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STEP 1 (2) > Cardiovascular Pharm > Flashcards

Cardiovascular Pharm Flashcards

1
Q

How should HTN in pregnancy be tx?

A

-hydralazine, labetalol, methyldopa, nifedipine

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2
Q

What are the dihydropyridine CCBs (act on peripheral smooth muscle)?

A

-ipines (e.g. amlodipine, nifedipine)

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3
Q

What are the non-dihydropyridine CCBs (act on heart)?

A

verapamil and diltiazem

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4
Q

How do CCBs work?

A

they block voltage-dependent L-type Ca2+ channels of muscle

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5
Q

How does hydralazine work?

A

it increases cGMP to cause smooth muscle relaxation and vasodilates arterioles to reduce afterload for tx of HTN

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6
Q

T or F. Hydralazine is safe in pregnancy

A

T.

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7
Q

What is hydralazine usually given with?

A

a BB to prevent reflex tachycardia

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8
Q

How does nitroprusside work?

A

it is short acting and increases cGMP via direct release of NO

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9
Q

The main toxicity of nitroprusside is _____

A

cyanide poisoning

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10
Q

How does fenoldopam help in HTN crises?

A

it is a dopamine D1 agonist that causes coronary, peripheral, renal, and splanchnic vasodilation

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11
Q

What are some common nitrates?

A

-nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

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12
Q

How do nitrates work?

A

vsaodilate by increasing NO in vascular SM increasing cGMP and predominantly working in VEINS (over arteries) to decrease preload

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13
Q

What are the main uses of nitrates?

A

angina, pulmonary edema

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14
Q

What are the AEs of nitrates?

A
  • reflex tachycardia (give with a BB)
  • hypotension
  • flushing, HA
  • tachyphlyaxis
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15
Q

What is the goal of antianginal therapy?

A

reduction of myocardial O2 consumption by decreasing either end-diastolic volume, BP, HR, or contractility

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16
Q

What determinants of angina do nitrates affect?

A

decrease end-diastolic volume, BP, ejection time, and MVO2

increase HR

dont affect contractility

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17
Q

What determinants of angina do BBs affect?

A

decrease end-diastolic volume, BP, Contractility, HR, and MVO2

increase ejection time

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18
Q

What determinants of angina do BBs AND Nitrates affect?

A

no effect on end-diastolic volume, contractility, HR, or ejection time

decreased BP

**drastically decrease MVO2**

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19
Q

What are some HMG-CoA reductase inhibitors?

A
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20
Q

How do statins affect LDL, HDL, and triglycerides?

A

LDL- reduced

HDL- increased

TAGs- decreased

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21
Q

How do statins work?

A

they inhibit conversion of HMG-CoA ro mevalonate, a cholesterol precursor

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22
Q

What are the AEs of STATINs?

A

elevated LFTs

myopathy when used with fibrates or niacin

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23
Q

What are some bile acid resins used to decrease cholesterol uptake?

A

cholestyramine, colestipol

colesevelam

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24
Q

How do bile acid resins affect LDL, HDL, and triglycerides?

A

LDL- decrease

HDL and TAGs- slightly increase

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25
How does Ezetimibe work?
it prevents cholesterol absorption at the small intestine brush border (only affects LDL- decreases)
26
What are the fibrates?
gemfibrozil clofibrate, bezafibrate, fenofibrate
27
How do fibrates affect LDL, HDL, and TAGs?
LDL- decrease HDL- increase TAGs- greatly decrease
28
How do fibrates work?
they upregulate LPL to increase TAG clearance and activate PPARa to induce HDL synthesis
29
How does niacin work?
inhibits lipolysis in adipose tissue and reduces hepatic VLDL synthesis to decrease LDL and increase HDL
30
What are the AEs of niacin?
- niacin flush - hyperglycemia - hyperuricemia
31
How does digoxin work?
it directly inhibits Na/K ATPase to indirectly inhibit the Na/Ca exchanger in myocytes to prevent efflux of calcium and thus act as a positive inotrope it also stimulates the vagus nerve to decrease HR
32
What are the uses of digoxin?
HR (increases contractility) and a. fib (decreases conduction at AV and SA node)
33
What are the AEs of digoxin?
- cholinergic- N/V, diarrhea, blurry ision, AV block - hyperkalemia
34
What things predispose to digoxin toxicity?
**renal failure, verapamil, amiodarone, and quinidine** all decrease clearance
35
How do Class I Antiarrhythmics work?
slow conduction by decreasing the slope of _phase 0 depolarization_ by acting as **Na+ channel blockers**
36
What are the Class IA AAs?
Quinidine, Procainamide, Disopyramide 'the **Qu**een **Proc**laims **Diso**'s **pyramid**"
37
How do Class IAs work?
- increase AP duration - elongate effective refractory period (ERP) in ventricular action potential - **increase QT interval**
38
What are the uses of Class IAs?
both atrial and ventricular arryhthmias, especially re-entrant and ectopic SVT and VT
39
AEs of Class IAs?
- cinchonism (headache, tinnitus with quinidine) - SLE like syndrome (procainamide) - HF (Disopyramide) - **torsades de pointes** **-**thrombocytopenia
40
What are the Class IBs?
Lidocaine, Mexiletine
41
How do Class IBs work?
decrease the AP duration, preferrably affecting ischemic or depolarized Purkinje and ventricular tissue.
42
What are the uses of Class IBs?
acute ventricular arrythmias (especially post-MI) digitalis-induced arryhthmias
43
AEs of Class IBs?
CNS modulation CV depression
44
What are the Class ICs?
Flecainide, Propafenone
45
How do Class ICs work?
significantly prolongs ERP in AV node and accessory bypss tracts (no effect on ERP in Purkinje and ventricular tissue) minmal effect on AP duration
46
What are the uses of Class ICs?
SVTs, including a fib.
47
AEs of Class ICs?
porarryhthmic in ischemic (post-MI) and structural heart disease
48
What are the Class II AAs?
BBs (metoprolol, propranolol, etc.)
49
How do BBs work?
decrease SA and **AV** nodal activity by decreasing cAMP and Ca2+ currents and decrease the slope of phase 4 depolarization
50
What are the AEs of beta blockers?
impotence, exacerbation of COPD and asthma, bradycardia, AV block, etc. may mask the signs of hypoglycemia
51
What are the Class III AAs?
**A**miodarone, **I**butilide, **D**ofetilide, **S**otalol ## Footnote **AIDS**
52
What are the AEs of amiodarone?
pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism (40% iodine by weight) - can act as a hapten - bradycardia, heart block
53
What does amiodarone do if it acts as a hapten?
contributes to corneal deposits, blue/gray skin depositis resulting in photodermatitis
54
What are the uses of Class III AAs?
a. fib, a. flutter, ventricular tachycardia (amiodarone, sotalol)
55
T or F. Class III can cause TDP
TRUE. Prolong the QT interval
56
What are the Class IV AAs?
CCBs - verapamil and diltiazem
57
What is the DOC for abolishing supraventicular tachycardia?
adenosine
58
How does adenosine work?
it increases K+ efflux to hyperpolarize the cell and decrease Ica activity
59
Adenosine
-very short acting (15 sec) effects blunted by theophylline and caffeine (both are adenosine receptor antagonists)
60
What are the AEs of adenosine?
flushing, hypotension, chest pain, sense of impending doom bronchospasm

STEP 1 (2) (16 decks)

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