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77 Cards in this Set
- Front
- Back
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thick tubules are probbaly more proximle bc of brush border (left side of pic)
note how tubules are back to back; this is good; as you get disease they start to drop out and get farther apart |
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mesangium; produce basement membrane matrix; support glomeruli;
podocytes are on the outside of the loops notice symmetry; no fibrous deposits on one side vs the other not cellularity, not a lot of touching between nuclei (if they were = hypercellular) endothelial cells =inside of capillary loop podocytes = outside of capillary loop |
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mesangium = meso = middle, angium = blood vessels => supports blood vessels
endothelial cells inside vessel podocyte cells outside vessel loops |
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spikey parts = podocytes
mesangium next to capillary lumen which has blood cells in it |
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two layers of basement membrane = lamina rare externa/interna
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glomerular slit diaphragm: deficiencies in nephrin or podocin = proteinuria bc these compounds are very important for holding back protein
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Non-collagenous disease
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IgG anti-NC1, which is a component of the basement membrane collagen
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azotemia
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accumulation of nitrogenous wastes
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increased BUN in GI bleeding
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rbc breakdown in gi tract
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increased BUN in increased protein intake
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protein breakdown in gi tract
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creatinine laboratory evaluation
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not much creatinine secreted into tubules (10%);
you can lose alot of kidney function 50-60% and still have normal creatinine |
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BUN/Creatinine ratio
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10/1 Normal
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BUN:Cr >= 20:1
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Pre-renal azotemia likely; sluggish flow of circulation around tubules allows for more BUN resorption
Tubular secretion of creatinine persists blunting the marked rise serum creatinine (stone, clot, stenosis, low blood pressure) |
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BUN: Cr = 10:1
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Something wrong in kidney because nothings working right so both BUN:Cr are not being reabsorbed preferentially
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BUN:Cr > 20:1
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early phase BUN:Cr 20:1 in early phase urea absorbed from sluggish urine flow
Later phase BUN:Cr approximately 10:1, pressure from backup of urine can damage kidneys This will then result in intrinsic disease |
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foamy urine
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protein
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upper limit of 24 hour protein excretion in normal adults
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150mg
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which proteins are dipstick sensitive too
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only albumin; wont be sensitive to other proteins (benz-jones proteins for ex)
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dysmorphic rbc; rbc going through diseased kidneys
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Hematuria; intact rbc; indicates bleeding in kidney since it is not a rbc cast
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tubular cell cast; indicative of tubular casts
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granular cell casts; indicative of tubular diseaes
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uric acid crystals
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cystine crystals
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oxylate crystals; look like envelopes
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why cant you just look at urine volume to evaluate kidneys
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GFR-reabsorption = urine volume
BUT both could be low and thus still urinating normal volumes |
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Memorize this chart
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a. global
b. segmental c. diffuse focal/mesangial |
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poststreptococcal glomerular nephritis; big hump is pathonomonic
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Type I RPGN
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antiglomerular basement membrane antibody; linear deposition (IgG +/- C3); can go to lung and cause pulmonary hemorrhage
Goodpasture antigen = noncallagenous portion of the alpha 3 chain of type IV collagen |
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Type I RPGN
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antiglomerular basement membrane antibody; linear deposition (IgG +/- C3); can go to lung and cause pulmonary hemorrhage
Goodpasture antigen = noncallagenous portion of the alpha 3 chain of type IV collagen |
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Type IIII RPGN
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Pauci-immune
c-ANCA: Wegners (cytoplasmic staining) p-ANCA: polyangitis ANCA may direct against the MPO and PR3 |
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Crescents in RPGN; parietal epithelial cells proliferate and squeeze off glomerulus
fibrin proteins when spilled out into bowmans capsule promotes proliferation of parietal cells |
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mc systemic causes of nephrotic syndrome
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diabetes, amyloidosis, SLE
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Spike and dome
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membranouS Spikes (membranous nephropathy)
IC deposit between podocytes; BM grows around it = spikes |
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minimal change diease (lipod nephrosis)
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normal glomeruli on EM + nephrotic syndrome
effacement of foot processes |
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focal segmental glomerulosclerosis
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Type I MPGN
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localization in glomerulus activates complment/alternative pathway
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Type II MPGN
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decreased levels of C3 w/ normal C4 (bc it snot involved in the classic)
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Membrano proliferative glomerulonephritis
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subendothelial IC with granular IF
basement membrane laid on top of IC deposits; IC deposition = granular |
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Left: Type I: Subendothelial deposits, tram tracking
Right: Type II: Ribbon like deposits of electron dense material |
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Where does IgA deposit
