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Cardiology > Renal Agents > Flashcards

Renal Agents Flashcards

1
Q

Filter approximately 1300 mL blood per min or 700 mL plasma

A

Kidneys

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2
Q

In the kidney, the peritubular capillary network surrounds the

A

Convoluted tubules

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3
Q

Passes close to the glomerulus between the afferent and efferent arterioles

A

Distal Convoluted Tubule

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4
Q

Osmotic diuretics that promote water retention in the tubular fluid

A

Mannitol or glucose

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5
Q

Water permeability in collecting duct is controlled by

A

ADH

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6
Q

Inhibits ADH secretion by the pituitary

A

Alcohol

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7
Q

A carbonic anhydride inhibitor that blocks sodium bicarbonate reabsorption, resulting in decrease in NaCl reabsorption

A

Acetazolamide

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8
Q

Acetazolamide functions on the

A

Proximal tubule

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9
Q

Osmotic agents act on the thin descending limb to promote

A

Water retention

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10
Q

Block the NKCC2 cotransporter

-Act on thick ascending limb

A

Loop diuretics (i.e. furosemide)

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11
Q

Relatively impermeable to water

A

DCT

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12
Q

Blocks the electrically neutral Na+/Cl- cotransporter NCC

A

Thiazides diuretics

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13
Q

Reabsorption in DCT is via parathyroid hormone regulated apical Ca2 channel and a basolateral Na+/Ca2+ exchanger

A

Ca2+

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14
Q

The site of mineralcorticoid and ADH action

A

Collecting tubule

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15
Q

The major site of K+ secretion

A

Collecting tubule

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16
Q

Sodium bicarbonate reabsorption by the PCT is initiated by the action of the

-Allows Na+ to enter the cell

A

Na+/H+ exchanger NHE3

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17
Q

Inhibits carbonic anhydride and acts predominantly in the proximal tubule by blocking sodium bicarbonate reabsorption

A

Acetazolamide

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18
Q

The bicarbonate loss from carbonic anhydride inhibitors can cause a

A

Hyperchloremic metabolic acidosis

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19
Q

The portion of acetazolamide that can cause allergic reactions, bone marrow depression, and skin toxicity

A

Sulfonamide group

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20
Q

Carbonic anhydride inhibitors should be avoided in patients with

A

Hepatic Cirrhosis

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21
Q

Used to treat glaucoma, acute mountain sickness, metabolic alkalosis, and to alkalinize the urine

A

C.A. Inhibitors

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22
Q

Raise CO2 content of tissues, which in turn stabilizes deoxyhemoglobin

-Useful for counteracting acute mountain sickness

A

C.A. Inhibitors

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23
Q

Osmotic diuretics such as mannitol act in the

-Where the cells are freely permeable to water

A

PT and Descending limb of Henle’s loop

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24
Q

Causes loss of water, reduced intracellular volume, and hypernatremia risk

A

Mannitol

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25
Q

Function to increase water excretion in preference to Na+ excretion

  • Reduces intracranial and intraocular pressure
  • Promotes prompt removal of renal toxins
A

Osmotic Diuretics

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26
Q

Water expansion into the extracellular compartment causing hyponatremia

-Effect of osmotic diuretic toxicity

A

Extracellular volume expansion

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27
Q

Can complicate congestive heart failure and may produce florid pulmonary edema

A

Extracellular Volume Expansion

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28
Q

Excessive use of osmotic diuretics w/out carefully monitoring serum ion composition and fluid balance can lead to

A

Dehydration and Hypernatremia

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29
Q

Loop diuretics act in the loop of Henle and block the

A

NKCC2 cotransporter

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30
Q

Loop diuretics cause an increase in the excretion of

A

Mg2+ and Ca2+

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31
Q

Furosemide, bumetanide, ethacrynic acid, and torsemide are the

A

Loop Diuretics

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32
Q

The most effective diuretics currently available

A

Loop diuretics

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33
Q

A phenoxyacetic acid derivative containing an adjacent ketone and methylene group

A

Ethacrynic Acid

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34
Q

What is the duration of effect for

  1. ) Furosemide
  2. ) Torsemide
A
  1. ) 2-3 hours

2. ) 4-6 hours

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35
Q

Block tubuloglomerular feedback by inhibiting salt transport into the macula densa

A

Loop Diuretics

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36
Q

Induce synthesis of renal prostaglandins by expressing COX-2

A

Loop Diuretics

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37
Q

Inhibit cyclooxygenase and can reduce prostaglandin synthesis in the kidney and interfere with loop diuretics

38
Q

Can both relieve pulmonary congestion and reduce LV filling pressures in CHF before a measurable increase in urinary output occurs

A

Furosemide and ethacrynic acid

39
Q

Most important indications are acute pulmonary edema, other edematous conditions, and acute hypercalcemia

A

Loop Diuretics

40
Q

A major adverse effect of loop diuretics is

A

Hypokalemic metabolic alkalosis

41
Q

Can also cause impaired carbohydrate tolerance, hyperglycemia, dehydration, and hyponatremia

A

Loop diuretics

42
Q

Both loop diuretics and thiazides can cause

A

Hypokalemic metabolic alkalosis

43
Q

Is mostly just used for patients sensitive to sulfonamides

A

Ethacrynic acid

44
Q

Furosemide, bumetanide, and torsemide may demonstrate cross reactivity in patients who are sensitive to other

