppression test Cushing DISEASE Management
*Adrenal Cushing Syndrome: •Large purple striae, thin skin •Syndrome: 1mg @ 11pm-check cortisol •surgical removal of pituitary tumor
Gland •Exogenous long- •Hirsutism, male hair loss at 8am: (+) if cortisol elevates >5 •Hyperandrogenism: Flutamide
term ortisol excess •Muscle weakness proximally •Hypercortisolism: Metrypone
•Elevated BP, immune suppression •Disease: high ACTH and suppression •HTN: K+ sparing diuretics, CCB
Cushing Disease: of cortisol on high dose
•Increased ACTH Monitor/treat cortisol related conditions:
secretion from •24 hour urine free cortisol osteoporosis, psych, DM, hypokalemia,
anterior pituitary *most specific (+) if 3x normal muscle weakness, infections

Causes: •Late night 11pm salivary cortisol

•Iatrogenic (steroid)
•Pituitary adenoma •Serum ACTH
•Ectopic ACTH <20  adrenal CT
•Tumor (SCLC, >20  MRI pituitary
medullary thyroid)

ENDO
Type I DM no insulin due to destruction of beta-cells (islet 3 Ps: Monitor: •insulin (multiple-dose basal bolus)
cells of the pancreas) *antibodies •polyuria (pee) •check glucose 3x daily -short acting: Humalog, Novalog
•polydipsia (thirst at home, increase fiber -basal: Glargine, Lantus, Levemir
•Islets of Langerhans infiltrated by lymph •polyphagia (hunger) •GFR + urine albumin/yr •Pramlitide (Symlin) *adjunct only
islet cell autoantibodies, T-lymph proliferate,
release of cytokines within infiltrated islets Labs: Dawn Phenomenon:
•Weight loss (low
•nml glucose  HIGH at 2am-8am
water) • glucose >200
preproinsulin (A, B, and C)  proinsulin (A & •decreased insulin sensitivity & nightly hormones
B)  insulin (C chain cleaves off) •postural hypotension •fast>126 (GOLD) •TX: bedtime injection of NPH, increase dose
•weakness, blurred •A1C >6.5%, GGT
Type IA (MC): autoimmune vision, neuropathy, •C-pep/Insulin ratio (low) Somogyi effect:
Type IB: non-autoimmune beta cell destruction fatigue *longer t ½ then insulin •hypOglycemia  rebound HYPER due to GH
(+)GAD-65 with type IA •TX: decreased night NPH, move earlier, or snack

Type II DM Risks: •polyuria, polydipsia •glucose >200 1st line-Metformin + diet + exercise
•(+) fhx; N. American, AA, Hispanics, Asians •blurred vision •fast>126 (GOLD) GLP1:“-tide”, DDP4: “-gliptin” SGLT2: “-glifozin”
•overweight (obese), birth wt >9lbs •poor wound heal •A1C >6.5%, GGT
•hyperglycemia •neuropathy Hypoglycemia: Sulfon, Meglit, Insulin
•dry and itchy skin •check glucose 1-2x/d Affordable: Metformin, Sulfonylureas
Insulin functions: glucose transport; stops •weight loss (5-10%) Weight Loss: GLP-1, SGLT2 inhibitors;
protein & TG breakdown, and gluconeogenesis •caloric restriction Weight Gain: Sulfonylureas, TZDs, insulin
•eye exam, neuropathy
•A1C 2x/year Screening:
Incretin: hormone that stimulates the release of
ADA: All adults 45+ q3 years or any adults with
insulin and decrease blood glucose
BMI 25+ and 1 additional risk fractor
 Yearly eye exams USPSTF: 40-70yo q3yr if overweight or obese

Diabetic •metabolic acidosis 1+ days of ↑ thirst with •Glucose: 350-900 1-Fluid: 1L/hr 0.9% NS or LR 1-2h
Ketoacidosis •insulin insufficiency and counterregulatory polyuria and polydipsia •pH: acidic (6.8-7.3) *if Na rises, change to 0.45%
hormone imbalance
GI: N/V, fruity breath •Potassium nml or ↑ 2-IV regular insulin 0.1U/kg/hr
•Relative/absolute insulin def. •Sodium ↓Bicarbonate ↓ *change to dextrose when glucose 200mg/dL
•Excessive counter hormones Cardio: ↓ BP, ↑ HR Goal glucose: 150-200mg/dL
•↓ Bicarbonate b/c depleted by ketoacids Renal: ↑BUN/Cr, ↓GFR
•↓ Insulin, ↑Glucagon Neuro: alert, drowsy, 3-Potassium 10meq if <5.2
-↑ hepatic gluconeogenesis and glycogenolysis confusion, coma Ketones: acetone, 4-Bicarb if pH <7.0 (50meq/L/2hrs)
-↑ free FA release -> ↑ ketones acetoacetate, B-hydroxy *important in determining sevirty of DKA
*triggered during increased physiologic need Respiratory: kussmaul *serum checks B-hydroxy,
SIPS: saline, insulin, potassium, search for cuase

Hyperglycemi Insulin deficiency and inadequate fluid intake polyuria, polydipsia, Glucose: 600-1200 1-Fluid management
a weakness, decreased oral pH: nml or minimal acid Infusion 1-3L/hr 0.9% NS 1-3h *Na >150  0.45%
Hyperosmolar Triggered by stress: intake, wt loss
State •infection (MC for both), infarction, ↓ water •K+ and bicarb nml 2-IV regular insulin 0.1U/kg/hr *NO if K <3.3
•Neuro: altered mental *change to dextrose when glucose 250mg/dL
Renal: ↑BUN/Cr, ↓GFR Goal glucose: 250-300mg/dL
•Cardio: ↓ BP, ↑ HR
Osmolality: 330-380 3-Potassium-10meq/hr, ↑ if K+ <3.5

Drug MOA Advantages Disadvantages Contraindications

Binguanides Inhibits hepatic gluconeogenesis Improves glucose N/V/diarrhea, anorexia, metallic taste Allergy
Metformin Decreases intestinal absorption *no hypoglycemia B12 deficiency *check levels! Acidosis
*FIRST LINE Inexpensive BBW: lactic acidosis CHF
Weight loss *avoid CRF, liver failure, ETOH CKD (GFR <30)
Improves lipids (especially TG) Nephrotoxicity: STOP if hospitalized, Hospitalization
dehydrated, or contrast Radiocontrast

Thiazolidinediones “unlock” muscle and fat cells and help Improves glucose Weight gain Allergy, CHF
“Locksmiths” them ultize glucose *no hypoglycemia Peripheral/macular edema, CHF
Rosiglitazone  Improve insulin sensitivity Pioglitazone improved HDL Rosiglitazone worsens TC, LDL, increases Caution:
Pioglitazone  Increase glucose uptake HDL Osteoporosis
BBW: both-CHF, Ros-MI Liver disease

Sulfonylureas “Electricians”: Improves glucose Associated with hypoglycemia Allergy to sulfa

Glimepiride “zap” pancreas to stimulate increased Inexpensive *Glipizide and glumpiperide lower risk Diabetic ketoacidosis
Glipizide, Glyburide production of insulin Short onset Weight gain
Meglitinides Caution:
Repaglinide Bind to K+ channels of B-cells -> Liver/renal disease
Nateglinide depolarization -> insulin release Cardiovascular disease
 a-Glucosidase “Block” the breakdown of starches in Improves PPBG Flatulence, elevated LFTs Allergy
Inhibitors intestine *no hypoglycemia hypoglycemia w/ sulfons or insulin Diabetic ketoacidosis
“Offensive Linemen”  Delayed carb absorption Cirrhosis
Acarbose, Miglitol  Lower postprandial glucose Caution: CKD, liver disease Major Chronic GI!

SGLT2 inhibitors “Halt” renal glucose absorption Lower glucose ind. Of insulin Dehydration GFR <45-60, Allergy
“The Traffic Cops” increase renal excretion by inhibiting the Weight loss (2-5kg) Genital yeast infections & UTIs
*end in –glifozin” protein Can lower blood pressure Increased LDL Caution:
Act of proximal tubule Masks ketoacidosis Osteoporosis, CKD

GLP-1 Agonists “mimic” incretin GLP-1 Improves both FBG and PPBG *INJECTION! Allergy
“Imitators” increase insulin release, decrease *no hypoglycemia Risk of hypoglycemia with sulfons Phx, fhx thyroid CA or
all in end “-tide” glucagon release, decrease gastric Weight loss 3kg N/V/D, slows motility MEN2
empyting, increase satiety Decreased appetite BBW Thyroid Cancer

DDP-4 Inhibitors “stretch” out the effects of endogenous Improves FBG and PPBG GI SE *less than GLP-1 allergy
“Stretchers” incretin GLP-1 Weight neutral May be expensive
*similar to GLP-1s but oral dosing Pancreatitis

Amylin Analogs “impersonate” the effects of amylin Improves FFBG and PPBG SC injection! Allergy
“Impersonators” decrease glucagon release, decrease weight loss BBW-hypoglycemia with insulin Gastroparesis
Pramlintide (Symlin) gastric emptying, increase satiety may be used with T1DM or T2 Nausea, vomit, anorexia Unknown hypoglycemic

SECOND LINE: SGLT2 inhibitors, GLP-1 agonists, DDP-4 inhibitors

Insulin Drugs Onset Insulin Coverage

Rapid-Acting Lispro (Humalog) Onset: 5-15 min Peak: 45-57 minutes Duration: 2-4 hours •Given at the same time of the meal
Aspart (Novolog) *usually with intermediate or long acting

Short-Acting Regular Insulin Onset: 30 min Peak: 2-4 hours Duration: 5-8 hours •Given 30-60 minutes prior to meal
*usually with intermediate or long acting

Intermediate NPH Onset: 2 hours Peak: 4-12 hours Duration: 8-18 hours •Covers insulin for ½ day
Lente *combined with rapid or short actin
*NPH usually given at bedtime

Long Acting Detemir Onset: 2 hours Peak: 3-9 hours (Detemir), no peak (Glargine) •Covers insulin for 1 full day
Glargine Duration: 6-24 hours (Detemir), 20-24 hours (Glargine) •Glargine causes less hypoglycemia than NPH
Lantus, Levemir *Should no be mixed with other insulin in same syringe

Complication DM About Characteristics Treatment

Hypoglycemia Blood glucose <70 Autonomic: sweating, tremors, palpitations, nervous, tachy, cool •15-20 G fast-acting carbs
CNS: HA, lightheaded, confusion, slurred speech, dizzy, irritable •IV D50W or glucagon
 Diabetic Retinopathy Nonproliferative: initial stage Non-proliferative: Microaneurysms, Dot hemorrhage, Retinal exudates
*leading cause of blindness •Retinal capillaries leak proteins, lipids, or RBC
Proliferative: same plus growth of new vessels, cotton wool spots
•Proliferative: new capillaries release VEGF

Diabetic Nephropathy *more likely in T1DM Initial: proteinuria  24hr urine for protein=best
*can lead to nephrotic syndrome with massive
proteinuria, edema, HLD, hypoalbuminemia Biopsy: Kimmel-Wilson leasion (pink hyaline material)

Peripheral Neuropathy Distal symmetric: most common! Distal symmetric:

•Denervation of foot muscles -> toe clawing and •Symmetric, bilateral loss of sensation, vibratory sense, and temp
displaced fat pabs  ↑pressure  ulcer • “stocking-glove” distribution, Charcot arthropathy

Autonomic Neuropathy •Gastoparesis: delayed gastric emptying •Urinary: incomplete bladder emptying *control hyperglycemia
DX: upper endoscopy  nuclear scintigraphy •Orthostatic hypotension
TX-botox, Metoclopromide, Erythromycin •Erectile dysfunction

Cardiovascular •5x risk of complications •Hyperglycemia, hyperlipidemia, inflammation, HTN, oxidative stress,
•3x risk of cerebrovascular complications abnormal platelet function and coagulation
•30x risk of gangrene of the feet •Treat: aspirin if >10% 10-yr risk

Immune More frequent, more severe infections •Impaired phagocytosis; impaired flow  immune cells cant travel
•High glucose helps organism growth

Skin •Candida
•Eruptive cutaneous xanthomas
•Pigmented pretibial papules/diabetic
dermopathy/shin spots
•Acanthosis nigricans
•Necrobiosis lipidica diabeticorum

TSH: best test for screening, Free T4: metabolically active hormone, ordered when TSH is abnormal , Free T3: use if TSH low and T4 normal
Thyroid Antibodies: Graves (Anti-TSI), Hashimoto (Anti-TG and anti-TPO)
Primary: HIGHs TSH and low T4, Secondary: low TSH, low T4
Radioctive Iodine: diffuse uptake: Graves, TSH adenoma; decreased uptake: thyroiditis; hot nodule: toxic adenoma; multiple: toxic multilobar; cold: r/o malignancy

Subblicnical Hypothyroidism: elevated TSH alone, normal free T3/T4; treatment is observation

ENDO Etiology Clinical Presentation Complications/Management

Cretinism Untreated congenital •mental development delays •high TSH •Levothyroxine
hypothyroidism •short stature •low T3, T4
•microglossia, coarse facial features, umbilical
Causes: hernia
•lack of maternal iodine •hypotonia (decreased DTRs)
•dysgenesis of thyroid gland •jaundice, feeding problems

Subacute •Likely due to viral infection (URI) •Acute enlargement of thyroid •↑ ESR level High-Dose aspirin, NSAIDS
(Granulomatous •hyper  euthyroid  hypothyroid •Pain: worse with head movements & swallow •(-) antithyroid antibody titer +/- corticosteroids if severe
 , DeQuervans) •starts in lower neck and radiates to jaw & ear BB for acute symptoms
Thyroiditis *MC-young & middle-aged women •Dysphagia Biopsy: granulomatous
*summer •Malaise, low-grade fever, Thyrotoxicosis inflammation with Severe: iodinated contrast agents
multinucleated giant cells

Suppurative Bacterial infection of thyroid gland by
Thyroiditis Gram (+) Staph. aureus
*only two causes of painful thyroids
are subacute and suppurative
•Severe pain, tenderness, redness, and
•fluctuance
•Fever, chills, pharyngitis
•↑ ESR level; ↑ leukocytes •Antibiotics
•Normal thyroid & antibodies •Surgical drainage of abscess
Thyroid US-abscess presence Complications:
•Abscess
FNA biopsy + gram stain + Cx •Chronic sinus tract formation

Riedel •systemic fibrosis of thyroid and
Thyroiditis adjacent neck structures
•middle aged or elderly women
•Asymmetric, stony, adherent gland •TSH varies •Tamoxifen and/or steroids
•non-tender, rapid growth •IgG4
•Dysphagia, dyspnea, pain, hoarse •surgery for decompression
Biopsy: dense fibrosis
*clinically similar to anaplastic thyroid CA *distinguish from anaplastic CA

Sick Euthyroid abnormal thyroid function studies in MANY! •Cardo, renal, pulm, GI, liver •decrease T3
Syndrome the setting of severe non-thyroidal •Sepsis disease •increased reverse T3
illness •Starvation/anorexia •Inflammatory •normal T4
•Burns •Trauma •TSH varies
Pathophysiology •Cancer •Surgery
•severe illnesses decrease peripheral *rT3 ↑ with stressor
conversion/deiodination of T3/T4

Toxic Adenoma •multiple hyperfunctioning •symptoms of thyrotoxicosis •decreased TSH and high T4 •RAI ablation
autonomous nodules •obstructive symptoms: dyspnea, dysphagia, •surgery for compressive sx
hoarsness, stridor RAI: multiple areas of iodine
•palpable thyroid gland uptake “hot nodules”

Thyroid Ultrasound: nml or decreased vascularity; RAI Uptake: typically low RAI uptake; Thyroiditis Complications: thyrotoxicosis, thyroid storm, hypothyroidism, depression, cancer
ENDO
Hyper- Causes: HIGH BMR, increased DTRs Thyroid labs: Treatment: PTU
thyroidism •Graves Disease (MC) •Heat intolerance •Primary: ↓TSH, ↑ FT4
•Toxic multinodular goiter •Weight loss, hyperglycemia Hypercalcemia, ↑ alk phos, Anemia Graves: radioactive iodine
•TSH secreting pituitary adenoma •Warm, moist skin & hair Decreased granulocytes
•Excess intake •Hyperactive: anxiety, tremor, nervous,
•Iatrogenic thyrotoxicosis fatigue, weakness •Graves-(+) TSI,(+) anti-TPO, anti-Tg Thyroid Storm Definitive tx:
•Amiodarone •Tachycardia, high output HF, A-Fib increased RAI and vascularity radioactive iodine surgery
•Scanty period, diarrhea
Graves: •Thyroiditis: ↑ ESR
•autoimmune disease of TSH receptor Eyes: lid lag with downward gaze
antibodies target and stimulate TSH
receptor Graves dermopathy (pretibial
myxedema): red, rough plaques
 Thyroid •Potentially fatal complication of
Storm untreated thyrotoxicosis
Triggers: surgery, trauma, infection,
illness, pregnancy
Hypo- Causes:
thyroidism •Iodine deficiency
•Hashimotos thyroiditis (autoimmune)
•Potpartum thyroiditis
•Pituitary hypothyroidism
•Hypothalamic hypothyroidism
Primary: failure of thyroid T3, T4
Secondary: failure of pituitary TSH
Tertiary: Failure of hypothalamus TRH
Hashimoto Autoimmune thyroid disease due to anti-
s TPO and anti-TG
*most common thyroid disorder
painless postpartum: autoimmune
Painless sporadic:
subacute form of Hashimoto, not
associated w/ pregnancy
Myxedema •extreme form of hypothyroidism
Coma
MC in elderly women with
hypothyroidism in the winter
Disease Signs/Symptoms
Thyroid >90% of nodules are benign
Nodules and Follicular adenoma MC benign
Goiters
Risks:
•exteme ages
•history head/neck radiation
Symptoms:
•most are asymptomatic
•compressive symptoms (large
multinodular goiters)
Exam:
HYPERMETABOLIC
•N/V/D, high fever
•Tremors, psychosis (AMS)
•Lid lag
•Palpitations, tachycardia
•Liver failure
LOW BMR, decreaed DTRs
•Cold intolerance
•Weight gain, hypoglycemia
•Constipation, menorrhagia
•Dry, thick skin; brittle nails
•Loss of outer 1/3 eyebrows
•Non-pitting edema (Myxedema)
•Hypoactivity: fatigue, sluggish,
memory loss, depression
•Bradycardia, low CO
•Diffusely, enlarged, firm, finely
nodular thyroid WITHOUT pain
•Hypothyroid sx, depression, fatigue
•loss of outher 1/3 of eyebrow
•+/- galactorrhea
•Goiter symptoms: hoarseness, dyspnea
Postpartum-hyper  hypo
Sporadic: hyper x1-2mo hypo
•bradycardia & obtundation
•hypthermia
•hypoventilation, hypotension
•hypoglycemia, hyponatreamia
Labs
Order TSH *FIRST TEST
•if normal or high  FNA biopsy
Thyroid US: *usually after labs
•determines if FNA is needed
•concerning-irregular margins, hypoechoic,
central vascularity, growth, >1cm
FNA Biopsy *BEST TEST
•nodules >1.5cm with normal TSH or
highly suspicious nodules
RAI Uptake *hyperfunctioning tissue
•Insulin resistance
•Increased free T3 & T4
•Decreased TSH
•serum TSH +/- FT: ↑ TSH, ↓ FT4
Hashimoto:
• (+) (anti-TPO) *MC and (=) anti-Tg
Imaging:*not indicated in simple cases
•thyroid US
•CT MRI views gland
(+) anti-TPO and (+) anti-Tg
RAI: diffuse decrease uptake:
Thyroid US: diffuse heterogenous density
FNA biopsy: lymphocytes, hurthle cells
Postpartum: (+) anti-TPO
•LOW Na+ and glucose
•increased TSH, LOW T4
Imaging Results
Multinodular Goiter
•Multiple hyperechoic nodules
•Enlargement of isthmus and
thyroid lobes
Thyroid nodule
•Single nodule, color flow Doppler
Solitary Thyroid nodule
•Discrete hypoechoic nodule
Multinodular Goiter
•SVC compression
1. Propranolol *reduce cardiac
sx
2. PTU *block new T3/T4
3. Iodine *blocks hormone relase
4. Glucocorticoids *reduce
peripheral conversion
Definitive: radioactive iodine
Treatment: Levothyroxine
•Treament Myxedema:
IV levothyroxine (LT4)
•Supportive Myxedema: blankets,
intubation, tx underlying
Observe if asymptomatic
Hypothyroidism-•Levothyroxine
Large gland/goiter
•Levothyroxine suppression
*higher risk of spontaneous
miscarriage in 1st trimester
•IV levothyroxine
•warming, supportive
Management
•Follow-up with regular palpation
and •US every 6mo
•LT4 suppression for nodule >2cm and
normal or high TSH
*reduces emergence of new nodules
•Ethanol Injection *shrink benign
nodules
Toxic Multinodular Goiter:
•Methimazole +/- BB
•Surgery
 •benign: varies
•malignant: rapid, fixed, no
movement with swallowing
•hypofunction=cold, high cancer risk
•hyperfunction=hot, low cancer risk
•Tracheal deviation
Cancer, Hyperfunction, Toxic: Surgery
Toxic adenoma, Tosic MNG, Graves
•RAI therapy *shrinks nodules by
~60%

