Renal from Review

jdlevenson's version from 2015-05-07 14:28


Question Answer
Most potent loop diureticFurosemide/ loop diuretic.
Loop diuretic clinical indicationsEdema/ volume removal, CHF, HTN, Hyperkalemia, Hypercalcemia (Ca relies on ROMK)
AmiolorideK+ sparing diuretic; ENaC inhibitor
Best loop diuretic for HTNHydrochlorothiazide.
Hydrochlorothiazide usesHTN, edema, nephrogenic DI
HTZ a/eHypokalemia, metabolic alkalosis, hypercelcemia; hyponatremia
Amioloride usesLiddle’s; with a loop diuretic to spare K
Spironolactone side effectHigh K+, metabolic acidosis, gynecomastia
Mannitol usesIncreased ICP, fulminant hepatic failure; NOT CHF.
Hypothyroid leads toEuvolemic hyponatremia.
Psychogenic PolydipsiaHyponatremia with low Una and low Uosm.
Pseudohyponatremia may be fromHyperlipidemia and or Multiple Myeloma.
Hypovolemic Hyponatremia is fromGI losses or polyuria.
Hypervolemic hyponatremia may be fromNephrotic syndrome, cirrhosis and CHF.
Water diuresis may be fromCentral DI, nephrogenic DI or psychogenic polydipsia.
Solute diuresis may be fromHyperglycemia and post-obstructive and renal failure.
Common to all nephrotic syndromes under microscopeFused and effaced foot processes.
What cause intracellular shifts of KInsulin, alkalosis, Beta2agonists.
What causes GI losses of potassiumDiarrhea, diuretics
What causes extracellular shifts of KBeta antagonists, acidosis, rhabdomyolysis.
How do beta receptors increase K+ within cellsBeta agonists increase Na/K ATPase
To stabilize hyperkalemiaCaGluconate, get K into cell (insulin, beta 2 agonists), Bicarb, Kayexalate.
Cl- sensitive metabolic alkalosis (Ucl < 15), three causesContraction alkalosis (loss of acid; vomiting) and Renal causes (diuresis) or Bartter syndrome (like Furosemide)
Cl- resistant metabolic alkalosis, UCl?>20
Cl- resistant metabolic alkalosis causesHigh BP? RAS, FMD, Renin secreting tumor, Licorice/ Syndrome of Apparent Mineralocorticoid Excess, Cushing’s. Normal BP? Exogenous bicarbonate/ milk alkali.
Cl- sensitive metabolic alkalosis, UCl?<15.
Normal anion gap acidosisRenal Tubular Acidosis or Diarrhea. HYPERCHLOREMIC.
Prerenal AKI, Uosm?High because reabsorbing as much as possible.

Section 2

Question Answer
Renal Tubular AcidosisA disorder of the renal tubules that leads to normal anion gap (hyperchloremic) metabolic acidosis.
Renal Tubular Acidosis, type 1, pH? where?Distal, urine > 5.5. Defect in ability of α intercalated cells to secrete H+ -> no new HCO3− is generated -> metabolic acidosis. Associated with hypokalemia, increased risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover).
Renal Tubular Acidosis, type 1, causessjogrens, lupus, sickle cell disease, lithium, amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract.
Renal Tubular Acidosis, type 1, treatmentBicarb. Potassium.
Renal Tubular Acidosis, type 2, pH?urine <5.5, proximal
Renal Tubular Acidosis, type 2, where?Defect in PCT HCO3− reabsorption-> increased excretion of HCO3− in urine and subsequent metabolic acidosis. Urine is acidified by α-intercalated cells in collecting tubule. Associated with hypokalemia, increased risk for hypophosphatemic rickets.
Renal Tubular Acidosis, type 2, causes?Causes: Fanconi syndrome and carbonic anhydrase inhibitors.
Renal Tubular Acidosis, type 4, ph?urine <5.5
Renal Tubular Acidosis, whatHypoaldosteronism -> hyperkalemia -> decreased NH3 synthesis in PCT -> decreased NH4+ excretion.
Renal Tubular Acidosis type 4 causesDecreased aldosterone production*** (e.g., diabetic hyporeninism*****, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance (e.g., K+-sparing diuretics, nephropathy due to obstruction, TMP/SMX.