Cv Pharmacology, Usmle Step 1

Front 1

Which diuretic can cause hypokalemia, mild hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia?

Back 1

Hydrochlorothiazide

Front 2

Which class of diuretics can cause potassium wasting, metabolic alkalosis, hypotension, and ototoxicity?

Back 2

Loop diuretics

Front 3

Which sympathoplegic antihypertensive drug can cause dry mouth, sedation, severe rebound HTN?

Which patients is it commonly used in?

Back 3

Clonidine, an alpha-2 agonist which causes decreased sympathetic outflow.

Patients with renal HTN are commonly treated w/ clonidine.

Front 4

Which sympathoplegic antihypertensive drug can cause sedation, salt and water retention, hepatic necrosis, and autoimmune hemolytic anemia?

Back 4

Methyldopa, which can be given to pregnant women. Causes you to make IgG Abs against your own Rh Ags (type II hypersensitivity rxn) --> extravascular (spleen) hemolysis.
Will have pos Coomb's test.

Should give w/ diuretic to decrease salt and water retention.

Front 5

Which sympathoplegic antihypertensive can cause sedation, depression, flushing, nasal stuffiness, diarrhea?

Back 5

Reserpine, which blocks uptake of NT's into storage vesicles --> depletion of catecholamines and serotonin. Don't use in pts w/ hx of depression!

Front 6

Which sympathoplegic antihypertensive can cause orthostatic and exercise hypotension, sexual dysfxn (retrograde and premature ejactulation), diarrhea?

Back 6

Guanethidine, which inhibits release of stored NE and depletes peripheral NE stores (no CNS effects).

Front 7

Which sympathoplegic antihypertensive can cause 1st dose orthostatic hypotension, dizziness, HA?

Back 7

Prazosin

Front 8

Which class of sympathoplegic antihypertensives can cause impotence, asthma, bradycardia, CHF, AV block, CNS effects (sedation, sleep alterations)?

Back 8

beta-blockers.

Front 9

Which vasodilator can cause nausea, HA, lupus-like syndrome, reflex tachycardia, angina, salt retention?
What other classes of antihypertensive should this drug always be used with and why?

Back 9

Hydralazine (increases cGMP --> smooth muscle relaxation. vasodilates arterioles > veins; afterload reduction. use for severe hypertension, CHF; first line therapy for HTN in preg, w/ methyldopa; contraindicated in angina/CAD due to tachycardia).
Should use w/ beta blockers to prevent reflex tachy and w/ diuretics to block salt retention.

Front 10

Which vasodilator can cause hypertrichosis, pericardial effusion, reflex tachy, angina, salt retention?

Back 10

Minodoxil (K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle; used for severe HTN)
Always use w/ beta blockers to prevent reflex tachy and w/ diuretics to block salt retention.

Front 11

Which vasodilator can cause dizziness, flushing, constipation, AV block, nausea, edema?

Back 11

Verapamil

Front 12

Which vasodilator can cause dizziness, flushing, nausea, edema?

Back 12

Nifedipine

Front 13

Which vasodilator can cause cyanide toxicity (releases CN), and what are the symptoms?

Back 13

Nitroprusside, which is used in malignant HTN and acute CHF (decreases both preload and afterload). acts by increasing cGMP via direct release of NO...vasodilates both arterioles and venules. Symptoms of cyanide toxicity include psychosis, muscle spasm, tissue hypoxia, nausea.

Front 14

Which vasodilator can cause hyperglycemia (reduces insulin release, hypotension)

Back 14

Diazoxide, opens K+ channels, hyperpolarizes, and thus relaxes smooth muscle cells (--> vasodilation of resistance arterioles --> sodium and water retention) and prevents insulin release (so sometimes used to treat insulinomas)...also used for hypertensive crisis.
Minodoxil is another vasodilator with the same effect.

Front 15

Which class of antihypertensives can cause hyperkalemia, cough, angioedema, taste changes, hypotension, pregnancy probs (fetal renal dmg), rash, increased renin.

