Week 2

Question 1

• thick ascending limb of Henle
• Na/K/2Cl transporter inhibitor
• ex: furosemide, bumetanide, ethacrynic acid

Answer 1

loop diuretics

Question 2

• distal tubule
• Na/Cl cotransporter inhibitor
• chlorothiazide, benzothiadiazine, metolazone

Answer 2

thiazide type diuretic

Question 3

• principal cells of collecting tubule
• spironolactone antagonist of Aldosterone, others Na channel blocker
• ex: spironolactone, amiloride, tramtirene

Answer 3

K+ sparing diuretics

Question 4

• proximal tubule
• carbonic anhydrase inhibition, bicarb reabsorption reducer
• ex: acetazolamide, methazolamide

Answer 4

carbonic anhydrase inhibitor

Question 5

• all tubule segments
• create osmotic gradient
• ex: mannitol

Answer 5

osmotic diuretics

Question 6

sudden decreases in kidney function that lead to fluid imbalance, electrolyte problems, accumulation of nitrogen waste
-complications: pulm edema, hyperkalemia (arrhythmias, metabolic acidosis, confusion)

Answer 6

acute kidney injury

Question 7

decreased perfusion, no immediate damage, blood shunted away and decreases GFR
-caused by low CO, MI, dehydration, vasodilation

Answer 7

pre-renal acute kidney injury

Question 8

damage to blood vessels, glomeruli, tubules, intersititum

• large vessels: obstruction due to cholesterol, hypertrophy, tearing, clot in vein
• small vessels: glomerulonephritis, hemturia, vasculitis, HTN, clots
• tubules: acute tubular necrosis, due to nephrotoxins (myoglobin, uric acid crystals, chemo, contrast dyes)
• interstitium: infectious, allergic nephritis common with antibiotics, WBC casts

Answer 8

intra-renal acute kidney injury

Question 9

obstruction of urine, reversible

• due to stones, tumors, enlarged prostate, seen by renal US
• asymptomatic if unilateral

Answer 9

Post-renal acute kidney injury

Question 10

hyperkalemia (wide QRS), pulmonary edema unresponsive to diuretics, seizures, aspirin OD, severe metabolic acidosis

Answer 10

indications for hemodialysis

Question 11

• polyuria, dehydration, hypokalemia, glucosuria, metabolic acidosis
• caused by genetics (glycogen storage, Wilson’s), heavy metals, tetracyclines, toluene
• damage proximal tubule (Na/K/ATPase)

Answer 11

Fanconi syndrome

Question 12

• defect in chloride transporter
• polyuria, poor muscle tone, heart problems, hypokalemia, alkalosis, hypocalciuria
• overuse of furosemide diuretics, Na/K/2Cl defect

Answer 12

Bartter syndrome

Question 13

• affects distal tubule, NaCl defect, ECF contraction
• hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria
• thiazide diuretic overuse

Answer 13

Gitelman syndrome

Question 14

-overaction of Enac, ECF expansion, HTN, decreased renin-ald, metabolic alkalosis

Answer 14

Liddle syndrome

Question 15

• V2 receptor or aquaporin mutation, non repsonsive to ADH
• excessive water intake –> polyuria, dilute urine, dehydration
• caused by lithium, affects collecting duct

Answer 15

nephrogenic diabetes insipidus

Question 16

• proximal and collecting duct, decreased pH, muscle weakness, kidney stones, bone resorption, growth retardation
• mutation in Na/H exchanger or proton pumps and carbonic anhydrase

Answer 16

tubular acidosis