Renal Pharmacology Flashcards

(82 cards)

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
How permeable to H2O is the thick ascending limb of the loop of Henle?
It is impermeable to H2O
26
How would you expect creatinine levels to change immediately after administration of an angiotensin-converting enzyme inhibitor?
Transient elevation (decrease in efferent arteriole pressure)
27
What adverse effects can occur with angiotensin-converting enzyme inhibitors?
Cough, Angioedema, Teratogenicity (fetal renal malformations), increased Creatinine (due to decreased GFR), Hyperkalemia, Hypotension (captopril's CATCHH)
28
Where are Ca2+ and Mg2+ reabsorbed by the nephron?
The cortical portion of the thick ascending limb of the loop of Henle
29
Thiazide diuretics cannot be prescribed for patients with which allergy?
Sulfa allergy
30
How does aliskiren affect angiotensinogen, angiotensin I (AT I), and angiotensin II (AT II) levels, respectively?
Angiotensinogen increases, AT I decreases, AT II decreases
31
How can an angiotensin-converting enzyme (ACE) inhibitor cause cough and/or angioedema?
By preventing inactivation of bradykinin, a potent vasodilator (increased bradykinin levels can cause angioedema)
32
When would ethacrynic acid (a phenoxyacetic acid derivative) be used?
Diuresis in patients allergic to sulfonamide (sulfa) drugs; ethacrynic acid is a nonsulfonamide drug
33
When would ethacrynic acid (a phenoxyacetic acid derivative) be used?
Diuresis in patients allergic to sulfonamide (sulfa) drugs; ethacrynic acid is a nonsulfonamide drug
34
How does hydrochlorothiazide reduce levels of Ca2+ in the urine?
Increases distal convoluted tubule reabsorption of Ca2+
35
Why can patients with bilateral renal artery stenosis develop renal failure when taking an angiotensin-converting enzyme (ACE) inhibitor?
These patients are dependent on angiotensin II to maintain their glomerular filtration rate; ACE inhibitors lower angiotensin II levels
36
What electrolyte change would you be most worried about in a patient taking amiloride or spironolactone?
Hyperkalemia (these are both K+- sparing diuretics)
37
What mechanism underlies volume contraction alkalosis?
Volume contraction increases angiotensin II, thus increasing Na+/H+ exchange in proximal convoluted tubule (PCT) and HCO3- reabsorption
38
How do thiazide diuretics change serum Ca2+ levels?
Thiazide diuretics increase serum Ca2+ levels
39
What class of drugs do candesartan, losartan, and valsartan belong to?
Angiotensin II receptor blockers (ARBs)
40
What medication replacement would you suggest for a patient experiencing a dry cough while taking lisinopril?
An angiotensin II receptor blocker (eg, losartan) because it is less likely to cause coughing as a side effect
41
How does an angiotensin-converting enzyme (ACE) inhibitor slow diabetic nephropathy?
Decreasing intraglomerular pressure with an ACE inhibitor slows glomerular basement membrane thickening
42
What is the mechanism of action of candesartan?
Selectively blocks binding of angiotensin II to AT1 receptor
43
Why should treatment of hypertension with hydrochlorothiazide be avoided for a patient with gout and diabetes?
Hydrochlorothiazide increases levels of both uric acid and glucose, which may worsen gout and diabetes, respectively
44
Which part of the nephron is freely permeable to H2O but not to electrolytes?
The thin descending limb of the loop of Henle
45
Name 4 potassium-sparing diuretics that act on the cortical collecting tubule.
The potassium (K+)–sparing diuretics include Spironolactone, Eplerenone, Amiloride, Triamterene (Keep your SEAT)
46
Serum levels of which substances are increased as a result of the effects of thiazide diuretics such as metolazone?
Glucose (hyperGlycemia), lipids (hyperLipidemia), uric acid (hyperUricemia), and calcium (hyperCalcemia) (hyperGLUC)
47
What happens to blood pH with overuse of loop and thiazide diuretics?
Loop diuretics and thiazides raise blood pH
48
On which part of the nephron do loop diuretics act?
Loop diuretics act on the ascending limb of the loop of Henle, in both the cortex and medulla
49
What is the mechanism of action of thiazide diuretics?
Reduce the diluting capacity of the kidney nephron by inhibiting NaCl reabsorption in the early distal convoluted tubule
50
What acid-base abnormality is associated with thiazide diuretic use?
Hypokalemic metabolic alkalosis
51
NSAIDs have an inhibitory effect on what aspect of loop diuretic activity?
They inhibit PGE-induced afferent arteriole vasodilation (loop diuretics stimulate PGE release)
52
Name 2 clinical uses for mannitol.
