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Renal > Renal Pharmacology > Flashcards

Renal Pharmacology Flashcards

1
Q

How does acetazolamide make cystine stones less likely to form?

A

Acetazolamide alkalinizes urine

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2
Q

What are some adverse effects associated with acetazolamide?

A

Hypokalemia, formation of calcium phosphate stones, paresthesias, NH3 toxicity, sulfa allergy, proximal renal tubular acidosis

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3
Q

How do serum levels of angiotensin II (AT II) differ with angiotensin-converting enzyme (ACE) inhibitors vs angiotensin II receptor blockers (ARBs)?

A

ACE: decreased AT II levels, ARB: increased AT II levels

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4
Q

How do loop diuretics and thiazide diuretics differ in their effect on serum calcium?

A

Loop diuretics decrease serum Ca2+; thiazide diuretics increase serum Ca2+

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5
Q

On which part of the nephron do thiazides act?

A

Thiazide diuretics act on the distal convoluted tubule, located in the cortex

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6
Q

On which segments of the nephron does mannitol exert its major diuretic effects?

A

Proximal convoluted tubule and a portion of medullary part of the descending limb of the loop of Henle

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7
Q

What type of kidney stones can be adversely formed as a result of acetazolamide use?

A

Calcium phosphate stones

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8
Q

What are 3 (general) clinical uses for loop diuretics?

A

Hypertension, edematous states (heart failure, cirrhosis, nephrotic syndrome, pulmonary edema), and hypercalcemia

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9
Q

By what mechanism, involving all cells, does K+ loss lead to alkalemia?

A

K+ exits all cells (to maintain a normal serum level) in exchange for H+ entering cells (causing alkalemia) to maintain plasma concentration of K+

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10
Q

How does acetazolamide cause acidemia?

A

Causes the kidney to decrease HCO3- reabsorption, thereby decreasing the body’s pH and leading to acidemia

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11
Q

Name at least 4 toxicities associated with use of loop diuretics.

A

Ototoxicity, Hypokalemia, Hypomagnesemia, Dehydration, Allergy (sulfa), metabolic Alkalosis, Nephritis (interstitial), Gout (OHH DAANG!)

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12
Q

All diuretics cause what changes to serum and urine sodium?

A

Decrease serum sodium, increase urine sodium (strength varies based on potency of diuretic effect)

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13
Q

What is the mechanism of action of triamterene and amiloride?

A

Triamterene and amiloride block Na+ channels in the cortical collecting tubule

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14
Q

Name 2 contraindications to aliskiren use.

A

Current treatment with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (relative contraindication), pregnancy (full contraindication)

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15
Q

Hydrochlorothiazide, chlorthalidone, metolazone are examples of drugs of which class?

A

Thiazide diuretics

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16
Q

How does a low K+ state lead to alkalemia and a paradoxical aciduria?

A

H+ rather than K+ is exchanged for Na+ at the cortical collecting tubule

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17
Q

What is the mechanism by which K+-sparing diuretics cause acidemia?

A

Aldosterone blockade prevents K+ and H+ secretion; also, hyperkalemia causes K+ to enter all cells (H+/K+ exchanger) while H+ exits

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18
Q

What are the adverse effects of mannitol?

A

Dehydration, pulmonary edema, hyponatremia or hypernatremia

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19
Q

How do angiotensin II receptor blockers affect levels of renin, angiotensin I (AT I), and angiotensin II (AT II)?

A

Renin, AT I, and AT II levels are all increased

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20
Q

What adverse effects can occur with aliskiren?

A

Decreased glomerular filtration rate, hypotension, angioedema, hyperkalemia

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21
Q

What is the most concerning toxicity of ethacrynic acid, especially as compared with other loop diuretics?

A

Ethacrynic acid (a nonsulfonamide) is much more ototoxic than the sulfonamide loop diuretics

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22
Q

What are the mechanisms of action of spironolactone and eplerenone?

A

Spironolactone and eplerenone competitively antagonize the aldosterone receptor in the cortical collecting tubule

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23
Q

What are clinical uses for thiazide diuretics?

A

Hypertension, heart failure, idiopathic hypercalciuria, osteoporosis, nephrogenic diabetes insipidus

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24
Q

Name some clinical indications for acetazolamide.

A

Altitude sickness, glaucoma, idiopathic intracranial hypertension, metabolic alkalosis

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25
Q

How permeable to H2O is the thick ascending limb of the loop of Henle?

A

It is impermeable to H2O

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26
Q

How would you expect creatinine levels to change immediately after administration of an angiotensin-converting enzyme inhibitor?

A

Transient elevation (decrease in efferent arteriole pressure)

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27
Q

What adverse effects can occur with angiotensin-converting enzyme inhibitors?

