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USMLE > Pharm1 - Pharm1 > Flashcards

Pharm1 - Pharm1 Flashcards

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USMLE® Step 1 flashcards
1
Q

MOA mannitol

A

creates an osmotic diuresis because it can’t leave the tubule inhibits Na and Cl reabsorption in PC and ascendin loop

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2
Q

clinical uses of mannitol

A

to decrease intractranial pressure or intraocular pressure through volume depletion

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3
Q

side effects of mannitol

A

can cause pulmonary edema d/t extracellular volume expansion, pulling water out of cells hypernatremia

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4
Q

contraindications of mannitol

A

CHF pulmonary edema anuria severe renal failure severe dehydration

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5
Q

how is mannitol administered?

A

parenterally (poorly absorbed PO)

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6
Q

MOA spironolactone

A

K sparing diuretic, antagonizes aldosterone in the DCT, inhibiting Na reabsorption

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7
Q

what effect does spironolactone have on Ca

A

decreases serum Ca levels by directly inhibiting its transport in the DCT

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8
Q

clinical uses of spironolactone

A

HTN pulmonary edema edema from CHF or cirrhosis, nephrotic syndrome primary hyperaldosteronism

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9
Q

side effects of spironolactone

A

gynecomastia (and other anti-androgenic effects) hyperkalemia hyponatremia hypochlroemic acidosis (blocks aldosterone’s effect on Na/H antiporter)

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10
Q

MOA amiloride

A

K sparing diuretic, directly inhibits Na reabsorption, independent of aldosterone increased Ca reabsorption

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11
Q

uses of amiloride

A

treats ca stones

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12
Q

differences between amiloride and triamterene?

A

MOA similar, but triampterene has shorter t1/2

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13
Q

MOA furosemide

A

loop diuretic, blocking NKCC increased urinary excretion of K, Mg, Ca increases RBF without altering GFR

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14
Q

clinical uses for furosemide

A

edema to increase urine output in ARF (although it doesn’t alter the course of ARF) hypercalcemia hyperkalemia

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15
Q

side effects of furosemide

A

K wasting metabolic alkalosis Mg depletion ototoxicity hyperuricemia

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16
Q

why does hyperuricemia result from furosemide use?

A

increases urate reabsorption d/t increased proximal Na reabsorption

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17
Q

contraindication of furosemide

A

sulfa allergy

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18
Q

which is the only loop diuretic without a sulfa group?

A

ethacrynic acid

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19
Q

MOA HCTZ?

A

block NaCl transport at the DCT Enhanced Ca reaborption (because Na and Ca compete for ATP dependent reabsorption at DCT)

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20
Q

clinical uses of HCTZ?

A

HTN edema DI (by inducing mild volume depletion) to stop recurrent renal calcium stones

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21
Q

contraindication of HCTZ

A

sulfa allergy

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22
Q

side effects of HCTZ

A

hyperglycemia hyperlipidemia hyperuricemia hypercalcemia melabolic alkalosis Mg depletion

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23
Q

MOA acetazolamide

A

Carbonic anhydrase inhibitor so it inhibits the reabsorption of HCO3- in PCT also CA is in ciliary body of eye and in choroid plexus cells, so it decreases aqueous humor production and increases CSF production

24
Q

uses for acetazolamide

A

acute altitude sickness glaucoma treatment for alkalosis facilitate eexcretion of weak acid (as seen in tumor lysis syndrome)

25
Q

side effects of acetazolamide

A

encephalopathy (from decreased excretion of NH3 in urine) renal stones b/c calcium phosphate is less soluble in alkaline urine hyperchloremic metabolic acidosis

26
Q

contraindications of acetazolamide

A

sulfa allergy hepatic or renal dz hyperchloremic acidosis hyponatremia hypokalemia

27
Q

what effect does furosemide have on the following serum levels: K HCO3 Ca Mg urate

A

decreased increased decreased decreased increased

28
Q

what effect does thiazide have on the following serum levels: K HCO3 Ca Mg urate

A

decrease increase increased decreased increased

29
Q

what effect does spironolactone have on the following serum levels: K HCO3 Ca Mg urate

A

increased decreased decreased none none

30
Q

what effect does amiloride have on the following serum levels: K HCO3 Ca Mg urate

A

increased decreased increased none none

31
Q

what effect does acetazolamide have on the following serum levels: K HCO3 Ca Mg urate

A

decreased decreased none none none

32
Q

which diuretics decrease Mg?

