Brainscape's Knowledge GenomeTM

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


See full index

Pharma drugs > Cardio/Renal > Flashcards

Cardio/Renal Flashcards

1
Q 
Antiarrhythmics class 1a
Drug names
A

Quinidine
Procainamide
Disopyramide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q 
Antiarrhythmics class 1b
Drug names
A

Lidocaine
Mexiletine
(Phenytoin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q 
Antiarrhythmics class 1c
Drug names
A

Flecainide

Propafenone

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

Na channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q 
Antiarryhythmics class 1a
MOA
A

Na channel blockers
Inc. AP duration
Inc. ERP (some K-channel blocking effects).
Prolongs QT interval.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q 
Antiarrhythmics class 1a
Clinical use
A

Na channel blockers
Atrial/ventricular arrhythmias (AFib, A-flutter; SVT, Vtach)
(esp. re-entrant and ectopic SVT, VT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q 
Antiarrhythmics class 1a
Toxicity
A

Na channel blockers.
>Cinchonism (headache, tinnitus; Quinidine).
>SLE-like syndrome (procainamide).
>Heart failure (disopyramide).
>Torsades de pointes (prolonged QT interval).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q 
Antiarrhythmics class 1b
MOA
A

Na channel blockers
Dec. AP duration (preferential for ischemic or depolarized Purkinje and ventricular tissue).
Dec. ERP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q 
Antiarrhythmics class 1b
Clinical use
A 
Na channel blockers.
Ventricular arrhythmias (post-MI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q 
Antiarrhythmics class 1b
Toxicity
A

Na channel blockers
CNS stimulation/depression
Cardiovascular depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q 
Antiarrhythmics class 1c
MOA
A

Na channel blockers

Markedly prolongs phase 0 depolarization.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q 
Antiarrhythmics class 1c
Clinical use
A

Na channel blockers
Life-threatening SVTs (atrial fibrillation).
Last resort in refractory Vtach.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q 
Antiarrhythmics class 1c
Toxicity
A

Na channel blockers

Pro-arrhythmic (CI in post-MI)

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

Beta-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q 
Antiarrhythmics class 2
Drug names
A

Metoprolol, Propanolol
Esmolol, Atenolol
Timolol, Carvedilol

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

B-blockers (B1 antagonists at low doses, atenolol)
Dec. SA/AV node activity (dec. cAMP – dec. Ca – dec. phase 4 slope, dec. depolarization).
Inc. PR interval – dec. conduction through AV node.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q 
Antiarrhythmics class 2
Clinical use
A

B-blockers
SVT
Ventricular rate control of A-fib and A-flutter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q 
Antiarrhythmics class 2
Toxicity
A 
B-blockers.
Impotence.
Exacerbated COPD, asthma.
CVS effects (bradycardia, HF, AV block).
CNS effects (sedation, sleep disturbance).
Can mask hypoglycemic signs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q 
Antiarrhythmics class 3
Type
A

K channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q 
Antiarrhythmics class 3
Drug names
A

Amiodarone
Ibutilide
Dofetilide
Sotalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q 
Antiarrhythmics class 3
MOA
A 
K channel blockers.
Prolongs phase 3 repolarization.
Prolongs AP duration.
Prolongs ERP.
Prolongs QT interval (ventricular contraction).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q 
Antiarrhythmics class 3
Clinical use
A

K channel blockers.
A-fib, A-flutter
Vtach (amiodarone, sotalol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q 
Antiarrhythmics class 3
Toxicity
A

K channel blockers.
Torsades de pointes (sotalol, ibutilide).
B-blockade (sotalol).
>Amiodarone: pulmo fibrosis, hepatotoxicity, hypo/hyperthyroidism (40% iodine); photodermatitis, corneal deposits (acts as a hapten); CNS effects, CVS effects – check LFT, PFT, TFT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q 
Antiarrythmics class 4
Type
A

Ca channel blockers (nondihydropyridine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q 
Antiarrhythmics class 4
Drug names
A

Verapamil

Diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q 
Antiarrhythmics class 4
MOA
A 
Ca channel blockers.
Prolongs phase 2.
Dec. conduction velocity -- slow rise of AP, slow closing of Ca channels.
Inc. ERP.
Inc. PR interval.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q 
Antiarrhythmics class 4
Clinical use
A

Ca channel blockers
Prevents nodal arrhythmias (SVT)
Rate control in A-fib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q 
Antiarrhythmics class 4
Toxicity
A 
Ca channel blockers
Constipation, flushing, edema
CVS effects (HF, AV block, sinus node depression)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Digoxin

Type

A

Cardiac glycoside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Digoxin

MOA

A

Inhibits Na/K ATPase – indirect inhibition of Na/Ca exchanger – Inc. intracellular Ca – positive inotropy (increases contractility)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Digoxin

Clinical use

A

> HF (inc. contractility).

