Renal Endo GU Flashcards
(157 cards)
Oligohydramnios
Potter’s Sequence: Lung hypoplasia, flat face/ears, limb defects.
Pre-renal azotemia Labs
Increased Serum BUN:CR > 15. FeNA<1%, normal Urine Anion gap, high urine osmality (kidneys are working)
Post-Renal Azotemia Labs
Initially you get absorption of BUN (cuz tubules are working thus BUN:CR 15. FeNA>2%, (cuz kidneys have broken)
Intrarenal injury labs
Elevated BUN and Cr (decreased GFR) thus Serum BUN:CR < 15. FeNA>2%, (cuz kidneys have broken) and no urine anion gap
Ischemic ATN location?
Proximal tubule and Medullar segment of ascending limb
Nephotoxic ATN location and causes?
-Proximal Tubule -Aminoglycosides, heavy metals, myoglobin (crush injury), ethylene glycol, radiocontrast
Eosiniphils in urine?
Acute interstial nephritis leading to Acute renal failure. Drug induced: PCN, NSAIDS and diuretics
Gross Hematuria and Flank pain?
Renal Papillary Necrosis. dt progression of acute interstial neprhitis. From Long term analgensic use, DM, Sickle cell trait, severe acute pylenephritis
Nephrotic Syndrome Presentation
Edema, infeciton, coagulation, poor lipid profiles from: Hypoalbunimemia, hypogammaglobulinemia, hypercoagulable state (loss of ATIII), hyperlipidemia and hypercholesterolemia (“liver trying to compensate for thin blood”)
First and second most common renal issue in SLE?
1) Diffuse proliferative glomeruloneprhitis 2) Membranous nephropahty
Renal diseases with granular immunoflourecence?
Immune complex deposition: (look for word membranous) MGN, MPGN
Puffy face in kid?
Minimal Change disease (losing albumin but no IgG due to cytokine induced effacement of podocytes)
Focal Segmental Glomerulosclerosis is associated with which populations? Positve or negative immunoflourescence?
AA, Hispanics, HIV, Herion, sickle cell disease. Negative immunoflor.
Spike and dome appearance? Where? Condition associated with?
1) Membranous nephropathy. Subepithelial side of BM. Immunocomplex dep. 2) Hep B/C, solid tumors, SLE, drugs.
Tram Track appearance? Location?
1) MPGN Type 1 > Type 2 (2 associated with C3 nephritic factor stabilizing C3 converatse = compliment acitvation). 2) Type 1 (Subendo); Type 2 (BM)
Diabetic Mechanism of Renal Damage
Non-enzymatic Glycosolation of BM allowing for hylanie arteriolosclerosis. Preferentially of efferent arteriole leading to hyperfiltration injury.
Round lesions in glomeruli? Associated with which condition? Other findings?
Kimmelstein Wilson nodules (christmas ball sclerosis) in DM. Increased PAS+ staining eosinophilic material.
Mechanism for general nephritic syndromes?
Immune complex deposition activating C5–>C5a which attrachs neutrophils causing hypercellular inflamed glomerulus
Child who was recently sick with throat infection, has risk for what renal disease? Virulence factor? Histology?
Post-strep glomerulnephritis. Group A beta hemolytic strep (pyogenes) with M protein factor (M causing N-ephritic). Supepiethelial humps
Cresents on histology indicative of? Made of what?
Rapidly progressive glomeulonephritis. Made up of inflammatory debris (macros and fibrin).
Family with hearing, vision, and hematuria
Alport syndrome, X linked, defect in Type 4 collagen. “Can’t see, can’t hear, can’t pee)
Bugs in cystitis
E coli. Staph Saprophyticus (in young sexually active females, novobiocin resistant)
Fever, flank pain, wbc casts, leukocytosis
Pyleonephritis. Ecoli, kleb, enterococcus faecalis
Cortical scarring with blunted calyces.
Chronic Pyelonephritis. Can also show thyroidization of kidney from eosinpholic proteinaceous material with waxy casts in urine