CPT OSCE Reviewer: I, III, V

– Through autoregulation, blood flow to the heart changes

rapidly as a result of higher demand. T
CASE #1 – the most important mediators involved in myocardial perfusion
– Mr Solomon, male, 55 year old real estate broker are adenosine (a potent vasodilator), other nucleotides, nitric
– Presents to the clinic following an episode of “chest pain” oxide, prostaglandins, carbon dioxide, and hydrogen ions.
that he experienced earlier in the day during a game of tennis
– Described as more of a discomfort or heaviness, localized to
the breast bone and does not radiate
– Pain subsided after a period of rest.
– Episodes of chest heaviness tend to occur following large
meals, jogging, and heavy alcohol intake. Not lasting more
than 15 minutes.
– Past episodes of burning sensation in the chest described as
being “like acid behind my breast bone”, occurs at night
when he lays down especially after a large meal.
– Has a history of hypertension (20yrs) and gout (10 years)
– Smokes 1 pack of cigarettes per day, drinks 2-3 cocktails every
night.
ANGINA PECTORIS

– is a medical term for chest pain or discomfort due to coronary

heart disease.
– i occ hen he hea m cle doe n ge a m ch blood a
it needs.
– Usually causes uncomfortable pressure, fullness, squeezing or
pain in the center of the chest.

TYPES OF ANGINA PECTORIS

1. STABLE ANGINA
– Episodes of chest discomfort are usually predictable
– They can occur during exertion or during mental and emotional
stress
– Chest discomfort is relieved with rest
2. UNSTABLE ANGINA
– Chest pain occur anytime, often while a person is resting.
– Discomfort may be more severe and lasts longer than in typical
angina.
3. VARIANT ANGINA
– Rare form, occurs in younger patient than those who have
other kinds of angina
– Transient spasm of localized portion of these vessels
– Occurs spontaneously and often at rest, between midnight and
early morning
– Responds to nitrate and CCB
4. MICROVASCULAR ANGINA
– Causes spasm within the wall of these very small arterial blood
vessels
– Symptoms occur with exertion or at rest and lasts longer than
30 minutes
– With shortness of breath, fatigue and lack of energy
PATHOGENESIS
– When atherosclerotic plaques are present, blood flow is
impeded
– but the process of autoregulation can compensate to a degree.
– Autoregulation is the dilation of the myocardial vessels in
response to decreased oxygen delivery.
DIAGNOSTICS
1. ECG OR EKG
– is a test that measures the electrical activity of the heart beat
– used to diagnose heart abnormalities such as arrhythmias or to
show ischemias
2. STRESS TEST
– used to evaluate how well the heart performs with activity
– during a stress test, a patient will usually be asked to perform
physical exercise, like walking on a treadmill
– an ECG is recorded during the period of exercise
3. CARDIAC BIOMARKERS
– proteins that are released when cells are damaged, ordered to
help differentiate angina from a heart attack
– Troponin most commonly ordered and cardiac specific of the
markers.
– If the levels are normal, it is much likely that the symptoms
and chest pain are due to heart muscle damage and more
likely the pain is due to stable angina
– CK-MB one particular form of the enzyme creatine kinase.
Used less frequently now.
4. CHEST XRAY
– Help rule out other sources of chest pain
5. CT OF THE CHEST
– More sensitive than chest xray that can identify other causes of
of chest pain such as aortic disease or blood clots.
 TREATMENT CASE #3
NON PHARMACOLOGIC – FDM, 57 yr old female, complains of a left sided chest pain.
– Patient was diagnosed with stage IIIA infiltrating intraductal
– Lifestyle modification adenocarcinoma of the left breast 5 years ago
smoking cessation – Lab exam revealed ER negative/PR negative, HER-2/neu
weight management positive
alcohol and sodium consumption should be limited. – Underwent modified radical mastectomy with axillary node
– Lipid Management dissection followed by 6 cycles CMF chemotherapy
LDL cholesterol should be <100mg/dL – 2 weeks PTC, px experienced increasing shortness of breath,
cough, mild-moderate pain on her left chest that is worse at
PHARMACOLOGIC night and not relieved by lying down or sleeping
– Has hypertension (10 years) controlled by Verapamil 240mg
DRUG MOA SIDE EFFECTS taken daily
Releases nitric oxide Orthostatic – Has Diabetes mellitus (8years) taking glyburide 5mg bid
in smooth muscle hypotension, – S/P cholecystectomy at age 40
which activates tachycardia, – Has family history of breast cancer
guanylyl cyclase and headache
increases cGMP
BREAST CANCER
Nonselective Acute heart failure, – Malignant proliferation of epithelial cells lining the ducts or
competitive sedation lobules of the breast
antagonist at Beta – Most common cause of cancer in women
adrenoreceptors – Clonal disease
– BRCA1 and BRCA2 genes involved in the development of
breast ca

Nonselective block of Atrioventricular block,

L type calcium acute heart failure, MALIGNANT DISEASE OF THE BREAST
channels in heart and constipation, edema
vessels. EFFECT:
Reduces vascular 1. INFILTRATING DUCTAL CA
resistance, cardiac
rate and force results – Most common invasive cancer in both males and females
in decrease oxygen – Common in perimenopausal and postmenopausal women
demand – Presentation: Hard, fixed mass, peau d o ange, lce a ion of
Excessive overlying skin, bloody nipple discharge, inverted or retracted
Block of vascular L hypotension nipple
type calcium
channels. 2. INVASIVE LOBULAR CARCINOMA
EFFECT: same with
Verapamil and – Second most common type of invasive breast cancer
Diltiazem but with – Originates from the terminal ducts cells
less cardiac effect – Has a high likelihood of being bilateral
Inhibits late sodium QT interval – Ill defined thickening of the breast
current in heart. prolongation, nausea,
Reduces cardiac constipation AGE NI LE OF DISEASE
oxygen demand
– 2% of invasive breast cancer
– Tender, eczematous, itchy nipple with or without bloody
discharge

4. INFLAMMATORY BREAST CANCER

– Most rapidly lethal malignancy of the breast
– Poorly differentiated
– Characterized by dermal lymphatic invasion

RISK FACTORS
– Age
– Estrogen 3 incidence that have a major impact on breast ca.
this is due to longer exposure of estrogen
o Early age of menarche
o Late age of first full-term pregnancy
o Age at menopause
– Race
– Oral contraceptives
– Estrogen replacement therapy
– Diet increased total caloric and fat intake
– Radiation
 PROGNOSTIC AND PREDICTIVE FACTORS – Radtiotherapy it is an effective approach to alleviate specific
sites of painful bones metastasis
– Axillary nodal status is the most significant prognostic factor. – Chemotherapy, common systemic treatment for bone mets
– Tumor size it correlates with the presence or absence of
involved axillary lymph nodes
– Tumor type/grade
– Lymphatic and vascular invasion 2. LUNG METASTASIS
– Proliferation markers – Chemotherapy which can destroy fast growing cells in the body
– Ethnicity – Hormonal therapy a cancer treatment that controls cancer cell
– ER/PR status growth by lowering the levels of certain hormones the cancer
– HER2/neu needs to grow
EVALUATION OF BREAST MASS – Targeted therapy this attempts to treat cancer with more
precision than chemo.
– Radiation reduce the symptoms to con ol he cance g o h

