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Flashcards in Pharm1 - Pharm1 Deck (57)
1

MOA mannitol

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

2

clinical uses of mannitol

to decrease intractranial pressure or intraocular pressure through volume depletion

3

side effects of mannitol

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

4

contraindications of mannitol

CHF pulmonary edema anuria severe renal failure severe dehydration

5

how is mannitol administered?

parenterally (poorly absorbed PO)

6

MOA spironolactone

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

7

what effect does spironolactone have on Ca

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

8

clinical uses of spironolactone

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

9

side effects of spironolactone

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

10

MOA amiloride

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

11

uses of amiloride

treats ca stones

12

differences between amiloride and triamterene?

MOA similar, but triampterene has shorter t1/2

13

MOA furosemide

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

14

clinical uses for furosemide

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

15

side effects of furosemide

K wasting metabolic alkalosis Mg depletion ototoxicity hyperuricemia

16

why does hyperuricemia result from furosemide use?

increases urate reabsorption d/t increased proximal Na reabsorption

17

contraindication of furosemide

sulfa allergy

18

which is the only loop diuretic without a sulfa group?

ethacrynic acid

19

MOA HCTZ?

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

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clinical uses of HCTZ?

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

21

contraindication of HCTZ

sulfa allergy

22

side effects of HCTZ

hyperglycemia hyperlipidemia hyperuricemia hypercalcemia melabolic alkalosis Mg depletion

23

MOA acetazolamide

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

uses for acetazolamide

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

25

side effects of acetazolamide

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

26

contraindications of acetazolamide

sulfa allergy hepatic or renal dz hyperchloremic acidosis hyponatremia hypokalemia

27

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

decreased increased decreased decreased increased

28

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

decrease increase increased decreased increased

29

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

increased decreased decreased none none

30

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

increased decreased increased none none

31

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

decreased decreased none none none

32

which diuretics decrease Mg?

furosemide HCTZ

33

which diuretics increase urate?

furosemide HCTZ

34

contraindication of spironolactone

acute renal failure

35

MOA nitroprusside

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

36

clinical uses of nitroprusside

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

37

side effects of nitroprusside

hypotension reflex tachy CN release

38

contraindications for nitroprusside

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

39

MOA nitroglycerine

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

uses of nitroglyceride

treats angina (decresae coronary asospasm) CHF HTN

41

side effects of nitroglycerine

hypotension, tachycardia, throbbing HA from meningeal arterial dilation

42

MOA captopril

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

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uses of captopril

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

44

side effects of captopril

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

45

contraindications of captopril

renal insufficiency bilateral renal artery stenosis

46

MOA losartan

AII receptor blocker

47

uses of losartan

HTN CHF

48

side effects of losartan

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

49

MOA milrinone

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

uses of milrinone

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

51

side effects of milrinone

ventricular arrhythmias hypotension hepatotoxicity

52

MOA sildenafil

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

MOA digoxin

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

uses of digoxin

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

55

side effects of digoxin

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

56

contraindication of digoxin

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

57

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

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