A

Cough, Angioedema, Teratogenicity (fetal renal malformations), increased Creatinine (due to decreased GFR), Hyperkalemia, Hypotension (captopril’s CATCHH)

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28
Q

Where are Ca2+ and Mg2+ reabsorbed by the nephron?

A

The cortical portion of the thick ascending limb of the loop of Henle

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29
Q

Thiazide diuretics cannot be prescribed for patients with which allergy?

A

Sulfa allergy

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30
Q

How does aliskiren affect angiotensinogen, angiotensin I (AT I), and angiotensin II (AT II) levels, respectively?

A

Angiotensinogen increases, AT I decreases, AT II decreases

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31
Q

How can an angiotensin-converting enzyme (ACE) inhibitor cause cough and/or angioedema?

A

By preventing inactivation of bradykinin, a potent vasodilator (increased bradykinin levels can cause angioedema)

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32
Q

When would ethacrynic acid (a phenoxyacetic acid derivative) be used?

A

Diuresis in patients allergic to sulfonamide (sulfa) drugs; ethacrynic acid is a nonsulfonamide drug

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33
Q

When would ethacrynic acid (a phenoxyacetic acid derivative) be used?

A

Diuresis in patients allergic to sulfonamide (sulfa) drugs; ethacrynic acid is a nonsulfonamide drug

34
Q

How does hydrochlorothiazide reduce levels of Ca2+ in the urine?

A

Increases distal convoluted tubule reabsorption of Ca2+

35
Q

Why can patients with bilateral renal artery stenosis develop renal failure when taking an angiotensin-converting enzyme (ACE) inhibitor?

A

These patients are dependent on angiotensin II to maintain their glomerular filtration rate; ACE inhibitors lower angiotensin II levels

36
Q

What electrolyte change would you be most worried about in a patient taking amiloride or spironolactone?

A

Hyperkalemia (these are both K+- sparing diuretics)

37
Q

What mechanism underlies volume contraction alkalosis?

A

Volume contraction increases angiotensin II, thus increasing Na+/H+ exchange in proximal convoluted tubule (PCT) and HCO3- reabsorption

38
Q

How do thiazide diuretics change serum Ca2+ levels?

A

Thiazide diuretics increase serum Ca2+ levels

39
Q

What class of drugs do candesartan, losartan, and valsartan belong to?

A

Angiotensin II receptor blockers (ARBs)

40
Q

What medication replacement would you suggest for a patient experiencing a dry cough while taking lisinopril?

A

An angiotensin II receptor blocker (eg, losartan) because it is less likely to cause coughing as a side effect

41
Q

How does an angiotensin-converting enzyme (ACE) inhibitor slow diabetic nephropathy?

A

Decreasing intraglomerular pressure with an ACE inhibitor slows glomerular basement membrane thickening

42
Q

What is the mechanism of action of candesartan?

A

Selectively blocks binding of angiotensin II to AT1 receptor

43
Q

Why should treatment of hypertension with hydrochlorothiazide be avoided for a patient with gout and diabetes?

A

Hydrochlorothiazide increases levels of both uric acid and glucose, which may worsen gout and diabetes, respectively

44
Q

Which part of the nephron is freely permeable to H2O but not to electrolytes?

A

The thin descending limb of the loop of Henle

45
Q

Name 4 potassium-sparing diuretics that act on the cortical collecting tubule.

A

The potassium (K+)–sparing diuretics include Spironolactone, Eplerenone, Amiloride, Triamterene (Keep your SEAT)

46
Q

Serum levels of which substances are increased as a result of the effects of thiazide diuretics such as metolazone?

A

Glucose (hyperGlycemia), lipids (hyperLipidemia), uric acid (hyperUricemia), and calcium (hyperCalcemia) (hyperGLUC)

47
Q

What happens to blood pH with overuse of loop and thiazide diuretics?

A

Loop diuretics and thiazides raise blood pH

48
Q

On which part of the nephron do loop diuretics act?

A

Loop diuretics act on the ascending limb of the loop of Henle, in both the cortex and medulla

49
Q

What is the mechanism of action of thiazide diuretics?

A

Reduce the diluting capacity of the kidney nephron by inhibiting NaCl reabsorption in the early distal convoluted tubule

50
Q

What acid-base abnormality is associated with thiazide diuretic use?

A

Hypokalemic metabolic alkalosis

51
Q

NSAIDs have an inhibitory effect on what aspect of loop diuretic activity?

A

They inhibit PGE-induced afferent arteriole vasodilation (loop diuretics stimulate PGE release)

52
Q

Name 2 clinical uses for mannitol.

A

Elevated intracranial or intraocular pressure, drug overdoses

53
Q

How does a loop diuretic affect K+ in the serum and urine?

A

Lowers serum K+ and raises levels of K+ in the urine

54
Q

Name some clinical indications for angiotensin II receptor blockers.