Thyroid papillary thyroid carcinoma *MC
Cancer •single thyroid nodule, painless
•MC after radiation exposure
•least aggressive, slow, confined
Follicular Thyroid Carcinoma
•metastasize (distant MC)
• ↑ iodine uptake
Medullary Thyroid Carcinoma
•Secrete calcitonin, prostaglandins,
5HT, ACTH, CRH, other chemicals
•Local mets, NO good iodine uptake
Anaplastic Thyroid Carcinoma
•Most aggressive, worst survival
•Rapidly enlarging mass in MNG
•Does not have good iodine uptake
•hard rock thyroid mass
•Palpable, firm, nontender nodule/mass Serum Tg
•↑-metastatic papillary and
Symptoms: follicular
•Anaplastic-s/s of metastasis
•Medullary-flushing, diarrhea Serum Calcitonin
*Medullary can be associated with Men IIa •↑-medullary thyroid carcinoma
and b
Serum CEA
MC Met Sites: lung, lymph, bone •↑-medullary thyroid carcinoma
Thyroid US *size, location of mass
RAI Scan *use after thyroidectomy
•reveal metastatic tissue
High uptake: follicular
CT or MRI: Distant metastases
CA: COLD & LOW uptake
Surgery-First Line
>1cm cancer: total
<1cm cancer: lobectomy
<4cm inderterminate: lobectomy
>4cm indeterminate: total
RAI therapy
CI-prego, nursing
*low iodine diet for 2wkbefore
Chemo: aggressive CA

TSH •benign pituitary adenoma that •diffuse goiter HIGH TSH and T4 •transphenoidal surgery
Secreting secretes TSH •hyperthyroidism SX •somatostatin analogs
Pituitary •compression os structures  bitemporal Radioactive iodine: DIFFUSE
Adenoma hemianopsia (optic chiasm), headache
Order MRI to detect adenoma

PHARMACOLOGY ***all BBW against the use for obesity *don’t take with food Monitoring: TSH every 4-8wks after change/start, then q6-12h
Drug Indication/MOA Monitor SE CI
Levothyroxine (T4) Hypothyroidism Monitor: Cardio: angina, palpitations, tachycardia, arrhythmia, CHF, Hypersensitivity
(Synthroid, Levoxyl, TSH suppression •check TSH levels every 6 weeks flushing Acute MI
Levothroid) Thyrotoxicosis
MOA: synthetic •best taken in the morning on an EMPTY CNS: anxiety, fatigue, insomnia, irritability, Adrenal insufficency
FIRST LINE thyroxine (T4) STOMACH pseudotumor cerebri (peds)

Endocrine: menstrual irregularities, wt loss

GI: abd cramps, diarrhea, vomiting, ↑appetite

Liothyronine (T3) Hypothyroidism 25mcg qd; titrate 12.5-25mcg/1-2wks Cardio: hypotension, tachycardia, arrhythmia, MI, CHF
(Cytomel, Triostat) Myxedema *take with water 1hr before food
Goiter suppression CNS: twitching, nervousness, irritability,
elderly/CAD-
 5mcg qd, titrate 2mcg per 2wks Endocrine: menstrual irregularities, wt loss
GI: abd cramps, diarrhea, vomiting

Liotrix Hypothyroidism 25/6.25mcg daily; titrate every 2-3wks Cardio: tachycardia, arrhythmia, HTN, palpitation Hypersensitivity
(Levothyroxine/ *take with water 1hr before food Thyrotoxicosis
Liothyronin) CNS: anxiety, insomnia, nervousness, irritability Adrenal insufficiency
(Thyrolar) elderly/CAD-
12.5/3.1, titrate 2-3wk Endocrine: menstrual irregularities, wt loss
GI: abd cramps, diarrhea, vomiting
Desiccated Thyroid Hypothyroidism 15-30mg daily; titrate every 6wks Cardio: angina, palpitation, tachycardia, arrhythmia, CHF Hypersensitivity
(armour thyroid, *take with water 1hr before food Thyrotoxicosis
nature-throid, CNS: anxiety, fatigue, insomnia, irritability, Adrenal insufficiency
westhroid) *don’t use in elderly Beef or pork allergy
Endocrine: menstrual irregularities, wt loss
65mg=100mcg levo GI: abd cramps, diarrhea, vomiting, ↑ appetite

Thiourea Drugs MOA SE CI &Monitoring

Methimazole Inhibits organification of iodine, blocking formation of thyroid hormone Methimazole carries greater risk of teratogenicity and Hypersensitivity
(tapazole) goes more into break milk than PTU Breast Feeding (Canada)
•prevents thyroid hormone synthesis •Pruritis, rash, urticarial, Joint pain *PTU only
•Abnormal taste, N/V, fulminant hepatitis
USE IN 1st TRIMESTER & STORM •Agranulocytosis, aplastic anemia Monitor:
•Thyroid
Propylthiouracil Inhibits organification of iodine, blocking formation of thyroid hormone PTU greater risk hepatotoxicity than methimazole •LFT
(PTU) AND decreases conversion of T4 -> T3 BBW hepatotoxicity •CBC
*first line for prego or breast feeding

PSYCH 5%-insomnia

Disorder About Presentation Findings Treatment

Anorexia •Refusal to maintain a normal body weight LOW BMI (>17.5kg/m2) or body weight <85% ideal •metabolic alkalosis 1st line-multimodal
Nervosa •Morbid fear of gaining weight •Leukocytosis & leukopenia (therapy, SSRI, nutrition)
•distorted body image •emancipation (thin), depressed, fatigue •hypogonadotropic
•MC in women and teenage girls •bone pain, osteoporosis, amenorrhea hypogonadism Hospital:
•highest death rate of all psych conditions! •abd pain, constipation •Anemia •<75% ideal body wt
•hair loss, brittle nails, lanugo •Hypokalemia •electrolyte imbalances
Types: •Russel Sign •Hypothyroidism •cardiac abnormalities
•Restrictive: reduced calorie intake, dieting, •hypothermia, decrease HR and BP •Increased BUN
excessive exercise, diet pills (dehydration)
•Purging: primarily engages in self-induced
vomiting, diuretic, laxative, enema
Bulimia •MC in females and late-teens •NORMAL/HIGH BMI •Metabolic alkalosis 1st line-multimodal
Nervosa •Recurrent binging & compensation •abdominal pain, constipation, hair loss •Hypokalemia •therapy
ONCE WEEKLY x3 MONTHS •teeth pitting or enamel erosion •Hypomagnesemia •SSRI-Fluoxetine
•increased heart rate •increased amylase •nutrition
Types: •puffy cheeks (parotid gland)
*self-worth influenced by
•purging: laxatives, vomiting, diuretics
shape and body weight
•non-purging: low kcal, diet, fast, exercise Russels Sign: calluses on dorsum of hand from vomit

Disorder About Criteria Treatment

Intimate •1/4 women, 1/7 men one in lifetime Clues: •screening, assessing, referring
Partner •women who leaves abusive partner has 70% > risk of being killed •contusions to chest ,breast, abdomen, face, neck •adress pateints directly with non-
Abuse •pregnancy abuse can make up 10% pregnancy-related hospital •MSK and “accidental injuries” threatening questions
admissions •multiple injuries in various stages of healing

Sexual •common ages 9-12 years old Clues:

Abuse •MC perpetrators: males, relatives, known by child •children with sexual knowledge
•initiate sex acts with peers or show knowledge
•bruises, pain, pruritis in genital or anal area

Physical •abuser often female and primary caregiver •cigarette burns, burns in stocking glow pattern
Abuse •laceration, healed fracture, subdural hematoma
•multiple bruises, retinal hemorrhages

Child •failure to provide basic needs of a child •malnutrition, failure to thrive, withdrawal, poor
Neglect hygiene

Disorder About & Criteria Symptoms Treatment

General •MC in females •restless/on edge •irritable •SSRIs (Paroxetine, Escitalopram,
Anxiety •fatigue •sleep disturbance Fluoxetine), SNRI (Venlafaxine)
Disorder •Excessive worry or worry a majority of days for •difficulty concentrating •headaches •Buspirone as adjunct *NO sedation
(GAD) 6+ MONTHS with 3+ symptoms •muscle tension •shakiness •Benzos *short term
•CBT x6-12 months
Panic Panic Attacks: Panic Attacks: 4+ hallmark sx of sympathetic overdrive Panic Attacks:
Attacks/ •Episode of intense fear or discomfort that develops •rule out life-threatening conditions (MI, thyrotoxicosis) •Benzos (Lorazepam, Alprazolam)
Disorder abruptly; usually peaks within 10min, last <60min
Physical Symptoms: Panic Disorder
•dizzy, trembling, choking, paresthesias, sweating, SOB, CP, •SSRI (Paroxetine, Sertraline,
Panic Disorder: chills, fear of losing control, fear of dying, palpitations, Fluoxetine, Citalopram)
•average age 20s, MC in females tachycardia, nausea, depersonalization or derealization •CBT
•Recurrent, unexpected panic attacks •combo is best
•2+ attacks x1 month and 1+ criteria sx (concern
 about future, persistent worry, maladaptive behavior) Panic Disorder Criteria Symptoms Acute Attacks: Benzos
•4/13 physical symptoms •persistent concern/worry of another attack
•worry of losing control during attack
•maladaptive behavior

Phobic •Symptoms 10-15min prior to specific stress event •out of proportion 1st line: CBT/exposure therapy
Disorder •causes fear 2nd line: SSRI, Benzos
•6+ MONTHS of fear/anxiety about an situation •actively avoided, distress Specific, predictable trigger: Benzos

Social •6+ MONTHS of intense fear of social situation or •MC type of phobia-public speaking •CBT (1st line), SSRI/SNRI or both
Phobia/ performance where you can be scrutinized Performance: Beta Blockers
Anxiety
Agoraphobia •Fear of going into places where you cant escape Scenarios: •SSRI, CBT, or both
•public transportation •open or closed spaces
•6+ MONTHS of fear/anxiety about 2+ scenarios •crowd/lines •outside home

Disorder About Criteria Treatment

Bipolar I/II Risks: FHX, men=women, 20-30 year old
Mania: abnormal or persistently elevated, expansive or
irritable mood for at least 1 WEEK
Hypomania: mania sx for < 1 week; no impairment
Bipolar I: 1+ FULL MANIC or mixed episode and
occasional depressive
•marked impairment in social/occupational function
•mood (euphoria), thinking (racing thoughts,
disorganized, distracted, grandiose), behavior (no
sleep, impulsive)
•1st line Mood Stabiliziers: Lithium
*reduces SI risk
•Others: atypical antipsychotics
(Ripseridone, Quetiapine, Olanzapine,
Ziprasidone)

Mixed: criteria for one and 3+ sx of other Bipolar II: 1+ MDD and 1+ hypomania episode
*Antidepressants may precipitate mania
Rapid: 4+ ep/yr

Cyclothymic •Similar to bipolar II but less severe 2+ YEARS of hypomania and depressive symptoms •Mood stabilizers (Lithium) and
•Gender: men=women (no more than 2 free consecutive months neuroepileptics

Drug MOA Indication Side effects DDI CI

Benzodiazepines Enhance GABA •Anxiety, panic •Drowsiness •ETOH •Pregnancy
Short: at receptor •insomnia, •dizziness •Opioids •Allergy
-Midazolam •ETOH withdrawal •decreased motor coordination •CNS depressants •Myasthenia gravis
-Triazolam •agitation •decreased libido •Anticonvulsants •Glaucoma
Long: •seizure •disinhibition •antidepressants
-Diazepam •procedural sedation •rebound anxiety, SI •antifungal
-Flurazepame
-Chlordiazepoxide Rare: respiratory depression

Buspirone •5HT-1a Anxiety •Dizziness, headache •Other Psych meds Allergy

receptor agonist •Drowsiness, nausea, HA •CNS depressants
•dopamine *NO SEDATION •Serotonin Syndrome
receptors
 Hydroxyzine Histamine •Anxiety •Drowsiness •Potassium Allergy
(Vistaril, Atarax) receptor •muscle relax •dizziness •MAOIs 1st trimester prego
antagonist •antihistamine •dry mouth •CNS depressants *only use po route
•antiemetic •rash
•insomnia •respiratory depression

•Antidepressants take about 4-6 weeks to reach efficacy

•Duloxetine first line if depression + neuropathic pain

Serotonin Syndrome: increased serotonergic activity in the CNS due with initiation or change in srotonergic drugs (SSRI, SNRI, TCA, MAOI, Buspirone, triptans or combo)
- AMS, agitation, confusion, hyperthermia, tachycardia, diarrhea, N/V, spontaneous/inducible conus, hypertonia (increased DTR), tremor, mydriasis (dilated pupil)
- TX: discontinue medication, supportive care; NO antipyretics for hyperthermia

Disorder About Criteria Treatment

Major Risks: FHX, female, 20-40yo 2+ WEEKS of 5+ SX •Psychotherapy
Depressive •must include anhedonia or depressed mood
Disorder Screen: •SSRI x4 weeks
(MDD) •PhQ2  PhQ9 if (+) •other symptoms: depressive mood, anhedonia, fatigue, *if not affects after 4 weeks then adjust
•Zung Self-Rated insomnia or hypersomnia, guilt or worthlessness,
recurring thoughts of death, psychomotor agitation,
Pathophysiology: weight loss, appetite change
•Alteration in neurotransmitters serotonin, epi, norepi, •Somatic SX: constipation, skin changes, pain
dopamine, ach, histamine
•Neuroendocrine dysfunction (adrenal, thyroid, GH) Catatonic: motor immobility, stupor, withdrawal
Melancholia: anhedonia, lack of reactivity, depression,
weight loss, excessive guilt, agitation
Seasonal •depressive symptoms at the same time each year •SSRI, light therapy, Buproprion
Affective (MC is winter “winter blues”)
Disorder
Atypical •mood reactivity (improved mood) in reposonse to •weight gain, appetite increase •MAO inhibitors (Phenelzine,
Depression positive events •hypersomnia Tranylcyprimine, Isocarboxazid)

Persistent •Patients are usually able to function Persistently depressed for 2+ YEARS with 2+ •SSRI and therapy
Depressive •No SX of hypomania, mania, or psychotic features symptoms (no more than 2 consecutive free months)
Disorder
(Dysthymia) •MC in women and teens/early adulthood

Grief •altered emotional state in response to loss •usually resolves in 6 months to 1 year •Psychotherapy
Reaction •peak in the first couple months •short course Benzos for insomnia
5 Stages: denial, anger, bargain, depression, acceptance Abnormal Grief: >1 year or positive SI

Premenstrua PMS: cluster of physical, behavior, and mood changes with •Physical: bloating, fatigue, breast swelling or pain •lifestyle modifications
l Dysphoric cyclical occurrence during luteal phase of menstrual cycle •Emotional: irritability, depression, anxiety, hostility, •SSRI (1st line for emotional)
Disorder libido hanges, aggressiveness •OCPs (Drospirenone contain)
PMDD: severe PMS with functional impairment •Behavioral: food cravings, poor concentration

Diagnosis: onset 1-2 weeks before menses, relevied

day 2-3 menses, 7 days free during follicular

Suicidal •recognizing the problem, assessment of risk, and SADPERONS: 5+ points is high risk Low risk: indicates remorse, shame or
Patient development of a treatment plan S: sex: male *female more often, male more affective embarrassment at suicide attempt
A: age: middle (45-64)
Recognition of SI D: depression High risk: sits quietly, engages poorly with
variable presentation: P: previous attempt *strongest predicitive factor physician, voices regret for surviving
•obvious attempt to cause self-harm E: ethanol use •require hospital admission to psych
•less obvious presentation: MVA or exchange of gunfire R: rational thinking loss service or medical with psych consult
•vague complaints, unwillingness to expand on thoughts S: social support lacking
O: organized plan Assure patient safety
• general questions about the patients emotional state N: no spouse (alone)
“what are your feelings about dying? S: sickness
“what has stopped you from killing yourself so far?”

Depression MOA CI Side effects Differences

SSRIs Selectively decreased •Allergy •N/D, anorexia •Sertraline: diarrhea, less QT, drowsy
FIRST LINE action of 5-HT reuptake •MOAI w/n 2 weeks •Sleep changes, HA, anxiety, dizziness •Citalopram/Escitalopram: more QT, least liver
*Fluoxetine 5wks •Decreased libido, anorgasmia, ED •Fluvoxamine: shorted t ½ and CYP
•Prolonged QT, WT gain, bleeding •Fluoxetine: long t ½ and don’t use with Tamoxifen
•Serotonin syndrome, increased SI •Paroxetine: anticholingeric SE, CYP, don’t use with
Tamoxifen *panic disorders 1st line
SNRIs Block reuptake of 5-HT •Allergy •N/D/V, constipation, dry mouth •Venlafaxine: high SE, elevated BP
2nd line if cant and NE (Milnacipran and •MOAI w/n 2 weeks •Sleep changes, HA, anxiety, dizziness •Desvenlafaxine: less HTN
tolerate SSRIs Levomilnacipran greater) •Angle closure •Decreased libido, anorgasmia, ED •Cymbalata: least associated with BP
glaucoma •Diaphoresis, HTN, SS syndrome •Milnacipran/Levomilnacipran: anticholinergic SE
•LESS SEX and NO WEIGHT GAIN!

