Cardiology Drugs - Sheet1 Flashcards

1
Q

Amlodipine

A

Dihydropyridine CCA - peripheral vasdilatory effects, good for HTN, side effect of face flushing, contraindicated post MI, CHF due to reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Nifedipine

A

Dihydropyridine CCA - peripheral vasdilatory effects, good for HTN, side effect of face flushing, contraindicated post MI, CHF due to reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

-ipine

A

dihydropyridine CCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diltiazem

A

Non dihydropyridine CCA, acts of l-type calcium channel, works to depress conduction and excitability in slow response tissues, effective in SVT not so much in HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Verapamil

A

Non dihydropyridine CCA, acts on l-type calcium channel, works to depress conduction and excitability in slow response tissues, used in paroxysmal SVT, angina and HTN, side effect = constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

HCTZ

A

Thiazide diuretic - acts at distal convoluting tubule as a diuretic, natriuretic, and kalluretic, possibly also vasdilates, esp effective in AA and elderly, drug of choice for uncomplicated HTN, toxicities: sulfa allergy, hypokalemia, increased insulin resistance and TG, LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Furosemide

A

Loop diuretic - acts in distal convoluting tubule as a diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Losartan

A

ARB - targets AT1 specifically (allows for potential positive side effects of AT2) but you lost bradykinin, less side effects than ACEI, not additive with ACEI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Enlalapril

A

ACEI - prevents conversion of angiotensin I to angiotension II and prevents breakdown of bradykinin, side effect includes cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Phenoyxbenzamine

A

Non selective alpha blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Prazosin

A

selective alpha blocker - results in vasodilation, decrease in PVR and BP, also used to encourage voiding in pts with GU obstruction (GU dilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Clonidine

A

central alpha agonist, decreases downstream alpha activity, vasodilation, side effects: drowsiness and bradycardia. good for those with diabetic autonomic neuropathy - stabilizes autonmic output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Spironolactone

A

aldosterone antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hydralazine

A

Arterial vasodilator - decreases svr, used with beta blocker to prevent reflex tachycardia, toxicity: excessive vasodilation, SLE-like syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sodium nitroprusside

A

Arterial vasodilator - metabolized by SMCs into NO - used for HTN emergencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Nitrates

A

Venodilators - used for angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Propranolol

A

Non-selective beta-blocker - used for MI, HTN and CHF because it decreases myocardial oxygen demand, reduces sympathetic action on heart (prevents adverse remodeling) and results in vasodilation (decrease in RAAS activity) - danger of bronchoconstriction due to beta 2 activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Metoprolol

A

Selective beta blocker - used for MI, HTN and CHF because it decreases myocardial oxygen demand, reduces sympathetic action on heart (prevents adverse remodeling) and results in vasodilation (decrease in RAAS activity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Carvedilol

A

alpha1 and non-selective beta blocker - used for MI, HTN and CHF because it decreases myocardial oxygen demand, reduces sympathetic action on heart (prevents adverse remodeling) and results in vasodilation (due to decrease in RAAS activity AND alpha blocking effects)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Epinephrine

A

Inotrope/Pressor/Vasoactive Drug - mixed alpha 1, beta 1, beta 2 agonist, mostly increases heart rate and cardiac output with mixed effect on SVR, used in emergencies, codes

21
Q

Norepinephrine

A

Inotrope/Pressor/Vasoactive Drug - strong alpha 1 agonist with some beta 1 activity - mostly increases systemic vascular riesistance - used as a pressor in distributive shock

22
Q

Dopamine

A

Inotrope/Pressor/Vasoactive Drug - mixed alpha 1 and beta agonist with some delta 1 activity. Low dose - has isolated delta activity resulting in renal vasodilation. Intermediate dose has delta activity and beta 1 activity resulting in increased cardiac output w/o effect on SVR. High dose has dominant alpha action results in increase in SVR and HR

23
Q

Dobutamine

A

Inotrope/Pressor/Vasoactive Drug - Synthetic beta 1 agonist, increases contractility and therefore cardaic output without increasing SVR - great for CHF

24
Q

Isoproterenol

A

Inotrope/Pressor/Vasoactive Drug - Mixed beta 1 and beta 2 agonist, increases inotropy and chronotropy. Causes a decrease in SVR with an increase in CO and HR. Good for pacing after heart transplant or pacing before you can add a pacemaker.

