Usmle Step 1 Fa Cardiology-Pharmacology

Front 1

Major classes of antihypertensive drugs

Back 1

Diuretics
Sympathoplegics
Vasodilators
ACE inhibitors
Angiotensin II receptor inhibitors

Front 2

Major examples of antihypertensive diuretics

Back 2

Hydrachlorothiazide
Loop diuretics

Front 3

Major examples of antihypertensive sympathoplegics (mech)

Back 3

Clonidine (alpha 2 agonist)
Methyldopa (alpha 2 agonist)
Reserpine (prevent transport into vesicles leading to MAO metabolism)
Guanethidine (reduces release of catecholamines by inhibiting Na/ATPase dependent pump)
Prazosin (alpha 1 blocker veins and arteries)
Beta blockers

Front 4

Major examples of antiHTN vasodilators (mech)

Back 4

Hydralazine (incr influx of K, leading to membrane hyperpolarization of smooth muscle cells)
Minoxidil (open K+ATPase, hyperpolarization of SM cells)
Nifedipine (CCB selective for SM)
Verapamil (non selective CCB)
Nitroprusside (cause release of NO from RBC's-direct vasodilator)
Diazoxide (open K+ channels in SM and beta islet cells-decr insulin secretion)

Front 5

Major examples of antiHTN ACEI's

Back 5

Captopril
Enalapril
Fosinopril

Front 6

Major examples of angiotensin II receptor inhibitors

Back 6

Losartan

Front 7

Antihypertensive drug side effects: HCTZ

Back 7

Hypokalemia, mild hyperlipidemia, hyperuricemia, lassitude (weariness), hypercalcemia, hyperglycemia

Front 8

Antihypertensive drug side effects: loop diuretics

Back 8

Potassium wasting, metabolic alkalosis, hypotension, ototoxicity

Front 9

Antihypertensive drug side effects: clonidine

Back 9

Dry mouth, sedation, severe rebound hypertension

Front 10

Antihypertensive drug side effects: methyldopa

Back 10

Sedation, positive Coomb's

Front 11

Antihypertensive drug side effects: reserpine

Back 11

Sedation, depression, nasal stuffiness, diarrhea

Front 12

Antihypertensive drug side effects: guanethidine

Back 12

Orthostatic hypotension, dizziness, headache

Front 13

Antihypertensive drug side effects: prazosin

Back 13

1st dose orthostatic hypotension, sexual dysfct, diarrhea

Front 14

Antihypertensive drug side effects: beta blockers

Back 14

Impotence, asthma, CV effects (bradycardia, CHF, AV block) CNS effects (sedation, sleep alterations)

Front 15

Antihypertensive drug side effects: hydralazine

Back 15

Nausea, HA, lupus like syndrome, reflex tachy, angina, salt retention

Front 16

Antihypertensive drug side effects: minoxidil

Back 16

Hypertrichosis, percardial effusion, reflex tacycardia, angina, salt retention

Front 17

Antihypertensive drug side effects: nifedipine, verapamil

Back 17

Dizziness, flushing constipation (verapamil), AV block (verapamil), nausea, edema

Front 18

Antihypertensive drug side effects: nitroprusside

Back 18

Cyanide toxicity (release CN)

Front 19

Antihypertensive drug side effects: diazoxide

Back 19

Hyperglycemia (reduce insulin release, hypotension)

Front 20

Antihypertensive drug side effects: ACEI

Back 20

Hyperkalemia, cough, angioedema, taste change, hypotension, pregnancy problems (fetal renal damage), rash, incr renin

Front 21

Antihypertensive drug side effects: ARBs

Back 21

Fetal renal toxicity, hyperkalemia

Front 22

Hydralazine
(a) mechanism
(b) clinical use
(c) toxicity

Back 22

(a) increase cAMP which causes SM relaxation. Vasodilates arterioles>veins; afterload reduction
(b) severe HTN; CHF. First line therapy for HTN in pregnancy w/methyldopa
(c) compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, HA, angina. Lupus like syndrome

Front 23

Minoxidil
(a) mechanism
(b) clinical use
(c) toxicity

Back 23

(a) K+ chanel opener-hyperpolarizes and relaxes smooth muscle
(b) severe HTN
(c) hypertrichosis; pericardial effusion; reflex tachycardia; angina; salt retention

Front 24

CCB's
(a) major examples
(b) mechanism
(c) clinical use
(d) toxicity

Back 24

(a) nifedipine, cerapamil, dilitiazem
(b) block voltage dependent L type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.
(c) HTN, angina, arrhythmias (not nif), Pirnzmetal's angina, Raynaud's
(d) cardiac depression, peripheral edema, flushing, dizziness, and constipation

Front 25

Nitroglycerin, isosorbide dinitrate
(a) mechanism
(b) clinical use
(c) toxicity

Back 25

(a) vasodilate by releasing NO in smooth muscle causing incr cGMP and smooth muscle relaxation. Dilate veins>>arteries. Decr preload.
(b) angina, pulmonary edema. Also used as aphrodisiac and erection enhancer
(c) tachycardia, hypotension, flushing, HA, "Monday disease" in industrial exposure; tolerance during work week and loss of tolerance over weekend resulting in tachycardia, dizziness, and HA on reexposure

Front 26

Malignant HTN treatment (and mechs)

Back 26

Nitroprusside (short acting; increase cGMP via direct release of NO)
Fenoldopam (dopamine D1 receptor antagonist-relax renal vascular smooth muscle)
Diazoxide (K+ channel opener-hyperpolarizes and relaxes vascular smooth muscle)

Front 27

Antianginal therapy: Nitrates
Affect on:
(a) preload or afterload
(b) end diastolic volume
(c) contractility
(d) HR
(e) ejection time
(f) mycoardial O2 consumption
(g) BP

Back 27

(a) preload
(b) decrease EDV
(c) increase contractility (reflex resp)
(d) increase HR (reflex resp)
(e) decr ejection time
(f) decrease MVO2
(g) decr

Front 28

Antianginal therapy: beta blockers
(a) preload or afterload
(b) end diastolic volume
(c) contractility
(d) HR
(e) ejection time
(f) mycoardial O2 consumption
(g) BP

Back 28

(a) afterload
(b) EDV incr
(c) contractility decr
(d) HR decr
(e) Ejection time incr
(f) MVO2 decr
(g) BP

Front 29

Antianginal therapy: beta blockers + nitrates
(a) end diastolic volume
(b) BP
(c) contractility
(d) HR
(e) ejection time
(f) MVO2

Back 29

(a) no effect or decr EDV
(b) decr BP
(c) little/no effect on contractility
(d) decr HR
(e) ejection time little or no effect
(f) MVO2 drastically decreased

Front 30

Calcium channel blockers in angina: nifedpine vs verapamil

Back 30

Nifedipine has similar effects to nitrates
Verapamil has similar effects to beta blockers

Front 31

Major types of lipid lowering agents

Back 31

HMG CoA reductase inhibitors
Niacin
Bile acid resins
Cholesterol absorption blockers
"fibrates"

Front 32

HMGCoA Reductase inhibitors
(a) effect on LDL
(b) effect on HDL
(c) effect on TG's
(d) mechanism
(e) side effects/problems

Back 32

(a) effect on LDL:
(b) effect on HDL: +
(c) effect on TG's: decr
(d) mechanism: inhibit cholesterol precursor mevalonate
(e) side effects/problems: reversible incr in LFT's

Front 33

Niacin
(a) effect on LDL
(b) effect on HDL
(c) effect on TG's
(d) mechanism
(e) side effects/problems

Back 33

(a) effect on LDL: decrease
(b) effect on HDL: ++
(c) effect on TG's: decrease
(d) mechanism: inhibit lipolysis in adipose tissue; reduce hepatic VLDL secretion into circulation
(e) side effects/problems: red, flushed face which is decr by aspirin or LT use

Front 34

Bile acid resins
(a) major examples
(b) effect on LDL
(c) effect on HDL
(d) effect on TG"s
(e) mechanism
(f) side effects/problems

Back 34

(a) major examples: cholestyramine, colestipol, colesevelam
(b) effect on LDL: decrease
(c) effect on HDL: slightly incr
(d) effect on TG's: slightly incr
(e) mechanism: prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more
(f) side effects/problems: Tastes bad and causes GI discomfort; decr absorption of fat soluble vits; contraindicated in pts w/gallstones

Front 35

Cholesterol absorption blockers
(a) major examples
(b) effect on LDL
(c) effect on HDL
(d) effect on TG"s
(e) mechanism
(f) side effects/problems

Back 35

(a) major examples: ezetimibe
(b) effect on LDL: decrease
(c) effect on HDL: none
(d) effect on TG"s: none
(e) mechanism: prevent cholesterol reabsorption at small intestine brush border
(f) side effects/problems: rare incr LFT's

Front 36

"Fibrates"
(a) major examples
(b) effect on LDL
(c) effect on HDL
(d) effect on TG"s
(e) mechanism
(f) side effects/problems

Back 36

(a) major examples: gemfibrozil, clofibrate, bezafibrate, fenofibrate
(b) effect on LDL: decr
(c) effect on HDL:+
(d) effect on TG"s: majorly decr
(e) mechanism: upregulate LPL which increases TG clearance
(f) side effects/problems: myositis; incr LFTs

Front 37

Cardiac glycosides
(a) major example
(b) mechanism
(c) clinical use

Back 37

(a) digoxin (protein bound; urinary secretion)
(b) direct inhibition of NaK pump leads to indirect inhibition of Na/Ca antiporter. Increase intracellular Ca2+ positive inotropy. Also stimulates vagus.
(c) CHF to incr contractility; afib (decr conduction to AV node and depress SA node)
inhibition of Na/Ca antiporter. Increase intracellular Ca2+ positive inotropy. Also stimulates vagus.

Front 38

(a) ECG changes seen in digoxin toxicity
(b) side effects of digoxin toxicity
(c) enhancers for digoxin toxicity
(c) antidote

Back 38

(a) may cause incr PR, decr QT, scooping of ST, T wave inversion
(b) Incr parasymp; n/v/d. blurry yellow vision; arrhythmia
(c) renal failure (decr exretion), hypokalemia (digoxing competes with K+ binding at Na/K pump) and quinidine (decr dig clearance; displaces dig from tissue binding sites)
(d) slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab frags, Mg2+

Front 39

Class I antiarrhythmics
General effects

Back 39

Slow or block conduction esp in depolarized cells. Decr slope of phase 4 depol, incr threshold for firing in abnormal pacemaker. Are state dependent (selectively depress tissue that is frequently depolarized).

Front 40

Class IA
(a) examples
(b) effect
(c) clinical use
(d) toxicity

Back 40

(a) Quinidine, Procainamide, Disopyramide
(b) incr AP duration, incr effective refractory period, incr QT interval
(c) atrial and ventricular arrhythmias esp reentrant and ectopic supraventricular and ventricular tachycardia
(d) quinidine (HA, tinnitus, thombocytopenia, torsades de pointes due to prolonged QT); procainamide (reversible SLE like syndrome)

Front 41

Class IB
(a) examples
(b) effect
(c) clinical use
(d) toxicity

Back 41

(a) Lidocaine, Mexiletine, Tocainide
(b) decr AP duration; affect depolarized Purkinje and ventricular tissue
(c) useful in acute ventricular arrhythmias
(d) toxicities: local anesthetic. CNS stimulation/depression, cardiovascular depression

Front 42

Class I C
(a) examples
(b) effect
(c) clinical use
(d) toxicity

Back 42

(a) Flecainide, envainide, propafenone
(b) NO effect on AP duration
(c) useful in V tachs that progress to VF and intractable SVT; usually used as last resort in tachyarrhythmias; for patients without structural abn
(d) proarrhythmic esp post MI (CI); significantly prolongs refractory period in AV node

Front 43

Class II antiarrhythmics
(a) examples
(b) mechanism
(c) clinical use
(d) toxicity

Back 43

(a) beta blockers (-alolols)
(b) decr cAMP, decr Ca2+ currents, suppress abnormal pacemakers by decr slope of phase 4; AV node part sensitive (incr PR)
(c) Vtach, SVT, slow ventr rate during afib and aflut
(d) impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS (sedation, sleep alterations). May mask hypoglycemia signs. Metoprolol can cause dyslipidemia.

Front 44

Class III antiarryhthmics
(a) examples
(b) mechanism
(c) clinical use

Back 44

(a) Sotalol, ibutilide, amiodarone
(b) increase AP duration, incr ERP
(c) used when other antiarrythmics fail; incr QT

Front 45

Side effect: ibutilide

Back 45

Torsades

Front 46

Side effect sotalol

Back 46

Torsades, excessive beta block

Front 47

Side effect: bretylium

Back 47

New arrythmias hypotension

Front 48

Side effect amiodarone

Back 48

Pulmonary fibrosis
Corneal and skin deposits
Neuro effects
Constipation
CV effects (bradycardia, heart block, CHF)
Hypothyroidism, hyperthyroidism

Front 49

Class IV antiarrythmics
(a) examples
(b) mechanism
(c) toxicity

Back 49

(a) verapamil, diltiazem
(b) CCB' s that primarily affect AV node cells. Decr conduction velocity, incr ERP and PR interval. Used in prevention of nodal arrythmias (SVT)
(c) constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

Front 50

Adenosine
(a) mechanism of antiarrhythmic action
(b) clinical use
(c) toxicity

Back 50

(a) incr K+ out of cells hyperpolarizing cell and decreasing incracellular Ca+.
(b) drug of choice indiagnosing/abolishing AV nodal arrythmias
(c) flushing, hypotension, chest pain

Front 51

K+ use as an arrhythmias

Back 51

Depresses ectopic pacemakers in hypokalemia (e.g. digoxin toxicity)

Front 52

Mg2+ use in arrhythmias

Back 52

Effective in torsades de pointes and digoxin toxicity