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Adv Pharm Faculty Page (Smoller/Bose) > Cardiovascular Pharmacology 1 (Primary & Acute) > Flashcards

Cardiovascular Pharmacology 1 (Primary & Acute) Flashcards

1
Q

Treatment of Primary (Essential) Hypertension by drug type

A

thiazide diuretics

ACE inhibitors

angiotensin II receptor blockers (ARBs)

dihydropyridine Ca2+ channel blockers

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2
Q

why are ACE I inhibitors used for HTN with diabetes mellitus?

A

they are protective against diabetic neuropathy

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3
Q

name the Calcium channel blockers

A

amlodipine

clevidipine

nicardipine

nifedipine

nimodipine

verapamil

diltiazem

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4
Q

which calcium channel blockers act more on vascular smooth muscle?

A

amlodipine = nifedipine > diltiazem > verapamil

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5
Q

which calcium channel blockers act more on the heart?

A

verapamil > diltizem > amlodipine = nifedipine

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6
Q

Calcium channel blockers Dihydropyridines (except nimodipine)–clinical use

A

HTN

angina (including Prinzmetal)

Raynaud phenomenon

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7
Q

Calcium channel blockers Non-dihydropyridines–clinical use

A

HTN

angina

atrial fibrillation/flutter

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8
Q

Calcium channel blockers non dihydropyridine–toxicity

A

cardiac depression

AV block

hyperprolactinemia

constipation

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9
Q

Calcium channel blockers dihydropyridine–toxicity

A

peripheral edema

flushing

dizziness

gingival hyperplasia

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10
Q

Hydralazine–mechanism

A

increase cGMP–smooth muscle relaxation

vasodilates arterioles more than veins, so afterload reduces

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11
Q

hydralazine–clinical use

A

severe HTN (particularly acute)

HF (with organic nitrate)

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12
Q

what is hydralazine often coadministered with?

why?

A

beta blocker

to prevent reflex tachycardia

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13
Q

hydralazine–toxicity

A

compensatory tachycardia–so contraindicated in angina/CAD

fluid retention

headache

angina

Lupus like syndrome

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14
Q

Thiazide diuretic MOA and examples

A

§Mechanism of Action

§Inhibit Na and Cl transport→ reduces blood volume→ reduces cardiac output→ reduces peripheral resistance

§Common Drugs

§Hydrochlorothiazide

§Chlorthalidone

§Indapamide

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15
Q

name the nitrate drugs

A

nitroglycerin

isosorbide dinitrate

isosorbide mononitrate

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16
Q

nitrates–mechanism

A

vasodilate by increasing NO in vascular smooth muscle –> inc in cGMP and smooth muscle relaxation

dilate veins >> arteries, so dec preload

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17
Q

nitrates–use

A

angina

acute coronary syndrome

pulmonary edema

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18
Q

nitrates–toxicity

A

reflex tachycardia (treat with beta blockers)

HTN

flushing headache

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19
Q

name lipid lowering agents

A

HMG CoA reductase inhibitors

bile acid resins

ezetimibe

fibrates

niacin (B3)

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20
Q

what type of Lipid lowering agent decreases LDL the most?

A

HMG CoA reductase inhibitor

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21
Q

what type of lipid lowering agent increases HDL the most?

A

niacin (B3)

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22
Q

what type of lipid lowering agent decreases triglycerides the most?

A

fibrates

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23
Q

what type of lipid lowering agent has NO effect on HDL and triglycerides?

A

ezetimibe

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24
Q

what type of lipid lowering agent has the smallest effect on lowering LDL?

A

fibrates

25
Q

what type of lipid lowering agent only slightly elevates triglycerides?

A

bile acid resins

26
Q

HMG CoA reductase inhibitors–mechanism

A

inhibit conversion of HMG CoA to mevalonate (a cholesterol precursor)

dec mortality in CAD patients

27
Q

name 5 HMG CoA reductase inhibitors

A

(-vastatins)

atorvastatin

lovastatin

pravastatin

simvastatin

rosuvastatin

28
Q

HMG CoA reductase inhibitors–toxicity

A

hepatotoxicity (inc LFTs)

myopathy (especially when used with fibrates or niacin)

