Content:

‣ Cardiovascular overview
‣ Dyslipidemia
‣ Hypertension
‣ Stroke
‣ Arrhythmias
‣ Heart failure
‣ Anticoagulants
‣ VTE
‣ Anemia
‣ SCD
‣ DM
‣ Thyroid disorders
‣ Oncology
‣ Pain management
‣ Epilepsy
‣ alzheimer’s
‣ depression
‣ schizophrenia
‣ bipolar
‣ ADHD
‣ Anxiety
‣ Asthma
‣ COPD
‣ Goat
‣ Rheumatoid arthritis
‣ Osteoarthritis
‣ Osteoporosis
‣ Multiple sclerosis
‣ Renal disease
‣ Liver disease
‣ GI disease
‣ Pregnancy
‣ Contraceptives
‣ Glaucoma, conjunctivitis
‣ Migraine
‣ Infectious disease
‣ BPH and ED

‫بالتوفيق جمي ًعا‬

 Cardiovascular

(Physiology questions are mostly about CVS)

Heart Sounds:
• The typical “lub-dub” sound of the normal heart consists of the first heart sound (S1): which
precedes ventricular contraction and is due to closure of the mitral and tricuspid valves
• The second heart sound (S2), which follows ventricular contraction and is due to closure of the
aortic and pulmonic valves.

• The S3 occurs in early diastole as blood rapidly rushes into a volume-loaded ventricle (eg, with
decompensated congestive heart failure).
• The S4 occurs in late diastole and is caused by atrial contraction into a stiff, noncompliant
ventricle (eg, hypertrophy due to hypertension).
• Murmurs are auditory vibrations resulting from turbulent blood flow within the heart chambers
or across the valves.

MAP = 2/3 SBP + 1/3 DBP

CO = HR x SV

Markers of Myonecrosis:
Cardiac troponin (cTn) preferred marker for evaluating the patient suspected of having a myocardial
infarction, since it is the most sensitive and tissue-specific biomarker available.

Markers of Hemodynamic Stress:

B-type natriuretic peptide (BNP) released from ventricular myocytes in response to increases in wall
stress. As a result, their serum concentrations typically are increased in patients with CHF.

Scores

• CHADS2 - VASC score

Estimates stroke risk in patients with non-valvular atrial fibrillation and determine which oral
anticoagulants therapy is most appropriate.

Anticoagulants are given when score:

For Male = 1 or more
For Female = 2 or more

DOACs > warfarin

Q: calculate score from case

• TIMI score

• To determine the likelihood of ischemic events or

mortality in patients with unstable angina or non–
ST-segment elevation myocardial infarction
(NSTEMI).

• ASCVD score:
• To guide decision-making for many preventive
interventions, including lipid and blood pressure
management

Dyslipidemia

Q: which of the following should be

taking at night time?
Statins:
• MOA: work by competitively blocking the active site of the first and key rate-limiting enzyme in the
mevalonate pathway, HMG-CoA reductase. Inhibition of this site prevents substrate access, thereby
blocking the conversion of HMG-CoA to mevalonic acid. (Know the cholesterol synthesis pathway
for biochem questions)
• ADR: Rhabdomyolysis
• Monitor: CK, Liver function (at baseline, 3 months, yearly)
• Metabolism: majority by CYP3A4 ( drug-drug interaction with azoles, amiodarone, verapamil, …)
• Less drug-drug interactions: pravastatin and rosuvastatin are not significantly metabolised by
CYP3A4 and are less susceptible to CYP interactions.
• Most tolerated: simvastatin or pravastatin may experience fewer side effects.

The percentage of LDL reduction needed:

(current LDL − goal LDL)/current LDL × 100

Niacin: (vitamin B3)

Lower TG
• MOA: inhibits the lipolysis of triglycerides and retards the metabolism of free fatty acids (FFAs) to the
plasma
• ADR: Flushing, hyperglycemia, hyperuricemia, upper GI distress, hepatotoxicity
• Contraindications: Liver disease, severe gout, active peptic ulcer

Fibrates: Gemfibrozil, Fenofibrate

Lower TG
• MOA: Reduces rate of lipogenesis in the liver
• Contraindications: Severe renal or hepatic disease
Gemfibrozil with statins = severe rhabdomyolysis (side notes: also cyclosporine with statins cause
severe rhabdomyolysis)

Bile Acid Sequestrate: (Cholestyramine, Colesevelam)

Lowers LDL
• Contraindications: increased TG

Ezetimibe:
• MOA: Inhibition of cholesterol absorption
(Added benefit with statins; not used alone)

PCSK9 Inhibitors: Alirocumab and evolocumab

The best in lowering LDL,TC, non-HDL but not used as a first line
• ADR: local injection site reaction, influenza, nasopharyngitis, UTI, myalgia …
 Hypertension

Types of hypertension:
A. Essential (primary)
B. Secondary

Goal: < 130/80 mmHg

Stage2: consider 2 antihypertensive

agents of different classes.

Which agents to use? first-line agents include thiazide diuretics, CCBs, and ACE inhibitors or
ARBs.

Hypertension in Patients With Comorbidities:

Stable Ischemic Heart Disease (SIHD): beta blockers, ACE inhibitors, or ARBs ( if not controlled,
add dihydropyridine CCBs, thiazide diuretics, and/or Spironolactone)
Heart Failure With Reduced Ejection Fraction: Nondihydropyridine CCBs are not recommended
Heart Failure With Preserved Ejection Fraction: diuretics should be prescribed to control
hypertension ( if not controlled, ACE inhibitors or ARBs and beta blockers)
Chronic Kidney Disease: Albuminuria give ACE inhibitors ( if not tolerated, ARBs)
Valvular Heart Disease: treatment with agents that do not slow the heart rate (i.e., avoid beta
blockers) is reasonable.

Hypertension in pregnancy: should be transitioned to methyldopa, nifedipine, and/or labetalol

SHOULD NOT be treated with ACE inhibitors, ARBs (why? Decrease fluid around fetus; increases
risk of fetal renal damage)

Resistant hypertension: >130/80 and patient is on 3 agents at optimal doses.

1. exclude psudoresistance
2. Lifestyle modification
3. Maximize diuretics, add spironolactone, add other agents with different MOA, use loop diuretics in
CKD patients or patients using minoxidil
Hypertensive crises
Hypertensive Emergency: a subset of hypertensive crises, are characterized by acute, severe
elevations in blood pressure, often greater than 180/110 mm Hg associated with the presence or
impedance of target-organ dysfunction
Hypertensive urgencies: are characterized by a similar acute elevation in blood pressure but are not
associated with target organ dysfunction

The goal is to correct the BP to no less than 20% to 25% in the first hour.
Exceptional Goal:
Acute ischemic stroke ( don’t lower BP; unless it is ≥185/110 mmHg + candidate re-perfusion
therapy)
Acute aortic dissection (SBP is rapidly lowered to a target of 100 to 120 mmHg to be attained in
20 minutes)

Management:
Vasodilators: Sodium Nitroprusside, nitroglycerin IV, nicardipine, hydralazine
Adrenergic inhibitors: Labetalol, esmolol, phentolamine

Re-evaluation: Once stable, increase dose of chronic meds (or change meds, if appropriate) and follow
closely
Example: short acting medications (Captopril, Clonidine, Labetalol)

Pharmacology of Cardiovascular
Diuretics
1. Thiazide: Hydrochlorothiazide, Chlorothiazide
a. MOA: Inhibition of Na/Cl co-transporter in the distal convoluted tubule
b. ADR: hypokalemia, hyponatremia, hypercalcemia, hyperuricemia
1. Thiazide-like: Indapamide.
a. MOA: Inhibition of Na/Cl co-transporter in the distal convoluted tubule
b. ADR: hypokalemia, hyponatremia, hypercalcemia, hyperuricemia
2. Loop: Furosemide, Torsemide, Bumetanide
a. MOA: Inhibition of Na/Cl co-transporter in the thick ascending loop of henle
b. ADR: hypokalemia , hyponatremia , hypocalcemia, hyperuricemia
c. Dose conversion factor: furosemide IV to PO conversion 1:2
3. Aldosterone antagonist: spironolactone
a. MOA: mineralocorticoid receptor antagonist
b. ADR: hyperkalemia

Beta blockers
1. Non-selective: propranolol, nadelol, timolol
2. B1 selective: atenolol, metoprolol, bisoprolol
3. Non selective with alpha blocker activity: carvedilol, labetalol
4. For HF: Metoprolol, Bisoprolol, Carvedilol (MBC)
a. ADR: bradycardia, heart block, bronchospasm
b. Contraindications: decompensated HF, heart block, asthma or COPD ( severe or
uncontrolled).
ACE inhibitors
‣ Lisinopril, Captopril, Enalapril, Perindopril
MOA: block the conversion of angiotensin I to angiotensin II by blocking converting enzyme
Results in an increase of bradykinin (which metabolized by the same enzyme)
ADR: dry cough, hyperkalemia, renal insufficiency, angioedema
DDI: ARBs , NSAIDs
Contraindication: PREGNANCY (Q: patient is on Lisinopril and got pregnant?)
Captopril: shortest duration

ARBs
MOA: blocks AT1 receptors, thus blocking the vasoconstrictive effects of Ag II
Cough is not expected with ARBs (Q: patient on captopril and c/o dry cough?)
Contraindication: PREGNANCY

CCB
Dihydropyridine: Amlodipine, Nifedipine, Nicardipine (ADR: reflex tachycardia, peripheral edema)
Non-dihydropyridine: verapamil, diltiazem (ADR: bradycardia, peripheral edema)

Nitrates
MOA: Primarily venous dilators that reduce preload and subsequently myocardial oxygen demand.In
higher doses, they are also arterial dilators
ADR: headache
Sublingual nitroglycerin for angina: 0.3-0.6 mg q5 minutes up to 3 times; no relief? Seek medical
attention immediately.