TNM STAGING SYSTEM
– Developed by AJCC
– T extent of the tumor; N
presence of metastasis
DIAGNOSTICS
– Breast self examination this practice increases the likelihood
of detecting a mass at a smaller size
– Mammogram aimed at evaluating the rest of the breast
before a biopsy is performed. Screening mammography starts
at the age of 40. Abnormal mammogram
Microcalcifications
Densities
New or enlarging architectural distortion
– Breast ultrasound used to determine whether a new breast
lump is a solid mass or fluid-filled cyst
– Biopsy
Core needle biopsy procedure to remove a small
amount of suspicious tissue with a larger core
needle
Fine needle aspiration is chosen when the lump is
likely to be filled with fluid
Surgical biopsy
– MRI
TREATMENT
spread to the lymph nodes; M CONSIDERATIONS
LUMINAL A has the highest levels of ER expression. Universally
negative or low in HER2, and has low proliferative
thrust. Most likely to respond to endocrine therapy
with favorable prognosis
LUMINAL B Tend to be PgR negative and has higher
proliferative activity. Express HER2. Prognosis is
somewhat worst
HER2 Amplified Poor prognosis.
BASAL ER/PR negative and HER2 negative tumors. High
grade

STAGE 0 Surgery, Radiation therapy, Hormone therapy

STAGE 1 Surgery, Radiation therapy, Hormone therapy,
Chemotherapy
MANAGEMENT FOR METASTASIS STAGE 2 Surgery + combination therapy (radiation, chemo or
hormone)
STAGE 3 Surgery + neoadjuvant
1. BONE METASTASIS STAGE 4 Chemotherapy

– Bisphosphonates a drug that works best in cases where

metastasis is weakening the bones. May be given by mouth or 1. STAGE 1 AND 2
IV infusion every 3 to 4 weeks. – Systemic adjuvant chemotherapy with:
– It helps bones mets by slowing bone damage and reducing the – Cyclophosphamide forms DNA cross links, resulting in
risk of bone fractures, easing bone pain and reducing high inhibition of DNA synthesis and function. Can cause Nausea
levels of calcium in the blood and vomiting
 – Fluorouracil inhibits TS; incorporation of FUTP into RNA
resulting in alteration in RNA processing. Can cause nausea,
vomiting, diarrhea, bone marrow depression
– Doxorubicin oxygen free radicals bind to DNA causing single
and double strand DNA breaks. Causes nausea and red uring
– Tamoxifen competitive partial agonist of estradiol at the
estrogen receptor.

2. STAGE 3 AND 4
– Pertuzumab is a humanized IgG1 antibody that targets a
different epitope on the her2/new receptor
– Ipatinib small molecular inhibitor of the tyrosine kinase

BISPHOSPHONATES
– Most patients with metastatic disease and those with bone
involvement should receive concurrent bisphosphonates
– Alendronate, Risedronate, Ibandronate, Pamidronate,
Zoledronate
– MOA: Suppress the activity of osteoclasts via inhibition of
farnesyl pyrophosphate synthesis
– Inhibits bone resorption and secondarily bone formation
– Can cause possible renal failure and rare osteonecrosis of the
jaw

CASE #5
– YG, 40 years old, complains of vaginal pruritus, generalized
body weakness, feeling thirsty and hungry most of the time
with increased frequency of urination
– Urine has sweet odor
– Pruritus involving flexors of the upper and lower extremities
during excessive perspiration or warmer temperature
– Noticeable weight loss over the past few months despite the
increase in appetite
– Was diagnosed with gestational diabetes on her 2nd pregnancy
4 years ago
 CPT CASE 2 HYPERTENSION
HYPERTENSION/DYSLIPIDEMIA
BASIS OF THE DIAGNOSIS
I. Clinical Scenario
II. Hypertension – Age
III. Dyslipidemia
– Recurrent nape pain, headache and palpitation for 1 month
– Easy fatigability
– Known HPN for 10 years (incompliance w/ medications)
CLINICAL SCENARIO – BMI: Obese II
– Blood pressure: 170/90mmHg
– M.G, 55 year old, male – Family history: AMI, Stroke and Hypertension
– Consultation: recurrent nape pain, headache, and palpitation – Smoker, Alcoholic drinker, age, diet and physical activity
for 1 month
– Few weeks prior to consult: easy fatigability, and worsening
headache and nape pain WHAT IS HYPERTENSION?

Past Medical History

– Hypertension is the most common cardiovascular disease.
– hypertensive since 10 years but took antihypertensive
– Prevalence increases with advancing age
medication only for 2 months
– Causes pathological changes in the vasculature with endothelial
– Non-diabetic
dysfunction, hypertrophy of the LV and propensity for
– No previous hospitalization
atherosclerosis
– Major risk factor for CAD (MI and sudden cardiac death)
Personal and Social History
– Major contributor to cardiac failure, renal insufficiency and
– Lawyer in a known law firm
dissecting aortic aneurysm
– smoker for 30 years consuming 1 pack/day,
– Defined as sustained increase in BP>140/90 mmHg
– alcohol consumption twice a month (5-6 bottles/beer)
– Sustained arterial HTN damages blood vessels in heart, kidney
– dietary intake: meat, rice, fruits, not fond of vegetables
and brain
– no regular exercise, sleeps 4-5 hrs/day,
– Leads to increase incidence of renal failure, coronary disease,
cardiac failure, and stroke
Family History
– Father died of AMI at the age of 50,
Normal Regulation of Blood Pressure
– Mother died of stroke at the age of 60,
– Brother has obesity and hypertension. – Arterial Blood Pressure = CO x PVR
– Regulating volume of intravascular fluid
General survey: – Baroreflexes, act in combination with RAAS
– Conscious, coherent, obese, balanced gait, good posture, not in – Local release of vasoactive substances from vascular
cardio-pulmonary distress endothelium

Vital Signs: CLASSIFICATIONS

BP: 170/90 mmHg RR: 20/min T: 36.5C HR: 95/min
Weight: 110 kg; Height: 5’7” BMI 37.98 (OBESE II)

Chest and lungs: normal

Heart: apical beat at the 6th ICS left mid axillary line, strong S1 and S2.
Normal rate and rhythm. No murmur

LAB TESTS VALUE NORMAL (IM PLAT)

↑ SCr 76 mg/dL (62umol/L) 0.52-1.0 mg/dL
↑ HDL 30 mg/dL > 40 mg/dL
↑ LDL 180 mg/dL <130 mg/dL
↑ TC 240 mg/dL 150-199 mg/dL
↑ TG 200 md/dL <150 mg/dL
↑ FBS 110 mg/dL < 100 mg/dL
↑ SGOT 60 mg/dL 14-36 U/dL
↑ SGPT 55 mg/dL 9-52 U/dL

Patient has CARDIOMEGALY: MI complication of HTN MG’s CASE IS CONSIDERED STAGE 2 HTN

DIAGNOSIS OF HYPERTENSION
– Two or more elevated readings on at least 2 clinic visits over a
period of one to several weeks
– Definition – adults with:
o SBP > 140 mmHg, or
o DBP > 90 mmHg

WHISKY CPT CASE 2: HTN, DYSLIPIDEMIA CPT 1 | 8

 ETIOLOGY OF HYPERTENSION MANAGEMENT OF HYPERTENSION: From IM PLATINUM 2nd Ed

PRIMARY HYPERTENSION Screening for Hypertension:

