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CVS Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

Mention diuretics utilizing organic acid secretion

A

Loop
Thiazides
CAEI

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2
Q

Mention diuretics utilizing organic base secretion

A

Amiloride

Triamterene

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3
Q

Mention diuretics utilizing glomerular filtration to reach site of action

A

Osmotic diuretics

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4
Q

Mention diuretics utilizing peritubular circulation to reach site of action

A

Spironolactone

Eplerenone

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5
Q

Mention drugs acting at proximal tubule

A

CAEI

Osmotic diuretics

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6
Q

Mention drugs acting at distal tubule

A

Thiazide (early)

Spironolactone/eplerenone (late + collecting duct)

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7
Q

Mention drugs acting as loop of Henle

A

Loop

Osmotic diuretics

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8
Q

Site of action of diuretics

A

Intra-nephron

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9
Q

Dsecribe mechanism of action of Loop diuretics

A

Inhibit 2Cl-/K+/Na+ reabsorption, leading to excretion of 20% of Na+, also dec medullary hypertonicity leading to failure if reabsorption of water by des loop of Henle & collecting duct ubder ADH effect.
Inc PGs secretion leading to VD in afferent arteriole & inc GFR

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10
Q

Effect of loop on electrolytes

A

Inhibit Ca & Mg reabsorption

Increase exchange of Na in nephron for K or H in blood in DCT, leading to hypokalemia & alkalosis

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11
Q

Application of venodilator action of loop

A

Used in acute pulmonary edema

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12
Q

Describe districution & t1/2 of loop diuretics

A

Highly bound to plasma proteins

Short t1/2

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13
Q

Describe absorption of loop diuretics

A

Frusemide absorption is variable

Bumetandine & torsedmide are almost completely absorbed

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14
Q

Describe elimination of loop diuretics

A

Frusemide is excreted unchanged by kidney upto 65%

Bumentadine & torsemide are extensively metabolised hepatically

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15
Q

Mention emergency indications of loop diuretics

A

Potent dehydrating agent in hypertensive encephalopathy & acute pulmonary edema.
Electrolyte disturbances: hypercalcemia, hyperkalemia, hypervolemic dilutional hyponatremia, distal renal tubular acidosis.

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16
Q

Mention indications of loop in edema

A

REFRACTORY edema

CHF, renal insufficiency, acute renal failure (inc blood flow), liver cirrhosis after full dose of spironolactone

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17
Q

Mention metablic & electrolyte adverse effect of loop diuretics

A 
Hypovolemia, shock, collapse, hemoconcentration & thrombosis
Hypokalemia & alkalosis
Hypocalcemia
Hyperuricemia
Hypomagnesemia
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18
Q

Mention adverse effects of loop diuretics

A

Ototoxicity (esp w aminoglycosides)
Interstitial nephritis (esp w cephalosporins)
Cross hypersensitivity with sulphonamides
Myalgia w bumetanide

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19
Q

Descibe pharmacokinetic causes of refractoriness to loop diuretics & their treatment

A
  • Defective absorption in decompensated HF (Give IV loop)
  • Defective PPB in hypoalbuminic state, mix diuretic with albumin prior to effusion
  • Dec in diuretic excretion by acid secretory system in renal impairment due to accumulation of acids (inc dose of frusemide 5 folds)
20
Q

Describe pharmacokinetic causes of refractoriness to loop & treatment

A
  1. Hypertrophy of distal tubular cells inc Na reabsorption (add thiazide)
  2. Na is reabsorbed in exchange for K in distal tubule (add spironolactone)
21
Q

Decsribe mechanism of action of thiazide

A

Inhibit active NaCl reabsorption in early part of DCT, excretion if 5-10% of Na, dec plasma volume and cardiac output
Vasodilation 2ry to dec Na level in blood vessel wall, delayed.
Initial hypovolemic response is necessary for delayed response

22
Q

Describe effect of thiazide on blood electrolyte

A

Inc Na reabsorption in exchange for K or H in late part of distal tubule, hypokalemia & alkalosis
Increase Ca reabsorption & Mg excretion

23
Q

Mention therapeutic uses of thiazide diuretics

A

Hypertension
CHF
Nephrogenic type of DI
Idiopathic hypercalcuria & Ca stones (with amyloride)

24
Q

Mechanism of action of thizaide in HTN

A

Initially diuresis —> dec blood volume
Persistent effect due to VD
Preferred in elderly dec risk of osteoporosis

25
Q

Mechanism of action of thizaide in nephrogeinc type of DI

A

Paradoxical dec in urine output with chronic uses may be due to dec PG & dec GFR thus urine volume decreases.

