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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?

25
what type of lipid lowering agent only slightly elevates triglycerides?
bile acid resins
26
HMG CoA reductase inhibitors--mechanism
inhibit conversion of HMG CoA to mevalonate (a cholesterol precursor) dec mortality in CAD patients
27
name 5 HMG CoA reductase inhibitors
(-vastatins) atorvastatin lovastatin pravastatin simvastatin rosuvastatin
28
HMG CoA reductase inhibitors--toxicity
hepatotoxicity (inc LFTs) myopathy (especially when used with fibrates or niacin)
29
niacin--mechanism
inhibits lipolysis (hormone sensitive lipase) in adipose tissue reduces hepatic VLDL synthesis
30
niacin--toxicity
red, flushed fase, which is dec by NSAIDS or long term use hyperglycemia hyperuricemia
31
name 3 bile acid resins
cholestyramine colestipol colesevelam
32
bile acid resins--use
prevent intestinal reabsorption of bile acids liver must use cholesterol to make more
33
bile acid resins--toxicity
GI upset decrease absorption of other drugs and fat soluble vitamins
34
ezetimibe--mechanism
prevent cholesterol absorption at small intestine brush borders
35
ezetimibe--toxicity
rare inc LFTs; diarrhea
36
name fibrate drugs
gemfibrozil bezafibrate fenofibrate
37
fibrates--mechanism
upregulate LDL --\> inc triglyceride clearance activates PPAR alpha to induce HDL synthesis
38
fibrates--toxicity
myopathy--inc risk with statins cholesterol gallstones
39
name a cardiac glycoside
digoxin
40
cardiac glycosides--mechanism
direct inhibition of Na/K ATPase --\> indirect inhibition of Na/Ca exchanger increase concentration of Ca --\> positive intropy stimulates vagus nerve --\> dec HR
41
cardiac glycosides--use
HF (inc contractility) atrial fibrillation (dec conduction at AV node and depression of SA node)
42
cardiac glycosides--toxicity
cholinergic--nausea, vomiting, diarrhea, blurry yellow vision (think van Gogh), arrhythmia, AV block can lead to hyperkalemia, which indicates poor prognosis
43
factors that predispose to toxicity with cardiac glycosides
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
Beta blockers MOA
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
BB are most effective in treating heart rate problems that originate where?
atria/AV node
46
which BBs are cardioselective
atenolol, esmolol, metoprolol, bisoprolol, nebivolol
47
Common BB side effects
impotence exacerbation of COPD and asthma cardiovascular effects (bradycardia, AV block, HF) CNS effects (sedation, sleep alterations) may mask signs of hypoglycemia
48
Alpha Blocker MOA
Block the alpha 1 adrenergic receptor on vascular (arteriole and venule) smooth muscle and ↓ vascular resistance
49
Alpha blocker indications
HTN (not first line) BPH
50
Alpha blocker adverse effects
* First-dose phenomenon - hypotension * Reflex tachycardia * Orthostatic hypotension * dizziness, palpitations, headache, and lassitude * Stress incontinence in women No sexual side effects
51
class IV antiarrhythmic--toxicity
flushing constipation edema cardiovascular effects--HF, AV block, sinus node depression
52
Thiazide contraindications/cautions
§Renal/hepatic disease §Gout §Hypokalemia §Allergy to sulfa drugs
53
Thiazide adverse effects
§Hypokalemia §Dehydration §Hyperglycemia §Hyperuricemia §Hyperlipidemia §Impotence §Hyponatremia
54
K sparing diuretics MOA and common drugs
§MOA: Blocks Na+ movement in & also prevents K+ movement out of cells §Amiloride, triamterene, spironolactone
55
K sparing diuretics contraindications/caution
§Use caution with other meds that may increase K (i.e. ACEI/ARB) §Caution in renal impairment
56
Loop diuretic MOA
inhibit Na/K/Cl cotransporter in the Loop of Henle which inhibits reabsorption of sodium and chloride leading to increased water excretion
57
Loop diuretic adverse effects
§Risk of hypokalemia, hypocalcemia, hypomagnesemia, hyponatremia §Hyperuricemia §Hyperglycemia §Ototoxicity
58
Loop diuretic indications
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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