Centrally acting sympatholytics: clonidine, methyldopa

MOA: reduces sympathetic outflow to the heart thereby decreasing cardiac output by decreasing heart
rate and contractility.
This class of drugs is not option for monotherapy of hypertension due to the CNS effects
ADR: sedation, bradycardia, orthostatic hypotension
In pregnancy: methyldopa

Alpha1 blocker (Prazosin, Doxazosin, Tamsulosin, Terazosin, Alfuzosin)

MOA: Blockade of α1 adrenergic receptors inhibits vasoconstriction induced by endogenous
catecholamines
This class is NOT recommended for initial monotherapy in hypertension; Mainly used in Benign
Prostatic Hyperplasia (BPH)
Main ADR: Orthostatic hypotension

Direct acting vasodilators: hydralazine, minoxidil

not first line; anticipated tachycardia + fluid retention, usually given with BB and diuretics
Hydralazine ADR: lupus like syndrome
Minoxidil ADR: Hirsutism

Q:
 Acute Coronary Syndromes

1. Unstable Angina: symptoms at rest ( normal ECG, Normal Cardiac enzymes levels)
2. NSTEMI: + cardiac enzymes are elevated
3. STEMI: + ECG showing ST- segment elevation

TIMI scoring Invasive vs Conservative Strategy for the management of ACS

Management:
1. MONA
a. Morphine
b. Oxygen if O2 sat less than 90%
c. Nitroglycerin (sublingual; recall maximum dose mentioned above)
d. Aspirin
2. Revascularization
a. Invasive (PCI, or CABG)
b. Non invasive (Fibrinolytics, alteplase, If PCI is not possible within 120 minutes, fibrinolytic
therapy is recommended and should be given within 30 minutes of hospital arrival (door-
to-needle time)
3. Dual antiplatelet (Aspirin + P2Y12 inhibitors) + anticoagulants (LMWH, or UH)
4. Given within 24 hours as needed ( BB, ACE inhibitors)

Pharmacology:
1. Aspirin
a. MOA: inhibits platelet aggregation by inhibiting production of thromboxane A2 via
irreversible COX1 and COX2 inhibition
b. Treatment dose: 162-325 mg; Secondary prophylactic dose: 81 mg
2. Nitrates
a. MOA: produces dilation of coronary arteries
3. P2Y12 inhibitors
a. MOA: bind to ADP P2Y12 receptor on the platelet surface, preventing activation of
GPIIb/IIIa receptor complex
b. Ticagrelor dose: LD 180 mg, MD 90 mg BID for 1 year; then 60 mg BID
4. Fibrinolytics (alteplase)
a. MOA: colt breakdown by binding to fibrin and converting plasminogen to plasmin

Q: correct regimen for aspirin and ticagrelor with doses

 Stroke
Signs and symptoms: ACT F.A.S.T
(Face, Arms, Speech, Time)

1. Acute ischemic stroke

a. Goal: restore blood flow
b. Agent: Alteplase ( BP should be less than 185/110 mmHg before initiating)
c. Criteria for timing: FDA approved (within 3 hours); non FDA approved (within 4.5 hours of
symptoms onset); door-to-needle time (within 60 minutes of hospital arrival)
d. Contraindication: active internal bleeding, severe uncontrolled BP, recent history of stroke
(within the past 3 months), any prior intracranial hemorrhage
e. Secondary prevention: hypertension, dyslipidemia, diabetes control + dual antiplatelet
(Aspirin + clopidogrel)
2. hemorrhagic strokes (Intracerebral hemorrhage, subarachnoid hemorrhage, subdural hematoma)
a. ICH: treat based on presentation
1. Severe coagulation factor deficiency or severe thrombocytopenia: give replacement
therapy or platelet infusions
2. ICH caused by anticoagulants: reversal therapy
3. Increase ICP: give mannitol or hypertonic saline
4. Treat seizures but never give prophylactic agents

Arrhythmias

Physiology (important to know action potential and what each wave represent)

Normal heart rate = 60 - 100 bpm

Lower: bradycardia
Higher: tachycardia
1. Supraventricular Arrhythmias
a. Atrial fibrillation: an irregular heartbeat that occurs when the electrical signals in the atria
fire rapidly at the same time. Most common. High risk for clot formation causing stroke.
(Recall CHADS2 VASc score; and when to use Oral anticoagulants)
b. Atrial flutter: more organized and regular than A Fib. Can progress to A. Fib
2. Ventricular Arrhythmias
a. Premature ventricular contractions (PVCs): related to stress or caffeine (skipped
heartbeat)
b. Ventricular tachycardia
c. Ventricular fibrillation
3. QT prolongation & Torsade de pointes
a. QT consider prolonged when it is > 440 milliseconds
b. QT prolongation leads to Torsade and can cause sudden cardiac death.
c. Most common drugs that can prolong QT: class I and class III antiarrhythmics, quinolones
and macrolides, all Azole antifungals, TCAs, SSRIs (citalopram, escitalopram), SNRIs
(mirtazapine, most antipsychotics, donepezil, tacrolimus.
d. Increase risk with hypokalemia, hypomagnesemia, and hypocalcemia

Pharmacology of Antiarrhythmics

Q: this drug belongs to which class?

Treatment of Atrial fibrillation
1. Rate control: The goal resting HR is <80 BPM in patients with symptomatic; however, a more
lenient goal of <110 BPM may be reasonable in patients who are asymptomatic and have
preserved left ventricular function. Beta-blockers (preferred) or non-DHP calcium channel blockers
( CCBs) are recommended. Digoxin is not first-line for ventricular rate control, but can be added
for refractory patients. (Patient with HFrEF should not receive a non-DHP CCB)
2. Rhythm control: conversion or maintenance of normal signs rhythm. Most effective with direct
current cardioversion (high energy shock).
Pharmacological cardioversion: amiodarone, dofetilide, flecainide, propafenone
Q: which drug also has rate control effect? Amiodarone

When do we prefer rhythm control?

• Paroxysmal AF
• Newly detected
• More symptomatic
• <65 years or age
• CHF exacerbated by AF
• No previous antiarrhythmic failure

Pharmacology
1. Amiodarone:
a. MOA: class III blocks K+ that causes repolarization of heart muscle, which increases
action potential duration
b. ADR: pulmonary toxicity, hepatotoxicity, hyper- and hypothyroidism (most commonly
hypothyroidism), photosensitivity (Q)
c. Teratogenic
d. Antiarrhythmic DOC in heart failure
e. DDI: decease digoxin by 50% and warfarin by 30-50% when starting amiodarone
f. Avoid grapefruit
2. Non-DHP CCB: diltiazem and verapamil
3. Digoxin:
a. MOA: induces increase in intracellular sodium that will drive influx of Ca inducing
contractility (positive inotropic, negative chronotropic)
b. Typical dose: 0.125 - 0.25 mg PO daily
c. Toxicity:
1. Initial toxicity: N/V, loss of appetite and bradycardia
2. Severe toxicity: blurred/double vision, greenish-yellow halos
3. Hypokalemia, hypomagnesemia, hypercalcemia increases the risk of toxicity
 Heart failure

Occurs when the heart is not able to supply sufficient oxygen-rich blood to the body, because of
impaired ability of the ventricle to either fill or eject blood

Q: know how to
classify patients
based on symptoms

FYI:
 Most importantly know the 4 pillars:
1. SGLT2i: empagliflozin and dapagliflozin
(mortality reduction benefit)
2. MRA: spironolactone (mortality benefit)
3. BB: metoprolol, bisoprolol, Carvedilol
(mortality benefit)
4. ARNI: Entresto (Sacubitril / Valsartan)
Do not use with or within 36 hours of ACE
inhibitors use

Digoxin: no mortality benefit, it reduces hospitalization and improves symptoms

Hydralazine and nitrates: morbidity and mortality in black patients
Anticoagulation

Indirect thrombin

Works on vitamin k
dependent factors:
Factor II, VII, IX, X
Indirect factor Xa inhibitors

Classes: (know which one is direct and which one is indirect)

1. Vitamin K antagonists: warfarin
2. Factor Xa inhibitors
a. Direct: rivaroxaban, apixaban, edoxaban
b. Indirect: fondaparinux
3. Thrombin inhibitors
a. Direct: argatroban, bivalirudin, dabigatran
4. sulfated polysaccharide:
a. Heparin (unfractionated heparin, LMWH: enoxaparin, dalteparin)
b. Antithrombin dependent mechanism (inactivating thrombin and Xa)
c. Indirect thrombin inhibitor

Major side effect for all anticoagulants: bleeding

Unfractionated heparin
a. MOA: Binds to antithrombin, which then inactivates thrombin (factor II) and factor Xa
b. ADR: HIT, thrombocytopenia, hyperkalemia, osteoporosis
c. Efficacy monitoring: aPTT (activated partial thromboplastin time), 6 hours after initiation
d. Safety monitoring: platelets at baseline and daily ( >50% decrease from baseline suggests
possible HIT)
e. HIT antibodies have cross-sensitivity with LMWH
f. In case of HIT, immediately D/C heparin or LMWH, can use direct thrombin inhibitor (DOC
is Argatroban, oral option Dabigatran)
g. Antidote: protamine
h. Warning for fetal medication errors
Low molecular weight heparin
a. MOA: binds to antithrombin, inactivates factor II and Xa, greater effect on factor Xa
b. ADR: similar to heparin (HIT) + injection side reaction (Sub Q)
c. Black box warning: don’t give LMWH for patients receiving neuraxial anesthesia (epidural,
spinal) puncture, risk of hematomas and paralysis
d. Efficacy monitoring: (not required, more predictable response) but you can get anti-Xa
level for renally impaired, obese, pregnant patients ( 4 hours post dose)
e. Safety monitoring: platelets
f. Antidote: protamine

Heparin induced thrombocytopenia

‣ Immune-mediated IgG drug reaction
‣ Unexplained drop in platelet count > 50% drop from baseline
‣ Management:
• D/C all forms of heparin and LMWH
• If patient is on warfarin, D/C warfarin and administer vitamin K (since it will lower
platelet count too); don’t restart it until plt >150 k
• Start patient on direct thrombin inhibitor: Argatroban (drug of choice)
• Patient is at high risk of thrombosis.

Factor Xa inhibitors
a. Direct: Apixaban, edoxaban, rivaroxaban (DOACs)
b. Indirect: Fondaparinux (injectable synthetic pentasaccharide) inhibits factor Xa via
antithrombin
c. Not recommended for patients with prosthetic heart valve
d. Avoid (DOACs) in patients with moderate to severe hepatic impairment
e. Avoid (Fondaparinux) in severe renal impairment (CrCl < 30)
f. Antidote for Apixaban and Rivaroxaban: Andexanet alfa
g. No antidote for edoxaban and Fondaparinux

Direct thrombin inhibitors

A. Oral: Dabigatran (DOAC)
a. No cross reaction with HIT
b. Antidote: Idarucizumab
B. Injectable: Argatroban, Bivalirudin
a. No cross reaction with HIT
b. No antidote

(Recall mechanisms, ADRs, Drug-drug interactions and drug-food interactions and antidotes, most
SPLE Questions are about anticoagulants especially warfarin)
Vitamin K antagonist (Warfarin)
a. MOA: competitively inhibits the Cl subunit of the multi-unit vitamin K epoxide
reductase (VKORCl) enzyme complex. This reduces the regeneration of vitamin K
epoxide and causing depletion of active clotting factors II, VII, IX and X and proteins
C and S.
b. Racemic mixture of R- and S- enantiomer (S- more potent)
c. Counseling point: should be taken at the same time everyday. Consistent amount of
vitamin K.
d. Monitor: international normalized ratio (INR)
1. Goal INR 2-3: most indications (VTE, AFib, bioprosthetic mitral valve, mechanical
aortic valve)
2. Goal INR 2.5-3.5: high risk indications (mechanical mitral valve, or any 2 mechanical
heart valves)
3. Begin monitoring after initial 2 or 3 doses; after stable dose of warfarin, monitor every
4 (1 months); if consistently stable every 12 weeks (3 months)
e. Dose:
1. healthy patients: 10 mg daily for 2 day; then adjust dose per INR
2. Lower dose (5 mg) for elderly, malnourished, high risk of bleeding, liver disease, heart
failure, taking drugs that can increase warfarin levels.
f. Contraindication: pregnancy (except in mechanical heart valves) causes nasal hypoplasia
g. Warnings: tissue necrosis/gangrene, HIT, presence of CYP2C9*2 or*3 alleles and/or
polymorphisms of VKORC1 gene
h. ADR: bleeding/bruising, skin necrosis, purple toe syndrome
i. Antidote: vitamin K