A

Heart failure, proteinuria, hypertension, chronic kidney disease with intolerance to angiotensin-converting enzyme inhibitors (cough, angioedema due to ↑ bradykinin)

55
Q

On which segments of the nephron does acetazolamide exert its major diuretic effects?

A

Proximal convoluted tubule and the cortical part of the descending limb of the loop of Henle

56
Q

Which electrolyte abnormality can cause arrhythmias in patients taking captopril?

A

Hyperkalemia; captopril is an angiotensin-converting enzyme (ACE) inhibitor, and hyperkalemia is an adverse effect of ACE inhibitors

57
Q

What are some clinical uses for angiotensin-converting enzyme inhibitors?

A

Proteinuria, hypertension, heart failure, diabetic nephropathy, prevention of heart remodeling from chronic hypertension

58
Q

What are the adverse effects of angiotensin II receptor blockers?

A

Hyperkalemia, decreased renal function, hypotension, teratogenicity

59
Q

Secretion of K+ and H+ occurs in which part of the collecting tubule of the nephron?

A

The cortical part

60
Q

What is the mechanism of action of mannitol?

A

As an osmotic diuretic, it increases tubular fluid osmolarity and therefore urine flow rate, leading to decreased intracranial/intraocular pressure

61
Q

What clinical manifestation can be caused by the endocrine effects of spironolactone therapy, especially in male patients?

A

Gynecomastia (due to antiandrogen effects)

62
Q

What is the clinical use for aliskiren?

A

Hypertension

63
Q

How do loop diuretics dilate the afferent arterioles?

A

They dilate afferent arterioles by stimulating prostaglandin E (PGE) release

64
Q

What is the effect on urinary Ca2+ excretion of loop diuretics and thiazide diuretics, respectively?

A

Loop diuretics increase Ca2+ in urine (decreased paracellular reabsorption); thiazides decrease Ca2+ in urine (enhanced reabsorption)

65
Q

What is the mechanism of action of a drug such as lisinopril?

A

Lisinopril, an angiotensin-converting enzyme (ACE) inhibitor (like captopril, enalapril, and ramipril), inhibits ACE → decreased angiotensin II → reduced blood pressure

66
Q

What type of drug allergy is acetazolamide associated with?

A

Sulfa allergy

67
Q

What is the mechanism of action of acetazolamide?

A

Carbonic anhydrase inhibitor, causing self-limited NaHCO3 diuresis and a reduction in total body HCO3- stores

68
Q

Why are angiotensin-converting enzyme (ACE) inhibitors contraindicated for patients with C1 esterase inhibitor deficiency?

A

ACE inhibitors must be avoided to prevent the adverse effect of angioedema (from ↑ bradykinin, a potent vasodilator)

69
Q

What is the mechanism of aliskiren?

A

Direct renin inhibition, which blocks conversion of angiotensinogen to angiotensin I (aliskiren Kills Renin)

70
Q

What is the mechanism of action of loop diuretics?

A

Block cotransporters (Na+/K+/2Cl-) in thick ascending limb of loop of Henle, abolish medullary hypertonicity, prevent urine concentration, ↑PGE release (dilate afferent arterioles)

71
Q

Name some clinical uses of K+-sparing diuretics.

A

Potassium depletion, hyperaldosteronism, nephrogenic diabetes insipidus (amiloride), heart failure, hepatic ascites (spironolactone), antiandrogen (spironolactone)

72
Q

Why does a high serum renin level occur when angiotensin-converting enzyme inhibitors are administered?

A

Loss of negative feedback

73
Q

How does mannitol cause diuresis?

A

Osmotic diuresis (similar to glucose)

74
Q

What are 2 contraindications to mannitol use?

A

Anuria, heart failure

75
Q

What is the effect of the loop diuretic furosemide on Ca2+ handling in the kidney nephron?

A

Furosemide increases Ca2+ excretion (Loops Lose Ca2+

76
Q

In what part of the nephron does acetazolamide act?

A

Proximal convoluted tubule

77
Q

What are the main electrolytes absorbed and secreted by the site of the nephron on which K+-sparing diuretics act?

A

Na+ (reabsorbed), K+ (secreted), and H+ (secreted); they act on the cortical collecting duct

78
Q

Why are angiotensin-converting enzyme inhibitors contraindicated in pregnancy?

A

Because they are teratogens and can cause fetal renal malformations

79
Q

What are the main electrolytes/molecules reabsorbed at the proximal convoluted tubule?

A

Na+, sugars, amino acids, and HCO3-

80
Q

What class of diuretics acts on the boxed part of the nephron in the diagram?

A

Potassium-sparing diuretics (cortical collecting tubule)

81
Q

Which class of diuretics acts on the boxed part of the nephron in the image?

A

Loop diuretics (thick ascending limb of loop of Henle)

82
Q

Which class of diuretics acts on the boxed part of the nephron in the image?

A

Thiazide diuretics (early distal convoluted tubule)

Renal (4 decks)

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