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Mesangium
IgA nephropathy |
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Henoch-Schonlein Purpura
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vascular disease that results from immunological damage to the blood vessel walls
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differentiate henoch-schonlein purpura from IgA nephropathy
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HSP = lesions on butt + abdominal pain/vomiting, IgA affecting vessels in GI tract
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diabetic nephropathy pathogenesis
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NEG of GBM/capillary basement membrane -> increased permeability/thickening
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Kimmelstiel-Wilson Disease/DNP
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nofdulcar glomerular sclerosis; one of the ways in which diabetes will affect the kidneys; large balls of PAS positive material (christmas tree dz)
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Amyloidosis
giant tongue |
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maybe add a line for how they look grossly
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autosomal dominant (adult polycystic disease
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expand out and affect entire functioning
mutation in ADPKD and PKD1/2 gene lack of calcium signal causes abnormal growth signaling = cellular proliferation, apoptosis, interactions w ECM and secretory function of the epithelia keep building cells around a tube |
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autosomal recessive polycystic kidney disease; radial dilitation of collecting ducts
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also associated w biliary dsgenesis and portal tract fibrosis
gene mutation = PKHD1 gene -> messed up protein fibrocystin its on chromosome 6 |
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nephrononphthisis; type of medullary cystic disease
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ar and ends in ESRD within the first 3 decades of life; consider this is young kids
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medullary cystic kidney disease vs nephronopthisis
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know nephronophthisis NPH1-6 gene mutations
MCKD1 and MCDK2 in medullary cystic disease |
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mckd location
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hug corticomedullary region
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medullary sponge kidney
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dilated medulary and papillary collecting ducts which result in the medulla having a sponge like appearance; occur at tips of pyramids
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acquired (dialysis associated) cystic disease
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chronic renal failure (dialysis) associated with the development of renal cysts in cortex or medulla (seen anywhere)
renal cancer (seen in 7% of dialyzed pts seen for 10 yrs) |
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simple cysts
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usually on cortex; translucent; smooth membrane; most asymptomatic
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urinary tract obstruction
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can occur anywhere
dysfunction in concentrating ability if you get to tubules; obstruction can eventually cause interstitial inflammation -> fibrosis, GFR may decline |
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complications
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infection (stasis), stone formation, permanent renal atrophy
acute obstruction = renal colick |
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urolithiasis
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increased conc. beyond soluility = precipitates = stones
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ammonium magnesium phosphate
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2nd mcc kidney stone; infection w urease-positive bugs (proteus vulgaris, staph, klebsiela); can form staghorn calculus
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cystine stones
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most often 2 to cystinuria; hexagonal shape. Rarely, may form cystine staghorn calculi
associated w genetic defects (cystinuria) faintly radiopaque; tx w alkalnization of urine |
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urolithiasis
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can lead to severe complications such as hydronephoriss and pyelonephritis; tx and prevent by encouraging fluid intake
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ureterovesciular junction stone pain radiation
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urinary uregency and frequency
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stone in lower part of ureter
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radiate to ipsilateral testicle and labium in women
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stone in upper part of ureter
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anterior radiation
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renal papillary adenoma (lots of little papilla; seen histologically as little islands)
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cortical tumors arising from the renal TUBULAR epithelium
histologically they are indistinguishable from low grade papillary renal cell adenocarcinoma |
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skin manifestations of tuberous sclerosis
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shagreen patches in the lumbosacral region of patient + angiofibromas around nose + ash leaf macules (hypopigmentations) in a patient with tubule sclerosis
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oncocytoma
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mahogany brown surface
note large eosinophilic cells |
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von hippel lindau syndrome association (VHL gene at 3p25)
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AD syndrome w renal cell carcinoma association
also cerebellar hemangioblastoma retinal angiomas pheochromocytoma cysts in various organs |
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VHL gene location
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3p25; its a tummor supressor gene
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variants of renal cell carcinoma
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clear cell carcinoma
papillary carcinoma |
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clear cell carcinoma
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70-80% of RCC; many demonstrate loss of sequence on chromosome 3 (3p25); loss of VHL/tumor supressor gene
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papillary carcinoma
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Sporadic form (Trisomies 7, 16, 17)
Familia form (Trisomy 7) - chromosome 7 which encompasses the MET proto-oncogene |
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chromophobe rcc prognosis
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excellent prognosis
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know this chart
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renal cell carcinoma; towards the top/pole of kidney; yellow = lots of lipids
a. clear cell type b. papillary type c chromophone |
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note lots of blood vessels in rcc
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