Warfarin Drug interactions

Pharmacokinetics
a. Substrate of CYP2C9
1. Inducers = decrease INR
a. carbamazepine
b. phenobarbital
c. phenytoin
d. rifampin
e. St. John's wort
2. Inhibitors = increase INR (high)
a. Amiodarone (when starting amiodarone, decrease warfarin by 30-50%)
b. Azole antifungals (fluconazole, ketoconazole, voriconazole)
c. metronidazole
d. tigecycline
e. TMP/SMX
b. warfarin has a high protein binding, displacement may increase free concentration (risk of
bleeding)
Antibiotics: penicillins ( amoxicillin, some cephalosporin, quinolones, tetracyclines)
Phenytoin (high protein binding)
Pharmacodynamic
a. Increase bleeding risk, but the INR may not be increased
1. NSAIDs
2. Antiplatelet
3. SSRIs and SNRIs
b. Increase clotting risk
1. Estrogen and SERMs
 Warfarin Food interactions
1. Increase bleeding risk
a. The 5 Gs ( garlic, ginger, ginkgo, ginseng, glucosamine)
b. Vitamin E
c. Grapefruit
2. Increase clotting risk
a. Green tea
b. Co-enzyme Q10
c. St. John’s wort
d. Any additions of vitamin K will decrease INR (stay consistent)

Warfarin Reversal
a. Recall when to use vitamin K (phytonadione or phylloquinone) with doses.
b. Other option:

• Four factor prothrombin complex concentrate (factors II, VII, IX, X, protein C,S)

Venous thromboembolism (VTE)

Risk factors:
‣ Surgery
‣ Major trauma
‣ Immobility
‣ Cancer and chemotherapy
‣ Previous VTE
‣ Estrogen
‣ Increasing age
‣ Obesity

Prophylaxis
‣ Pharmacological: UFH, LMWH, fondaparinux, Rivaroxaban, Apixaban, dabigatran (all are
approved for prophylaxis)
‣ Mechanical: intermittent pneumatic compression (IPC) devices or graded compression
stockings
◦Commonly: Enoxaparin 30 mg SubQ q12h or 40 mg daily (CrCl<30: 30 mg daily)
‣ Treatment dose: 1 mg/kg SubQ q12h
Unfractionated heparin 5000 units SubQ q8-12h
Treatment
Duration for provoked: 3 months
Duration for unprovoked: extended (6 months)
 Anemia

Normal levels:
‣ Hemoglobin
• Male: 13.2-16.6 g/dL
• Female: 11.6 -15 g/dL
‣ Hematocrit
• Male: 38.3 - 48.6%
• Female: 35.5 - 44.9%

• Anemia caused by Vitamin B12 deficiency is also called pernicious anemia, it is a megaloblastic
anemia, happens due to Lack of intrinsic factor. Treatment: Cyanocobalamin (B12)
• Type of anesthetic can cause anemia? Nitrous oxide
• medications can cause hemolytic anemia in the newborn when used by a pregnant woman at full
term? Nitrofurantoin

Iron deficiency anemia

• Most common type, caused by inadequate dietary intake (vegetarian), blood loss, decrease iron
absorption (use of PPIs), increase requirement (pregnancy)
• Treatment: recommended dose 100-200 mg elemental iron on an empty stomach
• Most patients treated with oral, IV for patient on dialysis
‣ Most commonly: Ferrous sulfate 325 mg PO (65 mg elemental, 20%) daily to TID
‣ Avoid antacid, H2RA, PPIs (increase gastric PH) lower absorption of iron
◦Antidote for iron overdose: deferoxamine
• Intravenous iron: may cause fetal anaphylactic reaction; with iron dextran give a test dose
‣ Most commonly used IV iron: iron sucrose

Normocytic anemia: anemia of chronic kidney disease

Erythropoietin (EPO) is a hormone produced by the kidneys that stimulates the bone marrow to
produce RBCs. A deficiency of EPO causes anemia of chronic kidney disease.
• Treatment:
‣ Erythropoiesis-stimulating agents (ESAs): Epoetin alfa; initiate when Hgb<10
◦The goal for Hgb in CKD patients is > 11 g/dL (110 g/L); if patient is on ESA
decrease or interrupt dose when HgB exceeds 11 (due to increased mortality)
‣ Always give iron therapy with ESA
 Sickle cell disease

Resulting from a genetic mutation in the genes that encode hemoglobin. Abnormal hemoglobin, called
hemoglobin S (HgbS or sickle hemoglobin). This causes RBCs to be rigid with a concave "sickle"
shape. Sickled RBCs burst (hemolyze) after 10 - 20 days, which causes anemia and fatigue.
(Normal RBCs have a lifespan of 90 - 120 days)

Acute Complications:
‣ Anemia
‣ Vaso-occlusive crisis (VOC)
‣ Cholecystitis
‣ Acute chest syndrome
‣ Infections
‣ Stroke

Treatment
1. Non drug treatment:
a. Blood transfusion
b. Bone marrow transplant (the only cure for SCD)
2. Drug treatment
a. Risk of infections: vaccination is key (especially for <5 years old; prevent sepsis and
meningitis). Prophylactic penicillin for infants who screen positive for SCD at birth should
be on penicillin twice daily until age five years.
b. Analgesic: for mild to moderate, rest, fluids, warm compresses, and use of NSAIDs or
acetaminophen. For severe and VOC, IV opioids or patient-controlled analogesia (PCA)
c. Disease modifying drugs:
1. Hydroxyurea:
MOA: stimulates production of hemoglobin F (HgbF)
Indication: should be consider in all children > 9 months of age regardless of
severity. And adults with 3 or more moderate to severe pain crises in one year.
BBW: myelosuppression
Warning: avoid live vaccines
ADR: increase LFTs, alopecia
Response can take 3-6 months

Contraception requires during treatment and after discontinuation

For females: 6 months after D/C
For males: 12 months after D/C

Folic acid supplementation is recommended to prevent macrocytosis

 Diabetes mellitus

• Insulin is a hormone produced by beta-cells (islet cells) in the pancreas. It moves glucose
intracellularly to be used as energy, either moved to muscle cells (primarily) for immediate use, or
stored in liver cells (as glycogen) or adipose (fat) cells.
‣ Brain cells can uptake and use glucose without being stimulated insulin.

• Insulin is counter-balanced by glucagon; they have opposite effects. Glucagon is produced by

alpha-cells in the pancreas. Glucagon pulls glucose back into the circulation. If glycogen is depleted,
glucagon will signal fat cells to make ketones as an alternative energy source.

Type 1 DM
• Autoimmune destruction of beta-cells in the pancreas, insulin cannot be produced.
• Timeline when symptoms start to occur in type 1 diabetes, when 70% of the islets of langerhans of
the pancreas are destroyed.

‣ Without insulin, glucose cannot enter muscle cells, starvation mode, and starts to
metabolize fat into ketones, which are acidic. High ketone levels cause diabetic
ketoacidosis (DKA)

• Mostly diagnosed in children, C-peptide test is used to determine if pancreas still produces insulin.
• Must be treated with insulin

Type 2 DM
• Due to both insulin resistance (decreased insulin sensitivity) and insulin deficiency.
• Strongly associated with obesity, physical inactivity, family history and the presence of other
comorbid conditions.
‣ Management: Plate method as a lifestyle modification + Oral or injectable medications

Prediabetes
• Should follow dietary and exercise recommendations to reduce the risk of progression to diabetes.
• Metformin can be used, BMI ≥ 35, age <60, and women with hx of gestational diabetes.
• Annual monitoring

Diabetes in pregnancy
• BG goal is more stringent; to prevent babies from being born with diabetes and obesity
• Testing for gestational diabetes at 24-28 weeks using oral glucose tolerance test.
• DOC in pregnancy: insulin
 Screening
• Even without risk factors, should begin testing at age of 45.
• Overweight (BMI ≥ 25) with at least one risk factor, should be tested, if normal repeat every 3 years

Comprehensive evaluation of diabetic patient

Eye exam:
• T1D: every 5 years
• T2D: every year
Alternative Questions:
Herbal product that can enhance the effect of oral antidiabetic medication: American ginseng
Lower fasting blood glucose levels: aloe vera
Known as insulin plant: Costus igneus

Management of T2D

• Always start with metformin

• Recall maximum doses and know when to add and what to add as a second agent:
‣ For 500 mg IR and ER, maximum dose is 2000 mg per day
‣ For 850 mg IR, maximum dose is 2550 mg (TID per day is the maximum dose)
• Patient with heart failure = SGLT2i (dapagliflozin, empagliflozin)
• Contraindicated in heart failure = thiazolidinediones
• Weight loss = SGLT2I and GLP-1
• Weight gain = insulin
Pharmacology
1. Biguanide: metformin
a. MOA: decrease glucose hepatic production, absorption, and increase insulin sensitivity.
b. First line treatments for T2D (DOC)
c. Dose: 500 mg daily or BID , titrate weekly usual maintenance 1000 mg BID (Max dose
2000-2550 mg per day)
d. ADR: GI side effects (diarrhea, nausea). Warning for Vitamin B12 deficiency (supplement)
e. Counseling point: taken with a meal; to decrease GI side effects
f. Contraindication: eGFR <30. Don’t start if eGFR 30-45
2. Sodium Glucose co-Transporter 2 inhibitors (SGLT2i): Canagliflozin, Dapagliflozin, Empagliflozin
a. MOA: reduce reabsorption of glucose and increase urinary glucose excretion
b. ADR: weight loss, volume depletion (warning for AKI)
c. Benefits: reduction in HF and CKD progression
3. glucagon-like peptide 1 agonists (GLP-1): Liraglutide , Dulaglutide (weekly dosing)
a. MOA: increase glucose-dependent insulin secretion
b. ADR: weight loss, injection site reaction
c. benefits: ASCVD benefit
4. Sulfonylurea: Glipizide, Glimepiride, Glyburide
a. MOA: insulin secretagogues
b. Sulfa allergy
c. ADR: weight gain, high hypoglycemia risk
d. Glimepiride, Glyburide not recommended for elderly (hypoglycemia)
5. Meglitinides: Repaglinide, Nateglinide
a. MOA: insulin secretagogues
b. ADR: weight gain, high hypoglycemia risk
6. Dipeptidyl peptidase 4 inhibitors: Sitagliptin, Linagliptin, saxagliptin
a. Potential risk in HF patient with saxagliptin
b. Don’t use with GLP-1 agonists, overlapping mechanisms
7. Thiazolidinediones: Pioglitazone, Rosiglitazone
a. MOA: increase peripheral insulin sensitivity
b. Black box: exacerbate heart failure (Contraindicated in HF)
c. ADR: peripheral edema, weight gain

