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piggy > Renal - Pharmacology > Flashcards

Renal - Pharmacology Flashcards

1
Q

On what three segments of the kidney nephron do osmotic agents such as mannitol exert their diuretic effects?

A

Proximal convoluted tubule, thin descending loop of Henle, and collecting duct

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2
Q

On what segment of the kidney nephron do loop agents such as furosemide exert their diuretic effects?

A

The ascending limb of the Loop of Henle

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3
Q

On what segment of the kidney nephron do thiazides exert their diuretic effects?

A

Distal convoluted tubule

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4
Q

On what segment of the kidney nephron do potassium-sparing agents exert their diuretic effects?

A

Collecting tubule

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5
Q

On what segment of the kidney nephron do antidiuretic hormone antagonists exert their effects?

A

Collecting duct

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6
Q

In the proximal convoluted tubule, the filtrate is _____ (hypotonic/isotonic/hypertonic) to blood plasma.

A

isotonic

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7
Q

In the thin descending limb of the loop of Henle, the filtrate is _____ (hypotonic/isotonic/hypertonic) to blood plasma.

A

hypertonic

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8
Q

In the thick ascending limb of the loop of Henle and the distal convoluted tubule, the filtrate is _____ (hypotonic/isotonic/hypertonic) to blood plasma.

A

hypotonic

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9
Q

On what segment of the kidney nephron does the diuretic acetazolamide exert its effects?

A

Proximal convoluted tubule

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10
Q

What are the clinical uses of mannitol?

A

To treat shock, drug overdose, and elevated intracranial/intraocular pressure

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11
Q

What is the mechanism of action of mannitol?

A

Mannitol acts as an osmotic diuretic, increasing osmolarity within the renal tubules producing increased urine volume

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12
Q

What two toxicities are associated with mannitol?

A

Pulmonary edema and dehydration

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13
Q

In what two conditions is mannitol contraindicated?

A

Anuric renal failure, congestive heart failure

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14
Q

What four toxicities are associated with acetazolamide?

A

Hyperchloremic metabolic acidosis (ACIDazolamide causes ACIDosis), neuropathy, ammonia toxicity, and sulfa allergic reactions

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15
Q

What is the mechanism of action of acetazolamide?

A

It acts as a carbonic anhydrase inhibitor, causing self-limited sodium bicarbonate diuresis and a reduction in total-body bicarbonate stores

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16
Q

What are the four clinical uses of acetazolamide?

A

To treat glaucoma, metabolic alkalosis, and altitude sickness, and to cause urinary alkalinization

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17
Q

What are three (general) the clinical uses of furosemide?

A

To treat edematous states (congestive heart failure, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, and hypercalcemia

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18
Q

Name one loop diuretic.

A

Furosemide, also known as Lasix

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19
Q

What is the mechanism of action of furosemide?

A

It inhibits the sodium-potassium-chloride cotransport system in the thick ascending limb of the loop of Henle, thereby abolishing the hypertonicity of the medulla and preventing the concentration of urine

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20
Q

What is the effect of the diuretic furosemide on calcium handling in the kidney nephron?

A

Furosemide increases calcium excretion (remember: “loops lose calcium”)

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21
Q

Name six toxicities associated with use of loop diuretics; use the mnemonic “OH DANG!”

A

Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), and Gout

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22
Q

Ethacrynic acid has a mechanism of action similar to which other drug?

A

Furosemide

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23
Q

Which loop diuretic is used to diurese patients who are allergic to sulfa drugs?

A

Ethacrynic acid

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24
Q

Name five toxicities of ethacrynic acid.

A

Ototoxicity, hypokalemia, dehydration, and interstitial nephritis

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25
Q

Serum levels of which substances are increased as a result of the effects of hydrochlorothiazide?

A

Glucose (hyperGlycemia), lipids (hyperLipidemia), uric acid (hyperUricemia), and calcium (hyperCalcemia) (remember: HyperGLUC)

26
Q

What is the mechanism of action of hydrochlorothiazide?

A

It reduces the diluting capacity of the kidney nephron by inhibiting sodium chloride reabsorption in the early distal tubule

27
Q

_____ (Furosemide/Hydrochlorothiazide) increases calcium excretion, whereas _____ (furosemide/hydrochlorothiazide) decreases calcium excretion.

A

Furosemide; hydrochlorothiazide

28
Q

Name four clinical uses of hydrochlorothiazide.

A

To treat hypertension, congestive heart failure, idiopathic hypercalciuria, and nephrogenic diabetes insipidus

29
Q

Name seven toxicities associated with hydrochlorothiazide.

A

Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, and sulfa allergy

30
Q

What are the three clinical uses of potassium-sparing diuretics?

A

To treat hyperaldosteronism, potassium depletion, and congestive heart failure

31
Q

What is the mechanism of action of spironolactone?

A

It exerts its effects by competitively antagonizing the aldosterone receptor in the cortical collecting tubule

32
Q

What is the mechanism of action of triamterene and amiloride?

A

They exert their effects by blocking sodium channels in the cortical collecting tubule

33
Q

Name four potassium-sparing diuretics.

A

Spironolactone, triamterene, amiloride, and eplerenone (remember: the K+ STAys)

34
Q

What are the toxicities of the potassium-sparing diuretics?

A

Hyperkalemia (leading to arrhythmias) and endocrine effects with spironolactone (gynecomastia and antiandrogen effects)

35
Q

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

A

Hyperkalemia leads to potassium entering all cells via the H+/K+exchanger in exchange for H+exiting cells

36
Q

Which diuretics increase potassium excretion in the urine, thus causing a potential decrease in serum potassium?

A

All of them, except for the potassium-sparing diuretics

37
Q

Which two classes of diuretics may increase the blood pH?

A

Loop diuretics and thiazides

38
Q

Which type of diuretics increases urine calcium excretion?

A

Loop diuretics

39
Q

Which types of diuretic reduce urine calcium excretion and increases serum calcium?

A

Thiazides

40
Q

What is the mechanism by which carbonic anyhydrase inhibitors cause acidemia?

A

Acetazolamide causes the kidney to excrete more bicarbonate, decreasing the body’s pH

41
Q

By what two mechanisms does potassium loss caused by loop diuretics and thiazide diuretics lead to alkalosis?

A

Potassium loss leads to potassium ions exiting the cells in exchange for hydrogen ions entering the cell, leading to alkalosis; also, in a low-potassium state, hydrogen ions (as opposed to potassium ions) are exchanged for sodium ions in the cortical collecting tubule, which leads to alkalosis

42
Q

By what mechanism do loop diuretics cause increased excretion of calcium in the urine?

A

Loop diuretics abolish the lumen-positive potential in the thick ascending limb of the loop of Henle, causing decreased paracellular calcium reabsorption, leading to increased urinary calcium and hypocalcemia

43
Q

Which two classes of diuretics may reduce the blood pH?

A

Carbonic anhydrase inhibitors and potassium-sparing diuretics

44
Q

What mechanism underlies “volume contraction alkalosis”?

A

Volume contraction leads to increased angiotensin II, which causes an increased hydrogen-sodium exchange in the proximal tubule and increased bicarbonate reabsorption

45
Q

By what mechanisms do thiazide diuretics decrease urinary calcium?

A

Volume depletion leads to enhanced paracellular calcium resorption in the loop of Henle; the increased sodium gradient in the tubule leads to increased sodium/calcium exchange and increased calcium resorption

46
Q

The names of angiotensin-converting enzyme inhibitors typically end in what suffix?

A

The suffix -pril

47
Q

What enzyme do captopril, enalapril, and lisinopril inhibit?

A

Angiotensin-converting enzyme

48
Q

Losartan is an example of what class of drug?

A

An angiotensin II receptor antagonist

49
Q

Why is renin released from the kidneys when angiotensin-converting enzyme inhibitors are used?

A

There is a loss of feedback inhibition (ie, the lack of angiotensin II production and subsequent aldosterone release results in a drop in blood pressure, causing renin release)

50
Q

What class of diuretics can be used in place of angiotensin-converting enzyme inhibitors if cough is a problematic adverse effect?

A

Angiotensin II receptor antagonists such as losartan

51
Q

What is the mechanism by which angiotensin-converting enzyme inhibitors can cause angioedema?

A

Angiotensin-converting enzyme inhibitors prevent the inactivation of bradykinin, a potent vasodilator; increased bradykinin levels can lead to angioedema in susceptible individuals

52
Q

What electrolyte disturbance can result from angiotensin-converting enzyme inhibitor toxicity?

A

Hyperkalemia

53
Q

Name the adverse effects of angiotensin-converting enzyme inhibitors; use the mnemonic CAPTOPRIL.

A

Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, and Lower angiotensin II

54
Q

Angiotensin-converting enzyme inhibitors can cause acute renal failure (acute kidney injury) in patients with which condition?

A

Bilateral renal artery stenosis; these patients are dependent on angiotensin II to maintain their glomerular filtration rate

55
Q

What are three clinical uses of angiotensin-converting enzyme inhibitors?

A

To treat hypertension and congestive heart failure and to slow the progression of diabetic renal disease

56
Q

What exogenous substance can be used to calculate the glomerular filtration rate and why?

A

Inulin, because it is freely filtered and is neither reabsorbed nor secreted

57
Q

Clearance of what endogenous substance approximates glomerular filtration rate?

A

Creatine

58
Q

How is the glomerular filtration rate calculated if inulin is used?

A

Glomerular filtration rate = the urine concentration of inulin times the urine flow rate divided by the plasma inulin concentration (Uinulin × V/Pinulin)

59
Q

Creatinine clearance slightly _____ (overestimates/underestimates) the glomerular filtration rate because creatinine is _____ (secreted/reabsorbed) by the renal tubules.

A

Overestimates; secreted; the plasma concentration of creatinine is slightly lower than it would be from filtration alone

60
Q

What is the value of normal glomerular filtration rate?

A

Approximately 100 mL/min

61
Q

What is the formula for calculating the glomerular filtration rate that relates glomerular capillary and Bowman’s space pressures?

A

Glomerular filtration rate = Kf[(Pgc - Pbs) - (πgc - πbs)]; where Kfis the filtration constant; Pgc is glomerular capillary pressure; Pbs is Bowman’s space pressure; πgc is glomerular capillary colloid osmotic pressure; and πbs is Bowman’s space colloid osmotic pressure (normally close to a value of 0)

62
Q

Name four conditions associated with renal papillary necrosis.

A

Diabetes mellitus, acute pyelonephritis, chronic phenacetin use, sickle cell anemia

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