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Step 1 Pharm > Cardiac Pharmacology > Flashcards

Cardiac Pharmacology Flashcards

1
Q

What medications do we recommend to tx patients with Primary Hypertension?

A

Thiazide diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), dihydropyridine Ca2+ channel blockers.

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2
Q

Drugs used to treat Hypertenstion with Heart Fail

A

Diuretics, ACE inhibitors/ARBs, β-blockers (compensated HF), aldosterone antagonists.

*β-blockers must be used cautiously in decompensated HF and are contraindicated in cardiogenic shock.

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3
Q

Recommended treatment for pts with HTN and Diabetes Mellitus

A

ACE inhibitors/ARBs, Ca2+ channel blockers, thiazide diuretics, β-blockers.

*ACE inhibitors/ARBs are p_rotective against diabetic nephropathy._

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4
Q

What drugs are safe to use in Hypertension in people that are pregnant

A

Hydralazine, labetalol, methyldopa, nifedipine.

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5
Q

What is the Mechanism of Ca+ Channel Blockers?

A

Block voltage-dependent L-type calcium channels of cardiac and smooth musclemuscle contractility.

Vascular smooth muscle—amlodipine = nifedipine > diltiazem > verapamil.

Heart—verapamil > diltiazem > amlodipine = nifedipine (verapamil = ventricle).

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6
Q

When would we use Dihydropyridines (except nimodipine)

A

Dihydropyridines (except nimodipine): hypertension, angina (including Prinzmetal), Raynaud phenomenon.

Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm). Clevidipine: hypertensive urgency or emergency. Non-dihydropyridines: hypertension, angina, atrial fibrillation/flutter.

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7
Q

When would you prescribe Nimodipine (dihydropyridine) to a patient?

A

Nimodipine is used to tx Subarachnoid hemorrhage to prevent cerebral vasospasm

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8
Q

When would you prescribe a Non-Dihydropyridine (diltiazem, verapamil ) to a patient

A

Hypertension, Angina, Atrial fibrillation/flutter

~these guys act on the heart

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9
Q

What toxicities do we worry about when prescribing Calcium Channel Blockers?

A

Cardiac depression, AV block (non-dihydropyridines), peripheral edema, flushing, dizziness, hyperprolactinemia (verapamil), constipation, gingival hyperplasia.

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10
Q

What is the mechanism of action of Hydralizine and it’s clinical use?

A

cGMPsmooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction.

**HydrAlizine= arterioles and Afterload reduction

S_evere hypertension_ (particularly acute), Heart Fail (with organic nitrate). Safe to use during pregnancy.

Frequently coadministered with a β-blocker to prevent reflex tachycardia.

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11
Q

Why is Fenoldapam usefull during Hypertensive emergency

Why do we use Nitroprusside during a hypertensive emergency

A

Fenoldopam: Dopamine D1 receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation.BP, natriuresis.

Nitroprusside: Short acting;cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide).

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12
Q

What is the Mechanism of Action of Nitrates?

A

Vasodilate by Increased NO in vascular smooth muscle–> INCREASE in cGMP and smooth muscle relaxation.

Dilate veins >> arteries and DECREASE preload.

(opposed to hyrdrAlazine which dilates Arterioles and decreaes Afterload)

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13
Q

What can you use Nitrates for?

What toxicity do we worry about?

A

Angina, acute coronary syndrome, pulmonary edema.

Reflex tachycardia (treat with β-blockers), hypotension, flushing, headache, “Monday disease” in industrial exposure: development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekendtachycardia, dizziness, headache upon reexposure.

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14
Q

These drugs Decrease end diastolic volume, Decrease BP, have No effect on contractility, Increase HR, Decrease Ejection time and Decrease MVO2

A

Nitrates

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15
Q

These drugs have little effect on EDV, Decrease BP, Decrease Contractility, Decrease HR,

Incresease Ejection time

Decrease MVO2

A

B-Blockers

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16
Q

These guys will lower LDL by a ton, increase HDL a little and decrease TG a little

What is the Mechanism of Action?

A

HMG-CoA reductase inhibitors

(lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin)

Inhibit conversion of HMG- CoA to mevalonate, a cholesterol precursor; mortality in CAD patients

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17
Q

What is the side effect profile we worry about HMG-CoA reductase inhibitors

A

Hepatotoxicity (LFTs), myopathy (esp. when used with fibrates or niacin)

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18
Q

These drugs will lower LDL and slightly increase HDL and TGs

A

Bile acid resins (cholestyramine, colestipol, colesevelam)

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19
Q

What is the MOA and Side effect profile of Bile acid resins

A

Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more

GI upset,absorption of other drugs and fat-soluble vitamins

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20
Q

What drug will decrease LDL but have no effect on HDL and TG

sides are LFTs adn diarrhea

What is the MOA

A

Ezetimibe

MOA: prevents cholesterol absorption at small intestine brush border

21
Q

Drugs that are AWESOME at decreasing TGs, and slight LDL decrease and slight increase in HDL

A

Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

22
Q

What is the MOA of Fibrinates and the side effect profile

A

Upregulate LPL–> Increase TG clearance and Activates PPAR-α to induce HDL synthesis

Toxicity: Myopathy (risk with statins), cholesterol gallstones

23
Q

What drug will decreaese LDL, Increase LDL and can give you a very red and flushed face

A

Niacin

24
Q

MOA of Niacin and toxicity

A

Inhibits lipolysis (hormone- sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis

Red, flushed face, which is by NSAIDs or long-term use

Hyperglycemia, Hyperuricemia

25
Q

Direct inhibition of Na+/K+ ATPase–>indirect inhibition of Na+/Ca2+ exchanger.