25
Q

Phenylephrine

A

Inotrope/Pressor/Vasoactive Drug - synthetic alpha 1 agonist, increases SVR, great for increasing SVR (decreases HR and CO) - use as pressor in distributive shock

26
Q

Milrinone

A

Inotrope/Pressor/Vasoactive Drug - PDEI: MOA: PDEIs prevent camp breakdown increasing intracellular ca concentration; vasodilation; Effects: increase cardiac index, decrease SVR, used for CHF but careful with hypotension (pt must be volume overloaded)

27
Q

Digoxin

A

Inotrope/Pressor/Vasoactive Drug - Digoxin increases intracellular calcium by blocking the Na/K ATPase, increasing intracellular sodium which changes the gradient for the Na/Ca exchanger such that calcium is brought into the cell to pump sodium out. Toxicity is increased by hypokalemia due to the fact that digoxin and postassium compete for the same binding site on the Na/K ATPase. Elminiated renally (careful with renal dz!). Results in an increase in CO, LVEF, exercise tolerance, natriuresis and a decrease in LVEDP and neurohormonal activation. Can increase refractoriness of the AV node (careful with heart block) and increase automaticity of the ventricles (can cause arrythmias!). Important to keep doses low to avoid toxicity. Used in CHF to eliminate symptoms (not decrease mortality).

28
Q

Atropine

A

muscarininc antagonist - increases heart rate and decreases vasodilation, used to prevent vagal reaction and restore conduction with AV block delay

29
Q

acetylcholine

A

muscarinic agonist - natural mediator of PNS but not used much due to very low half life

30
Q

Edrophonium

A

acetylcholineesterase inhibitor - increases AV node refractoriness - used to diagnose and treat SVTs due to AV reentry or bypass, side effects include GI cramping

31
Q

Physostigmine

A

acetylcholineesterase inhibitor - increases AV node refractoriness - used to diagnose and treat SVTs due to AV reentry or bypass

32
Q

Neostigmine

A

acetylcholineesterase inhibitor - increases AV node refractoriness - used to diagnose and treat SVTs due to AV reentry or bypass

34
Q

Statins (-astatin)

A

HMG Co A reductase inhibitors - prevent cholesterol synthesis in the liver resulting in upregulation of LDLR, and decreased LDL in the blood. adverse effects include increases in alt/ast and muscle related effects

35
Q

Fibrates

A

Activate nuclear receptor PPAR-alpha, results in tissues decreasing VLDL production and increasing VLDL clearance, result is decrease in TF and increased HDL. Doesn’t decrease risk of CV events, but good for people with high TG to avoid pancreatitis. Adverse effects: increased alt/ast, muscle effects

36
Q

Niacin

A

Suppress lipolysis of adipose, results in increased HDL and decreased HDL, adverse effects: flushing, hepatotoxicity

37
Q

Cholesterol Absorption Inhibitor

A

inhibit cholesterol transporter NPC1L1, prevents cholesterol absorption, low cholesterol causes liver to upregulated LDLR, decreased LDL in blood. adverse effectrs include high ast/alt

38
Q

Bile acid dequestrant

A

large molecular weight resin that bind bile salts in the intestinal tract and prevent transport across intestinal lumen by IBAT1. Decreased cholesterol intake, liver upregulates LDLR, less LDL in blood. side effects: constipation, bloating, flatulence, can interfere with drug absorption, and raise TG

39
Q

Aspirin

A

Cox inhibitor - prevents platelet aggregation

40
Q

clopidogrel

A

platelet adp inhibitor - prevents platelet activation

41
Q

Glycoprotine IIB/IIIa inhibitor

A

prevent platelet activation and aggregation

42
Q

Thrombolytic drugs

A

Prevent thrombus formation - used in STEMI to rid occlusion (less good than PCI)

43
Q

Heparin

A

acts on antithrombin III to cause an invactivation of Factor Xa - prevents thrombus formation

44
Q

Procainamide

A

Class Ia anti-arrhythmic (Na, K channel blockers) - works best on fast response tissues (atria, ventricles), decreases excitability (Na activity) and increases action potential duration (Ka activity), highest potency of class Is

45
Q

Quinidine

A

Class Ia anti-arrhythmic (Na, K channel blockers) - works best on fast response tissues (atria, ventricles), decreases excitability (Na activity) and increases action potential duration (Ka activity), highest potency of class Is

46
Q

Lidocaine

A

Class Ib anti-arrhythmic (Na blocker) - works best on fast response tissues (atria, ventricles), lowest potency of class Is, decreases excitability (Na activity)

47
Q

Flecainide

A

Class Ic anti-arrhythmic (Na blocker) - works best on fast response tissues (atria, ventricles), middle potency of class Is, decreases excitability (Na activity)

48
Q

Amiodarone

A

Class III anti-arrhythmic (K blocker) - works best on fast response tissues (atria, ventricles), has some beta blocker activity, increases action potential duration (Ka activity)

49
Q

Sotalol

A

Class III anti-arrhythmic (K blocker) - works best on fast response tissues (atria, ventricles), has some beta blocker activity, increases action potential duration (Ka activity)

50
Q

Adenosine

A

Short acting adenosine receptor agonist - acts on slow response tissue (SA, AV nodes), increases potassium current resulting in cell hyperpolarization (less excitability)