– Abnormal cardiac and peripheral hemodynamics – US Preventive Services Task Force recommends screening for
– Impaired pressure natriuresis high blood pressure in adults > 18 years old
– Baroreceptor resetting – Screening:
– Abnormalities in the RAAS o Every 2 years if BP < 120/80 (normal)
– Abnormalities in other vasoregulatory systems o Yearly if BP 120-139 / 80-89 (pre-hypertensive)
o Endothelin
o Atrial natriuresis Peptide (ANP) Non-Pharmacological Management: Lifestyle Management
o Endothelium-derived relaxation factor (EDRF)
ASPECT GOAL SBP Reduction
SECONDARY HYPERTENSION Weight Reduction Maintain BMI < 25 kg/m2 5-10 mmHg
– Renovascular hypertension Salt Reduction < 6 g NaCl/day 2-8 mmHg
– Renal parenchymal diseases Adapt DASH-type Diet rich in fruits, vegetables, 8-14 mmHg
o Altered excretory function Dietary Plan and low-fat dairy products
o Altered renin-angiotensin-aldosterone activity Reduced content of saturated
– Endocrinologic causes and total fat
o Oral contraceptices Moderation of For those who drink alcohol: 2-4 mmHg
o Mineralocorticosteroid excess syndrome Alcohol o < 2 drinks/day in men
o Pheochromocytoma Consumption o <1 drink/day in women
o Miscellaneous causes (acromegaly, Physical Activity Regular aerobic activity (e.g., 4-9 mmHg
hyperparathyroidism, hyperthyroidism, coarctation brisk walking for 30 mins/ day)
of the aorta)
– Clues for Suspecting Secondary Hypertension Threshold and Goals of Pharmacological Therapy in Patients with
o Age of onset <20 or >50 years Hypertension
o No family history of HPN
o DBP >100-120 mmHg CLINICAL CONDITION BP THRESHOLD BP GOAL
o Sudden increase in BP with stable Stage I HPN (When to treat?) (What is the target?)
o Poor BP control, despite good compliance
General Population
o Systemic findings (e.g. weight loss/gain, potassium
Clinical ASCVD or 10 year
abnormalities) ≥130/80 mmHg
ASCVD risk ≥10%
<130/80 mmHg
No clinical ASCVD and 10-
DEFINITION OF TERMS ≥140/90 mmHg
year ASCVD risk <10%
Older persons (≥65 years) ≥130 mmHg (SBP) <130 mmHg (SBP)
White Coat At least three separate clinic-based measurements Patients with specific co-morbidities
Hypertension >140/90 mmHg and at least two non-clinic-based Diabetes mellitus
measurements <140/90 mmHg in absence of any
Chronic kidney disease
evident of target organ damage
Heart failure
Use ambulatory BP monitoring for more accurate
Stable ischemic heart
diagnosis ≥130/80 mmHg
disease
Resistant Defined as: <130/80 mmHg
Peripheral arterial disease
Hypertension  Office BP ≥ 130/80 and with ≥ 3 drugs at optimal
Secondary stroke
doses (including a diuretic), or
prevention (lacunar)
 Office BP <130/80 but requires ≥ 4 drugs
Secondary stroke
Orthostatic Fall in SBP >20 mmHg or in DBP >10 mmHg within 3 ≥140/90 mmHg
prevention
Hypotension minutes of assuming upright posture from a supine
position.
Patient has no comorbidity (DM, CKD) and is <60 y/o;
Masked Normal or even low BP, but with evidence of BP Goal is <130/<80 with initial drug of Thiazide or ACEi or ARB or CCB
hypertension hypertensive end organ damage.
Consider severe peripheral arterial disease causing
masked hypertension.
REPRESENTATIVE
MECHANISM OF DRUGS WITH DOSE
CLASS ADVERSE EFFECTS
PRINCIPLES OF ANTI-HYPERTENSIVE THERAPY: From Pharma Manual ACTION RANGE mg/day
(doses per day)
Diuretics
STAGE 1 HTN
Selectively of Na/Cl Hydrochlorothiazid
– Weight reduction Sexual impotence
symporter which acts e 6.25-50 mg OD
– Restricting sodium intake Hypokalemia
Thiazide on the distal Metolazone 2.5-5
– Increasing aerobic exercise Dyslipidemia
diuretics convoluted tubules, mg OD Indapamide
Hyperuricemia
– Moderating consumption of alcohol leading to enhanced
Hyperglycemia
1.5mg OD
NaCl excretion
Stage 2 HTN – Hypokalemia – Furosemide 40-
– Non-pharmacological approach – Acts on the thick – Metabolic 80 mg OD
Loop ascending limb of alkalosis – Bumetanide 0.5-
– drugs
diuretics the Loop of Henle – Ototoxicity 2 mg OD
– Hypocalcemia – Ethacrynic Acid
– hypoMg 25-100 mg BID

WHISKY CPT CASE 2: HTN, DYSLIPIDEMIA CPT 2 | 8

 – Spironolactone – Spironolactone capacitance & – Doxazosin 1-8
antagonizes action 12.5-100 mg OD resistance mg OD
– Hyperkalemia
of aldosterone – Amiloride 5-20 vessels
Potassium- – Gynecomastia
– Triamterene & mg OD Central – Activation of – Sedation – Clonidine 75-
Saving (only for
amiloride inhibit – Eplerenone 25- Sympatholytics A2-receptors – Xerostomia 150 mcg BID-
diuretics spironolactone)
Na-K exchange 100 mg OD-BID in the CNS – Impotence TID
mechanism – Triamterene 25- – CNS side effects – Methyldopa
100 mg OD – Rebound HPN on 250-500 mg
Beta Blockers (BB) withdrawal BID-TID
– Atenolol 25-100 Direct – Release of – Reflex tachycardia – Hyrdrazaline
mg OD Vasodilators nitric oxide, – Headache 25 mg TID
– Selectively leading to – Hypotension – Minoxidil 2.5-
– Metoprolol 50-
inhibits B1- arterial – Lupus-like 80 mg/day
400 mg/day
Cardioselect Receptors (less vasodilation syndrome (for
– Metoprolol XL
ive BB (B1) pulmonary hydralazine)
50-200 mg OD
effects) – Bronchospasm – Hypertrichosis (for
– Bisoprolol 2.5-20
– Bradycardia minoxidil)
mg OD
– AV block
– Esmolol IV
– Metabolic
Non- – Inhibits both B1 syndrome
– Propanolol 40- THERAPEUTIC OBJECTIVES
180 mg BID-TID
Selective BB and B2 receptors – Glucose
– Others: Pindolol,
(B1/B2) intolerance I. Immediate goal
Timolol, Nadolol
– Sleep To control both systolic and diastolic BP within normal range
– Combined A1 &
disturbance with minimum possible drugs and in lowest possible dose without causing
B-adrenergic – Cardvedilol 6.25-
– Depression hypertension and maintaining quality of life.
receptor 25 mg BID
blockade – Nebivolol 5-10
Vasodilating
– Nebivolol: mg OD II. Long term goal
BB (A1/B)
additional nitric – Others: to prevent complications such as MI, stroke, and damage to the
oxide Labetolol other target organ leading to LVH, angina and arteriosclerotic peripheral
potentiating
vascular disease.
effect
Calcium Channel Blockers (CCB)
III. Lifestyle Modification and Education
– Amlodipine 2.5-
– Blocks L-type – Tachyarrhythmi
10 mg OD
calcium channels a
Dihydropy – Felodipine 2.5-
– Vascular effect > – Edema DRUG OF CHOICE
ridine 20 mg/OD
AV-node effect – Headaches
– Nifedipine 30-
120 mg/day ACEi or ARBs
– AV block (2nd
– Blocks L-type and 3rd deg) – Diltiazem 120-
Non-
calcium channels – Trifascicular 360 mg/day
Dihydropy – Sodium reduction is recommended for adults with elevated
– AV node effect > block – Verapamil 120-
ridine BP
vascular effect – Severe LV 480 mg/day
dysfunction – Site of action of ARB: blood vessel
Drugs Acting on the Renin-Angiotensin-Aldosterone-System (RAAS) – Beta blockers, ACE inhibitors, ARBs retards cardiac remodeling
– Captopril 25-150 – Dyslipidemia affects the suitability of the DOC for HTN
mg BID-TID o Beta Blockers are not suitable to the patient due to
– Inhibits ACE
– Enalapril 2.5-20 dyslipidemia
– Result: – Cough
angiotensin-I is – Angioedema
mg/day o β Blockers increase concentrations of triglycerides in
ACE- – Lisinopril 5-20 plasma and lower those of HDL cholesterol without
not converted – Hyperkalemia
Inhibitors mg/day changing total cholesterol concentrations.
to – Renal agenesis
– Perindopril 2.5-
angiontensin-II – With the ASCVD risk of more than 10% in 10 years, the BP goal
10 mg/day
– Ramipril 2.5-10 for this patient based on AHA guidelines is <130/80 mmHg
mg OD – Do not combine ARB + ACEi
Angiotensin – Competitive – Hyperkalemia – Candesartan 8-
Receptor antagonism – Renal agenesis 32 mg OD NOTES:
Blockers with – Less cough and – Irbesartan 150- – In short term trials, weight loss and reduction of dietary intake
angiotensin-II angioedema 300 mg OD of NaCl has been showed to prevent the development of
– Losartan 25-100 hypertension. In hypertensive individuals, even if these
mg OD
interventions do not produce sufficient reduction in blood
– Olmesartan 5-40
mg OD pressure to avoid drug therapy, the number of medications or
– Telmisartan 20- doses required for blood pressure control may be reduced.
80 mg OD – Consuming three to more alcoholic drinks per day (a standard
– Valsartan 80-320 drinks contains 14g ethanol) is associated with higher blood
mg OD pressure and a reduction of alcohol consumption is associated
Direct Renin – Directly inhibits – Angioedema – Aliskiren 75-300 with a reduction of blood pressure
Inhibitor rennin, the first – Hyperkalemia mg OD – Regular physical activity facilitates weight loss, decrease blood
enzyme in the – Cough
pressure, and reduces the overall risk of cardiovascular disease.
RAAS – Hyperuricemia
Other Anti-Hypertensives Blood pressure may lowered by 30 mins of moderately intense
physical activity such as brisk walking, 6-7 days a week, or by
Alpha Blockers – Blocks the – Postural – Prazosin 1-5
more intense, less frequent workouts.
postsynaptic hypotension mg/day
A1-receptors – Reflex tachycardia – Terazosin 1-5 – Reference: Harrisons 20th edition page 1901
found in mg/day

WHISKY CPT CASE 2: HTN, DYSLIPIDEMIA CPT 3 | 8

WHISKY CPT CASE 2: HTN, DYSLIPIDEMIA CPT 4 | 8
 DYSLIPIDEMIA
BASIS OF THE PROBLEM

Risk Factors
– Gender (male)
– Smoker
– Hypertension (>140/90)
– BMI (>25kg/m2)
– Family history of premature Coronary Heart
Disease(<55:M;<60:F)

Laboratory Results
– High cholesterol (240mg/dl)
– High LDL (180mg/dl)
– High Triglyceride (200mg/dl)
– Low HDL (30mg/dl)

DYSLIPIDEMIA

– Collective term for disorders of lipoprotein metabolism.

– Generally characterized clinically by increased plasma levels of
cholesterol, TGs, or both, variably accompanied by reduced
levels of HDL cholesterol.
– Elevated Serum TG is an independent risk factor for CHD

Factors contributing to elevated TG:

– Obesity, Overweight
– Physical inactivity
– Cigarette smoking
– Excess alcohol intake (increases TAG)
– High carbohydrate diets (>60% of energy intake)
– Several diseases (T2DM, chronic renal failure, nephrotic
syndrome)
– Certain drugs (Corticosteroids, estrogens, retinoids. Higher
doses of beta-adrenergic blocking agents)
– Genetic disorders (Familial combined hyperlipidemia, familial
hypertriglyceridemia, familial dysbetalipoprotinemia

NON-PHARMACOLOGIC TREATMENT

– Limit total caloric intake

– Limit intake of saturated fats and cholesterol
2018 ACC/AHA Multisociety Guidelines
– Avoid alcohol intake
on the Management of Blood Cholesterol
– Complex carbohydrate and fiber intake
– Exercise and weight reduction

ACC/AHA 2013 Guide for Lifestyle Management for Reducing CV Risk

1. Diet
– High in fruits and vegetables, whole grains; low fat; limit sweets
– DASH diet (Dietary Approaches to Stop Hypertension):
o Rich in fruits, vegetables, whole grains, and low-fat
dairy foods
o Meat, fish, poultry, nuts and beans
o Limited in sugar-sweetened foods and beverages,
red meat, and added fats
2. Physical Activity
– 3-4 sessions a week, lasting 40 minutes per session
– Moderate-to-vigorous intensity physical activity

THERAPEUTIC OBJECTIVES

– Prevention of ASCVD and pancreatitis

– Lifestyle modification
– Lower down and monitor Lipid profile

WHISKY CPT CASE 2: HTN, DYSLIPIDEMIA CPT 5 | 8

WHISKY CPT CASE 2: HTN, DYSLIPIDEMIA CPT 6 | 8
 PLEASE NOTE:
ASCVD RISK OF PATIENT: 30.8%
Classification: Very high risk
Statin Therapy: High intensity therapy

* Renal Function should be monitored in

patients on statins

WHISKY CPT CASE 2: HTN, DYSLIPIDEMIA CPT 7 | 8

 THE ACC/AHA 2013 GUIDELINES ON THE
TREATMENT OF BLOOD CHOLESTEROL
- Statin therapy is recommended for
individuals at increased atherosclerotic
cardiovascular disease (ASCVD) risk who are
most likely to experience a net benefit
(benefit>harm)
- There is insufficient evidence to support
continued use of specific LDL-C and/or non-
HDL-C treatment “targets”
- Appropriate intensity of statin therapy
should be used to reduce risk in those most
likely to benefit
- Non-statin therapies (e.g., fibrates, niacin),
whether alone or in addition to statins,
provide little benefit in risk reduction

DRUG OF CHOICE

HMG-CoA Reductase Inhibitors:

HIGH INTENSITY STATIN THERAPY

ATORVASTATIN 40-80 mg
OR
ROSUVASTATIN 20-40 mg

MONITORING
– Fasting lipid profile within 4-12 weeks
after initiation or dose adjustment and every
3-12 months thereafter
– Indicators of anticipated therapeutic
response to the recommended intensity of
statin therapy (focus is on the intensity of the
statin therapy as an aid to monitoring)

WHISKY CPT CASE 2: HTN, DYSLIPIDEMIA CPT 8 | 8

 CPT CASE 4 PNEUMONIA
PNEUMONIA
BASIS OF THE DIAGNOSIS
I. Clinical Scenario
II. Pneumonia - Productive cough with rust-colored sputum
III. COPD
- Moderate to high grade fevers with chills
IV. Drug-induced Gastritis
- Chest pain
V. Alcohol Withdrawal Syndrome
- Vitals: tachycardia, tachypneic, fever
- Chest and lung findings: bi-basal rales and rhonchi, dullness
on the right lower lung field
CLINICAL SCENARIO - Chest X-ray: Right lower lobe consolidation
- Increased values of laboratory Findings
– FDM, male, 57 year old
– Fever, severe right-sided chest pain and difficulty of breath
ETIOPATHOGENESIS
– 2 days PTA: productive cough with rust-colored sputum, fever
until few hours
– Few Hours PTA: Increasing malaise, fever with chills, epigastric - Lower respiratory tract infection (pulmonary parenchyma)
pain described as burning aggravated by intake of prednisone acquired in the community within 24 hours to less than 2
weeks
Past Medical History - Results from the proliferation of microbial pathogens at the
– Long history of COPD with 2 inhalers, alveolar level and the host’s response to those pathogens
o metaproterenol 2-4 puffs PRN and - Most common access of microorganisms to the lower
o ipratonium 2-4 puffs PRN, respiratory tract is through aspiration from the oropharynx
– with prednisone 30mg PO daily tablet 2 months ago - Classic pneumonia (lobar pneumococcal) evolves through a
– Phenytoin 400 mg PO HS due to Alcohol Withdrawal Seizure series of changes