Insulin

‣ Glargine 24 hours
‣ Degludec 42 hours (longest acting insulin)
• Starting insulin for T1D:
‣ Typical dose is 0.5 units/kg/day
‣ 50% of total daily dose is administered as basal insulin; other 50% as prandial (bolus)
insulin, dividd among 3 meals
• Starting insulin for T2D:
‣ Add basal insulin 10 units or 0.1-0.2 units/kg/day; and if not controlled, add prandial insulin
4 units or 10% of basal dose once prior to largest meal

Administration
‣ Best absorbed in the abdomen
‣ Rotate injection site
 Thyroid disorders

Hypothyroidism
• Lab findings: low T4 and high TSH
• Most common cause of hypothyroidism is Hashimoto’s disease, an autoimmune condition
where the body start producing antibodies that attacks thyroid gland.
• Drugs cause hypothyroidism: amiodarone, lithium, carbamazepine
• Monitoring: TSH should be monitored every 4-6 weeks until levels are normal, then 4-6 months, then
annually
• DOC: Levothyroxine 25-50 mcg/day
‣ should be take at least 60 minutes before breakfast with water

‣ Levothyroxine is safe during pregnancy; dose should be increased since pregnant women
require about 25% higher doses ( some reference say 30-50% increase)
‣ Elderly may require higher dose
‣ Adjustment is based on TSH
‣ ADR: weight loss
Hyperthyroidism
• Lab findings: T4 high, TSH low
• Most common cause is Graves’ disease, which is an autoimmune disease producing antibodies
that stimulate the thyroid gland
• Drugs that may cause hyperthyroidism: amiodarone, iodine, interferons
• Management: surgery, radioactive iodine to destroy part of gland, symptom control by beta blockers
◦Thionamides: inhibits synthesis of thyroid hormone
‣ Propylthiouracil (PTU)
‣ Methimazole
• ADR: hepatotoxic, may cause agranulocytosis, lupus erythematosus
• Methimazole is considered as DOC; lower risk of hepatotoxicity
• PTU is preferred in thyroid storm
• In pregnancy: 1st trimester give PTU, 2nd and 3rd trimester give methimazole
‣ Avoid methimazole in 1st trimester due to increased risk of fetal
abnormalities
Thyroid storm
• life-threatening medical emergency characterized by decompensated hyperthyroidism.
• Signs/symptoms: fever, tachycardia, tachypnea, agitation, delirium.
• Management:
‣ PTU is preferred
‣ + Iodide therapy
‣ + Beta blocker (propranolol)
‣ + steroid (dexamethasone)
‣ + supportive (acetaminophen, fluids, electrolytes,…)
 Oncology
Terminology
‣ Carcinoma = skin or tissues lining or covering internal organs
‣ Leukemia = cancer of leukocytes (WBC); commonly referred to as blood cancer
‣ Lymphoma = cancer of Lymphatic system
‣ Myeloma = cancer of bone marrow
‣ Sarcoma = connective tissue e.g. osteosarcoma which is a bone cancer

‣ Adjuvant = treatment given after the primary therapy

‣ Neoadjuvant = treatment given before the primary therapy

Pharmacology

• Recall mechanisms of action for each drug

Cell cycle independent
1. Alkylating agents: work by cross-linking DNA strands
a. Cyclophosphamide
b. Ifosfamide
1. Both cause hemorrhagic cystitis; due to the production of a metabolite called
acrolein
2. Give mesna as a chemoprotectant
c. Carmustine
d. Busulfan
1. Both can cause pulmonary toxicity
2. Platinum based compounds: work by cross-linking DNA strands
a. Cisplatin
b. Carboplatin
1. Class side effect: peripheral neuropathy
2. Cisplatin is nephrotoxic and ototoxic
3. Carboplatin causes dose-related myelosuppression
3. Anthracyclines
a. Doxorubicin
1. Cardiotoxicity; to prevent doxorubicin-induced cardiotoxicity give Dexrazoxane
2. Potent vesicants = extravasation leading to tissue necrosis
3. Cause red discoloration of body fluids

Cell Cycle specific

1. Topoisomerase I inhibitors
a. Irinotecan
b. Topotecan
2. Topoisomerase II inhibitors
a. Etoposide
1. Infusion rate-related hypotension; infused over at least 30-60 minutes
b. bleomycin
1. Causes pulmonary fibrosis
2. Test dose must be given; risk of anaphylactic
3. Not myelosuppressive
4. Causes fever and chills; premeditate with acetaminophen
3. Vinca Alkaloids (M phase)
a. Vincristine
1. Causes more CNS toxicity
b. Vinblastine
1. More bone marrow suppression
2. Class ADR: peripheral sensory neuropathy; both are potent vesicants
3. Labeling of vinca alkaloids: for Intravenous use
only. Fetal if given by other routes.
4. Intrathecal administration will cause progressive
paralysis and death
5. Should be prepared in a small IV bag (a piggyback)
rather than in a syringe, to avoid inadvertent
intrathecal administration
4. Taxanes (M phase)
a. Paclitaxel
b. Docetaxel
1. May cause peripheral sensory neuropathy
5. Antimetabolites (S phase)
A. Pyrimidine analogs
a. Fluorouracil (5-FU)
b. Capecitabine (prodrug of 5-FU)
1. Given with Leucovorin; to increase efficacy
2. ADR: hand-foot syndrome
c. Cytarabine
d. Gemcitabine
1. ARD: pulmonary toxicity
B. Folate analogs
a. Methotrexate
1. Folic acid and vitamin B12 may be required to reduce toxicity
2. Leucovorin must be give with high doses of methotrexate as a rescue
3. ADR: nephrotoxicity (hydration and IV sodium bicarbonate must be given to alkalinize
urine and reduce toxicity), SJS/TEN, tumor lysis syndrome, teratogenic

Breast cancer
• Top risk factor: being female
• Early sign of breast cancer: painless lump
• Prevention: vitamin D
• Treatment:
‣ Hormone positive = based on menopausal status

Tamoxifen should be avoided

in pregnancy (teratogenic)

Aromatase inhibitors:
• Anastrozole
• Letrozole

‣ HER2 positive = Trastuzumab

‣ Women with breast cancer, Topoisomerase is elevated? Irinotecan

 Pain management

(Adjuvant therapy can

include the use of
Ganpentin, pregabalin for
neuropathic pain)

Acetaminophen
‣ Maximum dose: > 4000 mg/day
‣ Hepatotoxicity
‣ Antidote: N-acetylcysteine NAC, toxicity is due to glutathione depletion
• Rumack-mathew nomogram uses the serum acetaminophen level and the time since ingestion
to determine the likelihood of hepatotoxicity,

NSAIDs
‣ Non selective block both COX1 and COX2
‣ ADR: GI bleeding and ulcer, CV risk (MI, and stroke), reduce renal clearance (AKI), increase
BP, cause premature closure of ductus arteriosus
• (Recall indomethacin can be use to close ductus)
• None selective (GI and CV risk)
◦Ibuprofen:
‣ Max OTC dose = 1.2 g/day
‣ Max Rx dose = 3.2 g/day
◦Indomethacin
‣ High risk of CNS side effects
◦Naproxen
• Selective COX 2 (lower GI risk, high CV risk)
◦Celecoxib
‣ Sulfa allergy
◦Diclofenac
• Salicylate NSAIDs
◦Aspirin
‣ Avoid in children; risk of Reye’s syndrome
Opioid analgesics
‣ mu receptor agonists, which primarily cause pain relief, but also cause euphoria and
respiratory depression
‣ Use for moderate to severe pain
‣ Use of Risk Evaluation and Mitigation strategy (REMS) for ALL opioid to manage safety
concerns with using opioid
◦Terminology:
‣ Physical dependence: experience physical withdrawal symptoms when opioids are D/C
‣ Addiction: drug-seeking behavior
‣ Tolerance: a higher dose is needed to produce the same effect
◦General class ADR:
‣ Respiratory depression
‣ Constipation
• Codeine
‣ Don’t use in children <12 for any indication
‣ Don’t use for <18 following tonsillectomy
‣ FDA recommends to avoid codeine cough and cold products for <18
• Fentanyl
‣ Counseling points for patch:
• Apply one at a time at a hairless skin
• Don’t cover with heating pad
• Hydrocodone
• Hydromorphone
• Methadone
‣ Causes QT prolongation
• Morphine
‣ High risk of medication errors
‣ Pre medicate with antihistamine (diphenhydramine) to reduce pruritus
• Oxycodone

Opioid overdose = naloxone

Dosing conversion

• Steps
‣ Calculate total in 24 hours
‣ Use ratio from table to get total for new
drug in 24 hours
‣ General rule, you should reduce the dose
by at least 25%, always round down with
opioids for cross-tolerance
‣ Divide new dose with appropriate interval
given in the question

• For fentanyl patch, remember dose is calculated in mcg/hr

‣ Convert from mg to mcg by x1000
‣ Then divide by 24 hours
‣ Some clinicians use an estimation of morphine 60 mg/day = 25 mcg/hr fentanyl patch
 Epilepsy

Epilepsy is a chronic seizure disorder.

A seizure occurs when excitatory neurons

produce a sudden surge of electrical
activity in the brain.(Imbalance between
inhibitory and excitatory pathways)

Deficiency of the inhibitory NT, gamma-

aminobutyric acid (GABA), or an excess of
the excitatory NT, glutamate.

Pharmacology:

1. Na channel blockers
A. Phenytoin/fosphenytoin
a. Infuse slowly (rate shouldn’t exceed 50 mg/minute) to avoid hypotension and arrhythmias
b. Causes extravasation leading to purple glove syndrome
c. Avoid in patients with a positive HLA-B*1502 , increase risk of SJS/TEN
d. ADR: nystagmus, ataxia, and diplopia (dose-related), can cause gingival hyperplasia, hair
growth, hepatotoxicity
e. Monitoring serum level, should be corrected according to albumin level
f. Highly protein bond
g. Strong CYP inducer (mainly 2C9 and 2C19)
h. Pregnancy category D: cleft and facial palate
B. Carbamazepine
a. Causes SJS/TEN and serious skin reactions, don’t give if patient is HLA-B*1502 positive
b. Causes aplastic anemia, and agranulocytosis
c. Cause multiorgan hypersensitivity reactions (DRESS), and hyponatremia (SIADH)
d. Strong enzyme inducer and autoinducer
e. Pregnancy category D
C. Oxacarbazepine
a. HLA-B*1502
b. Weak inducer, not an autoinducer
D. Lamotrigine
a. Causes SJS/TEN and alopecia
b. Safe in pregnancy
E. Topiramate
a. Causes metabolic acidosis
2. GABA activity
A. Valproic acid
a. Contraindicated in pregnancy causes neural tube defects and lower IQ
b. Hepatotoxic (monitoring LFTs) , increase ammonia levels, causes thrombocytopenia,
weight gain and alopecia
c. Also used for bipolar and migraine prophylaxis
B. Benzodiazepines
a. Diazepam
b. Midazolam
C. Phenobarbital
3. Ca related mechanisms: Levetiracetam and ethosuximide
Selecting the best Antiepileptic agent:
• During pregnancy
◦Levetiracetam
◦Lamotrigine
• Breastfeeding
◦Levetiracetam
• Absence seizure
◦Ethosuximide
• Generalized tonic-clonic seizures
◦Valproate
◦Lamotrigine
◦Topiramate
• For focal seizure
◦Carbamazepine
◦Phenytoin
◦Lamotrigine
 Parkinson's disease