Atypicals Buproprion: •Buproprion:, seizure, Buproprion: *NO WT GAIN OR SEX

Buproprion dopamine and NE reuptake anoremia, MAOI 2 weeks •dry mouth, insomnia, nausea
Remeron inhibitor •seizures, tobacco cessation
•Remeron: MAOI 2 wks
Remeron: antagonizes Remeron:
alpha-2 and 5-HT2/3 •dry mouth, drowsiness, sex dysfunction
•wt gain, increased appetite

Serotonin Nefazadone/Trazadone: •Allergy HA, N/D, SI risk, serotonin syndrome •Nefazadone: BBW-hepatotoxicity
Modulators Antagonize 5-HT •MOAI w/n 2 weeks  Drowsiness, xerostomia, hypotension
*with initiation and increase in dose •Trazadone: SEDATION, dry mouth, WT NEUTRAL
Vilazadone/ Vortioxetine:  Rare: priapism, cardiac arrhythmia
Partial agonist 5-HT •Vialazdone/Vortioxetine: N/V/C/D, sex dysfunction
 Faster onset and less sexual dysfunction

MAOIs MAOa: Break down •Allergy *MANY DDI INTERACTIONS Selegiline (Eldepryl): low doses for Parkinsons
Parnate serotonin and NE •Serotonin w/n 2 weeks •hypotension  Less CI than other MAOIs
Nardil •Cardiovascular •GI, urinary hesitancy  Less hypertensive crisis with transdermal
Marplan MAOb: •Pehochromocytoma •HA, myoclonic jerks
Eldepryl Break down dopamine •Hepatic/renal •edema
•Hypertensive crisis-foods with
tyramine

TCAs Inhibits reuatake of •Allergy •Anticholinergic, drowsiness, sweating Nortiptyline and Desipramine: highest tolerability
5-HT and NE •MOAI w/n 2 weeks •sexual dysfunction, wt gain & appetite
•Acute recovery of MI •tremor, OD fatality Tertiary(5-HT): Amitriptyline, Doxepin, Imipramine
•Cardiotoxicity (QT) Secondary (NE): Nortrip, Despiramine, Protriptyline

TeCAs •Ludiomil: •Less anticholinergic and more *have extra cyclic ring
block NE & 5-HT antihistaminic than TCAs *last resort, don’t ever really prescribe
Ludiomil •SI risk
Asendin •Asendin: blocks NE,
dopamine

Bipolar Labs/Indication Side effects DDI CI

Lithium Indication: Acute: GI, tremor, thirst, polyuria, weight gain, •Diuretics •CKD, dehydration, sodium
•Acute mania/hypomania or loose stools •NSAIDS depletion
maintenance •ACEIs •cardiovascular disease
Long term: LITH-PA •Tetracyclines •pregnancy
•Antidepressant *several wk onset •Leukocytosis, insipidus (renal), tremor, •Metronidazole •Ebstein’s anaomly
•Reduced SI risk & relapse risk hypothyroidism, parathyroid, arrhythmia •theophylline •increased lithium toxicity
 Valproate •Bipolar I/II N/V, HA, hair loss, bruising, weight gain, •TCAs •Allergy
*Depakote tremor, dizziness •anticonvulsants •Liver
enteric coated Labs: •Mitochondrial
*increase GABA •Serum drug. LFT Rare: hepatotoxic, pancreatitis, low platelets •Pregnancy

Lamotrigine •Bipolar I/II Nausea, rash, pruritis, drowsiness, MANY Allergy

*inhibit *safest for pregnancy
glutamate Labs: Serum drug, LFT, renal Rare: multiorgan hypersensitivity. SJS, TEN

Carbamazepine •Bipolar I/II Nausea, rash, pruritis, hyponatremia, fluid MANY •Allergy
retention, leukopenia •TCAs
Labs: •MAOI w/n 2 weeks
•Serum drug levels Rare: bone marrow suppression, aplastic •Bone marrow suppression
•LFTs, CBC, sodium anemia, SJS, TEN •Pregnancy

Alcohol Dependence: When withdrawal symptoms develop or tolerance

Substance About Intoxication Withdrawal Treatment
Alcohol Drink: Alcohol Intoxication: •uncomplicated (6-24h): increased CNS Screening: CAGE 2+ is (+)
•12oz beer •8oz malt liquor •Slurred speech activity (tremors, anxiety, diaphoresis, C: cut down
•5oz wine •1.3oz spirits •incoordination, unsteady gait palpitations, insomnia) A: annoyed
•nystagmus G: guilt
At-Risk Drinking: •impairment in memory or attention •withdrawal seizure (12-24h): E: eye opener
Continuous use of alcohol •coma or stupor MC tonic-clonic
-men: 4 drinks/day or 14 drinks/week Withdrawal:
-women: 3 drinks/day or 7 drinks/week Wernickes TRIAD: •alcoholic hallucinosis (48h): hallucinations •Benzos, Clonidine,
confusion, ataxia, ophthalmalgia with normal vital signs Barbiturates, Anticonvulsants
Moderate-Severe Drinking: •IV fluids, Thiamine & Mg
•Recurrent use of alcohol despite risks Karsakoff: •delirium tremens (2-5d): delirium, •Glucose
amnesia, aphasia, apraxia, agnosia hallucinations, agitations, abnormal vitals
Tolerance: need for increased amounts Chronic use TX: Naltrexon,
of alcohol; diminished effect with S/S: sweating, tachycardia, increased hand Campral, Antabuse
continued use of same amount tremor, insomnia, N/V, hallucinations, •Thiamine
agitation, anxiety, seizure

Substance Intoxication Withdrawal Treatment

Marijuana •Takes effects in about 10-20 minutes Withdrawal *usually only with heavy use Urine drug test can detect for 4-6
•Cannabis binds to CB1/2 cannabinoid receptors •irritable days and up to 50d in chronic users
•insomnia & restless
Intoxication •diaphoresis Treatment:
Moderate dose: •diarrhea Symptomatic
•euphoria, giddiness •twitching
•dry mouth (cotton mouth)
 •conjunctival erythema Complications of long-term use:
•tachycardia, hypotension •laryngitis & rhinitis
•low testosterone and low sperm count
High Dose: hallucinations, paranoia, delusions

Tobacco Withdrawal Symptoms: (+) effects: decrease anxiety and appetite, increase mood, •Nicotine Replacement
•restless alertness, soling •Buproprion (Wellbutrin)
•anxiety •Verenicline (Chantix)
•irritable (-) effects: CA, DM, COPD, asthma, dental, infection
•sleep abnormalities
•depression Tolerance due to UP REGULATION of receptors
•nicotine craving
•weight gain

Alcohol Chronic Use

Drug MOA Side Effects CI/DDI
Thiamine •Low BP
(B1) •Effect glucose metabolism

Naltrexone Blocks dopamine release, antagonizes mu BBW: hepatocellular CI: opioid dependency
1st LINE receptor  decreases craving and reward •N/V/D/C, abd pain DDI: opioids
•dizzy, HA, anxiety, fatigue
Acamprosate Restores glutamate •Diarrhea, nausea, abd pain CI: renal (Cr <30)
(Campral)  Stops withdrawal S/S •fatigue, HA, amnesia, mood
1st LINE
Disulfiram Inhibits enzyme aldehyde dehydrogenase  •Metallic taste CI: heart or CAD, ethanol
(Antabuse) increases acetaldehyde  Fs you up •Effects of drug  sweating, HA, dyspnea, low BP, DI: “WAM”-warfarin, amitriptyline, metronidazole
2nd Line flushing, palp

Substance Intoxication Withdrawal Treatment

Hallucinogen PCP (NMDA receptor antagonist) *15-30 minutes PCP Labs: CK-MB, AKI, CBC, CMP.
PCP, LSD •S/S: euphoria, numbness, disorientation, physical S/S: depression, anxiety, irritable, restless, sleep disturbance urine drug test
detachment, body distortion, unusual strength, dilated
pupils, multidirectional nystagmus LSD Treatment:
•no withdrawal because it does not affect dopamine •Haloperidol
LSD (5-HT receptor) •Benzos
•S/S: visual hallucination, see sound as color, dilated •Low stimulus environment
pupils, delusions

Inhalent Intoxication Common Chemicals Antipsychotics if severe aggression

Paint, Mild/moderate: euphoria, slurring speech, confused, •Toluene
petroleum, hallucinations, watery eyes, impaired vision, rash •Butane, Propane
toluene, glue, •Fluorocarbons
nail polish High dose: cardiopulm failure, liver, kidney, bone •Chlorinated hydrocarbons
marrow suppression *all organ failure •Acetone

Opioid MOA: mu receptor agonist Withdrawal Intoxiation:

heroin, •lacrimation Naltrexone (1st line)
oxycodone, Intoxication: •HTN, tachycardia Methadone,
morphine, •euphora •pruritic Buprenorphine
meperidine, •sedation & impaired memory •piloerections (goose bumps)
codeine •slurred speech •pupil dilation OD: Nalaxone
•impaired social function •flu-like symptoms
•pupil constriction •yawning Withdrawal:
•respiratory depression Methadone
•bradycardia & hypotension Clonidine
•nausea, vomit, flushing Lofexidine
Suboxone
Biots breathing: quick, shallow inspirations  apnea

Sedative/ GABAa channel-increased frequency of opening Withdrawal: Intoxication:

Hypnotic/ •rebound anxiety •Flumazenil (GABA antagonist)
Anxiolytic Intoxication: •seizures and tremors
Benzos •respiratory depression Withdrawal:
•hypotension •long acting benzo (Clonazepam)
•ataxia, amnesia (forget things), coma, death

Stimulants Intoxication: Withdrawal: Intoxication: *do not restrain

Cocaine •mydriasis (pupillary dilation) •depression and SI •antipsychotics
Amphetamine •hyperactivity, euphoria •hyperphagia •benzos
Meth •perspiration •hypersomnolence & fatigue •antihypertensives (Labetolol)
•excessive talking  depression •craving •vitamin C
•weight loss, anorexia •vivid unpleasant dreams
•dry mouth Withdrawal:
•nose bleeds and sepal perforation (COCAINE!) Kindling: hallucination and paranoia •Bupropion •Bromocriptine

Opioid Overdose Treatment

 Drug MOA Dose Side Effects
Naloxone Short-acting opioid antagonist Cardiorespiratory: 2mg
ventilations: 0.05mg IV
Opioid Use Treatment
Drug MOA Dose Side Effects
Naltrexone Blocks dopamine release, antagonizes mu receptor 25-50mg daily BBW: hepatocellular
1st LINE  decreases craving and reward Vivitrol (IV): 380mg IM/4wks N/V/D/C, abd pain, dizzy, HA, anxiety, fatigue
*opioid antagonist, completely blocks effects

Methadone Long-acting opioid agonist 20-30mg po, titrate up (80-120mg) •Constipation, drowsiness, sweating
•peripheral edema, hyperalgesia
•reduced libido, ED
•QT prolongation, OVERDOSE

Buprenorphin Partial agonist *often in combo with Naloxone •HA, nausea, pain
e *take home therapy 4mg B/1mg N daily •insomnia
most stabile on 16-20mg/d B •withdrawal syndrome

Taper by reducing 2mg/1-2wk Rare: liver, necrosis, anaphylaxis

Tobacco Use Treatment

Drug Use Dose Side Effects
Transdermal Apply to skin once daily, avoid hair, change places each •>10 cig: 21 x6wk, 14 x2wk, 7 x2wk •Skin irritation
Patch day •10 or less cig: 14 x6wk, 7 x2wk •Insomnia, vivid dreams

Oral Nicotine DON’T CHEW •Smoke w/n 30 min: 4mg •Mouth irritation
Lozenge •All others: 2mg •N/V/D, HA, insomnia
•Max: 5 every 6hrs or 20/day •palpitations

Oral Nicotine Diminishes withdrawal •25+ cigs: 4mg •N/V/D, HA

Gum “chew and park” method •all others: 2mg •excess salivation, mouth irritation
*avoid TMJ, poor dentition, dental appliances

Nicotine Absorbs through mucosa 6-16 cartridges/d for 6-12 wk Oropharynx irritation, bronchospasm
Inhaler Satisfies behavioral & sensory cravings *avoid RAD (asthma)

Nicotine Absorbed through nasal mucosa 1-2 sprays/3mo •Nasal and throat irritation
Nasal Spray Max: 10 sprays/hr or 80/day •sneezing, tearing

Buproprion Blocks dopamine and NE reuptake 150mg/d x3d, 150mg BID x12wk •Insomnia, agitation
(Wellbutrin) Antagonizes nicotinic rec. •dry mouth, HA
*start 1wk before quite date
•CI: Epilepsy, seizure, h/o anorexia/bulimia

Varenicline Partial agonist of nicotinic rec. 0.5mg x3d, 0.5mg BID x4d, 1mg BID •Vivid dreams
(Chantix) -Decreases withdrawal x12wk •nausea, insomnia, syncope
-Interferes with reward *start 1wk before quite date
Serious: neuropsych (SI, mood, behavior)
 Disorder About & Criteria Symptoms Treatment
Post- •trauma at any time with symptoms > 1 MONTH AVOIDANCE (1+): effort to avoid measure, effort to avoid 1st line-CBT with exposure
Traumatic •Men: combat experience, urban violence reminders
Stress •Women: rape or assault •SSRI/SNRI
Disorder EXPOSURE (1+): direct experience, witness, learn it happened (Paroxetine, Sertraline, Fluoxetine)
(PTSD) PTSD Criteria: to someone close, extreme/repeated exposure
1. Exposure to actual or threatened death, serious •Trazadone is good to use insomnia
injury, sexual violence INTRUSTION (1+): distressing memories, distressing dreams,
- Direct experience of the event feeling or reoccurrence, psych reaction or stress
- Witness the event
- Learn the event happened to someone close NEGATIVE CHANGE IN MOOD/COGNITIVE (2+):
- Experience extreme or repeat exposure memory loss, exaggerated, distorted thoughts, negative state
2. Presence of symptoms (avoidance, exposure, constantly, inability to be positive, decreased interest,
intrusion, negative change, arousal/reactivity) detachment
3. ALL have to occur for ONE MONTH
AROUSAL/REACTIVITY (2+): irritable, reckless, startled
easily, sleep disturbance, difficulty concentrating

Acute Stress •traumatic event occurs <1 MONTH ago and •similar symptoms to PTSD •counseling & psychotherapy
Disorder symptoms last < 1 MONTH *different between the two is the timing

Adjustment •maladpative emotional or behavioral reaction to an •marked distress out or proportion to the severity of stressor •psychotherapy
Disorder identifiable stressor •may manifest as depressed, anxiety, conduct disturbance
•disproportionate response within 3 MONTHS,
usually resolves by 6 MONTHS

GU 5%-balanitis
GI
Hernia (Inguinal) Indirect (MC!):
•internal inguinal ring
•lateral to inferior epigastric
•persistent patent process
vaginalis
Femoral Hernia Protrusion of the contents
through the femoral canal
Umbilical Hernia Occurs after closure of the
umbilical ring
MC in women
Risks: mult pregnancies,
ascities, obesity, intra-
abdominal tumors
Ventral Hernia Herniation through weakness
(Incisional in the abdominal wall
hernia)
MC in ventral incisions in
obese patients
GU
Glomerulo- Inflam glomeruliprotein, RBC in urine
nephritis
*intrinsic Types:
renal injury IgA nephropathy (Buergers)-MCC
•young males after URI or GI
Post-Infectious(high ASO, low comp.)
•MC with Group A Strep
•2-14yo boys, facial edema, cola/dark urine
Membranoproliferative: lupus, hep(HCV)
Rapid Progressive (RPGN)
•crescent formation on biopsy
GoodPastures Disease (anti-GBM)
•glomerulonephritis + hemoptysis
Vasculitis: polyangitis (P-ANCA) and
wegeners (C-ANCA)
Pauci-Immune: churg-strauss
Masses About/ Causes Signs/ Symptoms
Direct: Incarcerated: •Surgical repair
•Hesselbachs triangle: “RIP: rectus abdominis, •painful, enlarged and
inferior epigastric, pouparts (inguinal) ligament irreducible •Strangulated are surgical
•medial to inferior epigastric emergencies
•Does NOT reach scrotum Strangulated: systemic toxicity
•below the inguinal ligament •often become incarcerate or
•MC in women strangualted b/c small ring
•Increases steadily in size High rate complications: Observation: usually resolve by 2yo
•Umbilical hernias usually contain omentum •large size of the hernia
•Incarceration and strangulation are common •old age or debility of pt Surgical repair
•obesity •persistent after age 5
•Umbilical hernias with tight rings are often •intra-abd disease
associated w/ sharp pain on coughing or straining
•Aching sensation
Risks: •Small incisional hernias should be
•Poor surgical technique, post-op complications treated early
•Postop wound infection •Elastic bind if CI to surgery
•advanced age, general debility, obesity
•placement of drains or stomas through primary *typically, surgeons do not fix this
operative fascial defect due to rectus abdominus fascia
•defects in collagen
Classic presentation: UA: •High dose corticosteroids
•HTN •hematuria, proteinuria (<3g) *slows immune process
•Edema •RBC casts
(scrotal, periorbital) •high specific gravity •Cytotoxic agents if cell mediated
•hematuria (cola or tea-
colored urine) Labs: high BUN/Cr •Plasma exchange: Goodpasture
•Proteinuria •Complement low in immune complex disease and pauci-immune
•RBC, WBC, RBC casts •ASO titers (post-infectious)
•Anti-GBM antibodies
•ANCA levels (Pauci-Immune)
Renal Biopsy: GOLD
•IgA: IgA mesangial deposits
•Poststreptococcal: immune humps, hypercell
•Goodpastures: IgG in basement membrane
Diagnosis Treatment
Testicular •MCC testicular tumor in 18-40
Tumor/
Cancer Types:
•germ cell: seminoma & non
•nonseminomas: high AFP & b-
hcg, resistant to radiation
•seminomas: 4s: simple (lack
AFP), sensitive (to radiation),
slow, stepwise spread
Risks:
•Cryptorchidism
•Exogenous estrogen in prego
•Infertility, Fhx HIV, ethnicity
•Painless enlargement of testis
-testicular or scrotal heaviness
-painless nodule on testicle
•acute testicular pain -10%
•metastatic symptoms-10%
MC site of metastasis-retroperitoneal
abdominal lymph nodes
-Back pain, cough/dyspnea, anorexia,
N/V, bone pain, LE swelling
Labs: •Inguinal exploration with vascular control
•Alpha-fetoprotein (AFP) of spermatic cord
*nonseminomas •Radical inguinal orchiectomy
•Hcg *nonseminomas •Radiation/chemo with seminoma
•LDH
•Advanced: anemia, LFTs, renal Follow-Up:
•Monthly for 1st 2 years, bimonthly 3rd yr
Imaging/diagnosis: •Tumor markers at each visit
•Scrotal US-initial evaluation •CXR and CT every 3 months
*transscrotal biopsy contraindicated •80% relapse in 1st 2 years after tx
•Definitive: -radical inguinal Prognosis: 90% + 5 years survival rates
orchiectomy

