Renal

Question 1

Why does liver failure → kidney dysfunction? (hepatorenal syndrome)

Answer 1

failure to make urea → kidney loses a substantial contributor to its osmotic gradient → can’t reabsorb water effectively

Question 2

Why do most diuretics cause hypokalemia and alkalosis?

Answer 2

When Na+ is not reabsorbed in the tubule, the aldosterone mechanism is upregulated in the collecting duct. Here, Na+ is exchanged at the expense of H+ and K+

Question 3

What would you give to a patient with rhabdomyolysis?

Answer 3

Mannitol to help clear myoglobin

Question 4

Why are CA inhibitors diuretics?

Answer 4

Na+ has to be absorbed in exchange for H+ in the PCT; no CA → no H+ generation

Question 5

What is the effect of CA inhibitors on bicarb? What is the effect on acid/base balance?

Answer 5

without the H+ produced by CA, bicarb can’t be reabsorbed → bicarbonaturia → metabolic acidosis

Question 6

What drug would you use to treat metabolic alkalosis?

Answer 6

acetazolamide

Question 7

If a patient has both hypokalemia and acidosis, what do you suspect?

Answer 7

they are taking acetazolamide

Question 8

Why does acetazolamide cause hyperchloremia?

Answer 8

since Na+ isn’t coming in with HCO3- in prox. tubule due to CA inhibition, it comes in with Cl- later in tubule

Question 9

Which diuretic can cause renal stones? What kind?

Answer 9

Acetazolamide → ↑ urine pH → struvite stones (same kind as urease + bugs cause) and calcium oxalate stones

Question 10

What is the drug of choice for acute pulmonary edema?

Answer 10

loop diuretics

Question 11

What are two methods by which loop diuretics lower BP?

Answer 11

1. volume loss → ↓ preload

2. promote production of prostaglandins → vasodilation (not clear if arteries, veins, both but inhibited by NSAIDS)

Question 12

What parts of drug names indicate that a sulfur/sulfa group is present? Which drugs don’t have the giveaway name?

Answer 12

latin: sulfa/sulfo (eg. sulfonylureas)
greek: thia/thio (eg. propylthiouracil)
Memorize: All CA inhibitors, most loop diuretics (except EA), celecoxib

Question 13

Which loop diuretic can we give to a patient with a sulfa allergy?

Answer 13

Ethacrynic acid

Question 14

What drug can be given to help break up Ca2+ kidney stones?

Answer 14

thiazide (↓ Ca2+ in urine)

Question 15

How do thiazides act on vessels to help treat HTN? What side effect does this lead to?

Answer 15

direct-acting vasodilation (like minoxidil/diazoxide): open ATP-dependent K+ channels → hyperpolarize arteriole sm. mm. → relaxation; side effect: hyperpolarizes pancreatic cells → ↓ release of insulin → hyperglycemia and hyperlipidemia

Question 16

Why do thiazides cause hypercalcemia?

Answer 16

↓[Na+]i in tubule cells → ↑ activity of Na+i/Ca+o exchanger on BL membrane

Question 17

How do thiazides help in the treatment of nephrogenic DI?

Answer 17

add salt back into free water delivered to CCD → ↑ aldosterone → ↑ salt + H2O reabsorption

Question 18

Which diuretic would you especially want to avoid using in patients with DM?

Answer 18

thiazides → ↓ insulin release from pancreas → hyperglycemia and hyperlipidemia (DM already ↑ risk for atherosclerosis)

Question 19

When is aldosterone released?

Answer 19

Hypovolemia and hyperkalemia

Question 20

What also must be present for spirinolactone to have any physiological action?

Answer 20

aldosterone

Question 21

Why does spironolactone have endocrine side effects? How can we avoid this?

Answer 21

it is a fairly non-selective steroid receptor inhibitor (the aldosterone receptor is a steroid receptor/transcription factor for Na+ channels); use a more selective AR inhibitor = eplerenone to avoid endocrine effects s.a. gynecomastia/antiandrogen

Question 22

How do you approach questions that give you urine electrolytes and ask what drug was given (focus on diuretics)?

Answer 22

1. if ↑ Na+: diuretic; →
2. if K+ normal or low: K+ sparing; if high →
3. if HCO3- is high: acetazolamide; if low/nml →
4. if Ca2+ is low: thiazide; if high: loop