Elevated intracranial or intraocular pressure, drug overdoses
53
How does a loop diuretic affect K+ in the serum and urine?
Lowers serum K+ and raises levels of K+ in the urine
54
Name some clinical indications for angiotensin II receptor blockers.
Heart failure, proteinuria, hypertension, chronic kidney disease with intolerance to angiotensin-converting enzyme inhibitors (cough, angioedema due to ↑ bradykinin)
55
On which segments of the nephron does acetazolamide exert its major diuretic effects?
Proximal convoluted tubule and the cortical part of the descending limb of the loop of Henle
56
Which electrolyte abnormality can cause arrhythmias in patients taking captopril?
Hyperkalemia; captopril is an angiotensin-converting enzyme (ACE) inhibitor, and hyperkalemia is an adverse effect of ACE inhibitors
57
What are some clinical uses for angiotensin-converting enzyme inhibitors?
Proteinuria, hypertension, heart failure, diabetic nephropathy, prevention of heart remodeling from chronic hypertension
58
What are the adverse effects of angiotensin II receptor blockers?
Hyperkalemia, decreased renal function, hypotension, teratogenicity
59
Secretion of K+ and H+ occurs in which part of the collecting tubule of the nephron?
The cortical part
60
What is the mechanism of action of mannitol?
As an osmotic diuretic, it increases tubular fluid osmolarity and therefore urine flow rate, leading to decreased intracranial/intraocular pressure
61
What clinical manifestation can be caused by the endocrine effects of spironolactone therapy, especially in male patients?
Gynecomastia (due to antiandrogen effects)
62
What is the clinical use for aliskiren?
Hypertension
63
How do loop diuretics dilate the afferent arterioles?
They dilate afferent arterioles by stimulating prostaglandin E (PGE) release
64
What is the effect on urinary Ca2+ excretion of loop diuretics and thiazide diuretics, respectively?
Loop diuretics increase Ca2+ in urine (decreased paracellular reabsorption); thiazides decrease Ca2+ in urine (enhanced reabsorption)
65
What is the mechanism of action of a drug such as lisinopril?
Lisinopril, an angiotensin-converting enzyme (ACE) inhibitor (like captopril, enalapril, and ramipril), inhibits ACE → decreased angiotensin II → reduced blood pressure
66
What type of drug allergy is acetazolamide associated with?
Sulfa allergy
67
What is the mechanism of action of acetazolamide?
Carbonic anhydrase inhibitor, causing self-limited NaHCO3 diuresis and a reduction in total body HCO3- stores
68
Why are angiotensin-converting enzyme (ACE) inhibitors contraindicated for patients with C1 esterase inhibitor deficiency?
ACE inhibitors must be avoided to prevent the adverse effect of angioedema (from ↑ bradykinin, a potent vasodilator)
69
What is the mechanism of aliskiren?
Direct renin inhibition, which blocks conversion of angiotensinogen to angiotensin I (aliskiren Kills Renin)
70
What is the mechanism of action of loop diuretics?
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
Name some clinical uses of K+-sparing diuretics.
Potassium depletion, hyperaldosteronism, nephrogenic diabetes insipidus (amiloride), heart failure, hepatic ascites (spironolactone), antiandrogen (spironolactone)
72
Why does a high serum renin level occur when angiotensin-converting enzyme inhibitors are administered?
Loss of negative feedback
73
How does mannitol cause diuresis?
Osmotic diuresis (similar to glucose)
74
What are 2 contraindications to mannitol use?
Anuria, heart failure
75
What is the effect of the loop diuretic furosemide on Ca2+ handling in the kidney nephron?
Furosemide increases Ca2+ excretion (Loops Lose Ca2+
76
In what part of the nephron does acetazolamide act?
Proximal convoluted tubule
77
What are the main electrolytes absorbed and secreted by the site of the nephron on which K+-sparing diuretics act?
Na+ (reabsorbed), K+ (secreted), and H+ (secreted); they act on the cortical collecting duct
78
Why are angiotensin-converting enzyme inhibitors contraindicated in pregnancy?
Because they are teratogens and can cause fetal renal malformations
79
What are the main electrolytes/molecules reabsorbed at the proximal convoluted tubule?
Na+, sugars, amino acids, and HCO3-
80
What class of diuretics acts on the boxed part of the nephron in the diagram?
Potassium-sparing diuretics (cortical collecting tubule)
81
Which class of diuretics acts on the boxed part of the nephron in the image?
Loop diuretics (thick ascending limb of loop of Henle)
82
Which class of diuretics acts on the boxed part of the nephron in the image?
Thiazide diuretics (early distal convoluted tubule)