Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/33

Click to flip

33 Cards in this Set

  • Front
  • Back
silver stain in normal glomerulus shows...
highlights BM, Cap wall, masangial cells
tubules in cortex are mostly...
proximal tubules
(90%)
visceral epithelial cells are...
podocytes
parietal epithelial cells are...
lining of BC
filter layer (most) responsible for Ultrafiltrate...
BM
size and charge filtered
(albumin small enough to come out otherwise)
negative charges in BM from
Type IV collagen, heparin sulfate, proteoglycans
layers of BM ONLY seen on...
EM
(or cartoon)
glomerular dz in adults
mostly secondary
-diabetic GN
-amyloidosis

primary dz is 60%
-Membranous GN
-FSGS
-minimal change
-membranoproliferative (mostly kids)
glomerular dz in children
95% are primary dz
-minimal change glomerulopathy (65%)
-FSGS
-membranoproliferative (kid only)
-membranous (SLE or inf)
-secondary
clinical manifestations of glomerular dz
1-asymptomatic proteinuria
2-nephrotic syndrome
3-asymptomatic hematuria
4-nephritic syndrome
*glomerulonephritis
*acute glomerulonephritis
*crescentic glomerulonephritis
*chronic glomerulonephritis
5-end stage renal dz
clinical picture of nephrotic syndrome
edema, proteinuria, hyperlipidemia
mechanism of edema in nephrotic syndrome
renal injury leading to:
-increased g cap perm
(proteinuria, decreased onc pressure)

-inappropriate RAS/aldost
(lowers plasma volume & increases RAS/Ald activation)

-decreased glomerular filtration fraction & impaired Na excretion
child
proteinuria
normal LM
IMFL neg for Ig's & C3's
Minimal Change dz
-oval fat bodies (from "proteinacious backup")
-EM shows fusion of foot processes
possible mechanism for primary minimal change disease
change in charge on BM
-loss of GC polyanions
-Lymphokines
prognosis & tx for minimal change dz
excellent prognosis
responds to steroids
conditions associated with minimal change GN
neoplasms
-Hodgkin's, NHL, carcinoma
Allergy
Drugs
-Li, NSAIDS, Probenecid
AIDS
Congenital Nephrotic synd
DM
other glomerular dz
"maltese cross figure"
oval fat bodies
in glomerular nephropathy
esp minimal change disease
most common cause of nephrotic syndrome in adults
membranous glomerulopathy
assoc'd w/RV thrombosis (hyperviscosity)
Immune complex deposition in kidney
glomerulopathy associated with hyperviscosity
membranous glomerulopathy
(assoc w/RV thrombosis)
LM with prominant/thickened cap loops "wire loops" and spikes

subepithelial deposits

effaced foot processess
membranous glomerulopathy
-IMFL w/pos IgG

need biopsy (EM) to disting primary vs secondary
primary membranous glomerulopathy
affects only BM
"subepithelial deposits"
secondary membranous glomerulopathy
affects BM, mesangial, etc

requires work up for malignancy and ANA
common cause of nephrotic syndrome in adults & children
FSGS- focal, segmental glomerular sclerosis
nephropathy associated with hyperperfusion injury
FSGS
primary causes unknown
secondary causes:
-HIV
-IV Heroine
-reflux nephropathy
-parenchymal shrink
-GN
LM with foam cells, podocyte effusion, enlarged glomeruli

IMFL pos for IgM & C3
FSGS

IgM & C3 on sclerotic BM & some mesangials
hypocomplementemia w/hematuria

LM: very cellular w/tram tracking, immune deposits w/trichrome

IMFL: pos for complement & IgG
membranoproliferative glomerulonephritis

mixed syndrome

Type I assoc w/Hep C, lymphoprolif, in-dwelling caths
EM: mesangial interposition & subendo Immune deposits

Type II high recurr rate w/renal transplants
EM: BM transformation
"Dense Deposit Dz"
Dense Deposit Disease
Type II membranoproliferative GN

cigar shaped dense deposits
Cigar Shaped Dense Deposits
Type II membranoproliferative GN
most common cause of end stage renal disease in USA
diabetic glomerulosclerosis

first presents as asymptomatic proteinuria

b/c glycosylation of IgG
LM: Nodular mesangial expansion

IMFL: linear staining of BM for IgG

EM: thick BM (densa), expanded mesangials
Diabetic G-sclerosis
"Kimmelstiel-Wilson Nodules"
LM:
congo red stain pos for mesang & vessel

cotton candy expansion of mesangium

apple green bifringence

EM: randomly oriented fibrilary tissue
renal amyloidosis

2 Types
- AA: assoc w/lt chain, pos for kappa & lambda

-AL: devoid of lt chain, kappa or lambda neg, assoc w/inflamm or hered states
beta sheets found in ...
amyloid dz
nephrotic syndrom associated dz's
minimal change dz
(children)
- oval fat bodies
-effused foot process on EM

membranous glomerulopathy
(adults)
- wire loops, spikes, imm complex

FSGS
(both)
-foam cells
-IgM, C3
-hyperperfusion inj

MPGN- mixed synd, complement activation, tram tracking
-type I: Hep C
-type II: "dense body" recurs in renal transplant

Diabetic glomerulosclerosis
-glycosylated IgG
-nodular mesangial expansion
-THICK BM

amyloidosis
-AL or AA
-polarizes (immunofixation)
-beta sheets (congo red mol's)