Back 15

ACE-I's (captopril, enalapril, fosinopril)

Front 16

Name an ARB that can cause fetal renal toxicity and hyperkalemia

Back 16

Losartan

Front 17

How do you treat cyanide toxicity from nitroprusside treatment?

Back 17

Give NITRITES, which reduce Hgb to methemoglobin, which binds cyanide, forming cyanomethemoglobin. This prevents cytochrome oxidase inhibition in the electron transport chain. BUT then you have to get rid of the cyanomethemoglobin by giving THIOSULFATE (allows excretion of cyanide as thiocyanate).

Front 18

Which calcium channel blockers can be used to treat SVT's?

Back 18

diltiazem, verapamil

Front 19

How do nitroglycerin and isosorbide dinitrate work?

Back 19

They cause the release of NO from smooth muscle, which leads to an increase in cGMP and smooth muscle relaxation. They dilate veins way more than arterioles, so biggest effect is decreasing preload. Used for angina, pulmonary edema. Also used as erection enhancer.

Front 20

What effect do nitrates have on EDV, BP, contractility, HR, ejection time, and MVO2

Back 20

Nitrates decrease EDV, decrease BP, decrease ejection time, decrease MVO2,
BUT increase contractility and HR (reflex)

Front 21

What effect do beta blockers have on EDV, BP, contractility, HR, ejection time, MVO2?

Back 21

beta blockers decrease BP, decrase contractility, decrease HR, and decrease MVO2,
BUT
increase EDV and ejection time.

Front 22

What effect do beta blockers PLUS nitrates have on EDV, BP, contractility, HR, ejection time, MVO2?

Back 22

no effect or decrease EDV, decrease BP, no effect on contractility, decrease HR, no effect on ejection time, but DRASTICALLY decrease MVO2.

Front 23

Name two partial beta agonists that are contraindicated in angina

Back 23

pindolol
acebutolol

Front 24

How does niacin work as a lipid lowering agent?

Back 24

Decreases lipolysis and decreases hepatic production of VLDL; must use chol to make more VLDL. great for type IIb hyperlipoproteinemia (high VLDL and LDL). increases HDL and decreases LDL.

Front 25

Which lipid lowering agent can cause hyperglycemia, and is thus not recommended for diabetics?

Back 25

Niacin.

Front 26

With which other drug should bile acid resins (cholestyramine, colestipol, colesevelam) be used, and in which patients should they NOT be used?

Back 26

They should be used w/ niacin, and they should NOT be used in patients w/ hypertriglyceridemia b/c bile acid resins can actually increase triglycerides!!! Bile acid resins are also contraindicated in patients with GALLSTONES!!

Front 27

How do fibrates (clofibrate, benzafibrate, gemfibrozil) work?
How do they cause some drug interactions?

Back 27

upregulate LPL, leading to increased TG clearance and lowering the VLDL.
They displace other drugs from albumin, leading to increased effects (e.g. phenytoin, warfarin). must monitor PTT in pts on both warfarin and clofibrate.

Front 28

Which 3 drugs are used in malignant HTN treatment, and how do they work?

Back 28

Nitroprusside (short acting, increases cGMP via direct release of NO --> relaxes arteriolar and venous sm so decreases preload and afterload).
Fenoldopam (dopamine D1 receptor agonist - relaxes renal vascular smooth muscle)
Diazoxide (K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle, esp. arterioles).

Front 29

How do quinidine, hypokalemia, and renal failure increase digoxin toxicities?

Back 29

Quinidine: decreases dig clearance, displaces it from binding sites.
Hypokalemia: normally, K+ competes w/ dig for binding site in Na/K/ATPase...if K+ is not there, dig has free reign!
Renal failure: decreased elimination.

Front 30

What EKG findings may be seen in dig tox?

Back 30

increased PR, decreased QT, T-wave inversion of EKG, scooping of ST segment.

Front 31

What are the class IA antiarrhythmics, and how do they work?
What types of arrhythmias are they indicated for?

Back 31

Quinidine, procainamide, disopyramide
All class I antiarrhythmics block Na+ channels, thus slow rate (decrease slope) of phase 4 depolarization.
Class IA antiarrhythmics slow rate of phase 0 depolarization, slow conduction, and prolong repolarization. The decrease the ERP and increase AP duration and increase QT interval. Work for both atrial and ventricular arrhythmias, espeically reentrant and ectopic SVT and ventricular tachy.

Front 32

What are some toxicities associated w/ quinidine, a type IA antiarrhythmic?

Back 32

cinchonism - HA, tinnitus, thrombocytopenia, torsades de pointes due to increased QT interval

Front 33

What is the main toxicity associated w/ procainamide, a type IA antiarrhythmic?

Back 33

reversible SLE-like syndrome

Front 34

What are the class IB antiarrhythmics, and how do they work?

Back 34

Lidocaine, mexiletine, tocainide. (I'd Buy Lidy's Mexican Tacos). Also phenytoin.
decrease AP duration by shortening phase 3 repolarization. little effect on depolarization. block inactivated sodium channels, so useful in d/o's where heart is hypoxic or deploarized (post MI ventricular arrhythmias or dig-tox).

Front 35

What are the class IC antiarrhythmics, and how do they work? When are they used?

Back 35

Flecainide, Encainide, Propafenone. No effect on AP duration, slows impulse conduction in all cardiac tissues, esp. his-purkinje system. Only used as last resort in refractory tachyarrhythmias, b/c is proarrhythmic, esp. post-MI...in pts w/ structural abnormalities, Class IC drugs can precipitate cardiac arrhythmia and arrest!!!

Front 36

What electrolyte abnormality increases toxicity for all class I drugs?

Back 36

hyperkalemia.

Front 37

What are the class II antiarrhythmics? How do they work? When are they used?

Back 37

beta blockers!!!
they decrease cAMP, which decreases calcium currents. they suppress abnl pacemakers by decreasing slope of phase 4. AV node is especially sensitive --> increased PR interval. Esmolol is super short acting.

Use in V-tach, SVT, slowing ventricular rate during A-fib and A-flutter.

Front 38

What are the class III antiarrhythmics (potassium channel blockers)?
How do they work?

Back 38

Sotolol, ibutilide, amiodarone.
increase AP duration, increase ERP. used when other antiarrhythmics fail. Increase QT interval.

Front 39

What is the toxicity of sotalol?

Back 39

torsades de pointes, excessive beta block

Front 40

What is the toxicity of ibutilide (class III antiarrhythmic)

Back 40

torsades de pointes

Front 41

What is the toxicity of bretylium (class III antiarrhythmic)?

Back 41

new arrhythmias, hypotension

Front 42

what is the toxicity of amiodarone (class III antiarrhythmic)?

Back 42

pulmonary fibrosis, corneal deposits, hepatotoxicity, skin deposits --> photodermatitis, neuro probs, constipation, bradycardia, heart block, CHF, hyper/hypo thyroidism

Front 43

What are the class IV antiarrhythmics, what is their mechanism, and when are they used?

Back 43

verapamil and diltiazem
primarily affect AV nodal cells. decrease conduction velocity, increase ERP, increase PR interval (like beta blockers). used in prevention of nodal arrhythmias (SVT)...also afib, a flutter. they have a negative inotropic effect, so don't use in pts w/ compromised CV function. also don't use verapamil in WPW syndrome (risk of v-fib)

Front 44

When is adenosine used as an antiarrhythmic, and how does it work?

Back 44

increases K+ out of cells, leading to hyperpolarization and decreased calcium. drug of choice in diagnosing and abolishing AV nodal arrhythmias. very short acting, about 15 seconds. toxicity includes flushing, hypotension, chest pain.

Front 45

How are potassium and magnesium used as antiarrhythmics?

Back 45

K+ depresses ectopic pacemakers in hypokalemia (digoxin toxicity).
Mg++ is effective in torsades de points and digoxin toxicity.