Personal and Social History PHASE DESCRIPTION

– Smoker for 25 years Edema - Initial phase with the presence of a proteinaceous
– Alcohol abuser (stopped with rehab 1 year ago) exudate and often of bacteria in the alveoli
– Allergic to Ampicillin Red - Erythrocytes in the cellular intraalveolar exudate
Hepatization - Neutrophil influx is more important from the
General survey: Diaphoretic, agitated, weak looking and in CR distress standpoint of host defense
Vital Signs: - Bacteria are occasionally seen in pathologic
BP: 140/90 mmHg RR: 35/min T: 39.5C HR: 125/min specimens
Weight: 65 kg; Height: 163 cm BMI 24.46 (OVERWEIGHT) Gray - No new erythrocytes are extravasating and those
Hepatization already present have been lysed and degraded
Physical Exam - The neutrophilis the predominant cell, fibrin
– CVS- tachycardia, regular rhythm deposition is abundant and bacteria have
– Chest and Lungs: prolonged expiratory phase, bi-basal rales and disappeared
rhonchi, dullness on the right lower lung field - This phase corresponds with successful containment
– GIT: (+) epigastric tenderness of the infection and improvement in gas exchange
– Neurologic: lethargic Resolution - Macrophage reappears as the dominant cell type in
(Final Phase) the alveolar space and the debris of neutrophils,
LAB TESTS VALUE NORMAL (IM PLAT) bacteria and fibrin has been cleared, as has the
↑ HCO3 33mEq/L (33mmol/L) 22-28 mEq/L inflammatory response
↑ BUN 59 (21) 7-17 mg/dL
↑ Creatinine 106.1 (1.2) 0.52-1.0 mg/dL CLINICAL MANIFESTATIONS
↑ Phenytoin 59.4mg/dL(15mcg/L) 10-20 mcg/L - Commonly presents with acute cough, abnormal vital signs of
↑ WBC 18.6 x 10ˆ9 4.5-11 x109/L tachypnea, tachycardia, and fever with at least one abnormal
RBC 4.5 x 10ˆ9 4.5-5.5 chest finding of diminished breath sounds, rhonchi, crackles or
↑ Hct 0.49 0.38-0.47 wheezes
↑ Hgb 180 12.0-16.0 g/dL
NOTES:
↑ PMN 0.88 0.40-0.75
– Review Classification per Etiology
↑ Leukocytes 0.22 0.20-0.40
o CAP, HAP, VAP
ABG Respiratory Acidosis
Partially compensated
- PO2 70 75-100
- PCO2 47 35-45
- pH 7.3 7.35-7.45
Peak Flow
- FEV1 60% (pre-B2-agonist)
- FEV1/FVC 70% (post-B2-Agonist)
Sputum Gram’s stain >50 leukocytes/hpf, 0-5 epithelial cells/hpf,
gram(+) cocci in pairs- many
GUIAC TEST Positive
Chest Xray Right lower lobe consolidation

WHISKY CPT CASE 4: PNEUMONIA CPT 1 | 7

 CLASSIFICATION AND DISPOSITION THERAPEUTIC OBJECTIVES

LOW-RISK CAP MODERATE-RISK HIGH-RISK – Stabilize the patients vitals

CAP CAP – To administer proper antimicrobial therapy for the patient
Vital Signs - Stable - Unstable - Any of the – Eradicate the causative pathogens
- RR <30/min - RR > 30/min criteria – Resolving the clinical signs and symptoms
- PR <125bpm - PR >125bpm under – Minimize hospitalization
- Temp 36-40C - Temp > 40C or Moderate – To prevent further complications of the disease
- BP > <36C Risk CAP, – Decrease mortality
90/60mmHg - BP < 90/60 plus:
mm/Hg NON-PHARMACOLOGICAL THERAPY
Features - No altered - Altered mental - Severe
mental state of state of acute sepsis and – Adequate hydration
acute onset onset septic shock – Oxygen therapy for hypoxemia
- No suspected - Suspected - Need for – Assisted ventilation when necessary are critical to successful
aspiration aspiration mechanical treatment
- No or stable - Decompensated ventilation – Adequate nutrition
comorbids co-morbidities – Smoking cessation
Chest X- - Localized - Multilobar – IMMUNIZATION
Ray infiltrates infiltrates
- No pleural - Pleural effusion MANAGEMENT
effusion - Abscess
- No abscess – For patients requiring hospitalization, empiric therapy should
Disposition - outpatient - ward admission - ICU be initiated as soon as possible after a diagnosis

Patient is classified as MODERATE RISK CAP: RISK POTENTIAL PATHOGENS EMPIRIC THERAPY
– Unstable vital signs Low-Risk Streptococcus pneumoniae Previously healthy:
– Altered mental state CAP Haemophilus influenza Amoxicillin or extended macrolides
– Uncompensated COPD Chlamydphila pneumoniae (suspected atypical pathogen)
Mycoplasma pneumoniae
DIAGNOSTICS OF CAP Moraxella catarrhalis With stable comorbid illness:
Enteric Gram-negative β-lactam / β-lactamase inhibitor
bacilli combination (BLIC) or second-
DIAGNOSTICS COMMENTS generation oral cephalosporin +
(among those with co-
Chest Radiography - Essential in the diagnosis of CAP, assessing extended macrolides
morbids)
severity, differentiating pneumonia from other
conditions and in prognostication Alternative:
- Best radiologic evaluation consists of standing 3rd-generation oral cephalosporin
posterioanterior and lateral views of the chest + extended macrolide
- Does not predict the likely etiologic agent Moderate Streptococcus pneumoniae IV non-antipseudomonal β-lactam
Sputum Gram Stain - Strongly influenced by the quality of collection, -Risk CAP Haemophilus influenza (BLIC, cephalosporin or
and Culture transport, and processing Chlamydphila pneumoniae carbapenem)
- Main purpose of gram stain is to ensure that a Mycoplasma pneumoniae + extended macrolide
sample is suitable for culture – an adequate Moraxella catarrhalis OR
sputum sample must have: Enteric Gram-negative
- >25 neutrophils/LPF bacilli; Legionella IV non-antipseudomonal β-lactam
- <10 squamous epithelial cells/LPF pneumophila; Anaerobes +IV extended macrolide or IV
Blood Culture - Yield is relatively low, therefore it is optional for (risk of aspiration) respiratory FQ
hospitalized patients High-Risk Streptococcus pneumoniae No risk for P. aeruginosa:
- Most common isolate: S. pneumonia CAP Haemophilus influenza
- Strongest indication for blood cultures: severe Chlamydphila pneumoniae IV non-antipseudomonal β-lactam
CAP (more likely to be infected with S.aureus, Mycoplasma pneumoniae +IV extended macrolide or IV
P.aeruginosa, other gram negative bacilli) Moraxella catarrhalis respiratory FQ
Invasive Procedures - Options for non-resolving pneumonia, Enteric Gram-negative With risk for P. aeruginosa:
(e.g., transtracheal, immunocompromised patients and in whom no bacilli
transthoracic, biopsy, adequate respiratory specimens can be sent Legionella pneumophila IV antipneumococcal
bronchoalveolar despite sputum induction and routine diagnostic Anaerobes (risk of antipseudomonal β-lactam + IV
lavage, protected testing aspiration) extended macrolide +
brush specimen) Staphylococcus aureus aminoglycoside
Pseudomonas aeruginosa OR
Pneumonia Risk Score (CURB-65): predicts mortality in CAP IV antipneumococal
antipseudomonal β-lactam + IV
C - Confusion of new onset - Interpretation: ciprofloxacin/levofloxacin (high-
U - Urea (BUN) ≥ 7mmol/L (19mg/dL) - 0-1: out-patient dose)
R - RR ≥30 breaths per minute - 2: admit
B - BP <90/60 - ≥3: consider ICU
65 - Age ≥ 65 years old