PD is neurological disorder occurs when neurons

in the substantia nigra die or become impaired,
leading lower production of dopamine.
Major symptoms abbreviated as TRAP

Pharmacology
• Dopamine replacement
◦Carbidopa/levodopa
‣ Levodopa is a precursor of dopamine, carbidopa inhibits dopa decarboxylase enzymes;
preventing peripheral metabolism of levodopa
‣ Counseling point: Iron and protein-rich foods can decrease absorption.
‣ Contraindicated with MAO inhibitors; two weeks washout period
‣ Avoid abrupt discontinuation
‣ Cause body fluid discoloration (dark brown)
‣ Causes nausea; lower the dose to manage or give Domperidone
• COMT inhibitors
◦Entacapone
◦Tolcapone (hepatotoxic; not commonly used)
‣ They inhibit enzyme catechol-O-methyltransferase (COMT) to prevent peripheral conversion
of levodopa
‣ Mainly used with Carbidopa/levodopa
• Dopamine agonists
◦Pramipexole
◦Ropinirole
‣ Cause orthostatic hypotension
• Dopamine reuptake inhibitor
◦Amantadine
‣ Causes Livedo reticularis (skin pigmentation)
• Selective MAO-B inhibitor
◦Selegiline
◦Rasagiline
‣ Serotonin syndrome
‣ Avoid tyramine containing foods
• Anticholinergic
◦trihexyphenidyl
◦benztropine
‣ Causes mydriasis and closed angle glaucoma

Drugs that worsens PD

• Antipsychotic (haloperidol, droperidol, risperidone, paliperidone, prochlorperazine)
• Metoclopramide

Treatment of Parkinson's disease psychosis: Pimavanserin, or quetiapine

Treatment of hallucinations and delusions in PD: Clozapine
 Alzheimer’s disease

The two pathologic hallmarks of Alzheimer disease are:

‣ Extracellular beta-amyloid deposits (in senile plaques)
‣ Intracellular neurofibrillary tangles (paired helical filaments)
The beta-amyloid deposition and neurofibrillary tangles lead to loss of synapses and neurons, which
results in gross atrophy of the affected areas of the brain, causing loss of memory

Cholinergic hypothesis: Acetylcholine (ACh) is decreased in both concentration and function in

patients with Alzheimer's disease impairing cholinergic innervation.

Screenings tools: MMSE according to DSM-5 criteria

Herbal products for AD:

• Ginkgo
• Vitamin E
• Caprylidene

Drugs worsening AD
Centrall acting anticholinergics (avoid in elderly due to acute cognitive impairment risks according to
Beers Criteria) e.g. benztropine

Management
• Acetylcholinesterase inhibitors: inhibit centrally acting acetylcholinesterase, blocking hydrolysis.
◦donepezil
‣ Mainstay of treatment, alone or with memantine in more advanced stages of the disease.
‣ Taken QHS (at bedtime) to reduce nausea
◦Rivastigmine
‣ Both cause bradycardia
• NMDA blocker: inhibits glutamate binding and decrease abnormal neuron activation
◦Memantine
‣ ADR: dizziness, confusion, headache
 Depression

Neurotransmitters believed to be involved in depression include

serotonin, norepinephrine, epinephrine, dopamine, glutamate and
acetylcholine.
Serotonin (5-HT) may be the most important involved with feelings
of well-being.

Drugs that may cause or worsen depression:

Beta blockers (propranolol), isotretinoin, methyldopa.

Screenings tools: Hamilton Depression Rating Scale (Ham-D) according to DSM-5 criteria

Herbal products for depression:

• St. John’s wort
• SAMe (S-adenosyl-L-methionine)
• Valerian
• 5-HTP (5-hydroxytrytophan)

Management
• Generally a suitable trial period of antidepressants is at least 4-8 weeks (average 6 weeks) to
assess efficacy.
• Can take 1-2 weeks to feel benefit, and 6-8 weeks to feel full effect
• For mild depression: should be treated with cognitive behavioral therapy (CBT)
• Moderate to severe: should be treated with antidepressants in addition to CBT
◦For most patients SSRI or SNRIs, choice is based on safety profile
◦In pregnancy, SSRIs except paroxetine, due to potential cardiac effect

Pharmacology
1. SSRIs (Selective serotonin reuptake inhibitors):
A. Citalopram
a. QT prolongation
B. Escitalopram
C. Fluoxetine
a. Taken in the morning (most activating)
D. Paroxetine
a. Taken in the evening (most sedating)
E. Sertraline
a. Preferred in patient with cardiac risk
2. SNRIs (serotonin and norepinephrine reuptake inhibitors):
A. Venlafaxine
B. Duloxetine
3. Tricyclic antidepressants: inhibit NE and 5-HT, and also block acetylcholine
A. Amitriptyline
B. Nortriptyline
a. As a class, considered to have worst safety profile. Cause QT prolongation, arrhythmia,
weight gain, orthostatic hypotension (beer criteria: avoid in elderly)
4. Dopamine and norepinephrine reuptake inhibitors
A. Bupropion
a. Contraindicated in seizure disorders
5. Miscellaneous antidepressants: Mirtazapine, and Trazodone
Selecting the best antidepressants:
• cardiac or QT prolongation risk
◦Preferred: Sertraline
◦Avoid: Citalopram, and Escitalopram
• For smokers
◦Preferred: bupropion
• For patients with seizure disorder
◦Preferred: SSRIs or SNRIs
◦Avoid: bupropion
• Pregnant women
◦Preferred:
‣ If mild-to-moderate: CBT
‣ If severe: citalopram, escitalopram, fluoxetine, sertraline
◦Avoid: paroxetine
• Patient complaining of daytime sedation:
◦Preferred: fluoxetine, bupropion (activating effect)
• Patient complaining of insomnia:
◦Preferred: paroxetine, mirtazapine, trazodone
 Schizophrenia

It is a heterogeneous syndrome of disorganized and

bizarre thoughts, delusions, hallucinations,
disorganized speech and impaired psychosocial
functioning.
Psychosis is a hallmark feature.

Goal of therapy
• Acute Phase: usually require hospitalization, relieve
psychotic symptoms,
• Stabilization phase: may take several months (for at
least six months), induce remission.

Herbal products: fish oil

Drugs that may cause psychotic symptoms: cannabis, cocaine, LSD

Management:
First line is second generation antipsychotics (lower risk of extrapyramidal symptoms EPS)

1. First generation antipsychotics

A. Haloperidol
B. Chlorpromazine
a. MOA: mainly block dopamine 2 receptors
b. ADR: EPS, anticholinergic side effects, QT prolongation
c.
2. Second generation antipsychotic: block dopamine and serotonin receptors (lower EPS)
A. Aripiprazole
a. Cause akathisia
B. Clozapine
a. Causes neutropenia/ agranulocytosis, seizure, cardiomyopathy
b. Patient must be enrolled in the clozapine REMS
C. Olanzapine
D. Quetiapine
a. Often used for psychosis in Parkinson disease
E. Risperidone

• Acute psychosis:
‣ IM 2nd generation (aripiprazole, ziprasidone, and olanzapine)
‣ Or oral 2nd generation +/- IM lorazepam
• Adjunctive medications
◦Schizoaffective disorder: mood stabilizers (lithium, Carbamazepine, Valproic acid)
◦Depressions: SSRIs
 Bipolar Disorder

Patients with bipolar disorder usually cycle between mania and depression.
The goal of treatment is to stabilize the mood without inducing a depressive or manic state.
Mood stabilizers, such as lithium and antiepileptic drugs (valproate, lamotrigine and carbamazepine),
considered first line

Acute treatment
• Manic episode: first-line treatment is valproate, lithium or an antipsychotic.
‣ A combination of an antipsychotic + lithium or valproate is preferred for severe episodes.
• Depressive episode: first-line treatment is lithium, but lamotrigine can be used as an alternative.

Maintenance treatment
• Lithium and valproate are preferred for maintenance monotherapy, but lamotrigine, carbamazepine
and 2nd generation antipsychotics are alternatives.

Pharmacology:
1. Lithium
A. MOA: reuptake of serotonin and/or norepinephrine or by moderating glutamate levels in
the brain.
B. ADR: serotonin syndrome, tremor, polyuria/polydipsia, weight gain, hypothyroidism
C. Toxicity manifestation: ataxia, hand tremor, vomiting, at higher levels, CNS depression,
arrhythmia, seizures, coma
D. Monitoring: lithium level, renal function, thyroid function
E. AVOID IN PREGNANCY, associate with cardiac malformations

In pregnancy:
• Lithium = cardiac malformations
• Valproate = neural tube defect
• Carbamazepine = facial abnormalities
◦Safer option in pregnancy: Lamotrigine

Attention Deficit Hyperactivity Disorder (ADHD)

Herbal product: fish oil

Management:
• First line: Stimulants
◦MOA: block the reuptake of norepinephrine and dopamine
‣ Methylphenidate
‣ Dexmethylphenidate
‣ Dextroamphetamine/ amphetamine (Adderall)
• Non-stimulant for ADHD :
‣ Atomoxetine (SNRIs)
 Anxiety

• Herbal products
‣ St. John’s worts (strong CYP3A4 inducer)
‣ Valerian (anxiety and sleep) (hepatotoxic; require monitoring)
‣ Passionflower
‣ Kava (hepatotoxic; not recommended)

• Non pharmacological: CBT

Management
• Acute: for fast relief = benzodiazepines
• First line = SSRIs (at least 4 week for noticeable effect)
• Second line = Buspirone, TCA, hydroxyzine, pregabalin, gabapentin
• Stage fright or performance = propranolol (not FDA approved)

Pharmacology
◦Buspirone
‣ MOA: affinity for serotonin receptors
‣ ADR: risk of serotonin syndrome, don’t use with MAO

For OCD use: Clomipramine

Or SSRIs
Benzodiazepines are NOT effective
 Asthma

Pathophysiology:
• Early phase: Bronchoconstriction
◦major role in acute exacerbations
‣ Allergen-induced, IgE dependent release of mediators
from mast cells
• Late phase: inflammatory response.
◦Primary mediators: white blood cells “Eosinophils” that stimulate
mast cell degranulation and release substances that attract other
white cells to the area.

