Renal Flashcards
Why does liver failure → kidney dysfunction? (hepatorenal syndrome)
failure to make urea → kidney loses a substantial contributor to its osmotic gradient → can’t reabsorb water effectively
Why do most diuretics cause hypokalemia and alkalosis?
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+
What would you give to a patient with rhabdomyolysis?
Mannitol to help clear myoglobin
Why are CA inhibitors diuretics?
Na+ has to be absorbed in exchange for H+ in the PCT; no CA → no H+ generation
What is the effect of CA inhibitors on bicarb? What is the effect on acid/base balance?
without the H+ produced by CA, bicarb can’t be reabsorbed → bicarbonaturia → metabolic acidosis
What drug would you use to treat metabolic alkalosis?
acetazolamide
If a patient has both hypokalemia and acidosis, what do you suspect?
they are taking acetazolamide
Why does acetazolamide cause hyperchloremia?
since Na+ isn’t coming in with HCO3- in prox. tubule due to CA inhibition, it comes in with Cl- later in tubule
Which diuretic can cause renal stones? What kind?
Acetazolamide → ↑ urine pH → struvite stones (same kind as urease + bugs cause) and calcium oxalate stones
What is the drug of choice for acute pulmonary edema?
loop diuretics
What are two methods by which loop diuretics lower BP?
- volume loss → ↓ preload
2. promote production of prostaglandins → vasodilation (not clear if arteries, veins, both but inhibited by NSAIDS)
What parts of drug names indicate that a sulfur/sulfa group is present? Which drugs don’t have the giveaway name?
latin: sulfa/sulfo (eg. sulfonylureas)
greek: thia/thio (eg. propylthiouracil)
Memorize: All CA inhibitors, most loop diuretics (except EA), celecoxib
Which loop diuretic can we give to a patient with a sulfa allergy?
Ethacrynic acid
What drug can be given to help break up Ca2+ kidney stones?
thiazide (↓ Ca2+ in urine)
How do thiazides act on vessels to help treat HTN? What side effect does this lead to?
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
Why do thiazides cause hypercalcemia?
↓[Na+]i in tubule cells → ↑ activity of Na+i/Ca+o exchanger on BL membrane
How do thiazides help in the treatment of nephrogenic DI?
add salt back into free water delivered to CCD → ↑ aldosterone → ↑ salt + H2O reabsorption
Which diuretic would you especially want to avoid using in patients with DM?
thiazides → ↓ insulin release from pancreas → hyperglycemia and hyperlipidemia (DM already ↑ risk for atherosclerosis)
When is aldosterone released?
Hypovolemia and hyperkalemia
What also must be present for spirinolactone to have any physiological action?
aldosterone
Why does spironolactone have endocrine side effects? How can we avoid this?
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
How do you approach questions that give you urine electrolytes and ask what drug was given (focus on diuretics)?
- if ↑ Na+: diuretic; →
- if K+ normal or low: K+ sparing; if high →
- if HCO3- is high: acetazolamide; if low/nml →
- if Ca2+ is low: thiazide; if high: loop