WHISKY CPT CASE 4: PNEUMONIA CPT 2 | 7

Common Antibiotics Used in CAP
COPD
GROUP COMMON ANTIBIOTICS
Extended macrolides - azithromycin dehydrate 500 mg OD PO or IV BASIS OF THE DIAGNOSIS
- clarithromycin 500 mg BID PO or IV
Oral β-lactam/β- - Amoxicillin-clavulanic acid 1g BID PO – Productive cough
lactamase inhibitor - Sulatamicillin 750 mg BID PO – Difficulty of breathing
(BLIC) - amoxicillin-sulbactam – Patient has long history of COPD
Oral second- - Cefuroxime axetil 500 mg BID PO – Patient is a smoker for 25 years
generation - cefaclor – General survey: Patient in cardiorespiratory distress
cephalosporin – Chest and lungs: Prolonged expiratory and ronchi is heard
Oral third-generation - cefdinir, cefixime, cefpodoxime proxetil upon auscultation
cephalosporin – Intake of Metaproterenol, Ipratropium Br, prednisone
IV non- - ampicillin-sulbactam 1.5g q6 IV
antipseudomonal β- - Cefuroxime 1.5g q8 IV ETIOPATHOGENESIS
lactam (BLIC, - Ceftriaxone 2g OD IV
cephalosporin or - Ertapenem 1g OD IV – Characterized by expiratory airflow limitation that is not fully
carbapenem) reversible (hallmark: airflow obstruction)
Repiratory - Levofloxacin 500-750mg OD PO or IV – Unusual in the absence of smoking or prior history of smoking,
Fluoroquinolones - Moxifloxacin 400mg OD PO or IV except for patients with A1-antitrypsin deficiency
IV antipneumococal, - Piperacillin-tazobactam 4.5g q6 IV – Elastase-Antielastase Hypothesis: remains a prevailing
antipseudomonal β- - Cefepime 2g q8-12 IV mechanism for its pathophysiology
lactam (BLIC, - Meropenem 1g q8 IV – Smoking tobacco is the main risk exposure for COPD
cephalosporin or
carbapenem) A. The Pathological Changes include:
Aminoglycosides - Gentamicin 3 mg/kg OD IV - Chronic inflammation
- Amikacin 15 mg/kg OD IV - Increased numbers of specific inflammatory cell types in
different parts of the lung
Duration of Treatment - Structural changes resulting from repeated injury and repair

ETIOLOGIC ORGANISMS DURATION OF TREATMENT B. Encompasses the Following Conditions:

Most Bacterial - 5-7 days (3-5 for azalides for S. - Emphysema: anatomically-defined condition characterized by
Pneumonias pneumoniae) enlargement and destruction of alveoli “pink puffers”)
Enteric Gram negative - Chronic bronchitis: clinical condition characterized by chronic
pathogens, S. aureus, cough and phlegm (“blue bloaters”)
P.aeruginosa - Small airways disease: condition where bronchioles are
- MSSA-CAP - 7-14 days (up to 21 days if bacterimic) narrowed
- MRSA-CAP - 7-21 days (up to 28 days if bacterimic)
- P.aeruginosa - 14-21 days (up to 28 days if bacterimic) CLINICAL MANIFESTATION
Mycoplasma and - 10-14 days
Chlamydophila CARDINAL SYMPTOMS SIGNS
Legionella - 14-21 days (10 for azalides) Most common: - May be normal in early stages
Cough, - Pink puffers (predominantly emphysema):
Discharge Criteria sputum production, thin, non-cyanotic, prominent use of
During 24 hours before discharge, the patient should have: exertional dyspnea accessory muscles
– Temperature of 36-27.5 deg C - Blue bloaters (predominantly chronic
– Pulse <100/min COPD may be punctuated bronchitis): heavy and cyanotic
– RR between 16-24/min by exacerbations (acute - “Tripod position”: to facilitate use of
– SBP >90 mmHg worsening of symptoms) accessory muscles
– Blood O2 saturation >90% - Signs of hyperinflation: barrel chest,
– Functioning GI tract (allowing use of oral antibiotics) enlarged lung volumes on percussion
(hyperresonance)
- Others: pursed-lip breathing, expiratory
DRUG OF CHOICE wheezing, systemic wasting, weight loss
- Signs of cor pulmonale (bipedal edema,
ascites) in severe cases
– Cephalosporin + Macrolide
- Clubbing is not a sign of COPD
– Cephalosporin + Respiratory quinolone

ROUTE OF ADMIN: DIAGNOSIS

– Cephalosporin: Ceftriaxone – IV
– Macrolide: Azithromycin – Oral - A clinical diagnosis of COPD should be considered in any patient
who has dyspnea, chronic cough or sputum production, and a
history of exposure to risk factors for the disease
- Risk factors: tobacco smoke (including popular local
preparations), smoke from home cooking and heating fuels,
occupational dusts and chemical

WHISKY CPT CASE 4: PNEUMONIA CPT 3 | 7

DIAGNOSTIC COMMENTS/EXPECTED FINDINGS Classification Based on Exacerbation
TEST - Exacerbation of COPD: defined as an acute event characterized by
Spirometry - Required to make the diagnosis worsening of the patient’s respiratory symptoms that is beyond
- Post-bronchodilator FEV1/FVC <0.70 confirms presence of normal day-to-day variations and leads to a change in medication
persistent airflow limitation - Best predictor of having frequent exacerbations (2 or more per year)
- FEV1, FEV1/FVC and all other measures of expiratory is a history of previously treated events
airflow are reduced
- TLC, FRC and RV may be increased indicating air trapping Modified Medical Research Council (mMMRC) Questionnaire for
- DLCO may be reduced
Assessing the Severity of Breathlessness
Chest - Useful for excluding other differential diagnoses
radiograph - Low flattened diaphragms
mMMRC DESCRIPTION
- Increase in the volume of retrosternal airspace
0 I only get breathless with strenuous exercise
(hyperinflation)
- Hyperlucent lung zones with possible bullae formation 1 I get short of breath when hurrying of the level or walking up a
and diminished vascular markings slight hill
CT scan - Not routinely requested 2 I walk slower than people of the same age on the level because of
- May be helpful when the diagnosis is in doubt to rule out breathlessness, or I stop for breath when walking on my own
concomitant diseases pace on the level
- Useful if surgical procedure such as lung volume reduction 3 I stop for breath after walking 100 meters or after a few minutes
is contemplated on the level
Pulse - To evaluate a patient’s oxygen saturation and need for 4 I am too breathless or I am breathless when I’m dressing or
oximetry supplemental oxygen therapy undressing
- Should be used to assess all stable patients with
FEV1<35% predicted or with clinical signs suggestive of THERAPEUTIC OBJECTIVES
respiratory failure or right heart failure
- If peripheral saturation is <92%, ABGs should be assessed Reduce symptoms:
Arterial - Resting or exertional hypoxemia - Relieve symptoms
blood gas - Increased alveolar-arterial oxygen tension gradient - Improve exercise tolerance
(ABG) - In long-standing disease, may have chronically increased - Improve health status
arterial PaCO2 but metabolic compensation (increased
Reduce risk:
HCO3) maintains pH near normal
- Prevent disease progression
- Prevent and treat exacerbations
CLASSIFICATION OF COPD - Reduce mortality

Classification based on Severity of Airflow Limitation in COPD using NON-PHARMACOLOGICAL THERAPY

Spirometry (Post-Bronchodilator FEV1)
Spirometry should be performed after the administration of an adequate
Smoking - Biggest impact in the natural history of COPD
dose of a short-acting inhaled bronchodilator (to minimize variability) Cessation - Nicotine replacement therapy (gum, inhaler, nasal
spray, transdermal patch) reliably increases long term
SPIROMETRY FINDINGS smoking abstinence rates
STAGE CLINICAL FINDINGS
FEV1/FVC FEV1 - Brief (3-minute) period of counseling to urge a
- Chronic cough and sputum smoker to quit results in smoking cessation rates of 5-
GOLD 1 production ≥ 80% 10% or enrolment in a smoking cessation program as
Mild - Patient unaware that lung predicted part of intervention
function is abnormal - Varenicline, bupropion, and nortriptyline: increases
- Chronic cough and sputum long-term quit rates, but should be used as part of a
production program
GOLD 2 - Shortness of breath on 50 – <80% - E-cigarettes as a smoking cessation aid: uncertain
Moderate exertion Post- predicted benefit at present
- Stage patients typically seek bronchodilator Oxygen Therapy - Only pharmacologic therapy demonstrated to
medical attention FEV1 / FVC unequivocally decrease mortality rates in COPD
- Greater shortness of breath <0.70 - For chronically hypoxemic patients
GOLD 3 - Reduced exercise capacity 30 – <50% - >15 hours / day (long term oxygen therapy)
Severe - Fatigue predicted Lung Volume - Segmentectomy or lobectomy of focal
- Repeated exacerbations Reduction Surgery emphysematous areas of the lung
- Signs or symptoms of
GOLD 4
respiratory failure (PaO2< 60 <30%
Very
mmHg + PaCO2>50 mmHg) predicted
Severe
- Cor pulmonale

GROUP SPIROMETRIC EXACERBATIONS

CLASSIFICATION PER YEAR
A Low exacerbation risk GOLD 1-2 ≤1
Less symptom severity
B Low exacerbation risk GOLD 1-2 ≤1
More symptom severity
C Low exacerbation risk GOLD 3-4 ≥2
Less symptom severity
D Low exacerbation risk GOLD 3-4 ≥2
More symptom severity

WHISKY CPT CASE 4: PNEUMONIA CPT 4 | 7

 PHARMACOLOGICAL THERAPY MANAGEMENT OF STABLE COPD

- None of the existing medications for COPD have been shown to Non-Pharmacologic Management of COPD
modify the long-term decline in lung function
- Bronchodilator medications are central to the symptomatic GRP ESSENTIAL RECOMMENDED DEPENDING ON
management of COPD (principal bronchodilator treatment includes LOCAL GUIDELINE
B2-agonists, anticholinergics and methylxanthines) A Smoking cessation Physical activity Flu vaccination
B-D Smoking cessation Pneumococcal
MEDICATIONS COMMENTS ADVERSE EFFECTS Pulmonary rehabilitation vaccination
Beta2 – Agonists - Alters airway smooth - Sinus tachycardia
muscle tone improving - Arrhythmias Pharmacologic Management of COPD
Short acting: emptying of the lungs - Tremors
Salbutamol - Effects usually wear off - Hypokalemia GRP Preferred Next Step if no Other Possible
Terbutaline within 4-6 hours (short Treatment improvement Treatment
acting) and >12 hours (long A Any Continue, stop or try Antioxidant
Long acting: acting) bronchodilator alternative class of mucolytics
Formoterol - Regular treatment with bronchodilator
Salmeterol LABA is more effective and B Start with LAMA LAMA + LABA if no Plus SAMA, SABA
Vilanterol convenient than treatment or LABA improvement
Olodaterol with SABA C Start with LAMA Use LAMA + LABA if Plus SAMA, SABA
Indacaterol - Appears to provide with further
subjective benefit in acute exacerbations
episodes but is not Alternative: LABA + ICS
necessarily helpful in stable D LAMA + LABA LAMA + LABA + ICS Plus SAMA, SABA
disease Alternative: try LABA + Consider PDE-4 inh if
ICS before going to FEV1 <50% predicted
Anticholinergics - Blocks acetylcholine’s effect - Dryness of the mouth triple therapy and patient has
(antimuscarinics) on muscarinic receptors - Bitter metallic taste chronic bronchitis
- Bronchodilating effects of - Arrhythmias Consider macrolide
Short acting: short-acting inhaled (in former smokers)
Ipratropium Br anticholinergics lasts longer
Oxitropium Br than that of short-acting
B2-agonists
OTHER NOTES:
Long Acting:
Tiotropium
- routine use of antibiotics during exacerbation of COPD because
Ulmeclidinium it frequently involves bacterial infection of the lower airways
Glycopyrronium o used in COPD with increased dyspnea, sputum
volume and purulence
Methylxanthines - Acts as nonselective - Tachycardia - Use for the relief of acute symptoms of COPD:
phosphodiesterase - Arrhythmias o Inhalation of SABA
Theophylline inhibitor - Seizures o Inhalation of anticholinergic drug
Aminophylline - Improves FEV1 and - Headaches - Bronchodilators are the mainstay treatment for symptomatic
Doxofylline breathlessness when added - Insomnia COPD
to salmeterol - Inflammation pays a key role in the pathophysiology of COPD
but use of and response to anti-inflammatory medications are
Inhaled - Addition of ICS to - Hoarseness different with that of asthma
corticosteroids bronchodilator treatment - Oral candidiasis
appropriate for:
Beclomethasone - Symptomatic patients
Budesonide with FEV1<50%
Mometasone predicted (Stages III, IV)
Fluticasone - Repeated
exacerbations
- Chronic treatment with
systemic glucocorticoids
should be avoided
- ICS combined with LABA in
moderate to severe COPD is
more effective than either
component alone

PDE-4 inhibitors - Improves lung function and - Anorexia

reduces moderate and - Weight loss
Roflumilast severe exacerbations in - Diarrhea
patients with chronic - headache
bronchitis or those who are
in fixed-dose LABA/ICS
combination

WHISKY CPT CASE 4: PNEUMONIA CPT 5 | 7

 PHARMACOLOGICAL THERAPY
DRUG-INDUCED GASTRITIS
I. ANTACIDS
BASIS OF THE DIAGNOSIS a. Neutralising buffering capacity of 2 hrs
b. Best given 1 hr after meals and at bedtime
- 2 days PTA, patient experienced epigastric pain described as c. AlOH, MgOH, NaHCO3, CaCO3
burning, aggravated by intake of prednisone (oral)
- Patient has long history of COPD and was prescribed with II. ACID SECRETORY INHIBITORS
prednisone 30 mg PO daily tablet 2 months ago a. PPI
- Smoker, Alcoholic drinker i. 24 hrs gastric acid inhibition
- Diaphoretic, tachycardic ii. Full acid inhibiting effect - 3 days
- GIT: (+) epigastric tenderness iii. Omeprazole, Pantoprazole, Rebeprazole,
Lansoprazole, Esomeprazole
THERAPEUTIC OBJECTIVES
b. H2RA
- To provide relief to patient signs and symptoms i. Blocks histamine receptors at parietal cells -
- To prescribe the patient with most effective, most suitable, reduce acid secretion
safest drug and cost-effective treatment for drug-induced ii. Cimetidine (CYP450 inhibitor), Ranitidine
gastritis (less CYP450 inhibitor), Famotidine,
- To provide a dietary and lifestyle management appropriate to Nizatidine
his diagnosis upon discharge
- To develop an appropriate monitoring and follow up plan for c. Antimuscarinics
his condition i. Decrease gastric acid secretion but also
- To treat drug-induced gastritis without the cessation of decrease mucus and bicarbonate secretion
causative drug ii. Pirenzipine, Telenzipine
- To potentiate mucosal defense mechanism and repair gastric
injury; and III. LOCAL MUCOSAL PROTECTIVE AGENTS
- To prevent further complications such as gastric ulceration or a. PG Analog
bleeding i. Misoprostol
ii. PGE1 analog that exogenously replaces PG
stores (PGE1 and PGE2)
NON-PHARMACOLOGICAL THERAPY
iii. Prevent NSAID induced ulcers
iv. Abortifacient
- Surgical treatment was originally designed to decrease gastric acid b. Sucralfate
secretion c. Carbenoxolone
- Vagotomy is a component of each of these procedures and is aimed d. Bismuth
at decreasing acid secretion through ablating cholinergic input to the
stomach.
- Both truncal and selective vagotomy (preserves the celiac and
hepatic branches) result in gastric atony despite successful reduction
of both basal acid output (BAO; decreased by 85%) and maximal acid
output (MAO; decreased by 50%).
- Drainage through pyloroplasty or gastroduodenostomy is required
in an effort to compensate for the vagotomy-induced gastric motility
disorder.
- To minimize gastric dysmotility, highly selective vagotomy (also
known as parietal cell, super-selective, or proximal vagotomy) was
developed. Only the vagal fibers innervating the portion of the
stomach that contains parietal cells is transected, thus leaving fibers
important for regulating gastric motility intact.
- Antrectomy is aimed at eliminating an additional stimulant of gastric
acid secretion, gastrin.
- Laparoscopic surgery has led several surgical teams to successfully
perform highly selective vagotomy, truncal vagotomy/pyloroplasty,
and truncal vagotomy/antrectomy through this approach.
- Endoscopic approaches for the treatment of peptic disease and its
complications has led to a substantial decrease in the number of
operations needed for this disorder with a drop of >90% for elective
IV. DOC: H2RA or PPI (PANTOPRAZOLE)
ulcer surgery over the last four decades
Pantoprazole:
Food to avoid:
- Spicy foods - Pantoprazole is less likely than omeprazole and esomeprazole
- Alcohol to interact with other drugs, in fact has no noted significant
- Coffee and other beverages that contains caffeine drug interaction at all.
- Fatty foods - In a patient with drug induced gastritis who required continued
- Fried food use of prednisone or other NSAID, Pantoprazole more reliably
promotes ulcer healing

WHISKY CPT CASE 4: PNEUMONIA CPT 6 | 7


ALCOHOL WITHDRAWAL SEIZURE
BASIS OF THE DIAGNOSIS
- Alcohol Abuser
- Stopped alcohol 1 year ago under rehabilitation
- Chills and sweating
- General Survey: Agitated
- Older Age (57 yrs old)
- Intake of Phenytoin for Alcohol Withdrawal Seizure
o Antiseizure activity
o Referred as diphenylhydantoin
o Have anti-arrhythmic activity
o MOA: Na+ channel blocker
o A/E: diplopia and ataxia
- Diaphoretic
- RR – 35/min (Increased)
- Febrile (39.5)
- (+) Guaiac test: indicate Alcohol withdrawal symptoms
ALCOHOL WITHDRAWAL SEIZURE
- A characteristic syndrome of motor agitation, anxiety, insomnia and
reduction of seizure threshold due to abrupt alcohol discontinuation
in an individual with alcohol dependence.
- Wide spectrum of manifestations – ranging from anxiety, decreased
cognition and tremulousness
- One of the most common causes of seizures in adults.
- Severity of the syndrome is usually proportionate to the degree and
duration of alcohol abuse.
- Can be categorized as mild, moderate or severe withdrawal,
withdrawal seizures and deliriumtremens
- Can occur 8 hours after the last drink but usually do not manifest
more than 48 hours after alcohol cessation
- Can during the first 1-5 days of withdrawal
- More prevalent in persons with history of withdrawal syndromes
- Seizures are generalized tonic-clonic seizures which are brief in
duration and resolve spontaneously
If the patient agrees to stop drinking, sudden decreases in alcohol intake
can produce withdrawal symptoms:
- Tremor of the hands (shakes)
- Agitation and anxiety
- Increase in pulse, Respiratory rate and body temperature
- Sweating
- Insomnia
- Abrupt cessation of alcohol intake after prolonged heavy drinking may
trigger alcohol withdrawal seizures.
- Increase risk in: older age, concomitant medical problems, misuse of
additional drugs, and higher alcohol quantities.
- Generalized tonic-clonic seizures are the most characteristic and severe
type of seizure that occur in this setting.
- One of the most common causes of seizures in adults.
- Several days later, individuals can develop the syndrome of delirium
tremens
WHISKY CPT CASE 4: PNEUMONIA
NON-PHARMACOLOGICAL THERAPY
Alcoholic rehabilitation
- Core components of the rehabilitation phase of treatment
include cognitive-behavioral approaches to help patients
recognize the need to change, while working with them to alter
their behaviors to enhance compliance.
Relapse prevention education
- Helps patients identify situations in which a return to drinking is
likely (e.g., spending time with heavily drinking friends or
stopping in a bar to meet friends but planning to only have a
nonalcoholic beverage), formulate ways to avoid the risky
situation and if not possible to mitigate the risks to which they
are exposed.
- It is also important to develop coping strategies that increase
the chances of a return to abstinence quickly after an episode
of drinking.
Self-help groups such as Alcoholics Anonymous (AA)
- To assist them in developing a sober peer group and to learn
how to deal with life’s stresses while remaining sober.
Counseling
- Focuses on areas of improved functioning in the absence of
alcohol (i.e., why it is a good idea to continue abstinence),
helping patients to manage free time without alcohol,
encouraging them to develop a nondrinking peer group, and
discussions of ways to handle stress without drinking.
THERAPEUTIC OBJECTIVES
Major objective: Prevention of seizures, delirium and arrhythmias
Potassium, magnesium, and phosphate balance should be restored as
rapidly as is consistent with renal function
PHARMACOLOGICAL THERAPY
Thiamine therapy is initiated in all cases
- Water soluble vitamin, combines with ATP to form thiamine
pyrophosphate, an essential coenzyme in carbohydrate
metabolism.
- Mild alcohol withdrawal does not need any other
pharmacologic assistance
- For severe cases – detoxification
- Administration of a long acting sedative-hypnotic drug for
alcohol and gradually reducing (tapering) the dose of the long
acting drug
- Benzodiazepines:
o Chlordiazepoxide and diazepam
o Lorazepam and oxazepam
DOC: BENZODIAZEPINES
- Help reduce agitation and prevent more severe withdrawal
symptoms, such as seizures and delirium tremens (DT)
- specific drug treatment for detoxification in more severe cases
- substituting a long-acting sedative-hypnotic drug for alcohol
and then gradually reducing (“tapering”) the dose of the long-
acting drug.
Assuming patient has no liver disease: DIAZEPAM
MOA: Positive allosteric modulator of GABAA receptors
Individuals with Alcohol Used disorder are often deficient in vital
nutrients, so medical treatment also includes:
- Thiamine (100mg)
- Folic Acid (1mg)
CPT 7 | 7