Diagnosis: spirometry and pulmonary function test

(Measure baseline, then after SABA, to test for reversibility- if the FEV1 increases by more than 12%
with the use of SABA-)

2018 guidelines (for SPLE recall the old guidelines)

GINA 2021 (for your reference)

Asthma exacerbation
• Target oxygen
saturation of 93-95%.
Pharmacology:
1. Short-acting Beta 2 agonists (SABA)
A. Salbutamol (Albuterol)
a. ADR: tachycardia, hypokalemia, hyperglycemia, insomnia
2. Long-acting Beta 2 agonists (LABA)
A. Salmeterol
B. Formoterol
a. Not used as monotherapy (higher mortality, and CVD)
3. Anticholinergics
A. Ipratropium bromide
B. Tioropium
a. ADR: dry mouth, tachycardia, bronchitis, sinusitis
4. Inhaled corticosteroids (ICS)
A. Budesonide
B. Fluticasone
C. Mometasone
a. ADR: oral thrush (candidiasis)
5. Systemic corticosteroids
A. Prednisone
B. Prednisolone
C. Methylprednisolone
D. Hydrocortisone
a. Short term (5-7 days) side effects: hyperglycemia, mood changes
b. Long term side effects: adrenal suppression, glaucoma, osteoporosis
c. Tapering is required if treatment given for more than 2 weeks
6. ICS/LABA combination
A. Diskus (fluticasone/ salmeterol)
B. Symbicort (budesonide/ formoterol)
C. Dulera (mometasone/ formoterol)
7. Methylxanthines
A. Theophylline
a. Not used
8. Leukotriene Modifiers
A. Montelukast
a. 2020 FDA warning: causes neuropsychiatric events
9. Monoclonal antibodies/biological therapy
A. Omalizumab
a. MOA: anti IgE
b. ADR: injection site reaction, thrombocytopenia, anaphylaxis

If you use ICS rinse you mouth with water after

inhalations, to prevent oral thrush
 COPD

Characterized by persistent airflow limitation that due to airway and/or alveolar abnormalities

Diagnosis: Spirometry is the gold standard

The presence of a post-bronchodilator FEV1/FVC < 0.70 confirms persistent airflow limitation and
thus of COPD. (<12 % improvement or no improvement after SABA)

Assess Symptoms: Validated

questionnaires
• COPD Assessment Test (CAT)
• The modified British Medical Research
Council (mMRC) scale.

COPD exacerbation
• Target oxygen saturation of 88-92%.
• Antibiotic treatment should be initiated for exacerbations based on cardinal
symptoms
 Gout

Buildup of uric acid (UA) crystals in the joints. UA is produced as an

end-product of purine metabolism. Purines are present in foods,
and they make up one of the base pairs of DNA

Drugs that increase uric acid:

Aspirin, calcineurin inhibitors (tacrolimus, cyclosporine), diuretic
(loop and thiazide) , niacin (vitamin B3) , pyrazinamide.

Goal of uric acid level to prevent attacks: < 6 mg/dL

Treatment of acute pain (attack):

• Colchicine
• Steroids (prednisone, prednisolone, methylprednisolone)
• NSAIDS (indomethacin, naproxen, celecoxib)

Chronic management to prevent attacks :

• First line: Xanthine oxidase inhibitors, Allopurinol
‣ Stops production of uric acid
‣ Screen for HLA-B*5801 allele, high risk of hypersensitivity reaction
• Second line: probenecid
 Rheumatoid Arthritis (RA)

• Chronic, progressive autoimmune disorder that affects joints.

• Bilateral, symmetrical disease is consistent with an RA diagnosis, in contrast to osteoarthritis
(OA), which presents unilaterally.

Management:
1. DMARDs (disease modifying anti-rheumatic drug)
A. Methotrexate
a. MOA: irreversibly binds and inhibits dihydrofolate reductase
b. Dose: 7.5-20 mg once weekly, never dosed daily due to higher risk of liver damage
c. ADR: hepatotoxic, myelosuppression, teratogenic, alopecia
d. Monitoring: CBC, LFT, hepatitis B and C serology, TB test
e. Give Folate to reduce side effects
B. hydroxychloroquine
a. ADR: irreversible retinopathy, hepatotoxic
b. Monitoring: eye exam every 3 months
C. Sulfasalazine
a. ADR: yellow-orange coloration of skin and urine
b. CI: sulfa or salicylate allergy
D. Leflunomide
a. MOA: inhibits Pyrimidine synthesis
b. Teratogenic
2. Anti-TNF biologic DMARDs
A. Etanercept
B. Adalimumab
C. Infliximab
D. Certolizumab
a. ADR: serious infections, such as TB; screen for latent before starting them, injection site
reaction, hepatotoxic, hepatitis B reactivation, heart failure, lupus-like syndrome
b. Monitoring: test for TB and HBV prior, CBC, LFT
c. Don’t use live vaccines
d. Considered as add-on therapy to first line (methotrexate)
3. Non TNF biologic DMARDs
A. Rituximab: depletes CD20 B cells, (add-on therapy)
B. Anakinra: IL-1 receptor antagonist

Osteoarthritis
 Osteoporosis

Complications:
• Hip fracture
• Vertebral compression fractures

Diagnosis:
• DXA (dual-energy X-ray Absorptiometry) is the
gold standard
• WHO T-score thresholds
‣ Osteopenia: T-score between −1 and
−2.5
‣ Osteoporosis: T-score at or below −2.5

• Who should be screened? Women ≥ 65 and men ≥ 70, or at younger age if risk factors are present

Non pharmacological
Smoking Cessation • Weight-Bearing Exercise • Minimize risk of falls and injuries • Diet

Pharmacological management:
• First line: bisphosphonates
‣ ADR: hypocalcemia
‣ Complete dental work prior, risk of jaw necrosis
‣ Taken in the morning with water 30 min before
food, upright position
◦Alendronate
‣ Prevention: 5 mg daily PO
‣ Treatment: 10 daily or 70 mg weekly PO
◦Risendronate PO
◦Ibandronate (IV every 3 months)
◦Zoledronic acid
‣ Prevention: 5 mg IV every 2 years
‣ Treatment: 5 mg IV once year
• For osteoporosis prevention in postmenopausal women:
◦Raloxifene
‣ MOA: selective estrogen receptor modulators
‣ Increase risk VTE and stroke in CHD patients
‣ CI : history or current VTE, pregnancy

Q: know doses in terms of which one is used on a daily or weekly or yearly basis
 Multiple sclerosis

To treat relapse: steroid

• Methylprednisolone 3-7 days

First line for management:

• Interferon Beta
‣ Warning: psychiatric disorders, injection site necrosis, thyroid dysfunction
• Glatiramer acetate
‣ Preferred in pregnancy
Second line:
• Fingolimod
• Teriflumomide
 Renal disease

• Proximal tubule: SGLT2 inhibitors

• Loop of henle: regulated by antidiuretic hormone
(Vasopressin). Loop diuretic work in thick ascending
(inhibits Na-K pump)
• Distal convoluted tubule: thiazide diuretic (inhibits Na-Cl)
• Collecting duct: potassium sparing diuretics

Drug induced kidney disease

Labs used to estimated kidney function : BUN and serum creatinine

Equation to estimate kidney function (CrCl): Cockcroft-gault equation for adults.
Schwartz for children

GFR is calculated using MDRD and CKD-EPI equations

KDIGO guidelines recommend using GFR and degree of albuminuria to determine the stage
KDIGO guideline recommendations for different disease states:
• Hypertension
◦ACE / ARB as a first line for CKD patients with albuminuria
‣ SCr is expected to increase by 30%, D/C if it exceeds 30%
‣ Monitoring potassium and SCr in 1-2 weeks after initiation
• Diabetes
◦First line treatment with metformin and SGLT2 inhibitors

Complications of CKD
• Mineral and bone disorders
◦Hyperphosphatemia
‣ Use of phosphate binders
‣ First line: calcium-based
• Ca acetate
• Ca carbonate
‣ Non-Ca based: sevelamer
◦Vitamin D deficiency and secondary hyperparathyroidism
‣ Using analogs such as calcitriol, calcifediol (cause hypercalcemia)
‣ Using calcimimetic such as Cinacalcet (cause hypocalcemia)
◦Anemia
‣ First line: Erythropoiesis-stimulating agents (Epoetin alfa, darbepoetin alfa)
• Only used when hemoglobin is <10 g/dl, and D/C when it exceeds 11
• Only effective with adequate iron levels, for dialysis patients IV iron
◦Hyperkalemia
‣ Insulin with dextrose, or albuterol to shift K intercellularly
‣ Sodium bicarbonate is used when metabolic acidosis is present
‣ ECG changes or to prevent arrhythmia give calcium gluconate
‣ K can be removed by dialysis

Dialysis
• For stage 5
• Two primary types: hemodialysis and peritoneal dialysis
• Factors affecting drug removal during dialysis:
‣ Molecular size, volume of distribution, protein binding
‣ Also dialysis factors like membrane type (high flux or high efficiency) and flow rate
 Liver disease
Hepatitis

• Hepatitis C preferred regimen: Velpatasvir + sofosbuvir

Cirrhosis
• Severity assessment: Child-Pugh classification. Another scoring system (MELD)

Herbal: milk thistle (limited data showing efficacy, but not harmful)
• Avoid KAVA

Drugs with boxed warning for liver damage:

Complications of liver disease and cirrhosis:
• Portal hypertension
◦Can lead to the development of esophageal varices
‣ First line for varices: band ligation or sclerotherapy
‣ Octreotide can be use to constrict the GI blood vessels
◦Non-selective BB used for primary and secondary prevention of variceal bleeding
‣ Titrated to maximal tolerate dose (target HR of 50-60 bpm) and continued indefinitely
• Propranolol or nadolol
• Hepatic encephalopathy
◦Accumulation of ammonia
‣ First line: lactulose
• Ascites
◦Spironolactone monotherapy or with furosemide (furosemide is not used alone)
• Spontaneous bacterial peritonitis
◦Ceftriaxone for 5-7 days
◦Secondary prevention: ciprofloxacin or Bactrim
• Hepatorenal syndrome
◦Treated with albumin, octreotide, midodrine
 Gastroesophageal Reflux Disease (GERD)

When to refer for further evaluation?