26
Q

Mechanism of action of thizaide in hypercalcuria

A

Dec GFR, inc Ca tubular reabsorption, dec Ca in urine.

27
Q

Mention adverse effects of thiazide

A
  1. Hypokalemia & alklaosis more than loop
  2. Hyperuricemia
  3. Hyperlipidemia inc LDL & dec HDL (coronary sclerosis)
  4. Hypomagnesemia & hyponatremia
  5. Impotence
  6. Hypersensitivity (sulphonamide derivative)
  7. Glucose intolerance (interfere with insulin secretion)
28
Q

Mention contraindications of thiazides

A

Edema of renal impairment & liver cell failure

29
Q

Mention thiazide preparation which:

  1. Can be used in renal impairment
  2. Used inHTN with less metabolic side effects
A
  1. Indapamide

2. Metolazone

30
Q

Describe the 2 mechanisms of action of K retaining diuretics & members which utilise each mechanism

A
  1. Indirect, antagonizing binding of aldosterone to its receptor, thus prevent formation of protein which stimulates Na pump (delayed, spironolactone/eplerenone)
  2. Direct, block Na channels directly (amiloride, triameterene)
31
Q

Mention effect of spironolactone on Mg

A

Inhibit its excretion

32
Q

Mention inidcations of K retaining diuretics

A

CHF, added to loop or ACEI to dec mortality (30%)
Edema of liver cirrhosis
Hypokalemia & hypomagnesemia

33
Q

GR: Spironolactone is used in edema of liver cirrhosis

A

As liver cirrhosis is associated with hyperaldosteronism, and it doesn’t cause hypokalemia or acidosis

34
Q

GR: Triameterene & amiloride are preferred in hypokalemia

A

As they are rapid & short acting, thus daily dose adujstment is possible

35
Q

GR: K sparing & losing diuretics are comines

A

To potentiate their diuretic action and anatagonizse their hypokalemic effect (more effective than K & Mg supplemets)

36
Q

Mention adverse effects of K sparing diuretics

A

Hyperkalemia & metabolic acidosis

Gynecomastia due to antiandrogenic effect of spironolactone but not eplerenone

37
Q

Describe mecahnsim of action of mannitol

A

Mannitol is freely filtered by GF and nor reabsorbed leading to inc osmotic pressure in nephron and water retenion thus urine volume is increased, the increased osmotic pressure partially prevents Na reabsorption by to much lesser extent than water.

38
Q

Mention the clinical application:

Mannitol prevents Na reabsorption to much lesser extent than H2O

A

Ineffective in edematous states with Na overload

39
Q

Describe the role of Mannitol as dehydrating agent

A
  1. Decrease intracranial pressure rapidly in cerebral edema caused by head injury or brain surgery
  2. Rapid decrease of intraocular pressure in acute congestive glaucoma
40
Q

Mannitol is used fir prophylaxis of …..

Why?

A

Acute renal failure

Maintaining high urine flow, preventing concentration of toxic agents which cause renal damage

41
Q

Describe mechanism of action of CAEI

A

Inhibit carbonic anhydrase enzyme causing inhibition of of Na/H exchange and inhibit NaHCO3 reabsorption resulting alklaline urine diuresis and metabolic acidosis due to loss of NaHCO3

42
Q

Mention inidcations of CAEI

A
  1. Emphysema & sickness of high altitude (acidosis)
  2. Epilepsy (acidosis)
  3. Glaucoma (dec formation of aqueous humour, Methozolamide)
43
Q

Mention adverse effects of CAEI

A
  1. Metabolic acidosis (drowsiness) & refractoriness to diuretic effect
  2. Calcium & phosphate stones
  3. Hypersensivity (sulphonamide derivatives)
44
Q

Mention site of vasopressin receptors

A

V1A & V2: perpherally, modulate BP & renal function reapectively
V1A & V1B: central nervous system

45
Q

Mention indications of vaptans

A

Euvolemic hyponatremia (SIADH), hypervolemic hyponatremia

46
Q

Mention drugs which cause marked reduction in GFR in renal hypoperfusion states

A

ACEI, inhibit efferent arteriole VC

NSAIDs, inhibit afferent arteriole VD

47
Q

…… toxicity is enhanced with ……

A

Lithium

Loop & thiazide

CVS Pharmacology (6 decks)

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