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Step One > Pharm-CV > Flashcards

Pharm-CV Flashcards

1
Q

What should be used to treat primary hypertension?

A

Thiazide diuretics, ACE inhibitors, ARBs, dihydropyridine Ca channel blockers

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2
Q

What should be used to treat hypertension with HF? Which should be used cautiously and why? When should it not be used?

A

Diuretics, ACEIs/ARBs, Beta blockers, aldosterone antagonists

Beta blockers must be used cautiously in decompensated HF and are contraindicated in cardiogenic shock

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3
Q

What should be used to treat hypertnesion with DM? Which is particularly useful?

A

ACEIs/ARBs (protective against diabetic nephropathy), Ca channel blockers, thiazide diuretics, beta blockers

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4
Q

What should be used to treat hypertension in pregnancy?

A

Hydralazine, labetalol, methyldopa, and nifedipine

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5
Q

What is the mechanism of amlodipine, clevidipine, nicardipine, nifedipine? Class of drug? Where do they act? What are they used to treat? Toxicity?

A

Dihydropridine Calcium channel blocker

Block voltage gated L type calcium channels of smooth muscle (decr. muscle contractility)

On vascular smooth muscle

Hypertension, angina (including prinzmetal), raynaud phenomenon

cardiac depression, peripheral edema, flushing, dizziness, constipation, gingival hyperplasia

-pine=piping (vessels)
hydro=fluid=vessels

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6
Q

What class of drug is nimodipine? How does it differ from the others in its class?

A

Dihydropridine Calcium channel blocker

Not used to treat what the others are used to treat
Treats subarachnoid hemorrhage (prevents cerebral vasospasm)

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7
Q

What is the mechanism of diltiazem, verapamil? Class of drug? Where do they act? What are they used to treat? Toxicity?

A

Non Dihydropridine Calcium channel blocker

Blocks voltage gated l type calcium channels of cardiac muscle leading to decr. muscle contractility

Hypertension, angina, A-fib/flutter

AV block, hyperprolactinemia (verapamil), cardiac depression, peripheral edema, flushing, dizziness, constipation, gingival hyperplasia

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8
Q

What class of drug is clevidipine? How does it differ from the others in its class?

A

Dihydropridine Calcium channel blocker

Treats hypertensive urgency or emergency in addition to its other functions

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9
Q

What is the mechanism of hydralazine? Clinical applications? What is it often administered with? Why? Toxicity? contraindications?

A

Incr. cGMP leads to incr. smooth muscle relaxation
Vasodilates arterioles > veins
Afterload reduction

Severe hypertension
HF (with organic nitrate)
Safe to use during pregnancy

Administered with beta blocker to reduce reflex tachy

Compensatory tachy (contraindicated in angina/CAD), fluid retention, headache, angina, lupus like syndrome

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10
Q

What drugs should be used in a hypertensive emergency?

A

Clevidipine, fenoldopam, labetalol, nicardipine, nitroprusside

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11
Q

What is the mechanism of nitroprusside? Clinical applications? Duration of action? Toxicity?

A

Incr. cGMP via NO release

Short acting

Hypertensive emergency

Cyanide toxicity

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12
Q

What class of drug is fenoldopam? Mechanism of action? Results? Clinical applications?

A

Dopamine D1 receptor agonist

Coronary, periph, renal, and splanchnic vasodilation

Decr. BP and Incr. natriuresis

Hypertensive emergency

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13
Q

What class of drug are nitroglycerin, isosorbide dinitrate, isosorbide mononitrate? What is their mechanism? Location? Clinical application? Toxicity? Explain monday disease.

A

Nitrates

Vasodilate by incr. NO in vasc. smooth muscle leading to an incr. in cGMP and SM relaxation.

Veins > arteries
Decr preload

Angina, acute coronary syndrome, pulm. edema

Reflex tachy, hypotension, flushing, headache
Monday disease (industrial exposure): tolerance throughout the week, lose it over the weekend, symptoms back on monday.
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14
Q

What is the goal of antianginal therapy? Mechanism?