‣ Not responding to lifestyle changes
‣ 2 weeks of OTC products
‣ Alarm symptoms (Odynophagia, dysphagia,
GI bleeding, weight loss)

Pharmacology
1. Antacids
A. Calcium carbonate
B. Magnesium hydroxide (milk of magnesia)
C. Sodium bicarbonate
a. MOA: neutralizing gastric acidity,
b. OTC, fast relief but short duration
c. ADR: calcium and aluminum based can cause constipation, magnesium cause diarrhea
d. Calcium based are preferred in pregnancy
2. Histamine 2 receptors antagonists
A. Famotidine
B. Ranitidine
C. Cimetidine
a. MOA: reversibly inhibit H2 receptors on gastric parietal cells, decrease acid secretion
3. Proton Pump inhibitors
A. Esomeprazole (60 minutes before meal)
B. Omeprazole
C. Lansoprazole
D. Pantoprazole
a. MOA: irreversibly bind to the gastric H/K-ATPase pump
b. Most effective, 8-week course to heal erosions
c. Warning: C. Difficile, hypomagnesemia, vitamin B12
deficiency
 Peptic ulcer

Three most common causes:

1. H. Pylori
2. NSAIDS
3. Stress ulcer

H. Pylori
• Diagnosis: urea breath test (UBT), D/C PPIs, bismuth, antibiotic 2 weeks prior
• Treatment: first line triple therapy (based on Clarth. resistance level) , or quadruple therapy
◦Triple therapy: taken for 14 days
‣ Amoxicillin 1000 mg BID + Clarithromycin 500 mg BID + PPI BID
• Penicillin allergy: replace amoxicillin with metronidazole 500 mg TID
◦Quadruple therapy: taken for 10-14 days
‣ Bismuth + metronidazole + tetracycline + PPI

NSAIDs induced ulcer

1. D/C NSAIDs
2. Test for H. Pylori
3. PPIs are effective in healing erosions, also for secondary prevention
4. Misoprostol (prostaglandin analog): appears to be as effective as PPIs for however, poorly tolerated
 Constipation
Defined as infrequent bowel movements (less than three per week) or difficulty in passing stools
Non pharmacological:
• Increase fluid intake
• Increase physical activity
• Foods high in fibers

Pharmacological
1. Bulk-forming (first line)
A. Psyllium (soluble fibers)
2. Osmotic
A. Polyethylene glycol (PEG)
a. May cause electrolyte imbalance
3. Stimulants
A. Senna
B. Bisacodyl
a. Used with chronic opioid
4. Emollients (Stool softeners)
A. Docusate
a. Preferred when straining should be avoided (postpartum)
5. Lubricants
A. Mineral oil
a. Contraindicated in pregnancy and age <6 years old
 Diarrhea
Non pharmacological
• Fluid and electrolyte to prevent dehydration

Pharmacological
1. Bismuth subsalicylate
2. Loperamide
A. Antimotility
B. Don’t use in children < 2 years
C. Warning for torsade de pointes

Inflammatory bowel disease

1. Ulcerative colitis (UC)
2. Crohn’s disease (CD)

Pharmacological
• For acute exacerbation:
◦Oral or IV steroids
‣ (Taper over 8-12 weeks once remission
is achieved, steroids not recommended
for maintenance)
 Pregnancy

Vitamins and minerals during pregnancy:

• Folate (vitamin B9) 600 mcg/day
◦To prevent birth defects of brain and spinal cord (neural tube defects)
• Calcium and vitamin D (1000 mg/day; 600 IU/day)
◦Required for the baby’s skeleton
Preferred during pregnancy? (important to know, majority of questions about pregnancy)
1. Motion sickness: Pyridoxine (vitamin B6) +/- doxylamine
2. GERD: antacid (calcium carbonate)
3. Flatulence: simethicone
4. Constipation: fiber (psyllium)
5. Cough, cold, allergies: First-line is Cromolyn, second-line 1st generation antihistamine
(chlorpheniramine). If ICS is needed, budesonide is preferred
6. Pain: acetaminophen, avoid NSAIDs (cause premature ductus closure)
7. Asthma: budesonide for maintenance, albuterol as a rescue inhaler
8. Hypertension: labetalol, methyldopa, nifedipine. ACE and ARBs are contraindicated
9. Diabetes: insulin is preferred (metformin and glyburide are commonly used).
10. Hypothyroidism: Levothyroxine (increase dose by 30-50%)
11. Hyperthyroidism: PTU in the 1st trimester, then switch to methimazole
12. VTE: LMWH is preferred for treatment
13. Mechanical valve: warfarin is teratogenic, switch to LMWH, the switch back to warfarin after the 1st
trimester
14. Infection: generally, amoxicillin, ampicillin, cephalosporin, erythromycin, azithromycin considered
safe. Avoid: tetracyclines (teeth discoloration), quinolones (cartilage damage)
15. UTI: treated even in asymptomatic bacteriuria. Cephalexin or ampicillin safe options. Nitrofurantoin
and Bactrim should be considered last line during 1st trimester + shouldn’t be used in the last 2
weeks of pregnancy
 Contraception
Methods of birth control:
• Abstinence is the only 100% effective way
• Condoms help protect against STDs
• Hormonal contraceptives: work by inhibiting the production of FSH and LH, which prevents ovulation
◦Combined contraceptives (contains both estrogen and progestin)
◦Progesterone only contraceptives
◦Long acting reversible devises ( intrauterine, copper IU, implant

1. Combination contraceptives
A. Contain estrogen ethinyl estradiol and a progestin
a. Monophasic = same dose of estrogen and progestin throughout the pill pack
b. Biphasic, triphasic, quadriphasic = the number of times the amounts of hormones
changes. They mimic the estrogen and progesterone levels during menstrual cycle
2. Progestin-only pills
A. Primarily used in women who are lactating, because estrogen decreases milk production.

Considerations for selecting a contraceptive:

• Breastfeeding: Progestin-only pills or non-hormonal
• Clotting risk (VTE, stroke,…): Progestin-only pills or non-hormonal
• Migraine with aura: Progestin-only pills or non-hormonal
• Fluid retention: drospirenone (it is a mild potassium sparing
diuretic)
• Uncontrolled hypertension: Progestin-only pills or non-hormonal
• Nausea: decrease estrogen or use Progestin-only pills
• Breakthrough bleeding:
‣ If early or mid cycle: increase estrogen
‣ If late in the cycle: increase progestin

Drug interactions: Decrease contraceptive’s efficacy

‣ Some antibiotics (rifampin)
‣ Anticonvulsant (Carbamazepine, phenytoin, topiramate, lamotrigine)
‣ St. John’s wort
‣ Smoking tobacco

Emergency contraception
• Copper IUD (most effective)
• Levonorgestrel
 Glaucoma
• Inraocular pressure (IOP) above normal range (12-22 mmHg), leads to damage of optic nerve and
loss of the visual field.

Two main forms:

1. Open-angle glaucoma
2. Closed-angle glaucoma (medical emergency, rapid increase of IOP)

Pharmacology:
1. Prostaglandin analogs: most effective in decreasing IOP
A. Latanoprost (brand name: xalatan)
B. Bimatoprost
a. MOA: increase aqueous humor outflow
b. ADR: darkening of iris, blurred vision
2. Beta blockers: preferred if the pressure in one eye only (don’t cause eye pigmentation like
prostaglandin analogs)
A. Timolol
3. Cholinergic: increase aqueous humor outflow by dilation of blood vessels
A. Pilocarpine

Conjunctivitis

Known as pink eye, can be caused by virus, bacteria, or an allergen

• Viral: caused by adenovirus. No treatment
• Bacteria:
‣ Moxifloxacin
‣ Ofloxacin
‣ polymyxin/trimethoprim drops
‣ Erythromycin
• Allergic:
‣ Antihistamines: azalastin
 Migraine

Herbal products:
• Caffeine for treatment (in combination with acetaminophen)
• For prevention: butterbur, feverfew, magnesium, riboflavin, peppermint, coenzyme Q10

Acute treatment:
• OTC: acetaminophen, ibuprofen, naproxen
• Prescription: serotonin receptor agonists (triptans), ergotamine

Pharmacology:
1. Triptans (first line)
A. Rizatriptan
B. Sumatriptan
C. Zolmitriptan
a. MOA: serotonin receptors agonists causing vasoconstriction of cranial blood vessels.
b. Contraindications: stroke, TIA , uncontrolled hypertension, ischemic heart disease
c. ADR: Increase BP, serotonin syndrome, paresthesia
2. Ergotamine drugs
A. Dihydroergotamine
a. MOA: nonselective agonist of serotonin receptors
b. Second line after triptan failure
c. Contraindications: uncontrolled hypertension, pregnancy, IHD

Prophylactic drugs
Consider when acute treatment is used ≥ 2 days/weeks or ≥3 times per month
1. Antihypertensive:
A. Beta blockers: best evidence with propranolol, timolol, metoprolol.
2. Antiepileptic:
A. Topiramate (causes weight loss)
B. Valproic acid
3. Antidepressants
A. TCA (most evidence with amitriptyline)
 Infectious diseases
Antibiotics pharmacology

1. Beta lactams (Class ADR: hemolytic anemia)

A. Penicillins ( as class they are not active against MRSA or atypical)
a. Natural penicillins
1. Penicillin V
2. Penicillin G
A. Active against gram positive
B. Penicillin V is first line treatment for strep throat and mild skin infections
b. Antistaphylococcal penicillins
1. Dicloxacillin
2. Nafcillin
3. Oxacillin
A. Covers MSSA
c. Aminopenicillins
1. Amoxicillin
2. Amoxicillin/clavulanate (augmentin)
3. Ampicillin
4. Ampicillin/sulbactam (unasyn)
A. Cover gram negative like Haemophilus, Neisseria, Proteus, E.coil
d. Extended-spectrum penicillins
1. Piperacillin/Tazobactam
A. Extended coverage of gram negative, covers pseudomonas aeruginosa
 B. Cephalosporin (Gram -ve spectrum increases with each generation)
a. 1st: cefazolin, cephalexin, cefadroxil
b. 2nd: cefuroxime, cefotetan, cefoxitin, cefaclor, cefprozil
c. 3rd: ceftazidime, ceftriaxone, cefotaxime, cefdinir, cefixime, cefpodoxime
d. 4th: cefepime
e. 5th: ceftaroline
f. Combinations: Avycaz (ceftazidime/ avibactam), Zerbaxa (ceftolozane/Tazobactam)
g. Siderophore cephalosporin: cefiderocol (Fetroja)
1. Key points:
A. Anti-pseudomonas: ceftazidime, cefepime
B. Cefotetan and cefoxitin cover anaerobic coverage (B. fragilis), used for surgical
prophylaxis
C. Ceftaroline covers MRSA
D. Ceftriaxone should not be used for neonate (causes hyperbilirubinemia; biliary
sludging)
C. Carbapenems
a. Doripenem
b. Imipenem/ cilastatin
c. Meropenem
d. Ertapenem
1. Reserved for MDR gram negative infections, cover ESBL-producing pathogens and
anaerobic pathogens. No coverage for atypical, MRSA, VRE
2. Ertapenem doesn’t cover pseudomonas, or acinetobacter
3. Doripenem should not be used for pneumonia
D. Monobactams
a. Aztreonam
1. Mainly gram negative coverage including pseudomonas, no gram +ve coverage
2. Aminoglycosides: inhibit protein synthesis through the 30S ribosome
A. Gentamicin
B. Tobramycin
C. Amikacin
D. Streptomycin
a. Generally not used as monotherapy, synergic effect when used with B-lactams or
vancomycin
b. Nephrotoxicity and ototoxicity
 c. Two ways of dosing
1. Traditional dosing: lower doses more frequently, peak and trough are drawn with the
4th dose and compare to a goal
2. Extended interval: uses higher doses less frequently, random level is drawn after the
first dose and plotted in the hartford nomogram. The nomogram is used to determine
the appropriate dosing interval
3. Quinolones: inhibit DNA gyrase
A. Ciprofloxacin
B. Levofloxacin
C. Moxifloxacin
D. Gemifloxacin
a. Levofloxacin, Moxifloxacin, Gemifloxacin are referred to as respiratory quinolones, they
cover S. pneumonia
b. Ciprofloxacin and levofloxacin have enhanced gram -ve coverage, including
Pseudomonas
c. ADR: QT prolongation, seizure, peripheral neuropathy
4. Macrolides: inhibits protein synthesis through 50S ribosome
A. Azithromycin
B. Clarithromycin
C. Erythromycin
a. They cover Atypical (legionella, chlamydia, mycoplasma, MAC) and haemophilus.
b. ADR: QT prolongation, hepatotoxic
5. Tetracyclines: inhibit protein synthesis through 30S ribosome
A. Doxycycline
B. Tetracycline
a. Contraindication: children <8 years old, pregnant women or breastfeeding
6. Sulfonamides: inhibition of the folic acid pathway
A. Sulfamethoxazole/Trimethoprim (Bactrim) (5:1)
a. Single strength: 80 mg TMP/ 400 mg SMX
b. Double strength: 160 mg TMP/ 800 mg SMX
c. Contraindication: G6Pd deficiency, risk of hemolysis, sulfa allergy
d. ADR: hemolytic anemia
7. Vancomycin: inhibits cell wall synthesis
A. Covers gram positive bacteria (MRSA) and C. Difficile
B. ADR: nephrotoxicity and ototoxicity, infusion reaction/ red man syndrome (infuse over 2 hr)
8. Daptomycin
a. ADR: myopathy and rhabdomyolysis
b. Don’t use to treat pneumonia; gets inactivated by surfactants in the lungs
9. Oxazolidinone: inhibit 50S subunit of the bacterial ribosome
A. Linezolid
a. Covers MRSA and VRE
b. ADR: thrombocytopenia, peripheral and optic neuropathy
c. It is a MAO inhibitor, avoid tyramine containing foods
10. Tigecycline
A. Covers MRSA and VRE, also gram negative, anaerobic, and atypical. Except 3Ps
(pseudomonas, Proteus, Providencia species)
11. Polymyxins
A. Colistin
B. Polymyxin B
a. Primarily MDR gram negative pathogens in combination with other antibiotics
b. ADR: nephrotoxicity, neurotoxicity
12. Clindamycin: reversibly binds to the 50S subunits of the bacterial ribosomes
A. BBW: C. difficile and colitis
13. Metronidazole
A. Active against anaerobes and protozoal infections, used for intaabdominal infections
B. Contraindication: 1st trimester
C. ADR: metallic taste
14. Fidaxomicin: inhibits RNA polymerase.
A. Used for C. Difficile. Not effective for systemic infections
15. Fosfomycin:
A. Activity against E. Coli, used for the treatment of uncomplicated UTI (cystitis)
16. Nitrofurantoin:
A. Covers E. Coli, klebsiella, VRE. Used for uncomplicated UTI (cystitis)
B. Contraindicated: renal impairment CrCl<60, (best to be avoided in third trimester)
C. ADR: hemolytic anemia, G6PD, brown urine discoloration
Infectious diseases:
• Preoperative antibiotics:
◦Generally first line: cefazolin or cefuroxime
◦Penicillin allergy: clindamycin
◦MRSA risk or suspension: vancomycin
◦Colon or colorectal surgeries: cefotetan or cefoxitin, or you can use cefazolin + metronidazole
• Meningitis