Disease Causes/Risks Signs/Symptoms Labs/Imaging Treatment

Benign •More common with increasing age
Prostatic *more sensitive to androgens & GF,
Hyperplasi stops nml cell death
a (BPH) •Increase in both glandular and stromal
component
Risks:
•Genetics (African americans more
likely, Asians less likely)
•Increase Risk: Higher PSA levels,
prostatitis, heart disease, BB use, lack of
exercise, obesity
•Decreased risk: NSAIDS, excessive
ETOH, smoking, exercise
*alcohol & smoke suppress T
Usually begin slowly, progress gradually
Obstructive voiding-hesitancy,
decreased force, incomplete bladder
emptying, double voiding (urinating
within 2 hr), straining, post-void dribble
Irritative: urgency, frequency, nocturia
*detrusor muscle hypertrophy and
hyperplasic, collagen deposit
DRE: smooth, firm, symmetric, elastic
enlargement of prostate
Neuro: r/o neurogenic bladder
Lower abd exam: evaluate distention
Labs:
•UA: normal, possible hematuria
•PSA: can be elevated in BPH
2 mechanisms of obstruction:
•Mechanical: narrowed urethral
lumen or bladder neck
•Dynamic: A-receptor stimulation
causing increased tone
(constriction) to prostatic urethra
Pharm:
•Alpha-1 Blockers: Tamsulosin
•5-alpha Reductase: Finasteride
*reduce size of prostate
Surgical Procedures:
•Transurethral Resection of the
Prostate (TURP) *MC!
*can cause retrograde ejaculation
•Tranasurethral Incision (TUIP)
•Open Simple Prostatectomy
Minimally Invasive:
•Laser Therapy (TULIP)
•Transurethral Needle Ablation of
Prostate (TUNA)
•Transurethral Electrovaporization
•Hyperthermia
•Implant to Open Prostatic Urethra
Drug Class Drugs in class MOA SE Notes
SELECTIVE Prazosin (Minipress) Help with •Orthostatic hypotension, dizziness, combo of alpha blocker and 5-alpha reductase is
Alpha-1-blockade Doxazosin (Cardura) symptoms tiredness, retrograde ejaculation, rhinitis, HA first line
“-osin” Terazosin (Hytrin)
*doxazosin and Terazon more •Intraoperative floppy iris syndrome
effective but more SE

NON-SELECTIVE Sildosin (Rapaflo) DDI: Antihypertensives & PDE-5 inhibitors

Alpha-1a-blockade Tamsulosin (Flomax) *drop BP when taken with alpha blockers
“-osin” Alfuzosin (Uroxatral)

5-alpha-reductaste Finasteride reduces size of •Decreased libido •Don’t work overnight and may take up to 6 months
inhibitors Dutasteride *more efficacious prostate gland •Erectile or ejaculatory dysfunction to see treatment
Jalyn (combo of dutasteride and *more effective for very large prostates because
tamsulosin) reduce PSA by 50% and size by ~20%

PDE 5 Inhibitors Tadalafil (Cialis) BPH + ED •Not covered well by insurance

Phytotherapy Saw Palmetto •If doesn’t want to take meds- try this
*approved in Europe

GU About Clinical Presentation Diagnostics Treatment

Renal Types: •Acute, severe pain (flank) Labs: Supportive: pain (NSAIDS, opioids), fluids, antiemetic
Calculi •Calcium oxalate- MC! •radiate to abdomen or groin •hematuria (micro or gross)
(Nephro- •Uric Acid: protein, gout, chemi •Urgency and frequency •<5.5: uric acid or cysteine Pharm:
lithiasis) •Struvite: Mg Ammonium Ph •Nausea/Vomiting • 5.5-6.8: calcium oxalate •Alpha-1 blocker-Tamsulosin
•Cysteine: rare •Hematuria • >7.2: calcium phosphate/struvite •Steroids-Prednisone 10mg daily for 3-5d

Risks: Exam: CVA tenderness Frequent or + family history: Surgery:

•high protein and salt
•inadequate hydration
•humidity & elevated temp.
•sedentary lifestyle
•GI malabsorption syndromes
•HTN, obesity, gout
•<5mm pass spontaneously
•10mm+ do NOT pass
*stone size does NOT
correlate with severity
•Low Na & protein, high fluid
Diagnostics:
•KUB abdominal xray (cheapest)
•Renal US (good if noradiation)
•Non-Contast Spiral CT-BEST!
•extracororeal shock wave lithotripsy
•uretroscopy w/ w/o stent  immediate relief if obstruct
•percutaneous nephrolithotomy  large >10mm, struvite
Prevention:
•Increase fluids-best thing to do! (1.5-2L of urine/day)
•Diet (Eat bran to decrease calciuria)
*do not need to decrease calcium!

GU About Presentation Diagnostics Treatment

Acute •non-gonococcal v gonococcal
Urethritis
Bugs:
•Neisseria gonorrhoerae (MC!)
•Chlamydia trachomatis (2nd MCC)
•Mycoplasma genitalium
•Trichomonas vaginalis
Risks: men, young & sexually active
MC route: ascent up urethra
Epididymitis •often occur simultaneously due to an
and Orchitis underlying bacterial etiology
Orchitis:
•isolated orchitis is often viral of
syphilitic (rare to find alone)
•viral orchits MC due to mumps
(5d post parotitis; unvaccinated)
Epididymitis
•bacterial infection is most common
•men <35: G/C *h/o sexual risk
•men >35: E. coli and Klebsiella
Acute Bugs: Gram – rods most common
Bacterial •>35 years old: E. coli, Pseudomonas,
Prostatitis Proteus, Klebsiella, Enterobacter
•<35 years old: G/C
MC route: ascent up urethra
Risks: catheter, biopsy, stricture, UTIs
Chronic Bugs:
Bacterial •Gram – rods most common
Prostatitis •E. coli
•Pseudomonas, Proteus, Klebsiella,
•Enterococcus
MC route: ascent up urethra
Type of Stones Causes
•Irritative voiding (dysuria)
•Pain/pruritus at urethral meatus
•Urethral discharge:
-nongonococcal: scanty/thin/watery
-gonococal: thick/purulent/copious
Exam:
•+/- inflammation at urethral meatus
•Thick, purulent, copious discharge
*gonorrhea
•gradual onset of milt to severe
unilateral testicular pain
-lower abd, inguinal canal, scrotum
•+/- fever, dysuria, discharge (UTI)
•affected testis will hang low
*inflammation and edema pull down
Exam:
•swollen, tender, warm
•cremasteric reflex normal
•Phren (+)
•Fever, chills, malaise
•Pain-perianal, sacral, suprapubic
•Irritative & obstructive voiding
Digital rectal exam (DRE): *KEY!
hot, exquisitely tender prostate
*prostatic massage CI due to sepsis
•Dull, poorly located, in suprapubic,
perineal or low back pain
•Irritative & obstructive voiding
•HX UTI or (+) cultures
DRE: nml (MC), may see boggy
(spongy), tender, enlarged, and/or
indurated prostate
About/Diagnosis
Labs:
•>2 WBC/hpf
•Gram (-) intracellular
diplococci
Nucleic Acid: BEST TEST
•first catch or first void
UA:
•+ WBC esterase & pyuria >10
•+/- hematuria
Ultrasounds of Scrotum
•r/o torsion
•enlarged epididymis
•increased blood flow
UA with C/S: pyuria
Nucleic Acid Amplification
•test for G/C
Labs:
•CBC: leukocytosis, left shift
•UA: pyuria, bacteriuria,
hematuria
•Urine culture: + for bacteria
Imaging: rarely indicated
Labs:
•Prostatic secretions: increased
WBCs (>10) with a (+) culture
UA: nml unless cystitis a
Urine culture: negative; + for
organism AFTER massage!
Treatment
Empiric treatment
*usually treat both G & C together
Gonorrhea:
•Ceftriaxone250mg IM x 1 dose
Chlamydia:
•Azithromycin 1g po x 1 dose
•Doxycyline 100mg po BID x7days
Outpatient
<35: Ceftriaxone+Azithromycin or Doxy
>35: Fluoroquinalone, Bactrim
•elevation, ice, NSAIDs, stool softener
•avoid lifting heavy objects and straining
•follow up with urology in 5-7d f
Admission  toxic or septic
•fever, hypotension, tachycardia (shock)
-workup: CBC, CMP, blood culture
<35: Ceftriaxone + Azithromycin
>35: Bactrim OR Levofloxacin
IV: fluroquinalone +/- aminoglycoside, or
amp/gent
Oral (MC): Bactrim 800-160mg BID or
Fluoroquinalone (Cipro)
Fluoroquinolones or Bactrim x6wk
SE of prolonged use:
C. diff, CNS, tendinopathy
Supportive: anti-inflam, sitz baths
Hypercalciuric •Absorptive hypercalciuria
Stones *calcium •Resorptive hypercalciuria
•Renal hypercalciuria
Absorptive hypercalciuria: Increased urinary Calcium even without high •Absorptive hyperclacuria-thiazide diuretics or
dietary calcium intake, high absorption in S.I. cellulose phosphate (bind to Ca)
Resorptive hypercalciuria: secondary to hyperparathyroid Resorptive hypercalciuria-treat elevated PTH
Renal hypercalciuria: normal or low serum Ca Renal hypercalciuria-thiazide diuretics

Hyperuricosuric Dietary purine excess or uric •Allopurinol (gout medication)

Stones *calcium acid metabolic defects

Hyperoxaluric Primary intestinal disorders H/o chronic diarrhea, usually have IBD •Stop diarrhea, avoid excess ascorbic acid
Stones Absorb oxalate more than calcium *cut down vit C tablets and/or orange juice
*calcium •Calcium carbonate

Hypocitraturic Chronic diarrhea, chronic •Reduce potassium citrate supplements

Stones *calcium HCTZ treatment, acidosis •Oral lemonade
Uric Acid Calculi Hyperuricemia, Urinary pH consistently <5.5 •Increase pH > 6.2 *helps treat patients
myeloproliferative disease, •Potassium citrate (alkalizes urine)
cancer, abrupt weight loss Xray: Pure uric acid is radiolucent *cant see on xray •Allopurinol 200mg/day if hyperuricemia

Struvite Calculi MC-women w/ recurrent UTIs Urease-producing: Proteus, pseudomonas, providencia “PPP” *usually cause staghorn calculi
Cystine Calculi Abnormal cystine excretion Xray: radiolucent; “smooth-edged ground glass” Urinary volume foal 3-4L, goal pH >7.0

About Presentation Diganosis Treatment

Acute Bugs: •Irritative voiding (dysuria) Labs: Short term antimicrobial Therapy
Cystitis •E. coli •Frequency urgency & frequency •Pyuria •Nitrofurantoin 100mg po BID x5-7d
“Bladder •Proteus •Suprapubic pain •Hematuria *safe in pregnancy
Infection” •Klebsiella •+/- gross hematuria •Bacteriuria •Bactrim 800/160mg po BID x3d
“UTI” •Pseudomonas •Leukocyte esterase •Fosfomycin (Monurol) 3g po x1
•Staph saprophyticus Exam: •Urinary nitrate •FQs, Augmentin, Cephalosporins
•Suprapubic tenderness •Urine culture + bacteria
MC route: ascent up urethra •NO CVA! Analgesics: Phenazopyridine (Azo)
•NO TOXICITY! COLONY COUNT >100,000 Other: baths, fluids +/- juice, probiotics
Risks: women, sex, spermicides, pregnancy *epithelial cells indicate
(P and E), elderly, infants contamination *DO NOT TREAT IF NO SX

Acute Bugs: •Irritative void (dysuria) Labs: Outpatient:

Pyelo- •E. coli •Suprapubic pain •Pyuria, hematuria, bacteriuria •1st line: FQ (Cipro or Levo),
nephritis •Proteus •+/- gross hematuria •+/- WBC Casts Bactrim, Augmentin
“kidney •Klebsiella •Fever, chills, N/V/D •Leukocyte esterase & Urinary
infection” •Pseudomonas •Flank pain nitrate •Adjunct/Pregnancy Tx:
•CX: + heavy growth of bacteria 1g Ceftriaxone (Rocephin)
MC route: Exam: •CBC: leukocytes w/ left shift
ascent up urethra •Fever Inpatient:
hematologic route •Tachycardia Imaging: •IV ampicillin/gentamicin, FQ
•CVA tenderness •CT: renal inflam, abscess •IV carbapenem (Imipenem)
•US: hydronephrosis, abscess •IV cephalosporin (Cefepime)
HEME 4%

HEME
Iron •MC anemia worldwide •Fatigue, weakness, dyspnea, exercise •High TIBC, RDW Ferrous Sulfate
Deficiency intolerance •Low iron, ferritin, transferrin *take with Vitamin C
Microcytic Causes: •hair thinning •Low MCV, low MCH, nml MCHC
•MCC blood loss (menstruation, GI) •pallor, pica, cheilitis *microcytic, hypochromic
•decreased absorption (diet, celiac) •koilycia, plummer vinson syndrome
Bone marrow: absent iron stores
Pathophysiology: *DEFINTIIVE
•decreased RBC production due to lack of
iron and decreased ferritin (iron stores)

Lead Pathophysiology: Neuro: ataxia, fatigue, learning Serum lead: >10 •removal of the source of lead
Poisoning •enzymes cause cell death  shortening disabilities, difficulty concentrating Capillary initial  venous best
Anemia life span of RBCs •wrist or foot drop <44mcg: outpatient follow-up and
•causes acquired sideroblastic anemia Smear: microcytic hypochromic lifestyle modfications
GI: abdominal pain, vomit, anemia with basophilic stippling
constipation, loss of appetite •ringed sideroblasts inmarrow 45-69mcg: succimer

Butrons lines: thin, blue-black line at X-rays: lead lines

base of the gums near the teeth

Alpha •Decreased alpha-globin •¼-silent •microcytic hypochromic •Moderate: folate, avoid oxidative
Thalassemia •MC in S.E. Asians •2/4- minor (trait) •normal/increased iron, ferritin stress, avoid iron supplementation
•¾- HbH (Heinz bodies)
Microcytic -Symptomatic at birth Smear: target cells •Severe: transfusions, splenectomy
-HSM, pigmented gallstones iron chelation (IV Deferoxamine),
-Frontal bossing Electrophoresis: all equal
•4/4- hydrops fetalis •HbH with ¾ deletion

Beta •Decreased beta-globin •½: Minor (trait)-asymptomatic electrophoresis: Minor: no treatment

Thalassemia •MC in Mediterranean •2/2: major (cooleys) •increased HbA2 and HbF,
-symptomatic around 6 months Major:
Microcytic HbF=2a2y -HSM, Frontal bossing & maxillary smear: target cells, nucleated cells •blood transfusions
HbA=2a2b, HbA2=2a2d growth, osteoporosis, cardiac (high •folate & vitamin C supplements
output HF) X-ray: crew-cut skull appearance •iron chelating (Deferoxamine)
“hair on end” appearance from
extramedullary hemtopoieses Definitive=bone marrow transplant
 HEME/ONC
Folate Pathophysiology: •fatigue, exercise intolerance, pallor Labs: Folate supplement
Deficiency •folate required for DNA synthesis •Glossitis, cheilosis •high MCV and homocysteine
Macrocytic •deficiency causes abnormal synthesis of •NO NEUROPATHY •normal MMA
DNA, nucleis acis, metabolism
Smear: hypersegmented neutrophils,
Causes: macro-ovalocytes
•MCC=diet  leafy greens, alcoholic
•increased requirements (prego, infant,
malignancy)
•impaired absorption
•impaired metabolism: MTX,
Trimethoprim
•loss from dialysis
B12 Source: animal meat, eggs, dairy •fatigue, exercise intolerance, pallor Labs: B12 (Cobalamin) Injections
Deficiency •glossitis, diarrhea, malabsorption •high MCV weekly until corrected  monthly
Macrocytic Pathophysioogy: •dereased B12
•intrinsic factor is released by the •NEUROPATHY (symmetric), loss of •high homocysteine & MMA •can switch to oral therapy after
stomach parietal cells which allows B12 vibratory, sensory, and proprioception symptoms resolve
absorption in ileum •decreased DTRS Smear: hypersegmented, macro- •if pernicious, then need lifelong IM
•B12 deficiency causes abnormal ovalocytes, basophilic stippling therapy
synthesis of DNA, nucleic acids, and
metabolism. B12 is needed to convert
homocysteine to MMA

Causes:
•decreased absorption: pernicious
anemia  damaged parietal cells  lack
of intrinsic factor
•diet (vegans)

HEME/ONC
Anemia of MCC of normocytic anemia •fatigue, exercise intolerance, pallor Labs: EPO if renal disease or low EPO
Chronic •normocytic normochromic anemia
Disease Pathophysiology: •increased hepcidin
Normocytic •increased hepcidin and decreased EPO •Increased ferritin
 not able to produce heme •Low iron and TIBC
•decreased RBC production

Caauses
•MCC: Chronic Kidney Disease (CKD)

Hemolytic Anemia: increased RBC destruction > bone marrow replacement

- Intrinsic (sickle cell, thalassemia, G6PD, spherocytosis); Extrinsic (autoimmune, DIC, TTP, HUS, PNH, hypersplenism)
- Labs: increased reticulocytes, increased INDIRECT bilirubin, low haptoglobin
HEME/ONC
Hereditary •autosomal dominant •varying degrees, may go undetected, Labs: All: folic acid (1mg daily)
Spherocytosis may present acute after infection •high reticulocytes
autoimmune Pathophysiology: •normal MCV, high MCHC Definitive: splenectomy
abnormally shaped RBC due to proteins in •anemia, jaundice, splenomegaly •(+) osmotic fragility, (-) coombs *could be partial
cytoskeleton  sphere instead of flexible •pigmented gallstones *delay until 5+yo or puberty
and biconcave  destroyed by spleen Smear: hyperchromic
microspherocytes -pneumococcal vaccine
-transfusions of EPO if severe
EMA binding: PREFERRED
•flow cytometry analysis
Sick Cell •Autosomal resessive •trait usually asymptomatic Electrophresis: •PCN at 2mo, folic acid at 1yr
Anemia •MC in African Americans •trait: HbA and HbS •supportive: folic acid, vaccines
Normocytic Disease: *begin as early as 6mo •disease: HbS
Types: •dactylitis-inflammation of •Hydroxyurea
•trait (heterozygous-AS) finger/toe joints Smear: Howell-Jolly, target cells, MOA: increases production of HbF,
•disease (homozygous-SS) •osteomyelitis (Salmonella) sickled RBC reduces RBC sickling
•aplastic crisis with parovirus B19 SE: myelosuppression, GI
Pathophysiology: •Jaundice, HSM, cardiomegaly Labs: increased reticulocytes
•Valine substitutes for glutamic acid on •Ill appearing, poor healing, Acute Crisis :
B chain  HbS has decreased solubility retinopathy, stroke, tibia skin ulcers Splenic Sequestration: HOP: hydration, oxygen, pain
under hypoxia  abnormal shape  •reticulocytosis
vaso-occlusive episodes  spleen Splenic Sequestration Crisus: *differentiates from aplastic crisis Definitive: allogenic stem cell
•acute splenomegaly •drop in hemoglobin
Triggers: SHITAE: stress, hypoxemia, •rapid decrease in hemoglobin •thrombocytopenia
infection, temperature changes, acidosis,
exercise Vaso-Occlusive Crisis:
•acute chest syndrome
•back, abdominal, bone pain
•priapism

G6PD •X-linked recessive; MC in AA males •EPISODIC hemolytic anemia Smear: Prevent: avoid oxidative drugs,
Normocytic •Jaundice, dark urine •Bite & Blister cells; Heinz Bodies triggers
•Deficit in G6PD enzyme •Malaise, weakness, pain
Labs: •Folic acid supplementation
•RBC is vulnerable to oxidative state  Triggers: •Low hgb & hct
hgb denatures  forms Heinz bodies  infection, food (fava beans), ABX •High reticulocytes & High MCH
damages membrane  spleen destroys •G6PD assay
Autoimmune •antibody forms against RBC (IgG) •abrupt, life-threatening Smear: Prednisone 1-2mg/kg/day orally
Hemolytic •fatigue, exercise intolerance, pallor •microspherocytosis *esp warm
Anemia Pathophysiology: •polychromataphils Severe: splenectomy
*autoimmune Warm:IgG, Cold:IgM for complement •hemolysis: hemoglobinuria,
• macrophages remove membrane  jaundice Labs: Comorbitities: treat underlying
spherocytes  destroyed by spleen •splenomegaly •low hgb, hct, RBC
•complement can tag Kupffer cells •high reticulocytes Transfusion: required
•high indirect bilirubin *give without type/cross matching
Causes:
•warm: idiopathic, meds, autoimmune DIAGNOSTIC: COOMBS (+)
•cold: infection (mycoplasma, EBV)
 HEME/ONC
Polycythemia Acquire disorder causing
Vera OVERPRODUCTION of ALL 3
hematopoietic cell lines
Pathophysiology: JAK2 gene mutation
Causes: radiation, toxins, men, 50-60yo
MCC of death=thrombosis
Primary v. Secondary Erythrocytosis:
Primary: low EPO, high WBC & plt
Secondary: high EPO, normal other
•Fatigue, HA, dizziness, vertigo
•Generalizes pruritus due to
histamine release
*worse in a warm shower/bath
•Bleeding-engorged vessels from plts
•Hypercoaguability
*increased blood viscosity and
platelet dysfunction
•abdominal pain, discomfort 
ulcers due to increased histamine,
hepatosplenomegaly
•Engorged conjunctival & retinal
vessels  vision changes
•Plethora-reddish uneven
complexion to the face, palms, nail
beds, mucosa
CBC:
•Elevated RBC, WBC, plt
•HCT> 54%males, 51% females
CMP: liver and renal
Peripheral Smear: normal
•Low EPO
•Genetic mutation: (+) JAK2
•Iron studies due to blood loss
Criteria:
3 major or 2 major + 1 minor
•Major: increased RBC mass
(hgb/hct), + BM biopsy, JAK2
•Minor: decreased EPO, increased
ALP, iron deficiency
Management: Refer to Hematology,
educate
Treatment:
Phlebotomy
•1unit decreased Hct by 3%
•Remove 1 units weekly until <45%
•ASA 81mg daily
•alternative=hydroxyurea
Myelosuppressive chemo if:
•Frequent phlebotomy
•High risk or mod/severe thrombosis
•Pruritis

Aplastic Failure of hematopoietic bone marrow
Anemia due to suppression or injury of stem cells
from T cell attack
MC: idiopathic autoimmune Diseases,
toxins, medications, infections (hepatitis
Pathophysiology:
Hypoplasia of hematopoietic bone
marrow  decrease WBC, RBC plts
•Decreased WBC-infection
•Decreased RBC-anemia, fatigue,
pallor
•Decreased platelets-bruising, bleed
Exam:
•pallor, purpura, petechial “3 Ps”
*no hepatomegaly, splenomegaly,
bone tenderness, lymphadenopathy
Labs:
•low WBC, RBC, platelets
•normal MCV, MCH
Bone marrow biopsy: BEST
•hypocellular fatty aspirate
•low/no hematopeitic precurosors
Supportive: RBC & PLT transfusion
Mild: bone marrow growth factors
•erythropoietic (EPO), myeloid
MOA: recombinant DNA
SE: HTN, thrombosis
BBW: vascular, heart issues, tumor
CI: uncontrolled HTN, aplasia
Severe: stem cell transplant

Primary Hemostatis:
Platelets form a plug at the site of vascular injury  platelet adhesion, activation, and aggregation
Platelets send out ADP and Thromboxane A  more platelets  platelet plug
- Diseases: ITP, TTP, HUS, DIC, vWF deficiency
- Labs: affects bleeding time, but NOT PT or PTT
- Classic Presentation: petechiae, mucocutaneous bleeding

Secondary Hemostasis:
Clotting factors respond in a cascade to form fibrin strains to strengthen platelet plug
Extrinsic pathways (1, 2, 5, 7, 10): prolongs PT *DIC, warfarin therapy, vitamin K deficiency, Intrinsic Pathway (1, 2, 5, 8, 9, 11, 12): prolongs PTT *heparin overdose
- Diseases: hemophilia, DIC, vWF
- Presentation: deep delayed bleeding (hemarthrosis), delayed bleeding after surgery
HEME About Clinical Presentation Diagnostics Treatment
Immune •antibodies against antigens on platelets •Bleeding, petechiae, bruising ISOLATED thrombocytopenia •Steroids
Thrombo- surface  destruction by spleen •mucosal bleeding <100,000
cytopenic Purpura •2nd line: IVIG, splenectomy
Causes: •NO splenomegaly •normal PT. PTT, INR
•primary: MC after URTI
•secondary: HIV, HCV, SLE, Marrow: megakaryocytes
antiphospholipid syndrome

Thrombotic platelets into thrombi in vessel  FATRN: Fever, anemia, Tests: Plasmapheresis with FFP
Thrombocytopenic shearing of erythrocytes thrombocytopenia, renal, neuro •vWF LOTS, ADAMTS13 low •removes antibodies, adds
Purpura (TTP) •LOW Hgb & platlets ADAMTS13 to serum
Pathophysiology: •Acute/subacute onset of neurologic •HIGH fibrinogen, bilirubin
Adults •low ADAMTS13 symptoms, anemia, or 2nd line: steroids,
Brain, Fever, vWF •high vWF thrombocytopenia Direct Coombs: negative (-) immunosuppression
*antibodies against ADAMTS13 •Fever 50% pts Smear: mod/severe schistocytosis
•Hemoglobinuria, splenomegaly 3rd line: splenectomy

Hemolytic-Uremic •Renal failure with microangiopathic •Prodromal gastritis Labs: Typical:

Syndrome (HUS) hemolytic anemia and (Fever, blood diarrhea for 2-7d •BMP: elevated BUN/CR Supportive care
thrombocytopenia  damages before onset of renal failure) •CBC: severe anemia, varying
Kids endothelial cells •Irritability, lethargy, Seizure thrombocytopenia Atypical:
Kidney •Acute renal failure, Anuria Plasma exchange ASAP
NO fever Typical: Shigella toxin, E. coli O157:H7 •HTN Smear: schistocytes (helmet cells)
Diarrhea •diarrhea in 2-3yo, acute renal failure •Edema *Antibiotics and anti-motility
•Pallor (due to anemia) •stool for E. coli and Shigella agents are avoided
Atypical: non-STx, sporadic or familial

Heparin Induced Pathophysiology: •Venous thrombosis: legs, cardiac, •new thrombocytopenia •anticoagulation: Argatroban
Thrombo- •Antibody to hapten of heparin and skin  necrosis, gangrene •platelet drop >50% *direct thrombin inhibitor
cytopenia (HIT) +PF4 forms neoantigen on platelet  •can be hypercoaguable because •venous or arterial thrombosis
antibodies  clearance  low destroyed platlets release granules •GOLD: 14-C-serotonin release
•onset 5-7d post therapy assay
HEME About Clinical Presentation Diagnostics Treatment
DIC Pathologic activation of coagulation system  •Widespread hemorrhage & thrombosis Labs: •Treat underlying cause
widespread microthrombi  consumes clotting •bleeding from venipuncture sites, •Increased PTT, PT/INR •FFP if severe bleeding
factors  thrombocytopenia and diffuse bleeding catheters, drains •Decreased fibrinogen •platelets if <20,000
*MC at venipuncture sites •Increased D-dimer
Causes: •gangrene or multi-organ failure •Thrombocytopenia
•infections (gram – sepsis)
•malignancies, obstetric (pre-eclampsia) Smear: fragmented RBC, shistocytes

vWF •Autosomal Dominant •recurrent nose bleeds, heavy •Decreased vWF, decreased VIII •DDAVP
Disease •MC inheritable bleeding disorder periods, prolonged wound bleeding •prolonged PTT and bleeding time •recombinant vWF or
•ineffective plt adhesion due to low vWF •family history •normal PT/INR Factor VIII
•use Celebrex for anti-
vWF function: promotes plt adhesion by GOLD: Ristocetin-induced platelet inflammatory
crosslinking GP1b receptor on plts with exposed aggregation *helps determine type
collagen on damaged epithelium
•factor VIII degradation

Hemophili •X-linked recessive; MC in children & males •hemarthrosis (joints, MC ankle) •prolong PTT & bleeding time • A: Factor VIII or DDAVP
a •A: factor VII deficiency (MC) •hemorrhage due to trauma •normal platelets • B: Factor IX
•B: Factor IX deficiency *christmas tree •possible purpura/petechiae • C: Factor XI
•C: factor XI deficiency *ashkenazi jews

HEME
Factor V Leiden •MCC inherited thrombophilia (hypercoag) •DVT, PE, Clotting •normal PT, PTT Anticoagulant indefinitely

Pathophysiology: Factor V: activated by thrombin and helps Activated protein C

•Mutation of Factor V  does not respond to convert prothrombin to thrombin resistance assay
protein C  does not turn off and keeps clotting  confirm with DNA test

Protein C/S •Autosomal dominant •DVT, PE •Protein C and S assay Indefinite anticoagulant
Deficiency •Vitamin K dependent anticoagulant proteins •purpura fulminans in newborns: red •plasma antigen levels
purpuric lesion at pressure points  eschar Necrosis: IV vit K, heparin,
•Protein C: risk warfarin induced necrosis protein C, FFP, Heparin

Anti-thrombin •Autosomal dominant •Venous thrombosis, DVT, PE •antithrombin III assay Thrombosis: high-dose IV
III deficiency Normal: inactivated thrombin, IIa, IXa, Xa •MC in deep veins and mesenteric veins heparin  oral

Antiphospholipi •Acquired hypercoaguable condition Cardiac: Libman-Sacks, endocarditis, Antibodies anticoagulation

d Syndrome •antibody (aPL) in plasmsa pulmonary HTN, thrombotic events
•necrosis of hip
HX: pregnancy complications •Livdeo reticularis, adrenal insufficiency
ONC
Hodgkins •Germinal B cells undergo
transformation
•2 peaks: 20s, 50s
Risks: EBV, smoking,
immunosuppressed
Types:
•nodular: MC, females
•mixed: EBV
•lymphocyte rich: MC in males
•lymphocyte poor: MC >60yo
Non-Hodgkins •Accumulate in lymph tissue
(spleen, nodes, thymus)
•malignant overgrowth of
lymphocytes; MC: B cells
Risks: increased age, radaiation,
fhx, immunosuppressed, infections
(EBV, HIV, HHV-8), autoimmune
•PAINLESS cervical/supraclavicular LAD •Staging: Ann Arbor Stage I-II: Combo Chemo
*alcohol may cause pain + radiation
•lymph spread in contiguous fashion •CBC normal, elevated ESR
(cervical MC) •CT/PET for staging Stage III-IV: combo
•Mediastinal mass, fatigue, wt loss ABVD: Adiramycin,
Biopsy: Reed Sternberg cells: large cells Bleomycin, Vinblastine,
•B SX: wt loss >10%, T >38C, sweats with bi/multi-lobed nuclei (owl-eye Dacarbazine
*indicate advanced disease appearance) & inclusions
MOPP: Mustine,
Exam: HSM, nephrotic syndrome, Oncovorin/Vincristine,
hyercalcemia PRocarbazine,
Prednisolone
•PAINLESS lymphadenopathy •viral serology Asymptomatic: no tx
*non-contiguous •CXR  CT of chest
•Cough, dyspnea, edema Stage I: Chemo
•Mediastinal mass, RLQ mass tissue biopsy: DIAGNOSTIC
•extranodal (GI MC) Intermediate/Aggressive:
•bone marrow RCHOP: Rituximab,
Types: Cyclophasphamide,
•Diffuse large B-Cell: MC, aggressive Doxorubicin,
•Folicular: slow growing, hard to cure Hydrochloride,
•Lymphoblastic: TT “teen, T-cells” ONcovorin, Prednisolone
•Burkitt: BBBB: boy, B-cells, belly,
chromosome B *EBV
•Large Cells: B and T cell
ONC
ALL •MC malignancy in children
•Leukemic BLASTS replace marrow
(immature cells)
AM •MC acute leukemia in adults
L •accumulation of BLASTS
Types:
•acute promyelocytic (APL): MC associated
with DIC, myeloperoxidase (+), auer rods
•acute megakaryoblastic: MC in children
<5yo and downs
•acute monocytic: infiltration in gums
(gingival hyperplasia)
CLL •MC LEUKEMIA IN US!
•mature B cell malignancy
Risks: old age, men
Complications:
•obstructive lymphadenopathy
•transformation into aggressive large cell
lymphoma (Richter syndrome)
CM •uncontrolled production of
L maturegranulocytes
•Single specific genetic mutation
(translocation) of gene 9:22
•PHILADELPHIA on PCR
First (Chronic): MC  mature cells
Second (Accelerated): cytogenic
Third (Terminal Blast): immature
•Fever, weakness, fatigue
•Bone pain, pallor, anemia
•Petechia, purpura, infection
Exam: HSM, weight loss, lymphadenopathy,
abdominal pain
•Fatigue(MC), infection, nodules, HSM
•pantocytopenia
Leukostasis reaction: MC w/ AML & CML
•increased viscosity  plug
microvasculature
•SOB, hypoxic, HA, dizzy, vision change
•WBC >100,000
•tre
•Slow onset! Usually found incidentally
•lymphadenopathy (MC!)
•recurrent infections (PNA, HSV, HZV)
•hepatosplenomegaly
*upper abdominal discomfort/fullness
•anemia/thrombocytopenia
•Fatigue! *often first symptom
•Low-grade fever, night sweats, wt loss
•abdominal fullness, bone tenderness
•pruritis, flushing
•GI ulcers with elevated basophils due to
histamine
PE: HSM, LAD
CBC: ANC <1000, WBC 5-100,000 Combination chemo
Smear: lymphoblasts (~25%) (anthracyclines,
Vincristine, steroids)
•Marrow FNA & biopsy DEFINTIVE
maintenance: 6-MP, MTX
CBC: low WBC & plt, normocytic Combo chemo
normochromic anemia
Smear: auer rod Leukostasis:
•leukapheresis
Bone Marrow Biopsy: GOLD
•>20% myeloblasts, auer rods
•pantocytopenia, WBC > 20,000 Low stage: observe
•Isolated lymphocytes (>5,000)
*small, well-differentiated, normal High stage/SX:
appearing with “smudge cells” chemotherapy
(Fludarabine, Rituximab,
FLOW CYTOMETRY: CONFIRMS Cyclophasphamide,
Confirms abnormal B-lymphocytes Chlorambucil)
BM Aspiration/Biopsy: small lymphocytes •stem cell transplant is
*not required curative
CBC: WBC 100-150,00 w/ left Chronic:
(neutrophilia, basophilia, eosinophilia) Tyrosine kinase inhibitor
(Imatinib, Nilotinib,
Alk Phos: low Dasatinib) “-tinib”
Smear: Accelerated: blast cells, Accelerate or Blast:
promyelocytes TKI + multidrug chemo
*possible stem cell
BM Aspiration/Biopsy: hypercellular with
increased granulocytes and progenitors
ID 4%

ID-Bacterial
Typhoid •Gram (-) Salmonella Typhi
(Enteric) Fever •MC in children, young adults
*Invasive
•Crosses intestinal epithelium through M
cells  Peyer’s patches; may colonize in
gallbladder
Transmission: fecal-oral, food, water, hx
travel to areas of poor sanitation
•headache, malaise, anorexia •culture •oral rehydration and electrolyte
•intractable fever, chills, abd pain replacement
•”pea soup” green diarrhea, non-bloody
ABX: Ciprofloxacin, Ofloxacin
Exam: •Azithromycin, Ceftriaxone
•fever with bradycardia
•rose spots (faint pain or salmon
macular rash from trunk to extremities)
•HSM, GI bleeding

Incubation: 5-21 days

Non-Typhoidal S. enteriditis, S. tymphimurium •nausea, vomiting, abdominal cramping •culture •oral rehydration and electrolyte
Salmonella •common cause of foodbourne illness •diarrhea “pea soup” brown-green replacement
*Invasive •abdominal cramping
Sources: •malaise, headache ABX: Ciprofloxacin, Ofloxacin
poultry, eggs, milk, reptiles (turtles)

Shigellosis •gram (-) rods: Shigella sonnei (MC) •lower abdominal pain, cramps •culture •oral rehydration and electrolyte
*Invasive S. flexneri, S. dysenteriae (enterotoxin) •high fever, tenesmus replacement
•explosive, watery diarrhea  mucoid •WBC >50,000
Transmission: fecal-oral, food, water and bloody diarrhea •avoid anti-motility drugs
Sigmoidoscopy:
Incubation: 1-7 days, Neuro: febrile seizure •punctate areas of ulceration Severe: ABX-Ciproofloxacin,
HIGHLY virulent Ceftriaxone, Azithromycin, Bactrim
Complications: reactice arthritis, HUS,
toxic megacolon

Spirochet
e
Lyme Borrelia burgdorferi Stage 1: early, localized *within 1 week Criteria: 1/2 •Doxycyline
Disease •MC tickborne illness •erythema migrans: bulls eye with central clear •developed erythema migrans
•MC in spring and summer •flu-like symptoms: HA, myalgia, fatigue •one late manifestation + one lab Alternative:
•MC in northeast & central US confirmation •Amoxicillin *pregnancy
Stage 2: early disseminated
Transmission: Ixodes tick (deer) •bacteremia, worsening flu-like sx, Serology: ELISA  western blot Late or Severe;
•cardiac: arrhythmias, heart block Use in patients if: •IV Ceftriaxone if AV block,
•neuro: aspetic meningitis, facial palsy (CN VII) -reside/travel in area syncope, dyspnea, chest pain,
-risk factor + symptoms CNS, meningitis
Stage 3: Late persistant *months-years after Not in:
•MSK (joint pain-arthritis), neuro, skin -pateints with erythema migran
-screening asymptomatic
Viral About Contagious Presentation Diagnostics/Treatment
Epstein-Barr •HHV 4 •malaise/fatigue, fever, sore throat, Heterophile Antibody: test of choice •Supportive: fluids, antipyretics
Virus (EBV, •tonsillar pharyngitis +/- exudates (Monospot) *IgM acute, IgG life •corticosteroids if airway obstruction
Mononucleosis) Transmission: •lymphadenopathy (posterior cervical) 
•Saliva, blood •splenomegaly Peripheral Smear: lymphocytosis >50%
• “kissing disease” •palatal petechial, maculopapular rash with 10% atypical lymphocytes AVOID TRAUMA & CONTACT
*Ampicillin increases rash SPORTS x3-4 WEEKS if HSM
•EBV antibodies

Viral
Influenza Transmission: respiratory droplets
(Viral) (sneezing, coughing, talking, breathing),
touching contaminated surfaces
3 types: A (most pathogenic), B & C
*A has more severe outbreaks than B
Increased Risk:
•age >65 years old *MC seen in children
•pregnancy
•immunocompromised
ABRUPT ONSET •rapid influenza nasal swab or Mild disease and healthy: supportive
•headache viral culture •Acetaminophen, fluids, rest
•fever, chills •RT-PCR (1-3d)
•malaise •NP viral culture (3-7d) Ostelamivir (Tamiflu) within 48 hours
•URI symptoms, pharyngitis MOA: neuramidase inhibitors A & B
•PNA •hospitalized patients
•myalgia: legs, lumbosacral •high risk of complications (age,
cardiovascular disease, pulmonary
Hemaglutinin: bind to epithelium disease, immunosuppression, chronic
(cellular infection) liver disease, hemoglobinopathies-sickle
Complications: PNA, respiratory cells, thalassemia)
Neuraminidase: cleaves bond failure, death, meningitis,
holdings new virions (spread of myocarditis encephalitis, rhabdo, Prevention:
infection) kidney failure •influenza vaccine (inactive): ages 6
months and above, x2 if <9yo
-CI: high fever, GB w/n 6wk, <6mo
•Chemoprophylaxis in long-term facilities
where outbreaks occur

PHARM MOA Route Dosing

Neuramidase Attaches to the receptor sites to prevent •oral Tamiflu: Rapivab 600mg IV
Inhibitor binding to the host cell  •capsules 75mg po BID x 5d •infuse 15-30min, adults 18+
•Diskhaler  •all ages (prophylaxis only
3mo+), age and wt based Relenza: 2 inhalations BID x5d
•ages 7+ (5+ for prophylax)
 Viral About
HIV Retrovirus: changes RNA into Acute seroconversion: •ELISA  western blot *offer to all HIV (+) pateints
(Viral) DNA via reverse transcriptase •flu-like illness •HIV RNA viral load >100K copies
•fever, fatigue, myalgia, sore throat -can be positive in window period Regimens:
Transmission: •nontender generalized lymphadenopathy •elevated LFTs, mild anemia, thrombocytopenia •NNRTI + 2 NRTIs
•sex •PI + 2 NRTIs
Suspected Early Infection: •INSTI + 2 NRTIs
•IVDU Opportunistic Infection: •combo antigen/antibody immunoassay +
•mother •oral and esophageal candidiasis HIV viral loading test (RT-PCR)
•blood contact •CMV •both (-) but high suspicion: repeat in 1-2wk
•PCP pneumonia •(-) immune, (+) viral: early HIV
AIDS: CD4 <200 •cryptosporidiosis •both (+): early/established infection
-confirm with a second test (repeat one)

Viral Drugs MOA Adverse EFfects

NRTIs Zidovudine Abacavir Inhbits viral replication by interfering with HIV •Zidovudine: bone marrow suppression
Lamivudine Emtricitabine viral RNA-depenent DNA polymerase •Abacavir: CI HLA B5701
Tenofovir Stavudine

NNRTIs Efavirenz Nevirapine Inhibits viral replication by interfering with •Rash

Delavirdine Rilpivirine HIV viral RNA-dependent DNA polymerase •Efavirenz: vivid dreams
Etravirdine

Protease Atazanavir Indinavir Inhibits HIV protease leading to production of •N/V/D

Inhibitor Darunavir Ritonavir noninfectious, immature HIV particles •Lipodystrophy, hyperlipidemia
s Nelfinavir Saquinavir

INTI Raltegravir Dolutegravir Orevents insertion of DNA copy into host •hyperlipdiemia, GI symptoms

Fusion Enfuvirtide Disrupts the virus from fusing with T-cells •hyperlipdiemia, GI symptoms
Inhibitor
s
CCR5 Maraviroc Blocks viral entry into WBC

HIV Prophylaxis:
CD4 <200: Pneumocystitis  Bactrim
CD4 <150: Histoplasmosis  Amphotericin B
CD4 <100: Toxoplasmosis  Bactrim
CD4 <100: Cryptococcus  Fluconazole
CD4 <50: MAC  Azithromycin or Clarithromycin
CD4 <50: CMV Retinitis  Valgangciclovir
NEURO
Bacterial Acute infections of the arachnoid
Meningitis mater and subarachnoid space
Adults:
•Community Acquired
•S. pneumo (children, adults >20)
•N. Meningitidis (10-19yo)
•GBS, Listeria Monoctogenes, H. flu
•Healthcare Acquired: Staph aureus
Pediatrics:
•Neonatal: GBS, E. coli, Gram (-)
•Children >1 month: S. pneumo, N.
meningitides, GBS, H. flu
Viral •MCC-Enterovirus
Meningitis
Risk factors:
•Infants <1 month
•Immunodeficient patient
•Exposure to someone
Historical features:
•travel and exposure history
•TB exposure
•ill contacts with similar sx/viruses
•vaccination history
•sexual history (HSV, HIV, syphilis)
Adults:
•Fever, HA, Nuchal, Meningeal
•N/V, photophobia, seizure
increased ICP:
-papilledema, N/V, LOC change
-meningococcal rash
Pediatrics:
•Fever, lethargy, seizure, resp. distress
•Jaundice, N/V/D
•Poor feeding/decreased appetite
•Restlessness/irritability
•Bulging fontanel (infants)
Present similar to bacterial meningitis
but less severe
•HA, nuchal rigidity, Photophobia
•Constitutional symptoms
•mildly diminished LOC
*NO seizures or focal neuro
•Blood cultures x2 + stain, C/S
•PROMPT LP first, UNLESS:
-immunocompromised
-history of CNS
-new onset seizure
-papilledema
-abnormal LOC
-focal neurologic deficit
•Meet any above=CT first!
*DO NOT DELAY ABX!
Lumbar Puncture:
•low glucose
•high protein & WBC
•cloudy, pressure 200-300
Work-Up: same as bacterial
Lumbar Puncture
•CSF analysis, Gram stain and
•PCR amplification
•clear, pressure <200, rest
nml/low
CT scan
-not needed in uncomplicated
indications: focal neuro,
immunocompromised
GOAL: TX WIHTIN 60min
Standard for all (3mo-55yo) ALL 3
1.Dexamethasone 0-20minutes
2.Ceftriaxone (Cefotaxime <1mo)
3.Vancomycin
PLUS ONE additional below:
•Acyclovir (HSV encephalitis)
•Doxycycline (tick season)
•Ampicillin (<3mo or >55yo)
•Metronidazole (OM, sinus, mastoid)
Duration of ABX:
•S. pneumo 10-14d
•N. mening & HiB 7 days
•S. aureus 14 days, L.mono 14-21 days
Rifampin or Cipro prophylaxis if:
•Exposure H. flu, S. pneumo, N.mening
•GBS (+) 35-37 weeks gestation
•Neurosurgery
•Most cases self-limited (7-10d) & tx is
supportive: fluids, rest, sx control
Specific treatments:
•HIV  refer; HSV  Acyclovir
Empiric ABX: old & immunocomp
Indeterminate diagnosis on CSF: 1 of 2
1. administer ABX after cultures
2. observe w/ repeat LP in 6-24h
Prevention: IPV, MMR, VAR/Zoster
URGENT CARE 4%
Heat Illness
Wasp, •stinging results in
Bee, Ants envenomation causing one of 3
presentation
-localized reaction
-systemic reactions
-anaphylaxis
Clinical Presentation:
•localized bee sting: MC
reactions
-small pruritis, painful,
erythematous, edematous
lesion at sthe sting site
-occasionalyl >5cm
Abortion
Scorpion •most scorpions produce
localized reactions
•bark scorpion
-only systemic toxic scorpion
-infants & child high risk
-southwestern US
Snake •large triable shaped head with
Bites (Pit a heat sensitive depression “pit”
Vipers) between their eyes
•venom is cytotoxic
•copperhead, rattlesnake
Heat Edema
Fire Ant Sting
•sterile pustule evolves of 6-24h
•may results in necrosis and scarring
Systemic/Toxic (nona-allergic)
•more common with >50 stings
•N/V/D with irticarial lesions distant from
site of string
•symptoms usually subside within 48h
•severe acses may lead to complications
-rhabdo, liver failure, hemolysis,
thrombocytopenia, DIC
Anaphylactic Reactions: allergic rxn
•occurs within 6hr (most within 15 min)
•itchy eyes, urticarial, cough, resp failure,
CV collapse
Presentation
•sting is painful without initial
erythema/swelling
•exquisite pain with light percussion
known as “tap sign”
•neuromuscular excitation
-spasms, CN dysfunction, roving eye
movement, diplopia, dysphagia
•fang marks wit hpain, edema,
hemorrhage and necrosis around bite
& extending distant from bite if severe
-usually within 30 minutes but may be
delayed up to 12h
-if no s/s after 12h: dry bite
Systemic:
•hemolysis, thrombocytopenia,
coagulopathy
•vomiting
•respiratory failure with CV and collape
Heat Syncope
Labs:
•ONLY FOR SYSTEMIC and
ANPHYLACTIC sx
•directed at complications:
-CBC, CMP, caogs, CK
Management:
Anaphylaxis
•intubation if needed
•Epinephrine 1:1000 (adults 0.3-0.5)
•IV Methylprednisolone
•IV Diphenhydramien (Benadryl)
•IV Famotidine (Pepcid)
•Nebulized albuterol
Localized reactions only:
•Benadryl
•oral pain control: NSAIDS, Tlenol
•systemic: IV methylpred, Benadryl,
famotidine
•complications: may require blood,
dialysis, and extensive hostpital care
Management
•most pateints can be managed
symptomatically
-oral or IV pain medication
-Benzo for motor control
•consult poison control
•cardiac monitoring and IV access
-administer fluids and resp support
Labs: CBC, CMP, coags, CK, urine
myoglobin, type and crossmatch
•Immobilize biten extremity
-EMS may apply contrisction band
-not effective from EBM
•serial (30 mintes) wound evaluation
-measure affected limb above and
Heat Cramps
Wound Management:
•do not delay tx of systemic reaction
to care for wound
•remove stinger w/ scraping technique
•wash wound
•ice and elevated
•tetanus update
Disposition:
•local: discharge home
•systemic
-admit child, elderly, comorbid,
50+ stings, or prolonged reactions
-otherwise can send home:
observe for 6 hours in the ED to
make sure not rebound sx, repeat
labs before discharge, RX
EpiPen, f/u with allergist
•antivenin (anascorp) indicated in
severe systemic toxicity
Antivenin (CroFab)
•approved for bites from rattlesnackes,
copperheads and cottonmouths/water
moccasins
•compare severity of envenomation to
SE of antivenin
-hypersensitvity reaction in 5-19%
-recurrent coagulopathy in 50%
•td upate
Disposition
•observe in ER for 8 hours, DC if no
 below bite and mark border progression, ICU if severe
-assess sx of compartment syndrome

Physical Exam Diagnostics Gastric Decontamination

Poisoned •mental status, vital signs, pupillary
Patient examination help classify excitation or
depression
Excitation:
•CNS stimulation, mydriasis
•tachy, increased BP, RR, temperature
•anticholinergics, sympathomimetic,
serotonin syndrome, hallucinogens
Depression:
•depressed mental status, miosis
•low BP, RR, temperature
•sedative-hynoptic agents, opiates,
cholinergic agents
Exam
•vital signs
•mental status
•general appearance: agitation,
confused
•skin (full exposure): cyanosis, flushing,
diaphoresis or dry, injury, ulcer, bullae…
•Eyes
-mydriasis: anticholinergics, sympatho
-miosis: cholinergics, opioids
-nystagmus: ethanol, phenytoin,
ketamine, PCP
-lacrimation: cholinergic
•mucous membranes
-hypersalivation: cholinergic
-dryness: anticholinergics
•heart
•lungs: bronchorrhea (cholinergic), wheeze
•abdomen:
-diminished: anticholinergic, opiate
-enlarged bladder; anticholinergic
-tender/rigid: ASA, anticholinergic
•neuro:
-tone, tremor: cholinergic, serotonin
-assess cogitation, CN, DTRs, strength,
coordination, gait
Abdominal X-ray:
•suspected body packer
•Bezoar formation: small stony
concentration form in stomach or
intestines (ASA, salicylates)
CXR: pulmonary edema
Toxicology:
•UNNECESSARY if non-
intentional ingestion,
asympatomatic, or have clinical
findings consistent with medical
history
•individual screen for lithium and
digoxin may be needed
Common Coigestatnts:
•APAP, ethanol, salicylate
*ALWAYS in unknown ingestion
UA: calcium oxalate crystals with
ethylene glycol (antifreeze)
activated charcoal *BEST!
•indicated if ingestion of toxic
substance within 1 hour prior to arrival
*can used after 1hr
if antichol or salicylates
•AC is not able to bind to metals,
corosives, alcohols
•CI: cant protect air  aspirate
Gastric Lavage
•removes non-absorbed toxins
•indication: <1hour, no antidote to
toxin, poor response to supportive care
•high risk of aspiration
Procedure
•insert 36-40F orogastric tube
•lie LLD w/ head of bed tilted down
•200ml warm tap water in stomach
Whole Bowel Irrigation
•indications: ingestion of chemicals
poorly absorbed to charcoal (lithium,
iron, lead) and ingestion of drug-filled
packets
•GoLYTELY to flush out
-administer NG tube 1-2L/ht
-continue until clear (2-5h)
CI: absent BS, ileus, obstruction

Poison Enhanced Elimination Decontamination/Contamination

TX Multi-Dose Activated Charcoal
indications: ingestion of toxic levels
of carbamazepine, dapsone,
phenobarbital, quinine, theophylline
CI: uprotected airway, absent BS
•caution in ingestions resulting in
reduced GI motility
Urinary Alkalinization
Urinary Alkalinization
•ionizes acidotic toxins preventing
resorption across the renal tubule
•indications: moderate-severe
salicylate toxicity
•cautions: hypokalemia
•Procedure:
-IV sodium bicarb +/- KCL
-monitor K+ and bicarb q2-4h
•maintain K+ between 4-4.5
-pH q15-20min with goal 7.5-8.5
Hemodialysis/Hemoperfusion
•hemodialysis: more effective at
clearing highly protein-bound drugs
and lipid-soluble drugs
•hemoperfusion: clear water-soluble
low molecular weight
•both require critical care setting and
are expensive and invasive
 complications
Decontamination: Inhaled
•administer oxygen
•water aerosol inhalation  dilute irritants
•delayed upper airway obstruction or
pulmonary edema
Decontamination: Eyes
•irrigate with plain water or NS
•assess pH after 2L irrigation
Contaminated Skin
•avoid direct self-exposure
•wash skin with water and dilute soap
•hydrofluoric acid burns are particularly