INCREASE [Ca2+]–> ipositive inotropy. Stimulates vagus nerve–> INCREASE HR.

A

Digoxin; cardiac glycosides

26
Q

What do we use Cardiac Glycosides for?

A

HF ( contractility); atrial fibrillation ( conduction at AV node and depression of SA node).

27
Q

Toxicity we see asociated with Digoxin

A

Cholinergic—nausea, vomiting, diarrhea, blurry yellow vision (think van Gogh), arrhythmias, AV block.

Can lead to hyperkalemia, which indicates poor prognosis.
Factors predisposing to toxicity: renal failure (excretion), hypokalemia (permissive for digoxin

binding at K+-binding site on Na+/K+ ATPase), verapamil, amiodarone, quinidine (digoxin clearance; displaces digoxin from tissue-binding sites).

28
Q

Class IA Antiarrhythmics mechanism of action

A

Sodium channel blockers: Quinidine, Procainamide, Disopyramide.

Increase AP duration, Increase effective refractory period (ERP) in ventricular action potential, Increase QT interval.

29
Q

Clincal use for Na+ channel blocerks

A

Both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.

Quinidine, Procainamide, Disopyramide.

30
Q

Aghhh! What toxicity do we worry about with IA Sodium channel blockers

A

Cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades de pointes due to QT interval.

31
Q

What is the MOA of Class IB antiarrythmics

A

Decrease AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Phenytoin can also fall into the IB category.

Lidocaine

32
Q

What is the clinical use of IB antiarrythmics and what toxicity do we worry about?

A

Acute ventricular arrhythmias (especially post- MI), digitalis-induced arrhythmias. IB is Best post-MI.

Toxicity: CNS stimulation/depression, cardiovascular depression.

33
Q

MOA of class IC antiarrythmics

A

Significantly prolongs ERP in AV node and accessory bypass tracts. No effect on ERP in Purkinje and ventricular tissue. Minimal effect on AP duration.

34
Q

Clincal uses of class IC antiarrhythmics

Flecainide, Propafenone.

A

SVTs, including atrial fibrillation. Only as a last resort in refractory VT.

35
Q

Toxicity we see with class IC (Flecainide) antiarrhythmics

A

Proarrhythmic, especially post-MI (contraindicated). IC is Contraindicated in structural and ischemic heart disease.

36
Q

What class of antiarrhythmics are :Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol.

Mechanism

A

Class II:

Decrease SA and AV nodal activity by Decreaed cAMP, Decreased Ca2+ currents. Suppress abnormal pacemakers by Decreased slope of phase 4.

AV node particularly sensitive— Increased PR interval. Esmolol very short acting.

37
Q

What are the clinical uses and Toxicity associated with B blockers

A

SVT, ventricular rate control for atrial fibrillation and atrial flutter.

Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, HF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia.

Metoprolol can cause dyslipidemia. Propranolol can exacerbate vasospasm in Prinzmetal angina. β-blockers cause unopposed α1-agonism if given alone for pheochromocytoma or cocaine toxicity.

Treat β-blocker overdose with saline, atropine, glucagon.

38
Q

Class III antiarrhythmics:

What are they?

What’s the MOA?

A

Amiodarone, Ibutilide, Dofetilide, Sotalol.

AP duration,ERP,QT interval.

39
Q

Clinical uses of class III antiarrythmics

A

Atrial fibrillation, atrial flutter; ventricular tachycardia (amiodarone, sotalol).

40
Q

What toxicity is assoicted with Sotolol?

A

Sotalol—torsades de pointes, excessive β blockade.

*Remember to check PFTs, LFTs, and TFTs when using amiodarone.

41
Q

What toxicity is associated with Amiodarone?

A

Amiodarone—pulmonary fibrosis,hepatotoxicity, hypothyroidism/ hyperthyroidism (amiodarone is 40% iodine by weight), acts as hapten (corneal deposits, blue/ gray skin deposits resulting in photodermatitis), neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, HF).

42
Q

What are class IV anti-arrhythmics?

What is the MOA?

What is the Clinical Use?

A

Verapamil, diltiazem.

Decreased conduction velocity, Increased ERP, Increased PR interval.

Prevention of nodal arrhythmias (e.g., SVT), _rate contro_l in atrial fibrillation.

43
Q

What toxicity do we worry about in class IV antiarrhythmics (Verapamil, Diltiaxem)

A

Constipation, flushing, edema, cardiovascular effects (HF, AV block, sinus node depression).

44
Q

What levels do we need to check when prescribing a pt Amiodarone

A

Check PFTs, LFTs, and TFTs when using Amiodarone

Concern is Pulmonary fibrosis, Hyper or Hypothyroidism, Hepatotoxic

45
Q

New drug for Hypertensive emergencies that is a dopamine-1-Receptor Agonist; causes arteriolar dilation and natriuresis leading to d_ecreased systemic vascular resistance_ and blood pressure reduction. Has

A

Fenoldopam

46
Q

What drug would you give to pts that’s having a hypertenstive emegency but is pregant. If you give this agent it can cause cause significant reflex sympathetic activation causing increased heart rate and contractility and extensive sodium and fluid retention

A

Hydralazine

The reflex sympt activation is why it’s a third line for hypertensive emergencies

47
Q
A
48
Q

What effect does B-Blockers have on an ECG?

A

Will prolongue the PR interval by slowing AV conduction

Delayed conduction through the AV node results in PR elongation

Step 1 Pharm (15 decks)

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