A

Reduction of myocardial O2 consumption by decreasing EDV, BP, HR, or Contractililty

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15
Q

Compare and contrast nitrates and beta blockers and a combo of them bohth in their effect on EDV, BP, Contr., HR, ejection time, and MVO2? How does verapamil fit into this? Which beta blockers should not be used in angina? Why ?

A

NITRATES

EDV: Decr.
BP: Decr.
CONTR: No effect
HR: Incr. (reflex)
EJECTION TIME: Decr.
MVO2: Decr.

BETA BLOCKERS

EDV: No effect or decr.
BP: decr.
CONTR: decr.
HR: decr.
EJECTION TIME: incr.
MVO2: decr.

COMBO

EDV: no effect or decr. 
BP: decr.
CONTR: little/no effect
HR: no effect or decr. 
EJECTION TIME: little to no effect
MVO2: decr. a lot

Verapamil has similar effects to beta blockers
pindolol and acebutolol-partial beta agonists

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16
Q

What class of drugs are lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin? What is their effect on LDL, HDL, and TGs? Mechanism of action? Results? Side effects? In what conditions?

A

HMG-CoA reductase inhibitors (5 or suffix)

LDL: 3x decr.
HDL: 1x incr.
TGs: 1x decr.

Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor

decr. mortality in CAD patients

Hepatotoxicity (incr. LFTs)
Myopathy (w/ fibrates or niacin)

17
Q

What class of drugs are cholestyramine, colestipol, and colesevelam? What is their effect on LDL, HDL, and TGs? Mechanism of action? Side effects?

A

Bile acid resins (3 or prefix)

LDL: 2x decr.
HDL: slight incr.
TGs: slight incr.

Prevent intestinal absorp f bile acids; liver must use cholesterol to make more

GI upset
DEcr. absorption of other drugs and fat soluble vitamins

18
Q

What class of drugs are gemfibrozil, clofibrate bezafibrate, fenofibrate? What is their effect on LDL, HDL, and TGs? Mechanism of action? Side effects?

A

Fibrates (4 or suffix)

LDL: 1x decr.
HDL: 1x incr.
TGs: 3x decr.

upregulate LPL which leads to incr. TG clearance
Activates PPAR-alpha t induce HDL synth

Myopathy (incr. risk with statins)
cholesterol gallstones

19
Q

What the mechanism of ezetimibe? What is their effect on LDL, HDL, and TGs? Side effects?

A

LDL: 2x decr.
HDL: none
TGs: none

Prevent cholesterol absorption at small intestine brush border

Rare incr. LFTs
Diarrhea

20
Q

What is the mechanism of Niacin? What is their effect on LDL, HDL, and TGs? Side effects?

A

LDL: 2x decr.
HDL: 2x incr.
TGs: 1x decr.

Inhibits lipolysis (hormone sensitive lipase) in adipose tissue
Reduces hepatic VLDL synth

Red, flushed face which is decr. by NSAID use
Hyperglycemia
Hyperuricemia

21
Q

What is the mechanism of digoxin? Class of drug? Clinical applications/mechanism of accomplishing it? Toxicity? What are some factors predisposing to toxicity? Antidote for toxicity?

A

Cardiac glycoside

Direct inhib. of Na/K ATPase leading to inhib. of Na/Ca exchanger leading to incr. intracellular calcium leading to positive inotropy.
Stimulates the vagus nerve leading to decr. HR

HF (incr. contractility)
A fib (Decr. conduction at AV node and depression of AV node=vagal nerve stim.)

TOXICITIES
Cholinergic: nausea, vomiting, diarrhea, blurry yellow vision (van gogh), arrhythmias, AV block
Hyperkalemia (poor prognosis)

PREDISP TO TOXIC.
Renal failure, hypokalemia (allows digoxin to bind), verapamil, amiodarone, quinidine

ANTIDOTE
slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+

22
Q

What is the function of class 1 antiarrythmics? Which cells are they selective for? Mechanism?

A

Sodium channel blockers

Decr. slope of phase 0 depol.

