Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CRRAB 1 > Drugs > Flashcards

Drugs Flashcards

1
Q

Class of enalopril, captopril, lisinopril, ramipril

A

ACE inhibitors

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

Name ACE inhibitors

A

End in -PRIL

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

Name ACE inhibitors and their MOA

A

Enalopril, captopril, lisinopril, ramipril; MOA: inhibitor angiotensin converting enzyme, less angiotensin II, decreased glomerular filtration rate by preventing constriction of efferent arterioles

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

Class of losartin, cadesartan, valsartan?

A

Competitive angiotensin II receptor blockers

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

Name Angiotensin II receptor blockers?

A

End in -ARTAN; Losartan, candesartan, valsartan

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

Name Angiotensin II receptor blockers and their MOA?

A

end in -artan; bind competitively to angiotensin II receptors located on smooth muscle, allowing them to relax (Lowers BP), also prevents Na reabsorption.

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

Class of Metoprolol, Propranolol, esmolol, atenolol

A

Beta blockers

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

Name beta blockers

A

End in -olol

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

Name beta blockers and their MOA

A

End in -olol; decrease SA and AV nodal activity by decreasing cAMP, decreasing calcium currents. Decrease slope of Phase 4

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

What is the selectivity of beta blockers?

A

Drugs that Block Beta-1 start with A through M, Drugs that block beta-2 start with N to Z. Nonselective (both alpha and beta) have modified suffixes (not “-olol”)

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

What is the MOA of digoxin?

A

Inhibits Na/K ATPase, increasing intracellular Na, which will decrease the activity of the Na/Ca exchanger, increasing intracellular calcium and increasing muscle contractility, stimulates vagus nerve decreasing HR

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

Name HMG-CoA reductase inhibitors

A

End in -statins

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

MOA of statins

A

Inhibit HMG CoA reductase, preventing its conversion into mevalonate, a cholesterol precursor

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

Name Bile Acid resins

A

Cholestyrimine, colestipol, colesevelam

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

Name Bile acid resins and their MOA

A

cholestyrimine, colestipol, colesevelam; Prevent intestinal reabsorption of bile acids, making liver use more cholesterol to make bile

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

MOA of Ezetimibe

A

Prevent cholesterol absorption at small intestine brush border

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

Name fibrates

A

Gemfibrozil, clofibrate, bezefibrate, fenofibrate

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

Name Fibrates and their MOA

A

gemfibrozil, clofibrtae, bezafibrate, fenofibrate; MOA: Upregulate LPL, increasing TG clearance, activates PPAR-alpha to induce HDL synthesis

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

MOA of Niacin (Vitamin B3)

A

Inhibits lypolysis (hormone-sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis

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

Side effects of niacin

A

Red, flush face, hyperglycemia, hyperuricemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

MOA of Nitroglycerin

A

Increase NO in smooth muscle –> Increase cGMP and smooth muscle relaxation –> Increased vasodilation –> decrease preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Name potassium-sparing diuretic?

A

Spironolactone, eplerenone, Triamterine, Amiloride (The K+ STAys)

23
Q

Name and MOA of potassium-sparing diuretic?

A

Spirinolactone, eplerenone, Triamterine, Amiloride; Competitive antagonism of aldosterone at the aldosterone receptor in the distal convoluted tubule

24
Q

MOA of Hydralazine?

A

Increased cGMP –> smooth muscle relaxation.

25
Q

Does hydralazine target arterioles or veins more?

A

Arterioles; Reduces afterload

26
Q

Name emergency hypertensive drugs?

A

Nitroprusside, fenoldopam

27
Q

Name thiazide diuretics?

A

Chlorothalidone, hydrochlorothiazide

28
Q

MOA of hydrochlorothiazide and chlorthalidone?

A

Inhibits Na/Cl transporter in the early segment of distal convoluted tubule, decreasing diluting capacity of nephron

29
Q

Name Loop diuretics?

A

Furosemide, bumetidine, torsemide

30
Q

Name and say MOA of loop diuretics

A

Furosemide, bumetidine, torsemide; MOA: Inhibit NKCC of thick ascending limb of loop of henle; prevents urine concentration; Stimulates PGE release (vasodilatory effects on afferent arteriole)

31
Q

MOA of acetazolamide?

A

Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and decreased total body HCO3- stores, results in decreased bicarbonate reabsorption

32
Q

Name Class IA drugs

A

Quinidine, Procainamide, Disopyrimide (The Queen Proclaims Diso’s PYRAMIDE)

33
Q

Names and MOA of Class IA drugs

A

Quinidine, Procainamide, Disopyramide; Increase AP duration, Increase effective refractory period, increases QT interval

34
Q

Name Class IB drugs

A

Lidocaine, Mexiletine (I’d Buy LIDdy’s MEXIcan Taco’s) AND PHENYTOIN

35
Q

Name and MOA of IB drugs

A

Lidocaine, Mexiletine and Phenytoin; Decrease AP duration, preferentially affect ischemic or depolarized purkinje and ventricular tissue, p

36
Q

Name Class IC drugs

A

Flecainide, Propafenone (Can i have Fries, Please)

37
Q

Name and MOA of Class IC drugs

A

Flecainide, Propafenone; MOA: Significantly prolongs ERP in AV node and accessory bypass tracts, No effect on ERP in purkinje and ventricular tissue, Minimal effect on AP duration

38
Q

Class I drugs in order of affecting the slope of Phase 0 (Most to least)

A

C, A, B

39
Q

Class I drugs in order of increasing ERP:

A

A, C, B (decreases)

40
Q

Class I drugs in order of Kinetics (rate of association)

A

B> A> C

41
Q

Name Class II drugs

A

Metoprolol, propranolol, esmolol, atenolol…

42
Q

MOA of Class II Drugs

A

Decrease SA and AV nodal activity by decreasing cAMP and Ca currents, suppress abnormal pacemakers by decreasing slope of phase 4

43
Q

Name Class III antiarrhythmics

A

Amiodorone, Ibutilide, Dofetilide, Sotalol (AIDS)

44
Q

Name and MOA of Class III antiarrhythmics

A

Amiodorone, ibutilide, dofetilide, sotalol; MOA: Increase AP duration, Increase EPR, Increase QT interval

45
Q

What Class III antiarrhythmic blocks all the channels?

A

amiodorone

46
Q

Name Class IV antiarrhythmics

A

Verapamil, Diltiazem

47
Q

Name and MOA of Class IV antiarrhythmics

A

Verapamil, diltiazem; Decrease conduction velocity, Increase ERP, Increase PR interval

48
Q

Name Class V antiarrhythmics

A

Adenosine, Mg2+

49
Q

MOA of Adenosine as an antiarrhytmic

A

Increase K out of cells–> hyperpolarizing cell and decreasing the I(calcium) channel

50
Q

Why is Mg2+ used as an antiarrhythmic?

A

Effective in torsade de pointes and digoxin toxicity

51
Q

Name ATP-dependent K-channel openers?

A

Minoxidil and Diazoxide

52
Q

Antihypertensive drug that inhibits renin and therefore inhibits the conversion of angiotensinogen to angiotensin I

A

Aliskiren

53
Q

What vasodilatory acts on both arterioles and veins?

A

Nitroprusside

CRRAB 1 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions