Pharmacology: Cardiovascular Flashcards

(51 cards)

1
Q

Hydralazine

A

Incr cGMP

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2
Q

Nifedipine

A

Dihydropyridine
Blocks v-gated L type calcium channels, decr muscle contractility
More selective in heart muscle

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3
Q

Amlodipine

A

Dihydropyridine
Blocks v-gated L type calcium channels, decr muscle contractility
More selective in heart muscle

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4
Q

Verapamil

A

Non-dihydropyridine, Class IV anti-arrhythmic
Blocks v-gated L type calcium channels, decr muscle contractility
More selective in vascular smooth muscle

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5
Q

Diltiazem

A

Non-dihydropyridine, Class IV anti-arrhythmic
Blocks v-gated L type calcium channels, decr muscle contractility
More selective in vascular smooth muscle

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6
Q

Which CCB affects vascular smooth muscles more? Heart?

A

Vascular: dHPs
Nifedipine > diltiazem > verapamil

Heart: non-dHPs
Verapamil > diltiazem > nifedipine

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7
Q

Nitroprusside

What toxicity to worry about?

A

Direct release of NO –> incr cGMP
Short acting
Cyanide toxicity! (Tx: Amyl nitrite, B12, thiosulfate)

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8
Q

Fenoldapam

A

Dopamine D1 receptor agonist

Relaxes renal vascular smooth muscle

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9
Q

Diazoxide

A

K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle

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10
Q

Nitroglycerin (PO)

A
Releases NO --> incr cGMP --> smooth muscle relaxation and vasodilation
Veins >> arterioles
Decrease preload (venous pooling)
SE: Reflex tachy, flushing 
"Monday disease"
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11
Q

Isosorbide dinitrate (PO)

A
Metabolized to isosorbide mononitrate
Releases NO --> incr cGMP --> smooth muscle relaxation and vasodilation
Veins >> arterioles
Decrease preload (venous pooling)
SE: Reflex tachy, flushing 
"Monday disease"
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12
Q

Which beta-blockers are contraindicated in treating angina?

A

Pindolol and acebutolol: are partial beta-agonists

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13
Q

Digoxin

A

Cardiac glycoside

  1. Direct inhibition of Na/K ATPase increases intracellular Ca and inotropy
  2. Increases PSNS activity by incr vagal tone –> decr HR
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14
Q

What can increase Dig toxicity?

A
  1. Renal failure (decr excretion)
  2. Hypokalemia (more binding to Na/K channel)
  3. Quinidine (decr dig clearance)
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15
Q

Treating Dig toxicity

A

Slowly normalize K, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+

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16
Q

Pt with CHF and blurry yellow vision. What does his EKG look like?

A

Dig toxicity.

Incr PR interval, decr QT, scooping, T inversions, possible arrhythmias

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17
Q

Nesiritide

A

Recombinant B-type natriuretic peptide –> incr cGMP –> vasodilation

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18
Q

Quinidine

A

Class IA antiarrhythmic

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19
Q

Procainamide

A

Class IA antiarrhythmic

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20
Q

Disopyramide

A

Class IA antiarrhythmic

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21
Q

Lidocaine

A

Class IB antiarrhythmic

22
Q

Mexiletine

A

Class IB antiarrhythmic

23
Q

Tocainide

A

Class IB antiarrhythmic

24
Q

Moricizine

A

Class IC antiarrhythmic

25
Flecainide
Class IC antiarrhythmic
26
Propafenone
Class IC antiarrhythmic
27
Propranolol
Class II antiarrhythmic
28
Esmolol
Class II antiarrhythmic
29
Metoprolol
Class II antiarrhythmic
30
Atenolol
Class II antiarrhythmic
31
Timolol
Class II antiarrhythmic
32
Ibutilide
Class III antiarrhythmic | K+ channel blocker
33
Sotalol
Class III antiarrhythmic | K+ channel blocker
34
Bretylium
Class III antiarrhythmic | K+ channel blocker
35
Amiodarone
Class III antiarrhythmic K+ channel blocker Check LFTs, PFTs, TFTs Has class I, II, III, and IV effects because it alters the lipid membrane
36
Dofetilide
K+ channel blocker
37
Adenosine
Incr K+ efflux (out of cells) --> hyperpolarizing cell, decr Ca conductance (Na/K ATPase works harder, drives Ca out more via Na/Ca exchange?)
38
What drug blocks the effects of adenosine? How? What is is used for?
Theophylline, a methylxanthine. Used for asthma, COPD. A non-selective adenosine R antagonist, in addition to being a competitive nonselective PDE-inhibitor that increases cAMP -->--> decreasing inflammation
39
Statins
HMG-CoA reductase inhibitors | Decrease LDL cholesterol!
40
Niacin
Inhibit lypolysis, reduces VLDL secretion - Main effect: increases HDL! - SEs: Flushing, hyperglycemia, hyperuricemia
41
Cholestyramine
Bile acid resin - Prevent intestinal reabs of bile so liver must use up CH to make more - Main effect: decr LDL - SE: bad taste! cholesterol gallstones
42
Colestipol
Bile acid resin - Prevent intestinal reabs of bile so liver must use up CH to make more - Main effect: decr LDL - SE: bad taste! cholesterol gallstones
43
Colesevelam
Bile acid resin - Prevent intestinal reabs of bile so liver must use up CH to make more - Main effect: decr LDL - SE: bad taste! cholesterol gallstones
44
Ezetimibe
Cholesterol absorption blocker - Prevent CH reabs at small intestine brush border - Main effect: decr LDL
45
Gemfibrozil
Fibrate - Upregulates LPL and increases TG clearance - Main effect: decrease TG! - SE: Cholesterol gallstones (from increased cholesterol in bile
46
Clofibrate
Fibrate - Upregulates LPL and increases TG clearance - Main effect: decrease TG! - SE: Cholesterol gallstones
47
Benzafibrate
Fibrate - Upregulates LPL and increases TG clearance - Main effect: decrease TG! - SE: Cholesterol gallstones
48
Fenofibrate
Fibrate - Upregulates LPL and increases TG clearance - Main effect: decrease TG! - SE: Cholesterol gallstones
49
Ciprofibrate
Fibrate - Upregulates LPL and increases TG clearance - Main effect: decrease TG! - SE: Cholesterol gallstones
50
The lipid-lowering agents that: 1. Decrease LDL cholesterol 2. Increase HDL cholesterol 3. Decrease TG
1. Statins, bile acid resins, cholesterol absorption blocker (exetimibe) 2. Niacin 3. Fibrates
51
The lipid-lowering agents that: 1. Cause heptatoxicity 2. Cause myopathy/myositis 3. Cuase hyperglycemia 4. Cause cholesterol stones 5. Cause flushing 6. Cause hyperuricemia 7. Taste bad!
1. Statins, fibrates 2. Statins, fibrates 3. Niacin 4. BAS, fibrates 5. Niacin 6. Niacin 7. BAS