Renal pre-exam 4

jdlevenson's version from 2015-05-07 15:32

Lecture 15

Question Answer
Musty urinePhenylketonuria/ PKU.
MyoglobinuriaRhabdomyolysis. Red urine.
Dilute specific gravity1.003 (dilute)
Concentrated specific gravity1.030 (concentrated)
Isosthenuria specific gravity1.010
Urine pH 4.5 – 7.8. If higherUrea splitting (urea -> ammonia) bacteria. Proteus or Klebsiella. OR distal RTA.
In super acidic urine what can formUric acid.
In super alkaline urine what can formCaP, struvite.
Urobilinogen formed whereSI and excreted in stool and urine from bile.
Normally bilirubin will be () in urine whereas urobilinogen will be ()Negative urinary bilirubin and positive urobilinogen.
LE from fromLysed granulocytes.
Nitrates concerted to nitrite by what bacteriaGram negative.
Ketones in urine reflectFasting state/ starvation, alcoholic ketoacidosis, DKA.
Normal protein excretion per day30-150 mg/day. 300-500 = proteinuria.
Renal tubular cell in urineATN.
Multi-lobar nuclei vs Unliobar nuclei in urineMulti-lobar – WBC, Pyuria. Unilobar – renal tubular epithleial cells.
Culture negative pyuriaINTERSTITIAL NEPHRITIS.
WBC Casts inPyelonephritis and intersitital nephritis.
Broad waxy castsDilated atrophic tubules. CKD.
Maltese cross/ fatty castsnephrotic syndrome.
Oxalate Crystals in setting of metabolic acidosis and AKIEthylene glycol.
Treating uric acid stonesAlkalinize urine.

Lecture 19

Question Answer
ADPKD geneticsPKD1* and PKD2
ADPKD prognosis50% develop end stage renal failure; 10% of all dialysis pts
ADPKD non kidney manifestationsIntracranial arterial aneurysms and cysts in liver and or pancreas.
ADPKD everyone will get bilateral cysts by age30. Diagnose with imaging.
ADPKD where in nephronEvery segment of nephron but do not communicate with rest of nephron.
Alport extra renalSensorineural hearing loss. Eye changes (protrusion of anterior portion of lens).
AlportX-linked. Collagen IV Alpha 5. Can be AR or AD.
Alport presentationRecurrent gross hematuria. By age 16-35.
Question Answer
Alport on pathLamellated thickened BM -> progressive glomerulosclerosis from abnormal BM assembly.
Tubulo-interstitial diseaseTubules, no proteinuria -> fibrosis/ collagen in interstitium. Increased space between tubules.
Renal failure with normal proteinuria?Tubulointerstitial disease. <1 g/ day.
Question Answer
AIN classic signs and symptomsRash, eosinophilia, fever. Eosinohpiliuria, WBC and sometimes RBC in urine as well and maybe acid-base or electrolyte abnormalities.
AIN usually allergic. Most often fromAntibiotics (beta lactams, sulfonamides, rifampin), NSAIDs, Sulfa-containing drugs. Also infections – bacteria, viruses.
ATN will have dark brown granular casts AND ?Evidence of tubular dysfunction - inability to concentrate urine, etc. Also mimnimal proteinuria and decreased urine output.
Drug induced ATNAminoglycosides, Amphotericin B, antivirals. CONTRAST.
Aminoglycoside risk of ATNIncreases with cumulative dose. Much higher if > 2 weeks.
Amphotericin B and AKI50% pts have acute renal failure. REVERSIBLE. A/w mortality. Electrolyte deranagements such as non-anion gap metabolic acidosis. May be from deoxycholate. Inserts into cell membranes and increases cell permeability.
Risk of contrast associated ARF is worse inDM and underlying renal insufficiency. Advanced heart failure. More ionic contrast.
Contrast associated ARF is thankfullySelf-limited. Peaks a few days after administration.
HIV med that causes ARFIndinavir. Poor solubility. Nephrolithiasis, AKI, Chronic.