29
Q

niacin–mechanism

A

inhibits lipolysis (hormone sensitive lipase) in adipose tissue

reduces hepatic VLDL synthesis

30
Q

niacin–toxicity

A

red, flushed fase, which is dec by NSAIDS or long term use

hyperglycemia

hyperuricemia

31
Q

name 3 bile acid resins

A

cholestyramine

colestipol

colesevelam

32
Q

bile acid resins–use

A

prevent intestinal reabsorption of bile acids

liver must use cholesterol to make more

33
Q

bile acid resins–toxicity

A

GI upset

decrease absorption of other drugs and fat soluble vitamins

34
Q

ezetimibe–mechanism

A

prevent cholesterol absorption at small intestine brush borders

35
Q

ezetimibe–toxicity

A

rare inc LFTs; diarrhea

36
Q

name fibrate drugs

A

gemfibrozil

bezafibrate

fenofibrate

37
Q

fibrates–mechanism

A

upregulate LDL –> inc triglyceride clearance

activates PPAR alpha to induce HDL synthesis

38
Q

fibrates–toxicity

A

myopathy–inc risk with statins

cholesterol gallstones

39
Q

name a cardiac glycoside

A

digoxin

40
Q

cardiac glycosides–mechanism

A

direct inhibition of Na/K ATPase –> indirect inhibition of Na/Ca exchanger

increase concentration of Ca –> positive intropy

stimulates vagus nerve –> dec HR

41
Q

cardiac glycosides–use

A

HF (inc contractility)

atrial fibrillation (dec conduction at AV node and depression of SA node)

42
Q

cardiac glycosides–toxicity

A

cholinergic–nausea, vomiting, diarrhea, blurry yellow vision (think van Gogh), arrhythmia, AV block

can lead to hyperkalemia, which indicates poor prognosis

43
Q

factors that predispose to toxicity with cardiac glycosides

A

renal failure–dec excretion

hypokalemia–permissive for digoxin binding to K+ binding site on Na/K ATPase

drugs that replace digxin from tissue binding sites

decreased clearance (eg. verapamil, amiodarine, quinidine)

44
Q

Beta blockers MOA

A

PD/MOA:

Block beta receptors which:

  • ↓ the workload of the heart through decreases in heart rate (chronotropy)
  • ↓ strength of myocardial contraction (inotropy) Used as prophylaxis for anginal attacks and post-MI
  • Blocks epinephrine/norepi. which ↓ vasocontriction
45
Q

BB are most effective in treating heart rate problems that originate where?

A

atria/AV node

46
Q

which BBs are cardioselective

A

atenolol, esmolol, metoprolol, bisoprolol, nebivolol

47
Q

Common BB side effects

A

impotence

exacerbation of COPD and asthma

cardiovascular effects (bradycardia, AV block, HF)

CNS effects (sedation, sleep alterations)

may mask signs of hypoglycemia

48
Q

Alpha Blocker MOA

A

Block the alpha 1 adrenergic receptor on vascular (arteriole and venule) smooth muscle and ↓ vascular resistance

49
Q

Alpha blocker indications

A

HTN (not first line)

BPH

50
Q

Alpha blocker adverse effects

A
  • First-dose phenomenon - hypotension
  • Reflex tachycardia
  • Orthostatic hypotension
  • dizziness, palpitations, headache, and lassitude
  • Stress incontinence in women

No sexual side effects

51
Q

class IV antiarrhythmic–toxicity

A

flushing

constipation

edema

cardiovascular effects–HF, AV block, sinus node depression

52
Q

Thiazide contraindications/cautions

A

§Renal/hepatic disease

§Gout

§Hypokalemia

§Allergy to sulfa drugs

53
Q

Thiazide adverse effects

A

§Hypokalemia

§Dehydration

§Hyperglycemia

§Hyperuricemia

§Hyperlipidemia

§Impotence

§Hyponatremia

54
Q

K sparing diuretics MOA and common drugs

A

§MOA: Blocks Na+ movement in & also prevents K+ movement out of cells

§Amiloride, triamterene, spironolactone

55
Q

K sparing diuretics contraindications/caution

A

§Use caution with other meds that may increase K (i.e. ACEI/ARB)

§Caution in renal impairment

56
Q

Loop diuretic MOA

A

inhibit Na/K/Cl cotransporter in the Loop of Henle which inhibits reabsorption of sodium and chloride leading to increased water excretion

57
Q

Loop diuretic adverse effects

A

§Risk of hypokalemia, hypocalcemia, hypomagnesemia, hyponatremia

§Hyperuricemia

§Hyperglycemia

§Ototoxicity

58
Q

Loop diuretic indications

A

Edema/fluid overload 2/2 CHF, cirrhosis, renal disease – most common use

Hypertension- less effective than thiazides at lowering BP

Adv Pharm Faculty Page (Smoller/Bose) (32 decks)

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