Pharm lecture 3 Flashcards

1
Q

osmotic diuretic

A

mannitol

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2
Q

MOA osmotic

A

filter at the glomerulus, water is held in the lumen by the osmotic effect producing diuresis

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3
Q

where does osmotic diuretic occurs

A

proximal convoluted tubule

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4
Q

main use of mannitol

A

rapid treatment of increased intracranial pressure

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5
Q

carbonic anhydrase inhibitor

A

-Acetazolamide
-Dorzolamide
-Brinzolamide
-Methozolamide

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6
Q

MOA of carbonic anhydrase inhibitor

A

inhibit the reabsorption of sodium and bicarb

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7
Q

Where is the carbonic anhydrase inhibitor

A

proximal convoluted tubule

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8
Q

therapeutic use of carbonic anhydrase inhibitor

A

metabolic alkalosis and glaucoma

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9
Q

Loop diuretics

A

-furosemide
-bumetanide
-torsemide
-ethacrynic acid

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10
Q

therapeutic use of loop diuretic

A

CHF, edema and kidney disease

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11
Q

which diuretic is the most potent

A

loop diuretic
- inhibit the reabsorption of sodium up to 25%

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12
Q

MOA of loop diuretics

A

inhibits sodium, potassium, chloride transporter and reduce sodium reabsorption in the ascending loop of hence

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13
Q

what ions are loss in the loop diuretics

A

sodium, chloride, water, potassium, magnesium, calcium

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14
Q

_____ is about 40 times more potent than ______

A
  1. bumetanide
    2.furosemide
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15
Q

which loop diuretic can be used if pt has allergy to other loop diuretics

A

ethacrynic acid

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16
Q

concern with ethacrynic acid

A

greater ototoxic than other loop diuretics

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17
Q

SE of loop diuretics

A

tinnitus (ototoxicity), limit the rate of infusion of furosemide to 4mg/min

18
Q

electrolyte disturbance in loop diuretic

A

hypokalemia, hypochloremia, hypomagnesemia, alkalosis

19
Q

adverse effect associated with hypokalemia

A

arrhythmia, potential for digoxin toxicity

20
Q

which diuretic cause increase risk of gout

A

loop diuretic

21
Q

thiazide diuretics

A

-chlorothiazide
-HCTZ
-metolazone
-chlorthalidone
-indapamide

22
Q

MOA of thiazide diuretic

A

inhibit the reabsorption of sodium and chloride ions in the distal convoluted tubules by blocking NA-Cl transporter

23
Q

therapeutic use of thiazide diuretics

A

HTN, edema, preventative treatment for hypercalcemia kidney stones

24
Q

SE of thiazide diuretics

A

hypokalemia, hypochloremia, hypomagnesemia, hyperuricemia

25
Q

Loop and thiazide

A

used together to optimize the diuretic efficacy by interfering with sodium reabsorption at the thick ascending loop and distal convoluted tubules
* used for diuretic resistance

26
Q

Potassium sparing diuretics

A

spironolactone and eplerenone
-amiloride, triamterene

27
Q

MOA of potassium sparing diuretics

A

competes with aldosterone in the collecting duct to reduce the synthesis of sodium channel resulting in loss of sodium and retention of potassium

28
Q

SE of spironolactone

A

gynecomastia

29
Q

Calcium channel MOA

A

blocks the influx of calcium in vascular smooth muscle and cardiac muscle resulting in decrease intracellular calcium

30
Q

CCB meds

A

Dihydropyridine
-amlodipine
-nifedipine
nondihydropyridines
-diltiazem
-verapamil

31
Q

therapeutic use of CCB

A

HTN, angina, arrhythmia

32
Q

which diuretic increase the risk of gout?

A

Loop diuretics

33
Q

which CCB cause bradycardia

A

Nondihydropyridines
-diltiazem, verapamil

34
Q

MOA BB

A

reduce HR and contractility by blocking the release of norepinephrine and epinephrine at b1

35
Q

mixed a and b blockers

A

block the action of norepinephrine at a-1 receptors and BB action

36
Q

therapeutic use of BB

A

HTN, angina, CHF, arrhythmia, cirrhosis

37
Q

What happens with chronic use of BB

A

increase in beta receptors, super sensitive to beta agonist action and possibly lead to MI if suddenly stop

38
Q

Meds of mixed a and B

A

carvedilol, labetalol

39
Q

Beta-blocker with ISA vs Beta blocker without ISA

A

BB with ISA doesn’t reduce the resting CO and HR as effectively as BB without ISA

40
Q

BB with ISA

A

Acebutolol, Sotalol, Pinodolol

41
Q

SE of BB

A

bradycardia, hypotension, mask signs of hypoglycemia, bronchoconstriction