A

Sulfonamides

45
Q

Diuretics of the thiazides class block the electrically neutral

A

NCC transporter

46
Q

NCC is the gene mutated in

A

Gitelman’s syndrome

47
Q

Enhance Ca2+ reabsorption

48
Q

Include hydrochlorothiazide, indapamide, chlorthalidone, and metolazone

49
Q

Some members of the thiazides retain significant

A

CA inhibitor activity

50
Q

Thiazides can be inhibited by

51
Q

Similar to CA inhibitors, thiazides has unsubstituted

A

Sulfonamide group

52
Q

Thiazides that is less lipid soluble and must be given in relatively large doses

-Slowly absorbed and has longer duration of action

53
Q

Indicated for hypertension, heart failure, nephrolithiasis, and nephrogenic DI

54
Q

In nephrogenic DI, reduce plasma volume to lower GFR which enhances proximal tubule reabsorption of NaCl and water

-Causes decreased delivery of fluid to the diluting segments

55
Q

Can cause hypokalemic metabolic alkalosis and hyperuricemia

56
Q

Also cause impaired carbohydrate tolerance, hyperlipidemia, hyponatremia, and allergic reactions

57
Q

Cause a 5-15% increase in serum cholesterol and increase LDLs

58
Q

An important adverse effect of thiazides. Due to a combination of hypokalemic-induced elevation of ADH, reduction in diluting capacity of kidney, and increased thirst

A

Hyponatremia

59
Q

Where we see 2-5% of NaCl reabsorption

-Determines the final Na+ concentration in the Urine

A

Late Distal Tubule and Collecting Duct

60
Q

The late distal tubule and collecting duct is the site of action for

A

Aldosterone

61
Q

Major site of K+ secretion and acidification of urine

A

Late distal tubule and collecting duct

62
Q

Major sites of Na+, K+, and H2O (ADH-sensitive) transport

A

Principal cells

63
Q

Diuretics that increase Na+ delivery to the late distal tubule and collecting duct will therefore increase secretion of

64
Q

Primary sites of proton secretion

A

Late distal tubule and collecting duct intercalated cells

65
Q

Increases expression and delivery of apical membrane channels and the basolateral Na+/K+ ATPase

A

Aldosterone

66
Q

Competitive antagonists of the aldosterone receptor

-“Potassium-sparing Diuretics”

A

Spironolactone and Eplerenone

67
Q

More selective and has less side effects

A

Eplerenone

68
Q

Block the ENaC Na+ channel in the apical cells of the collecting tubule

A

Triamterene and amiloride

69
Q

Also can be inhibited by NSAIDs

A

Triamterene and Spironolactone

70
Q

Promoted by hyperkalemia and high levels of AN-II

A

Aldosterone release

71
Q

Has high levels in cirrhosis w/ ascites, renalvascular hypertension, adrenal tumors, and cardiac or nephrotic edema

A

Aldosterone

72
Q

Most useful in states of mineralocorticoid excess, due either to primary hypersecretion or to secondary aldosteronism

A

Potassium sparing diuretics

73
Q

Can be used to treat hypertension in Liddle’s Syndrome

A

Triamterene and amiloride

74
Q

Can cause hyperkalemia

A

Potassium-sparing diuretics

75
Q

The risk of this complication is greatly increased in the presence of renal disease or other drugs that reduce renin

A

Hyperkalemia from aldosterone

76
Q

By inhibiting H+ secretion in parallel with K+ secretion, the K+-sparing diuretics can cause

A

Hyperchloremic metabolic acidosis

77
Q

Synthetic steroids may cause endocrine abnormalities by effects on other steroid receptors. One of these effects is

A

Gynecomastia

78
Q

These endocrine abnormalities can be avoided by using

A

Eplerenone

79
Q

Patients with renal insufficiency are especially vulnerable and should rarely be treated with

A

Aldosterone antagonists

80
Q

Patients with liver disease may have impaired metabolism of

A

Triamterene and spironolactone

81
Q

Strong CYP3A4 inhibitors (ketoconazole and itraconazole) can markedly increase blood levels of

A

Eplerenone

82
Q

Secreted by the posterior pituitary whenever the cardiovascular system is challenged by hypovolemia and/or hypotension

83
Q

Increases the permeability of principal cells to water by binding to V2 receptors, thus increasing the number of water channels (AQP2) on apical surface

84
Q

The cell that responds to ADH is the same cell that responds to aldosterone. This is the

A

Principal Cell

85
Q

ADH receptor antagonists

86
Q

Used to treat euvolemic hyponatremia

87
Q

A non-selective antagonist at V1a and V2 receptors

A

Conivaptan

88
Q

Oral agents selectively active against the V2 receptor

A

Lixivaptan and tolvaptan

89
Q

Both appear to reduce the formation of cAMP in response to ADH and also interfere w/ cAMP in collecting tubule cells

A

Li+ and Demeclocyline

90
Q

Are indicated to treat SIADH

A

ADH antagonists

91
Q

If serum Na+ is not monitored closely, ADH antagonists can cause severe hypernatremia and

A

Nephrogenic DI

92
Q

If Li+ is being used for an effective disorder, than we can treat the nephrogenic DI with

A

Thiazides diuretic or amiloride

Cardiology (27 decks)

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