State dependent: depress tissue that is frequently depolarized (tachy)

Slow or block conduction

23
Q

Which class of drug are amiodarone, ibutilide, dofetilide, and sotalol? What is their mechanism? Clinical applications? Clinical applications of just 1 and 3? Toxicity of sotalol (1)? Ibutilide (2)? Amiodarone (3)? What should be checked when taking amiodarone? How does it differ?

A

Antiarr=potassium channel blockers (class III)

Incr. AP duration, incr. ERP, incr. QT interval

Afib
A flutter
ventricular tachy (1,3)

1=torsades de pointes, excessive beta blockade

2=torsades de pointes

3=pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroid, acts as hapten (corneal deposits, blue/grey skin deposits), neuro effects, constipation, CV effects (bradycardia, heart block, HF)

3=check PFTs, LFTs, TFTs

3=lipophillic, all class effects.

AIDS=amiodarone, ibutilide, dofetilide, sotalol

24
Q

What class of drug are lidocaine, mexiletine? Mechanism? Clinical applications? Toxicity?

A

Class IB (sodium channel) (2)

Decr. AP duration
Ischemic or depol. purkinje and ventricular tissue

Acute ventricular arrhythmias (especially post MI)
Digitalis induced arrhythmias

CNS stim/depressin, CV depression

1B is Best post mI
I’d Buy LIDdy’s MEXIcan Tacos (IB=LIDocaine/MEXiliTine)

25
Q

What class of drug are metoprolol (1), propranolol (2), esmolol, atenolol, timolol, and carvedilol? What is their mechanism? What location is particularly senstive? What is the mechanism there? Clinical applications? What is the toxicity? Of just 1? Of just 2? How is overdose treated?

A

Class II antiarr (beta blockers) (6)

decr. SA and AV nodal activity by decr. cAMP and Ca currents.
Suppress abnormal pacemakers by decr. slope of phase 4.
AV node sensitive=Incr. PR interval

SVT, ventricular rate control for a fib and a flutter

Impotence, exacerbation of asthma and COPD, CV effects, CNS effects, mask signs of hypoglycemia

1=dyslipidemia
2=exacerbate vasospasm in prinzmetal angina

Saline, atropine, and glucagon

26
Q

What class of drugs are flecainide, propafenone? Mechanism? Location? Clinical use? Toxicity? When are they contraindicated?

A

Class IC (2)

Prolongs ERP in AV node and accessory bypass tracts.
No effect on ERP in purkinje and ventricular tissue
Minimal effect on AP duration

SVTs, including a fib.
Last resort in refractory VT

Proarrhythmic, especially post MI (contraindicated)

I Can have Fries, Please

IC is Contraindicated post mI

27
Q

What class of drugs are verapamil/diltiazem? Mechanism? Clinical applications? Toxicity?

A

Class IV antiarrythmics (2)

Decr. conduction velocity
Incr. ERP
Incr. PR interval

Prevention of nodal arrhythmias (SVT)
Rate control in a fib

Constipation flushing, edema, CV effects

28
Q

When is Mg2+ effective as an antiarrhythmic?

A

Torsades de Pointes and Digoxin toxicity

29
Q

What class of drugs are Quinidine (1), procainamide (2), disopyramide (3)? Mechanism? Clinical use? Toxicity? Toxicity for 1? For 2? For 3?

A

Class IA antiarrhythmics (3)

Incr. AP duration
Incr. ERP
Incr. QT interval

Atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT

1=Cinchonism (headache, tinnitus)
2=reversible SLE like syndrome
3=HF

thrombocytopenia
Torsades de pointes due to incr. QT

I Avow that Quetzalquatl Purchased Diego’s PYRAMIDe

30
Q

What is the mechanism of adenosine in antiarrythmia? When is it the drug of choice? Duration? What blunts its effects? Adverse effects?

A

Incr. K+ out of cells leads to hyperpolarizing of cell and thus decr. calcium current into cell.

Drug of choice in diagnosing/abolishing SVTs

Very short acting (15 sec)

Blunted by theophylline and caffeine

Flushing, hypotension, chest pain, sense of impending doom, bronchospasm

Step One (49 decks)

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