A

furosemide HCTZ

33
Q

which diuretics increase urate?

A

furosemide HCTZ

34
Q

contraindication of spironolactone

A

acute renal failure

35
Q

MOA nitroprusside

A

vasodilation of arteries and veins contact with RBC –> decomposition of drug and release of NO NO, via activation of guanylate cyclase –> vasodilation

36
Q

clinical uses of nitroprusside

A

HTN crisis aortic dissection (must be given with B blocker) CHF

37
Q

side effects of nitroprusside

A

hypotension reflex tachy CN release

38
Q

contraindications for nitroprusside

A

known inadequate cerebral circulation hepatic/renal dz (increases thiocyanate toxicity)

39
Q

MOA nitroglycerine

A

via guanylate cyclase –> increase cGMP which activates cAMP protein dependent kinases and leads to dephosphorylation of myosin light chains and decreased intracellular Ca –> relaxation of veins and increased venous capacitance

40
Q

uses of nitroglyceride

A

treats angina (decresae coronary asospasm) CHF HTN

41
Q

side effects of nitroglycerine

A

hypotension, tachycardia, throbbing HA from meningeal arterial dilation

42
Q

MOA captopril

A

ACE inhibitor blocks formation of AII and degradation of bradykinin so, inhibits constriction of efferent arteriole, and potentiates vasodilation caused by bradykinin also causes venous vasodilation

43
Q

uses of captopril

A

HTN CHF ischemic heart disease decreases proteinuria and progression of nephropathy in diabetics

44
Q

side effects of captopril

A

cough from increased bradykinin can cause renal insufficiency b/c GFR is not increased in low volume states

45
Q

contraindications of captopril

A

renal insufficiency bilateral renal artery stenosis

46
Q

MOA losartan

A

AII receptor blocker

47
Q

uses of losartan

A

HTN CHF

48
Q

side effects of losartan

A

no cough can’t maintain GFR by vasodilation of efferent arterioles

49
Q

MOA milrinone

A

inhibits PDE III –> dilation of arteries and veins PDE III inactivates cAMP, so this process is inhibited –> increased Ca reflux in myocardium, with increased cardiac contractility

50
Q

uses of milrinone

A

refractory CHF can increase mortality, and should ONLY be used if diuretics, digoxin, and vasodilators have failed a-fib

51
Q

side effects of milrinone

A

ventricular arrhythmias hypotension hepatotoxicity

52
Q

MOA sildenafil

A

blocks PDE V action (thus potentiating the action of cGMP dependent kinases that activate phosphatases that encourage the relaxation of smoooth muscle) also decreases the Ca concnetration –> smooth muscle relaxation

53
Q

MOA digoxin

A

blocks the Na-K pump –> increased Na intracellularly this inhibits the Na concentration gradient from forming, blocking the Ca from leaving the cells this improves cardiac contractility also slows the conduction through AV node

54
Q

uses of digoxin

A

CHF a fib, a flutter (slows conduction through AV node)

55
Q

side effects of digoxin

A

narrow therapeutic window visual disturbances, nausea, blurred vision a-tac and AV block can result

56
Q

contraindication of digoxin

A

hypokalemia 2nd/3rd degree heart block WPW who develop a-fib –> increased impulses through accessory pathway –> VF

57
Q

what abnormalities can be seen on the EKG on a person taking digoxin

A

incresaed PR, decreased QT, scooping of ST segments, T wave inversion

USMLE (16 decks)

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