• Acute otitis media

◦First line is amoxicillin
◦Treatment failure: amoxicillin/clavulanate
◦Ceftriaxone IM or IV if unable to tolerate oral
• URTI
◦Common cold: supportive no antibiotics
◦Influenza: Oseltamivir x 5 days
◦Pharyngitis: penicillin, or amoxicillin for 10 days; penicillin allergy (clarithromycin)
◦Sinusitis: amoxicillin/clavulanate
• Community acquired pneumonia (CAP)
• HAP/VAP

• Tuberculosis (diagnosis with tuberculin skin test TST)

◦Latent TB: no symptoms and not contagious
‣ Preferred regimen: INH and rifapentine once weekly for 12 weeks via DOT (Directly
observed therapy)
◦Active TB:

Pharmacology of TB medications:
• Isoniazid:
‣ ADR: hepatotoxicity, peripheral neuropathy, optic neuritis
‣ Use pyridoxine (vitamin B6) to reduce its toxicity
• Rifampin:
‣ ADR: hepatotoxic, hemolytic anemia, orange-red discoloration of body fluid
‣ Strong enzyme inducer (decrease the efficacy of contraceptives) (INR decrease if on
warfarin)
• Pyrazinamide:
‣ Increases LFTs, cause hyperuricemia (contraindicated in acute gout)
• Ethambutol:
‣ Increases LFTs, causes optic neuritis (dose-related) and color blindness (reversible)
Endocarditis
• Start empirically with vancomycin and ceftriaxone, to cover staph, strep, and enterococci, then
definitive treatment would depend on specific pathogen and the type of infected valve. Gentamicin is
added for synergy with prosthetic valve or when treating more resistant pathogens
• In general, treatment takes 4-6 weeks
• Definitive:

• Infective endocarditis: Dental prophylaxis

Treatment of intraabdominal infections:

1. Primary peritonitis also called spontaneous bacterial peritonitis (SBP)
A. Occurs in patients with liver disease, unlike secondary peritonitis (caused by a traumatic event
such as surgery)
B. Drug of choice: ceftriaxone for 5-7 days
C. Primary and secondary prophylaxis: SMX/TMP or Ciprofloxacin
2. Other intraabdominal infections (all except primary peritonitis)
A. Cover anaerobic pathogens
a. Mild to moderate: cefoxitin
b. Severe: Tazocin, carbapenems, or cefepime + metronidazole
Treatment of skin and soft tissue infections (FYI; most of ID Q about UTI, pneumonia, endocarditis )

Diabetic foot infection

Urinary tract infections:
• Uncomplicated = occur in non-pregnant women
• Complicated = in males
• For asymptomatic bacteriuria (bacteria detected without symptoms) = no treat; except in pregnant
women, you should always treat
• Common pathogen: E. Coli
• Treatment options:
◦Uncomplicated cystitis:
‣ nitrofurantoin 100 mg BID for 5 days
‣ Or SMX/TMP DS BID for 3 days
‣ Or fosfomycin 1 dose (low efficacy)
◦Acute pyelonephritis and complicated UTIs:
‣ Outpatient ( Ciprofloxacin or levofloxacin; or ceftriaxone)
‣ Inpatient (ceftriaxone, Tazocin, or a quinolone such as Ciprofloxacin or levofloxacin)
◦Asymptomatic bacteriuria in pregnancy:
‣ Amoxicillin +/- clavulanate
‣ Or oral cephalosporin
‣ In case of penicillin allergy, you can use Nitrofurantoin (avoid in 3rd trimester) or SMX/TMP
(also avoid later in pregnancy; can cause hyperbilirubinemia). You can use fosfomycin
◦Treatment duration:
‣ 7 days if there is prompt symptoms relief
‣ If not, extend to 10-14 days

Travelers’ diarrhea

C. Difficile infection:
• Rates have increased due to antibiotics overuse
• Risk factors: healthcare exposure, PPI, age, immunodeficiency, obesity, hx of C. diff
• Treatment:
◦1st episode
‣ Vancomycin
‣ Fidaxomicin
‣ If above not available, use metronidazole
◦Fulminant/complicated
‣ Vancomycin + metronidazole
◦2nd episode
‣ If vancomycin was used in the 1st episode … use Fidaxomicin or vancomycin pulsed
regimen
Sexually transmitted infections (STIs)

• Syphilis = penicillin G; alternative = doxycycline

• Gonorrhea = ceftriaxone
• Chlamydia = doxycycline or Azithromycin
• Bacterial vaginitis = metronidazole
• Trichomoniasis = metronidazole
• Genital warts = imiquimod cream

Other infectious diseases:

• Rocky Mountain fever = doxycycline
• Typhus = doxycycline
• Lyme disease = doxycycline

Fungal infections

Pharmacology of antifungals:
• Amphotericin B
‣ MOA: binds to ergosterol, altering cell membrane
‣ Amphotericin B deoxycholate is more toxic than lipid
formulations (less infusion reaction, and less
nephrotoxicity)
‣ Covers most candida and aspergillus
• Azole antifungals:
◦Fluconazole
◦Voriconazole
◦Posaconazole
◦Itraconazole
‣ MOA: decrease ergosterol synthesis
‣ All are Enzyme inhibitors; they increase effect of warfarin
‣ ADR: hepatotoxic, cause QT prolongation
‣ All azoles are cleared hepatically except fluconazole, which requires adjustment in renal
impairment
‣ Optic neuritis with voriconazole (V= Vision chances)
‣ Voriconazole is the DOC for Aspergillus
‣ C. Krusei is resistant to fluconazole; and also it has limited activity against C. Glabrata
• Echinocandins
◦Caspofungin
◦Micafungin
◦Anidulafungin
‣ MOA: inhibit synthesis of beta(1,3)-D-glucan, which leads to inhibits of fungal cell wall
‣ Active against most candida (including glabrata and krusei)
‣ ADR: increase LFTs, histamine-mediated symptoms
Empirical therapies of selected fungal infections
• Candida albicans causing oropharyngeal infection (thrush) = topical antifungals (clotrimazole,
miconazole)
• Candida albicans causing esophageal infection = fluconazole
• Candida krusei or glabrata, all candidemia = 1st line echinocandin
• Aspergillus = voriconazole
• Cryptococcus neoformans causing meningitis = Amphotericin B + flucytosine
• Dermatophytes causing nail bed infection = Terbinafine or itraconazole

Viral infections

• Influenza = neuraminidase inhibitors (oseltamivir; age > 12, zanamivir; age > 6 )
‣ They decrease the duration of symptoms by ~ 1 day
‣ Warning: neuropsychiatric events
• HSV and VZV = acyclovir and valacyclovir
‣ Caution: renal impairment
• Cytomegalovirus = ganciclovir or valaganciclovir
‣ ADR: myelosuppression
‣ If refractory use Foscarnet or cidofovir
• Epstein-barr virus = no drug or vaccine exists

Opportunistic infections

• Primary prophylaxis in HIV patients

Treatment of opportunistic infections

 Erectile dysfunction

Herbal products:
yohimbe, L-arginine and panax ginseng

First line treatment:

• Use PDE-5 inhibitors
◦Sildenafil
◦Tadalafil
‣ MOA: local release of nitric oxide, which increases
cGMP and causes smooth muscle relaxation
‣ ADR: hearing loss, vision loss, hypotension,
priapism, headache, flushing
‣ Contraindication: nitrates use

• Second line = Alprostadil

‣ MOA: it is prostaglandin E1, a vasodilator
‣ ADR: penile pain, priapism

Benign Prostatic Hyperplasia

Herbal products: saw palmetto

Lycopsne is used for prostate cancer prevention

Treatment:
• Alpha blockers (first line)
◦Selective:
‣ Tamsulosin
‣ Alfuzosin
◦Non selective
‣ Doxazosin
‣ Terazosin
• Can be used alone or in combination with PDE-5 inhibitor
(tadalafil), with or without Finasteride
• Non selective ones have more side effects
‣ They cause orthostasis, dizziness, headache

Finasteride: 5 alpha reductase inhibitors

• MOA: inhibit enzyme, which blocks the conversion of testosterone to dihydrotestosterone
• Improves symptoms and decreases the risk of UTI