Renal - Pharmacology

Question 1

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

Answer 1

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

Question 2

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

Answer 2

The ascending limb of the Loop of Henle

Question 3

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

Answer 3

Distal convoluted tubule

Question 4

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

Answer 4

Collecting tubule

Question 5

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

Answer 5

Collecting duct

Question 6

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

Answer 6

isotonic

Question 7

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

Answer 7

hypertonic

Question 8

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

Answer 8

hypotonic

Question 9

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

Answer 9

Proximal convoluted tubule

Question 10

What are the clinical uses of mannitol?

Answer 10

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

Question 11

What is the mechanism of action of mannitol?

Answer 11

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

Question 12

What two toxicities are associated with mannitol?

Answer 12

Pulmonary edema and dehydration

Question 13

In what two conditions is mannitol contraindicated?

Answer 13

Anuric renal failure, congestive heart failure

Question 14

What four toxicities are associated with acetazolamide?

Answer 14

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

Question 15

What is the mechanism of action of acetazolamide?

Answer 15

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

Question 16

What are the four clinical uses of acetazolamide?

Answer 16

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

Question 17

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

Answer 17

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

Question 18

Name one loop diuretic.

Answer 18

Furosemide, also known as Lasix

Question 19

What is the mechanism of action of furosemide?

Answer 19

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

Question 20

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

Answer 20

Furosemide increases calcium excretion

(remember: “loops lose calcium”)

Question 21

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

Answer 21

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

Question 22

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

Answer 22

Furosemide

Question 23

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

Answer 23

Ethacrynic acid

Question 24

Name five toxicities of ethacrynic acid.

Answer 24

Ototoxicity, hypokalemia, dehydration, and interstitial nephritis

Question 25

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

Answer 25

Glucose (hyper**G**lycemia), lipids (hyper**L**ipidemia), uric acid (hyper**U**ricemia), and calcium (hyper**C**alcemia) (remember: Hyper**GLUC**)

Question 26

What is the mechanism of action of hydrochlorothiazide?

Answer 26

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

Question 27

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

Answer 27

Furosemide; hydrochlorothiazide

Question 28

Name four clinical uses of hydrochlorothiazide.

Answer 28

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

Question 29

Name seven toxicities associated with hydrochlorothiazide.

Answer 29

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

Question 30

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

Answer 30

To treat hyperaldosteronism, potassium depletion, and congestive heart failure

Question 31

What is the mechanism of action of spironolactone?

Answer 31

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

Question 32

What is the mechanism of action of triamterene and amiloride?

Answer 32

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

Question 33

Name four potassium-sparing diuretics.

Answer 33

Spironolactone, triamterene, amiloride, and eplerenone (remember: the K⁺ **STA**ys)

Question 34

What are the toxicities of the potassium-sparing diuretics?

Answer 34

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

Question 35

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

Answer 35

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

Question 36

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

Answer 36

All of them, except for the potassium-sparing diuretics

Question 37

Which two classes of diuretics may increase the blood pH?

Answer 37

Loop diuretics and thiazides

Question 38

Which type of diuretics increases urine calcium excretion?

Answer 38

Loop diuretics

Question 39

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

Answer 39

Thiazides

Question 40

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

Answer 40

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

Question 41

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

Answer 41

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

Question 42

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

Answer 42

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

Question 43

Which two classes of diuretics may reduce the blood pH?

Answer 43

Carbonic anhydrase inhibitors and potassium-sparing diuretics

Question 44

What mechanism underlies "volume contraction alkalosis"?

Answer 44

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

Question 45

By what mechanisms do thiazide diuretics decrease urinary calcium?

Answer 45

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

Question 46

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

Answer 46

The suffix -pril

Question 47

What enzyme do captopril, enalapril, and lisinopril inhibit?

Answer 47

Angiotensin-converting enzyme

Question 48

Losartan is an example of what class of drug?

Answer 48

An angiotensin II receptor antagonist

Question 49

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

Answer 49

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)

Question 50

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

Answer 50

Angiotensin II receptor antagonists such as losartan

Question 51

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

Answer 51

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

Question 52

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

Answer 52

Hyperkalemia

Question 53

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

Answer 53

**C**ough, **A**ngioedema, **P**roteinuria, **T**aste changes, hyp**O**tension, **P**regnancy problems (fetal renal damage), **R**ash, **I**ncreased renin, and **L**ower angiotensin II

Question 54

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

Answer 54

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

Question 55

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

Answer 55

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

Question 56

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

Answer 56

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

Question 57

Clearance of what endogenous substance approximates glomerular filtration rate?

Answer 57

Creatinine

Question 58

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

Answer 58

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

Question 59

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

Answer 59

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

Question 60

What is the value of normal glomerular filtration rate?

Answer 60

Approximately 100 mL/min

Question 61

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

Answer 61

Glomerular filtration rate = K_f [(Pgc - Pbs) - (πgc - πbs)]; where K_f is 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)

Question 62

Name four conditions associated with renal papillary necrosis.

Answer 62

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