>A-fib (decr. AV node conduction, depresses SA node).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Digoxin

Toxicity, Antidote

A

> Cholinergic: N/V, diarrhea, changes in color vision (blurry yellow vision), arrhythmias, AV block.
Hyperkalemia (poor prognosis).
Antidote: slowly normalize K; Mg, anti-digoxin Fab fragments.

33
Q

Digoxin

Predisposing for toxicity

A

Renal failure.
Hypokalemia.
>Verapamil, Amiodarone, quinidine – decr. digoxin clearance, displaces digoxin at tissue-binding sites.

34
Q

Calcium channel blockers

Dihydropyridines

A

Amlodipine, Clevidipine
Nicardipine, Nifedipine
Nimodipine

35
Q

Calcium channel blockers

Non-dihydropyridines

A

Diltiazem

Verapamil

36
Q

Calcium channel blockers

MOA

A

Blocks L-type calcium channels on cardiac and smooth muscle (decrease contractility).
>Vascular smooth muscle: amlodipine = nifedipine.
>Heart: verapamil > diltiazem > amlodipine = nifedipine.

37
Q

Calcium channel blockers

Clinical use

A

> Dihydropyridines (except nimodipine): HTN, angina, Raynaud phenomenon.
Nimodipine: SAH (prevents cerebral vasospasm).
Clevidipine: HTN urgency/emergency
NDP: HTN, angina, A-fib/flutter.

38
Q

Hydralazine

MOA

A

Arteriolar dilator – reduces afterload.

Inc. cGMP – smooth muscle relaxation.

39
Q

Hydralazine

Clinical use

A

Severe HTN, HF.
Coadministered w/ B-blocker to prevent reflex tachycardia.
Safe in pregnancy.

40
Q

Hydralazine

Toxicity

A

> Compensatory tachycardia (due to inc. venous return from baroreceptor reflex; CI in angina/CAD).
Fluid retention (sympathetic activation of RAAS).
Lupus-like syndrome.

41
Q

Nitrates

Drug names

A

Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

42
Q

Nitrates

MOA

A

Venous dilator – reduces preload.

Inc. NO in vascular smooth muscle – inc. cCMP – smooth muscle relaxation.

43
Q

Nitrates

Clinical use

A

Angina, acute coronary syndrome

Pulmo edema

44
Q

Nitrates

Toxicity

A 
Reflex tachycardia (response to relative hypotension).
>"Monday disease" in industrial exposure: tolerance for vasodilating affect during work week, loss of tolerance over weekend (tachycardia, dizziness, headache upon exposure).
45
Q

Calcium channel blockers

Toxicity

A

Cardiac depression, peripheral edema.
AV block (NDPs)
Hyperprolactinemia (verapamil)
Gingival hyperplasia

46
Q

Mannitol

MOA

A

Proximal tubule
Osmotic diuretic.
Inc. tubular osmolarity – inc. urine flow.
Dec. ICP, IOP

47
Q

Mannitol

Clinical use

A

Elevated ICP, IOP (cerebral edema tx).

Drug overdose.

48
Q

Mannitol

[Toxicity, CI]

A

> Pulmo edema (rapid rise in volume, overall inc. in hydrostatic pressure in vessels).
CI: anuria, HF.
[ex. Pt w/ cerebral edema is given mannitol, so all the fluid in the brain is drawn back into BVs – rapid inc. in hydrostatic pressure – pulmo edema]

49
Q

Acetazolamide

MOA

A

Proximal tubule.
Carbonic anhydrase inhibitor.
Self-limited NaHCO3 diuresis – dec. total HCO3 stores.

50
Q

Acetazolamide

Clinical use

A

Glaucoma.
Urinary alkalization, Metabolic alkalosis.
Altitude sickness.
Pseudotumor cerebri

51
Q

Acetazolamide

Toxicity

A 
Hyperchloremic metabolic acidosis (dehydration).
NH3 toxicity (SE: urine alkalinization).
"ACIDazolamide causes ACIDosis"
52
Q

Sulfonamide Loop diuretics

Drug names

A

Furosemide
Bumetanide
Torsemide

53
Q

Sulfonamide Loop diuretics

MOA

A

Thick ascending limb of Henle.
Inhibit Na/K/2Cl cotransport.
Excess excretion of Na, Cl, H2O – no hypertonicity of medullary interstitium – prevents urine concentration.
Inc. Ca excretion (paracellular Ca reabsorption w/ Na/K/Cl cotransport).