Poison MOA and Examples
Opioid •heroin, morphine, methadone,
meperidine, hydrocodone, oxycodone
Sympthato- Mimic the effects of endogenous
mimetic agonists of the sympathetic nervous
system (epi, norepi, dopamine)
EX: cocaine, caffeine, amphetamines,
cathinones (bath salts)
Cholinergic Blocks acetylcholinesterase, leading to
excessive Ach
EX: organophosphate insecticides,
carbamate insecticides
Anti- Block the acetylcholine muscanaric
cholinergic receptors  inhibits parsympathetic
nerve impulses
Examples: Scopolamine, Atropine,
Antihistamines, TCAs, Antiparkinson,
Antispasmodics/
muscle relaxants
Disposition:
•discharge home if resolve in 6h
•admit with more significant symptoms
or those receiving physostigimine
Sedative/ 3 classes:
Hyponotic •benzos
•carisoprodol/alcohol.hypnotics
•barbituates
Disposition
•admit if sx after 6 hours
•consult psych for intentional OD
Serotonin •increased serotonergic activity
Syndrome
EX: MAOI, SSRI, Meperidine,
Dextromethorphan, TCAs, L-tryphtophan
Hallucinogenic •LSD, PCP, muschroom,
penetrating & corrosive10% Ca gluconate gel
Presentation Management
“physiologically depressed” •ventilation
•MC: CNS and respiratory depression, decreased BS, miosis •Naloxone
•hypothermia, bradycardia, orthostatic hypotension, bronchospasm,
pulmonary edema, seizures
•physiologic excitation •External cooling, sedation with benzos,
•MC: psychomotor agitation, diaphoresis, HTN, hyperthermia, hydration
mydriasis, tachycardia
•seizures, rhabdomyolysis, MI •CI: Beta Blockers
MC: salivation, lacrimation, diaphoresis, bronchorrhea, •airway protection and ventilation
urination & defecation, N/V, muscle fasiculations, weakness •Atropine: blocks Ach receptors
•bradycardia/tachycardia, rales, miosis/mydriasis, seizures, •Pralidoxine: Antidote
respiratory failure, paralysis •Diazepam: seizure, muscle fasiculations
MC symptoms: •activated charcoal to decrease drug
•hot as hades: hyperthermia absorption
•fast as a hare: tachycardia •address complications
•dry as a bone: no secretions or sweat -wide QRS: sodium bicarb
•mad as a hatter: AMS -agitation: benzos
•full as a tick: urinary retention -fluids: rabdo
•blind as a bat: mydriasis
•red as a beet: flushed skin supportive: treat hyperthermia with external
cooling methods
•decreased/absent BS, dysrhythmias, rhabdo, hypotension/HTN
•Physostimine: cholinesterase inhibitors
increases concentration of Ach
-if conventional therapies fail
•MC: slurred sppech, lethargy, CNS depression, respiratory Supportive
depression, confusion •venilation/intubation, 2 large bore IV
•bradycardia, hypotension, hypothermia, bradypnea, hyporeflexia •IV fluids bolus for hypotension
-dopamine or norepi if fails
•activated charcoal
•barbituates that don’t response
•benzos: confirmed benzo OD with
respiratory depression
-Flumazenil *get toxicity back 1st
•altered mental status, seizures, tremors/increased muscle tone •veniality support
•hyperthermia, tachycardia, HTN, tachypnea •benzos for agitation, tremors, seizures
•discontinue serotonergic drug
Labs: UA/CK, ABG *ADMIT ALL PATIENTS •Crypoheptadine if above fails
•disorientation, hallucination, anxiety, seizures, agitation, muscle •Benzo: agitation, hyperthermia, tachy, HTN
 dextromethorphan, ketamine
Poison About
Salycilate EX: ASA, pepto bismol,
liniments, flavoring agents
•ASA hydrolyzed to salicylic acid
 acid environment
•higher mortality with chronic
•risk for bezoar formation
Poison About
Tylenol Risks:
•chronic alcohol, AIDS
•anticonvulstants and anti-TB
Suggested When:
6 years old and older:
•ingests >10g (200mg/kg) over as
single ingestion or over 24hr
•>6g/day (150mg/kg) x2
consecutive days
Children <6 years old
•200mg/kg as single ingestion or
over 8hours
•150mg/kg per day
x2consecutive days
tension, N/V, HTN, tachycardia, tachypnea, hyperthermia, mydriasis
Presentation
Chronic
•fever, hyperventilation, AMS, volume
depletion, acidosis, hypokalemia
Acute
•<150mg: tinnitus, hearing loss,
dizziness, N/V
•150-300: high RR, hyperpyrexia,
diaphoresis, ataxia, anxiety
•>300: AMS, seizure, heart/lung/renal,
shock
Presentation
Stage 1 (day 1 after ingestion)
•anorexia, N/V, malaise, hypokalemia
Stage 2 (days 2-3 after ingestion)
•improvement in stage 1 sx
•RUQ abd pain, elevated LFTs and bilirubin,
prolonged PT
Stage 3 (Days 3-4 after ingestion)
•fulminant liver failure, metabolic acidosis,
coagulopathy, renal failure, encephalopathy,
pancreatitis, recurrent GI symptoms
Stage 4 (Day 5 and beyond)
•survival: improvement & recovery
•continued deterioration to multi-organ failure
and death
Diagnostics
salicylate level: >30 is toxic
-peak concentration may not
occur for 4-6 hours
-repeat every 1-2hr until peak
then every 4-6 hours
•CMP and magnesium
•ABG: mixed acid/base disturbance
-alkalemia w/ resp alkalosis and
metabolic acidosis
•assess for coingestants
-APAP, toxicology
•CXR and EKG for end-organ
•ABD image if bezoar suspected
-suspect is salicylate level
continue to rise despite tx with
gastric lavage or charcoal
Diagnostics
serum APAP level
•assess levels in asymptomatic
patients too due to delay
•peak serum concentration 30-
120min after acute ingestion
•Rumach-Mathhew nomogram
-determine clinical outcome
-only after one acute ingestion
between 4-24 hours post
•Nitropruss, phentolamine: refractory HTN
•aggressive IV fluids if rhabdo concern
Management
•ABCs
•correct volume depletion
•GI decontamination: activated charcoal
single dose
•reduce salicylate burden
-systemic/urinary alkalinization
with sodium bicarb
-FIRST LINE in mod-severe
Hemodialysis:
severe not responding to above
Management
•Activated charcoal
•Acetylcysteine: oral or IV
-prevents metabolite from
binding to hepatic cells (if within
8hr) & diminished necrosis
•Extra-corporal excretion
-patient with severe intoxication
who present too late to remove drug
-hepatic encephalopathy
Disposition:
•admit all patients requires
acetylcysteine
•discharge after 4-6h of observation if
acetylcysteine is not needed
DERM About Clinical Presentation Diagnostics Managment
Thermal Causes: scalding, direct thermal, flame burns Descriptions: •lab evaluation: assess Management:
Burn *based on % of BSA complications •supplemental O2 & intubation if needed
Depth •rule of 9s •ABG, CBC, CK, CMP •vitals: pulse ox may be falsely high by CO
•old: 1st, 2nd, 3rd, 4th degree •lund and broder •UA, carboxyhemoglobin •assess & treat trauma, inhalation, CO
•new systemic: superficial partial thickness, •palmar method: palm=1% •IV opiates for pain control
deep partial thickness, full thickness Complications •urinary cath: measure I&Os
•inhalation injury
•1st degree (sunburn): •carbon monoxide IV Fluids:
erythema, skin blanches with pressure •bacterial super infection •IV LR: 2 bore needle in unburned area
•sepsis •Parkland formula to determine fluid
•2nd degree (partial): red and blistered •multiorgan failure *½ over first 8 hours, ½ over 16 hours
-adults: 4ml x wt (kg) x %BSA
•3rd degree (full): tough, lethargy, non-tender -children: 3ml x wt (kg) x %BSA

•4th degree: bone and muscle Minor: clean with soap and water
Large Bullae >2cm: drain, debride, 1% silver
Moderate/Severe: dry sterile sheet & admit

About Signs and Symptoms/PE Tests and Stages Diagnostics and Treatment
Shoulder •most common joint to dislocate •visible or palpable deformity X-Ray: scalpular Y & Axillary views Treatment:
Dislocation •MC is ANTERIOR •swell, ecchymosis, pain, decreased ROM •Anterior: head anterior & inferior •reduction & immobilization
•hold affected limb close w/ elbow flexed •Hill Sach Lesion: groove fracture
Risks: young males •numb & weakness (neck & muscle spasm) •Bankart lesion: glenoid rim fracture 1st time anterior dislocations:
•AP: “light bulb sign” appearance of humeral •reduced then immobilized
Most Common Causes Anterior: abduction and external rotation head  posterior in neutral rotation for 3
•sports: football, hockey, volleyball Posterior: adduction and internal rotation weeks followed by PT
•trauma: during MVA, falls Complications: *focus on supraspinatous
•seizures: POSTERIOR dislocation •axillary nerve (MC)  anterior
AC Joint •MCC: fall on tip of shoulder
Dislocation •scapula moves downward due to
weight of arm  bump or bulge
above the shoulder
•pain over AC joint
•pain w/ lifting arm (esp abduction)
•deformity with type III – VI
•support arm in an adducted position
•clavicle prominence-esp with type II
Type I: AC joint partially, CC intact Type I & II: non-surgical
Type II: AC torn, CC intact, partial clavicle •ice, sling & analgesia
Type III: AC and CC complete, clavicle •full return within 4 weeks
separated from acromium
Type IV: clavicle posterior displaced Type III: nonsurgical
Type V: AC, CC, DT disruption
Type VI: inferior displacement or clavicle Type IV+: surgery

Arm About Presentation & Exam Diagnostics Treatment

Elbow •MC dislocation in children •extreme pain, swelling •AP and lateral x-ray Stable: REDUCE: steady, downward
Dislocation •>80% posterior •flexed elbow traction of forearm
•inability to bend elbow (extend) •posterior splint at 90 degrees flexion
Mehcanism: FOOSH •marked olecranon prominence •NSAIDS

•associated with ulnar collateral Physical Exam Unstale: ORIF

ligament disruption and fx of •extreme tenderness over elbow
radial head or medial epicondyle •deformity Refer: cant reduce, instability >3wk,
neurovascular injury

Radial Head •Subluxation of the radial head •child avoiding using the arm •X-rays are typically normal •Reduction
Subluxation due to sudden pulling force on -Usually not ordered unless - Flex elbow w/ forearm in supination
(Nursemaids) the child’s arm Physical Exam there is a hx of fall or trauma or the OR:
•Pain over the radial head & arm child continue not to use arm -Extension w/ forearm in pronation
Mechanism: lift, swing, pull slightly flexed

Medial •inflammation of the pronator •pain w/ wrist flexion & forearm •AP and lateral radiographs •activity modification, RICE. NSAIDS
Epicondyliti teres-flexor carpui radialis pronation •MRI is helpful in confirming •surgery if refractory (4-6 weeks)
s •tenderness over medial epicondyle *not necessary
“Golf Elbow” Causes: repetivite overuse, •pain worse with pulling activities
excessive wrist extension

Lateral •inflammation at tendon insertion •pain in the lateral elbow and forearm
Epicondyliti of extensor carpi radialis brevis with activities involving wrist extension
s muscle •more severe & occur at rest or with
“Tennis minimal activity (holding a cup)
Elbow”

About Clinical Presentation Diagnostics Treatment

Humeral Mechanisms: •pain, swelling, bruising, decreased ROM AP & axillary lateral views •minimally displaced < 1 cm
Fracture •FOOSH •arm held in adducted position •initial test -sling, analgesics, PT
•direct trauma
Physical Exam •2 part fx greater tuberosity > 0.5cm
Risks: young or elderly patient •if forearm & hand appear pale  r/o *proximal humerus/humeral head is -surgery
axillary artery injury common site for metastatic fx in breast
•the most common 2 part •RULE OUT RADIAL INJURY in CA Operative: ORIF for open, vascular or
fracture occurs at neck humeral hsaft pfracture nerve injury
Clavicle •most common bony injury
Fracture Causes: FOOSH, sports, MVAs
Groups:
I: midshaft (middle 1/3) (MC)
II: lateral (distal) third
III: proximal (medial) third
•pain increases with shoulder ROM AP and 10 degree cephalic tilt views
•swelling, tenderness, bruising, bulging confirm diagnosis
•grinding or crackling w/ ROM
•sagging of the arm downward and forward Complications:
•skin may appear tented •pneumothorax, hemothorax
•CC ligmanet disruption
•nerve injuries
non-surgically: figure 8 splint / sling
Proximal 1/3: ortho consult
•surgical repair for open, shortened or
fractures associated with neurovascular
compromise

Arm About Presentation & Exam Diagnostics Treatment

Distal Mechanism: FOOSH •swelling, echhymosis, deformity AP and lateral xray: FAT PADS Stable, nondisplaced:
Humeral •pain around the elbow •lateral fat pad: bleeding in joint •long arm posterior splinting x10days
Fracture Patterns: •worsens with flexion of elbow •posterior fat pad: always pathologic
“Supracondylar •complex •anterior fat pads: nml “sail sign: Displaced fractures: ORIF
Humerus •communiuted Types:
Fracture” •intra-articular A: fracture is non-articular Refer: displaced, neurovascular,
B: fracture is partially articular small patients that fail to regain motion
part remains in continuity with shaft
C: fractures are articular and no Complcations: medial & brachial nerve
fragment remains in continuity *Y and T injury  Volkmann ischemia (claw)
•radial nerve injury

Radial Head Mechanism: FOOSH
Fracture
Types:
Type I: Nondisplaced/minimal
Type II: Partial fractures with
displacement >2 mm
Type III: Comminuted fractures
Type IV: fracture of radial head
w/ dislocation of elbow joint
•Pain & swelling of the lateral aspect of AP and lateral Radiographs Type I and II: long arm 90 degrees
the elbow •FAT PADS: posterior or displaced
•May be concomitant with an elbow anterior Type III: ORIF
dislocation Type IV: closed reduction
•Crepitus with passive forearm
rotation Referral
•Type II or greater
•Failure of conservative TX or
persistent pain with limited ROM

Fracture •Easily fractured and occurs with
Olecranon a direct blow to the elbow
Mechanism: direct blow
•Pain worse on flexion
•May see ulnar nerve compression
•swelling of the entire elbow joint
•Tenderness of Olecranon Process
AP & Lateral x-ray
Non Displaced:
•Posterior long arm splint with elbow
in 90o flexion for 4-6 weeks
•F/u xray in 7-10
•Protected ROM in ~2-3 weeks
Nondisplaced: posterior long arm
splint w/ in 90 degree flexion x4-6wk
Displaced Fractures: ORIF
Referral
•displaced, open, malunion, neurovasc

Hand Exam and Diagnostics Treatment Bennett Fracture Rolando Fracture

Fracture of The most frequently occurring •Acute pain, tenderness, AP & lateral xray: forearm and wrist Stable: closed reduction
Distal fracture in adults swelling, and deformity *may want to due an xray of the elbow •sugar tong splint x2-3 weeks
Radius •pain worse with passive •Colles: dorsally displaced or angulated
(Colles and Mechanism: FOOSH motion •Smith: ventrally displaced or angulated Unstable/comminuted: ORIF
Smith)
Colles: distal fragment dorsal (back) Physical Exam Colles Complications:
•deformity and bruising •extensor pollicus longus tendon
 Smith: distal fragment ventral (front) • “Silver Fork Deformity” rupture (MC)
-fx of ulnar styloid Process •malunion or nonunion, median nerve
•Garden Spade (smith fx)

colles smith

Lunate •lunate does not articulate with both •swelling, pain of wrist AP view: lunate appears triangular Emergent closed reduction and splint
Dislocation the capitate and the radius • “peice of pie” sign  ORIF *EMERGENCY
and Fracture Fracutre:
*near pinky Mechanism: high energy while wrist •most serious carpal fracture Lateral View: volar displacement and tilt Fracture: immobilization
is extended and ularly deviated due to avascular necrosis • “spilled tea cup” sign

Fractures of •metacarpal fracture of base of thumb •pain with thumb movement AP and lateral x-ray Thumb splica splint
Base of •tenderness, swelling over •Bennet: fragment articulating with trapezium
Thumb (1st) Mechanism: the CMC joint •Rolando: Y sign Bennet: immobilization
Bennet and •axial force to flexed thumb
Rolando Rolando: ORIF, esternal fication,
Bennet: 2 pieces, oblique, non- closed reduction w/ pinning
comminuted
Rolando: Y-shape intra-articular Rolando-

fracture; comminuted Bennet

Fracture of •MC carpal bone fracture •pain worse ulnar deviation Ulnar Deviation PA/olique view •thumb spica splint
Scaphoid •MC in young adult males •Marked tenderness of the •may ne normal for 2 weeks •referred to orthopedic surgery
(Navicular) anatomical snuffbox (radial *if there is snuffbox pain then treat likfe FX
*near thumb Mechanism: FOOSH surface of wrist)
•Decreased ROM & strength
Complications: nonunion, avascular
necrosis (radial artery

Boxers •Fracture of the 5th metacarpal neck
Fracture •MC in distal phalanx
Mechanism: direct trauma against a
closed wrist (boxers)
•pain along 5th metacarpal •x-rays •ulner gutter splint 60 degree flexion
•swelling, ecchymosis •reductoin first if FX >25-30 degree
•distal fragment rotated angulation
>40 degree angulation: ORIF

Gamekeeper •tear of ulnar collateral ligament – •Pain and weakness of •clinical, xray •thumb splica splint and referral
(Skiers) instability at MCP joint pinch grasp (valgus stress)
Thumb •Pain, swelling, ecchymosis Complete rupture: surgery
Mechanism: forced abduction around thenar eminence

Pelvis Overview Clinical Presentation Diagnostics Adverse Outcomes and Treatment

Hip •occurs when femoral head is •severe pain in the hip/groin X-Ray: AP of pelvis, AP & lateral femur •EMERGENCY
Dislocation displaced from the acetabulum •unable to move LE •normal: femoral head and joint equal •reduction ASAP: closed reduction
•MC is posterior •other MSK injuries with it •posterior: head smaller & superior -rule out femoral head FX and intra-
•anterior: head larger, inferior, medial articular loose bodies before reducing
Cause: Physical Exam: •post-reduction xray/CT
•trauma (MVA, fall) •posterior: shortened, hip flexed, Complications: •neurovascular assessment

Mechanisms:
•Posterior (MC): axial loading
on adducted femur
•Anterior: axial load on
abducted & externally rotated
adduction, internal rotation
- sciatic nerve palsies
•anterior: mild flexion,
abduction, external rotation
- femoral nerve palsy
•osteonecrosis is MC early complication
-may not appear for 2-3 years Post-Reduction:
•sciatic nerve injury (posterior) •abduction exercises, use walking aid in the
•femoral nerve injury (anterior) OPPOSITE hand until walk without limp
•DVT
•bleed

Fracture •fracture of the pelvic ring and •pain in the groin, lateral hip, •AP xray of pelvis and oblique views A and B: conservative management
of the acetabulum or buttock with attempts at C/severe: traction and/or fixation (ORIF)
Pelvis weight bearing or inability Stable: involve one side
Mechanism: High energy: surgery
•high impact injuries (MVA) Low energy Unstable: disrupt ring at two sites as well as Low Energy: Stable, anlagesics
•low imapc injuries •pain with attempted ROM and involvement of the symphysis or SI structure
•fall straight leg raise, antalgic gait, Adverse Outcomes:
stance shortened •Grade A: stable, minimal displacement •GU injuries
Type: open book •Grade B: rotational unstable, vertical stable •distal neurologic injuries
High energy •Grade C: all unstable •chronic pain
•pain, swelling, deformity,
ecchymosis (perineal)

Femur Overview Presentation and Diagnostics Treatment

Fracture of •MC in elderly and osteoporosis pts
Proximal
Femur Mechanism:
“hip fracture” •minor/indirect trauma elderly
•high impact in younger patients
3 main types:
•femoral neck: above trochanters
*associated with avascular necrosis
•intertrochanteric: between greater and
lesser trochanter
•subtrochanteric: below trochanters
•limb externally rotated, abducted, short
•pain with attemting to rotate
•unable to SLR
Femoral Neck
•INTRASCAPULAR
•disruption of blood supply causing
nonunion FX or osteonecrosis
Intertrochanteric/Subtrochanteric:
EXTRASCALPULAR
•does NOT disrupt blood supply
•more extensive repair
xrays: AP of pelvis and cross-table
•MRI if xray normal
Proximal femur fractures can be
associated with thromboembolic
event, PNA, decubitus ulcers, UTIs
•ORIF
•surgery ASAP, delay no
more than 48h
•type of repaire depends on
location
•thromboembolic prophylaxis
Femoral Shaft:
•surgical treatment (open
reduction internal fixation

Femoral Mechanisms: •pain, swelling Complications: •immediate ortho consult

Condyle •axial loading •inability to bear weight •peroneal nerve injury: foot drop and •ORIF
Fractures •direct blow to the femur decreased sensation in web spaces
•popliteal artery injury

Knee About Presentation Diagnostics Treatment

Tibia •lower leg comprised of tibia and fibula
(Pilon) FX •tibia and fibula usually fractured together
•MC long bone fracture: tibial shaft
•swelling, pain, inability to bear weight X-ray: AP/lateral •urgent refer to ortho (1-2d)
•OPEN FX MOST COMMON Displaced: intramedullary nailing
emergent if: open, NV Nondisplaced: long leg cast x4-6wk
Compartment SX: increase and injury, compartment
unrelenting pain, tense swelling, pain syndrome, dislocation
with passive flexion/extension of toes
Fibula FX •fibula is non-weight bearing
•stabilizer of ankle against eversion
•twisting injury or direct blow
•deformity, shortening or angulation
*however, usually normal
•tenderness, swelling, bruising
X-ray: AP/lateral Distal FX: short leg cast
Proximal FX: long leg cast
Displaced/angulate, spiral,
comminuted: urgent ortho referral

F/A About Presentation Diagnostics Treatment

Fracture of •due to trauma with a
Metatarsals twisting or rotational force,
or blunt trauma (drop
something on foot)
•swelling, pain on weight
bearing
•ecchymosis and tenderness
X-ray: AP, lateral, oblique of foot
Ottawa Rules  Foot
•navicular bone (midfoot) pain
•5th metatarsal pain
•inability to walk >4 steps
nondisplaced metatarsal neck and shaft:
-short leg cast or fracture brace
•multiple fx, displacement, angulation, avulsion:
-surgery w/ open or closed reduction & fixation

Stress •fracture due to overuse or •localized aching pain, X-rays: usually negative •rest, avoid high-impact activities
(March) high-impact activities swelling, tenderness •ice, splint
Fracture •worse with activity
•3rd metatarsal is the MC •loaclized bone tenderness

Lisfranc 1+ metatarsal bones are •midfoot pain, swelling “Fleck Sign” avulsion fracture of medial REFER TO ORTHO
Injury displaced from the tarus •trouble bearing weight cuneiform or second metatarsal
•tenderness of TMT joints -FX to proximal metatarsal

Jones •transverse fracture through •pain over 5th metatarsal and x-ray: transverse fracture involving the •short leg cast x6-8 weeks
Fracture diaphysis of 5th metatarsal lateral border of foot metaphyseal-diaphyseal junction
at the metaphyseal-
diaphyseal junction

Pseudojones •fracture through base
Fracture (tuberosity) of 5th metatarsal
due to plantar flexion
Fractures of •involves proximal
Phalanges phalanx and is a result of
direct trauma *5th toe MC
•transverse abulsion fracture •walking cast x2-3 weeks
•ORIF id displaced
•pain, swelling, ecchymosis X-ray: AP radiographs •buddy taping the fractured toe to the adjacent toe
•limited ROM of toe •gauze pad placed between toes to absorb moisture

MSK About Presentation Diagnostics Treatment

Ankle Includes:
Fracture •lateral malleolus (distal fibula)
•medial malleolus (distal tibia)
•posterior tibia (malleolus)
•collateral ligament of talar dome
•ankle pain with weight bearing
•palpable gap
•tenderness over fractured site
Weber Classification: •minimally displaced fractures may not
A: below syndesmosis show on x-ray, if you are suspicious then
B: level of syndesmosis treat as fx
C: above syndesmosis
Stable: short or long leg cast
 stable: one side of joint Unstable/open: ORIF
unstable: both sides of ankle

Calcaneous/ Cause: severe trauma (MVA, fall) •severe pain, inability to bear X-ray: 3-view ankle xrays •posterior splint toe to upper calf
Talus FX •most involve articular surface and weight •CT •urgent referral
are unstable •swelling and tenderness •most require ORIF
compression of lumbar spine

Maisonneuv •spiral fracture of proximal third of •associated with distal medial •proximal x-rays
e Frature the fibula malleolar fracture or rupture of
deep deltoid ligament

Peds Fracture About Clinical Presentation Diagnostics Treatment

Greenstick •incomplete fracture
Fracture with angular deformity
and corticol disruption
•result of rotational force
•due to bone softness, there is a
fracture on one side of the bone and a
buckle on the other
•fracture line does not extend
completely through bone width
X-Ray: bowing •cast to prevent further movement are further
fracturing of the bone  stays on 4-6 weeks
•Tylebol

Torus (Buckle) •Incomplete fracture of •distal metaphysis where the bone is • stable and do not require surgical
Fracture one cortex more spongy intervention
•peds patients •may be very subtle so multiple xray •can apply simple splinting for ~3-4weeks
•MC site: distal dorsal views are needed •NSAIDs/analgesia
radius

Salter-Harris •fracture that involves S: slipped  type I straight across •goal is for anatomic reduction
Fracture the epiphyseal growth A: above  type II •fractures heal rapidly usually within 4-6
plate (physis) L: lower  Type III weeks
TE: through everything Type IV
Slipped(I) Above(II)
•females 12-14yo, males R: rammed  Type V •Type I/II: closed reduction & cast
14-16yo •Type III/IV: open reduction & fix (surgery)

If the fracture is 7+ days post injury,

reduction should be AVOIDED in children
Lower (III) <13yo because of risk of growth plate re-
injury and growth arrest

Through everything(IV) Rammed (V)

GI
Intussusceptio Telescoping of an intestinal segment into adjoining distal TRIAD: Ultrasound: BEST INTIAL •Barium enema with
n intestinal lumen •vomiting •donut or target sign pneumatic air or
•MCC of obstruction first 2 years of life •abdominal pain  draw legs up hydrostatic (saline)
 •6-12 months of age MC • bloody stool: “currant jelly” stools Abdominal x-ray: lack of gas
•fluid and electrolyte
Risks: idiopathic, meckels, enlarged lymph nodes, Exam: sausage shaped mass in RUQ Air or contrast enema: replacement  NG
tumors, FB, hamartomas Emptiness in RLQ (Dance’s sign) DIAGNOSTIC AND decompression
THERAPEUTIC
Hirschprung Congenital megacolon due to absence of ganglion cells •meconium ileus (failure of Contrast enema: transition zone Resection of affected
Disease  functional obstruction *MC in distal colon & rectum meconium to pass in >48h) bowel
•bilious vomiting Anorectal manometry: increased
Risks: male, downs, Chagas, MEN II •abdominal distention anal sphincter pressure and lack
•enterocolitis: vomit, diarrhea, toxic of relaxation
Pathophysiology:
•failure of complete neural crest  absence of enteric Rectal biopsy: DEFINITIVE
ganglion cells (auerbach plexus) *rectal suction biopsy

Meckels’ (Ileal) Persistent portion of embryonic vitelline duct (yolk •usually asymptomatic Meckel Scan: Surgical excision
Diverticulum stalk, omphalomesenteric duct) in the small intestine •painless rectal bleeding or •look for ectopic gastric tissue in
ulceration ileal area
Rule of 2s:
•2% population, 2% symptomatic Complications: Mesenteric arteriography or
•w/n 2 feet of ileocecal valve, 2in length •intussuception abdominal exploration
•2 tissues, 2 years old, 2x MC in males •volvus
•obstruction
Tissues: gastric (MC), pancreatic

GI
Paralytic Ileus Loss of peristalsis of the intestine
(STOP) without structural obstruction
Causes: surgery (abdominal and
pelvic), peritonitis, meds(opiates), illness,
infection, metabolic (low K, high Ca)
•N/V obstipation (severe const.) Labs: CBC, CMP •Complete bowel rest
•Abdominal distention with tympany  IV fluids/TPN, NG tube
Abd X-ray: dilated loops of •Slowly advance diet *gas=good
Exam:Diminished/absent BSs bowel with no transition zone •Activity
•Remove drugs that reduce
intestinal motility

Volvulus •Torsion bowel  bowel obstruction
Location: Sigmoid (MC!), cecum
•crampy abdominal pain, distention X-ray: “bent inner tube” •Endoscopic decompression
•N/V, constipation “coffeebean sign” (proctosignmoidoscopy) 
•tympanitic abdomen  U shaped appearance of the elective surgery
•fever, tachycardia, peritonitis air-filled closed loop of colon, •IV Fluids
loss of hausta
Neonates: bilous vomiting, colicky pain
GI series & CT: “birds beak”

Splenic Spleen is MC organ injured with trauma •abdominal pain, hypotension, shock FAST abdominal exam Incomplete rupture:
Rupture or endovascular embolization
Laceration Causes: L sided rib fracture, blunt •Kehr sign: referred left shoulder pain due
abdominal trauma, infectious mono to irritation of diaphragm and phrenic nerve Complete: splenectomy

GI
Toxic Total/segmental non-obstructive colonic •colitis present for at least 1wk XRAY (best!): •Complete bowel rest
Megacolon dilatation (>6cm) + toxicity prior to onset •Transverse or R colon is dilated, •bowel decompression: NG tube
•Profound bloody diarrhea 6-15cm supine •fluid and electrolyte replacement
 Causes: •abdominal pain, distention, N/V •broad ABX: Ceftriaxone +
•Complication of IBD (ulcerative colitis) •toxicity: fever, AMS, tachycardic, 3+ of following: Metronidazole
•infectious or ischemic colitis hypotension, dehydration •fever >38C
•volvulus •pulse >120
•diverticulitis PE: FAT BAT •neutrophil leukocytosis >10,500 •DC all antimotility agents (opiates,
•Fever, AMS, Toxic •anemia anticholinergics)
•BP low, abd pain, tachycardia
AND 1+ of following:
•hypotension
•altered mental status (AMS)
•dehydration
•electrolyte abnormalities

Chronic Ischemic bowel disaese due to mesenteric •chronic, dull abdominal pain that Angiography: DEFINITIVE Revascularization
Mesenteric atherosclerosis  decreased supply during is worse AFTER MEALS (Angioplasty with stenting or bypass)
Ischemia increased demand (eating) •anorexia (aversion to eating)
•weight loss
Risk: Atherosclerosis

Acute •Abrupt onset of small intestine •Crampy, abdominal pain Labs: leukocytosis, lactic •NPO, rest, fluids
Mesenteric hypoperfusion •Bloody diarrhea acidosis, increased hematocrit, •SURGERY-revascularization or
Ischemia *MC in superior mesenteric artery •N/V/D increased amylase resection
•Pain control, anti-emetics
Causes: emboli (A-Fib), thrombus, shock, •HALLMARK: pain out of DX:
cocain, vasopressors proportion •CT angiogram (initial)
•Arteriography: DEFINITIVE

Ischemia Decreased colonic perfusion  inflammation •LLQ pain, crampy CT Abdomen: 1st test •Restore perfusion
Colitis •Bloody diarrhea •”thumbprinting”  segmental •bowel rest
MCC: hypotension or atherosclerosis •abdominal tenderness bowel wall thickening •IV Fluids
*superior and inferior mesenteric arteries •observe for perforation
*MC splenic fixture & rectosigmoid junction Colonoscopy
•segmental ischemic changes in
Risks: elderly, DM, cardiac cath, MI, areas of low perfusion
sontipcation inducing medications

GI
Small Bowel Causes: “CAVO” •Leukocytosis on labs •NPO, IVF
Obstruction •post-surgical adhesions (MC) •crampy abdominal pain(mod/severe) •bowel decompression: NG tube
•incarcerated hernias, crohns, malignancy •abdominal distention Abdominal x-ray: multiple air •Surgery
(MCC of large bowel), intussusception •vomiting fluid levels in a “step-ladder”
 •obstipation (flatulence) appearance, dilated loops
Types:
•closed v open: closed-lumen occluded at Exam: CT scan: transition zone from
two points •High-pitched BS  hypoactive (late) dialted loops with contrast to no
•partial v complete: complete have •visible peristalsis (early) contrast
severe obstipation
•distal v parietal: distal is more
distention and less vomiting

Appendicitis •Obstruction of the lumen of the appendix •dull periumbilical or epigastric pain  •CBC, UA, pregnancy •Consult surgeon
 inflammation and bacterial overgrowth RLQ •CT scan: STUDY OF CHOICE •Appendectomy
•MCC of acute abdomen in ages 12-18yo •anorexia, nausea *don’t need contrast •IVF, ABX  Zosyn
•vomiting after pain *consult first in children to
Causes: •SX increase over 24h determine if imaging needed
•fecalith and lymphoid hyperplasia
(MCC) PE:
•inflammation, malignancy, foreign body •rebound tenderness, guarding
•McBurneys point: RLQ pain
Rectocecal: abd and flank pain •Rovsing: RLQ pain w/ LLQ palpation
Pelvic: tender abd and rectal pain •Psoas: RLQ pain with hip
flexion/extension (SLR)
•Obturator: RLQ pain with internal/external
rotation of hip with flexed knee

Small Bowel 24-40% adenocarcinomas in the •Abdominal pain: intermittent & crampy Diagnosis usually delayed  •Surgery
Carcinoma duodenum •N/V, wt loss, jaundice poor outcomes •Chemo if (+) lymph nodes
•Anemia
Risks: hereditary, CF, Crohns, alcohol, •CT scan
sugar, red meat, salt-cured, smoked foods • (+) CEA •Wireless capsule endoscopy

PULM About Presentation Diagnostics Treatment

Pneumo spontaneous:
-thorax •primary: no lung disease, atraumatic
-rupture of subpleural apical bleb
-tall, thin males 20-40yo
•secondary: underlying lung disease
traumatic: penetrating or blunt,
iatrogranic ((+) pressure, CPR)
tension (EMERGENT)
•air entering pleural sac
•MCC: cardiopulm, (+) pressure
•Sudden chest pain CLINICALLY Tension Pneumothorax:
-pleuritic, unilateral, non-exertion •Needle aspiration (14-16G)  chest tube
•Dyspnea CXR: expiratory view upright -2nd ICS at midclavicular line
•decreased peripheral markings •Oxygen 2-4L nasal cannula
Physical Exam: •companion lines (visceral pleural
•diminished breath sounds & TF line running parallel to ribs) Small Primary (<3cm):
•hyperresonance to percussion •deep sulcus sign •observation and oxygen; repeat CXR in 6hr
•mild tachypnea
•pneumothorax under tension Chest CT, bedside US: large or Large Primary (>3 cm):
-increased JVP unstable •needle or catheter aspiration v. chest tube
-systemic hypotension
-pulsus paradoxus Stable Secondary: chest tube + hospital

PULM
Pulmonary Obstruction of pulmonary blood flow due to a Symptoms: EKG: tachycardia, S1Q3T3 Oxygen, IV Fluids if needed
Embolism blood clot (thromboembolism) •Dyspnea (sudden onset)
•Pleuritic chest pain CXR: Stable
 Risks (Virchows Triad): •Hemoptysis (pulm infarction)
•venous stasis: immbolization, sitting > 4 hours, •Cough, wheeze
surgery
•intimal damage: trauma, infection, inflammation PE:
•hypercoagulability: medications, protein C or S •tachypnea, tachycardia
deficiency, Factor V Leiden, antithrombin III •hypoxemia; rales
deficiency, OCP use, pregnancy, malignancy •hypotension and syncope
•JVD & S3 and S4 sounds
•(+) homans: calf pain w/
dorsiflex
PERC (PE rule out criteria)
•age <50 years old
•HR <100
•O2 95% or greater
•no hemoptysis
•no estrogen use
•no prior DVT or PE
•no unilateral leg swelling
•no surgery/trauma requiring
hospitalization 4 weeks prior
•normal is MC
•atelectasis
•Hamptoms Hump: wedge
shaped infiltrate due to infarction
•Westmark Sign: avascular
markings distal to PE
ABG: respiratory alkalosis and
hypoxemia  acidosis
D-dimer: if low suspicion
VQ Scan:
*pregnant, increased creatinine
•poor perfusion, good ventilation
Helical (Spiral) CT: BEST
Pulmonary angiography: GOLD
Wells Score >6: high, 2-6: mod
+3: DVT, alt dx not likely
+1.5: HR >100, VTE hx,
immobilization for 4 weeks
+1: malignancy, hemoptysis
Anticoagulation
•Heparin or LMWH + Warfarin
•Dabigatran, Rivaroxaban,
Apixaban, Edoxaban
IVC Filters
•if anticoagulation is CI or
unsuccessful or RV dysfunction
seen on echo
Unstable:
BP <90, acute RB dysfunction
•Thrombolytics
•Thromboembolectomy (if TPA
is contraindicated)

PULM About Presentation Diagnostics Treatment

Acute MC form non-cardiogenic •rapid onset of profound CXR: •Non-invasive or mechanical ventilation
Respiratory pulmonary edema DYSPNEA within 12-48h af •bilateral pulm infiltrates -CPAP-full face ≥ 5 (mild disease)
Distress •SOB, tachypnea, intercostal •AIR BRONCHOGRAMS -PEEP ≥ 5 (mild, mod, or severe disease)
Pathophysiology: retractions, crackles •spares costophrenic angles •Treat underlying cause
 •diffuse alveolar damage and
surfactant
•increased permeability of the
capillary-alveolar barrier
•acute hypoxemic without
hypercarbia
Risks:
•critically ill (gram - sepsis)
•trauma, aspiration
FB Aspiration Common items: food (MC
peanuts), coins, toys, balloons
MC age is 2 years old
•hypoxemia (no response to O2)
•multiple organ failure: kidney,
liver, CV, CNS
HALLMARK: diffuse alveolar
damage
SUDDEN onset of choking,
cough, dyspnea, wheezing,
assymetric breath sounds
ABG: severe hypoxemia refractory
to supplemental O2
•Mild: PaO2/FiO2 201-300
•Mod: PaO2/FIO2 101-200
•Severe: PaO2/FIO2 <100
Absence of cardio pulmonary edema
•pulmonary wedge <18mmHg
CXR: air trapping
Rigid bronchoscopy:
DEFINITIVE DIAGNOSIS
PEEP ((+) end-expiratory pressure)
-prevents alveolar collapse
-give at lowest effective levels
-does not improve mortality
-risks: barotrauma, pneumothorax, auto-peep
Rigid Broncoscopy to remove FB
MC on the R side (wider, vertical, shorter
main bronchus)

OBGYN About/Rsiks Presentation Diagnostics Management

Placental Separation of the placenta either partially or •Sudden onset of •DIAGNOSIS OF EXCLUSION •fluids and blood if needed
Abruption totally from its implantation site before delivery abdominal PAIN •CBC, CMP, PT/PTT/INR, blood type •emergenct OBGYN consult
•vaginal bleeding -possibly emergent C-section
Cause: hemorrhage into decidua basalis •uterine tenderness •transabdominal US  TVUS
Complications:
Risks: MCC bleeding in THIRD •May be associated with elevated AFP •hypovolemic shock
•materal HTN TRIMESTER •DIC
•trauma, uterine fibroids, lupus Speculum and digital pelvic exam CI •AKI (hypovolemia)
•increasing maternal age, past aborption Exam: unltil US r/o placenta previa •Couvelair uterus: extravasation of
•Preeclampsia, smoking, cocaine •tender, rigid hypertonic blood into uterine musculature &
uterus beneath serosa
•NO PELVIC EXAM -myometrium “blue-purple” tone

Placenta Placenta that is implanted either over or near •PAINLESS vaginal

Previa internal cervical os bleeding usually after the C-Section performed in complete,
second trimester (28 wks) major degrees, and fetal distress
Classifications:
•Placental previa: os covered partial or complete *uterine body is
•Low-lying: implantation in lower uterine segment remodeling to form the
•partial: partial coverage lower uterine segment 
•marginal: adjacent to internal os (<2cm away) internal os dilates 
bleeding occurs
Risks: maternal age, mult. gestations, C-section,
smoking, high MSAFP, preveious previa