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Pharmacology > Pharmacology: Cardiovascular > Flashcards

Pharmacology: Cardiovascular Flashcards

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
Q

Flecainide

A

Class IC antiarrhythmic

26
Q

Propafenone

A

Class IC antiarrhythmic

27
Q

Propranolol

A

Class II antiarrhythmic

28
Q

Esmolol

A

Class II antiarrhythmic

29
Q

Metoprolol

A

Class II antiarrhythmic

30
Q

Atenolol

A

Class II antiarrhythmic

31
Q

Timolol

A

Class II antiarrhythmic

32
Q

Ibutilide

A

Class III antiarrhythmic

K+ channel blocker

33
Q

Sotalol

A

Class III antiarrhythmic

K+ channel blocker

34
Q

Bretylium

A

Class III antiarrhythmic

K+ channel blocker

35
Q

Amiodarone

A

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
Q

Dofetilide

A

K+ channel blocker

37
Q

Adenosine

A

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
Q

What drug blocks the effects of adenosine? How? What is is used for?

A

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
Q

Statins

A

HMG-CoA reductase inhibitors

Decrease LDL cholesterol!

40
Q

Niacin

A

Inhibit lypolysis, reduces VLDL secretion

  • Main effect: increases HDL!
  • SEs: Flushing, hyperglycemia, hyperuricemia
41
Q

Cholestyramine

A

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
Q

Colestipol

A

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
Q

Colesevelam

A

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
Q

Ezetimibe

A

Cholesterol absorption blocker

  • Prevent CH reabs at small intestine brush border
  • Main effect: decr LDL
45
Q

Gemfibrozil

A

Fibrate

  • Upregulates LPL and increases TG clearance
  • Main effect: decrease TG!
  • SE: Cholesterol gallstones (from increased cholesterol in bile
46
Q

Clofibrate

A

Fibrate

  • Upregulates LPL and increases TG clearance
  • Main effect: decrease TG!
  • SE: Cholesterol gallstones
47
Q

Benzafibrate

A

Fibrate

  • Upregulates LPL and increases TG clearance
  • Main effect: decrease TG!
  • SE: Cholesterol gallstones
48
Q

Fenofibrate

A

Fibrate

  • Upregulates LPL and increases TG clearance
  • Main effect: decrease TG!
  • SE: Cholesterol gallstones
49
Q

Ciprofibrate

A

Fibrate

  • Upregulates LPL and increases TG clearance
  • Main effect: decrease TG!
  • SE: Cholesterol gallstones
50
Q

The lipid-lowering agents that:

  1. Decrease LDL cholesterol
  2. Increase HDL cholesterol
  3. Decrease TG
A
  1. Statins, bile acid resins, cholesterol absorption blocker (exetimibe)
  2. Niacin
  3. Fibrates
51
Q

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!
A
  1. Statins, fibrates
  2. Statins, fibrates
  3. Niacin
  4. BAS, fibrates
  5. Niacin
  6. Niacin
  7. BAS

Pharmacology (15 decks)

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