54
Q

Sulfonamide Loop diuretics

Clinical use

A

Edematous states (HF, cirrhosis, nephrotic syndrome, pulmo edema).
HTN
Hypercalcemia

55
Q

Sulfonamide Loop diuretics

Toxicity

A

Ototoxicity (similar symporters in ear)
Hypokalemia
Dehydration, Allergy
Nephritis, Gout

56
Q

Thiazide diuretics

Drug names

A

Chlorthalidone

Hydrochlorothiazide

57
Q

Thiazide diuretics

MOA

A

Distal convoluted tubule.
>Inhibits Na/Cl cotransporter – no Na/Cl reabsorption – Na/H20 excretion.
>Dec. diluting capacity.
>Dec. Ca excretion (Ca/Na antiporter exchanges Na from blood w/ reabsorbed Ca – dec. intracellular Ca during exchange prompts further inc. Ca reabsorption).

58
Q

Thiazide diuretics

Clinical use

A

HTN, HF
Nephrogenic diabetes insipidus
Osteoporosis, Idiopathic hypercalciuria

59
Q

Thiazide diuretics

Toxicity

A

Hypokalemic metabolic alkalosis
Hyponatremia, Hypercalcemia (hypocalciuria)
Hyperglycemia, Hyperlipidemia, Hyperurecemia

60
Q

K-sparing diuretics

Drug names

A

Spironolactone, Eplerenone

Triamterene, Amiloride

61
Q

K-sparing diuretics

MOA

A

Collecting tubules.
>Spironolactone, eplerenone: competitive aldosterone receptor antagonists.
>Triamterene, Amiloride: Na channel blockers – block ENaC, w/c drives Na/K pump.

62
Q

K-sparing diuretics

Clinical use

A

Hyperaldosteronism
K depletion
HF

63
Q

K-sparing diuretics

Toxicity

A

Hyperkalemia (maybe arrhythmias).

Endocrine effects w/ spironolactone (gynecomastia, antiandrogen).

64
Q

ACE inhibitors

Drug names

A

Captopril, Enalapril

Lisinopril, Ramipril

65
Q

ACE inhibitors

MOA

A

Inhibit ACE – dec. ATII – prevent constriction of efferent arteriole – dec. GFR.
Inc. Renin.
Prevents bradykinin inactivation (vasodilator).

66
Q

ACE inhibitors

Clinical use

A

HTN, HF (prevent heart remodelling due to chronic HTN).
Proteinuria (no ATII, no vasoconstriction).
Diabetic nephropathy – dec. intraglomerular pressure – slow GBM thickening.

67
Q

ACE inhibitors

Toxicity

A

Cough, Angioedema (bradykinin accumulation –vasodilation).
Teratogen.
Inc. creatinine (due to dec. GFR).
Hyperkalemia, Hypotension.
*CI in bilateral renal artery stenosis – renal failure.

68
Q

Angiotensin II receptor blockers (ARBs)

Drug names

A

Losartan
Candesartan
Valsartan

69
Q

ARBs

MOA

A

Blocks binding of ATII to AT1 receptor – similar effects of ACEi (prevents peripheral vasoconstricting effects of ATII).
Dec. GFR, inc. renin.
Don’t inc. bradykinin.

70
Q

ARBs

Clinical use

A

For intolerance of ACEi (cough, angioedema).
HTN, HF
Proteinuria
Diabetic nephropathy

71
Q

ARBs

Toxicity

A

Hyperkalemia
Dec. renal function
Hypotension
Teratogen

72
Q

HMG-CoA reductase inhibitors (-statin)

[Names]

A

Lovastatin, Simvastatin
Pravastatin, Atorvastatin
Rosuvastatin

73
Q

HMG-CoA reductase inhibitors

[MOA, effect on lipid levels, toxicity]

A

> Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor).
Super dec. LDL, inc. HDL, dec. TGL.
Dec. mortality in CAD
Tox: hepatotoxic, myopathy (esp. w/ fibrates or niacin)

74
Q

Bile acid resins

[Names]

A

Cholestyramine
Colestipol
Colesevelam

75
Q

Bile acid resins

[MOA, effect on lipid levels, toxicity]

A

> Prevents intestinal reabsorption of bile acids – liver uses cholesterol to make more.
Dec. LDL, slightly inc. HDL.
SE: dec. absorption of other drugs and fat-soluble vitamins

76
Q

Ezetimibe

[MOA, effect on lipid levels]

A

> Prevents cholesterol absorption at SI brush border.

>Dec. LDL

77
Q

Fibrates

[Names]

A

Gemfibrozil
Clofibrate
Bezafibrate
Fenofibrate

78
Q

Fibrates

[MOA, effect on lipid levels, toxicity]

A

> Upregulates LPL – inc. TG clearance.
Activates PPAR-alpha to induce HDL synthesis.
Super dec. TG, inc. HDL, dec. LDL
SE: myopathy (inc. risk w/ statins), cholesterol gallstones

79
Q

Niacin (B3)

[MOA, effect on lipid levels, SE]

A

> inhibits lipolysis (HPL) in adipose, reduces hepatic VLDL synthesis.
Inc. HDL, dec. LDL
SE: red, flushed faced (PGs); Hyperglycemia, hyperuricemia

Pharma drugs (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions