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Flashcards in 102914 glomerular disease Deck (36)
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1
Q

mechanisms of glomerular disease

A

immunocomplex deposition-ciruculate then deposit in glomerulus(like lupus). activates complement resulting in neutrophil chemotaxis

antibodies against GBM or glomerular antigens

cytokine production by inflam cells

2
Q

glomerular disease that is diffuse is

A

affecting all glomeruli

3
Q

focal

A

affects a few glomeruli

4
Q

global

A

affects the entire glomerulus

5
Q

segmental

A

affects a portion of the glomerulus

6
Q

how does glomerular disease present?

A

loss of GFR
hematuria
proteinuria

7
Q

nephrotic syndrome

A

proteinuria greater than 3.5 g/day
hypoalbuminemia
edema
hyperlipidemia

lipiduria
hypercoagulability

8
Q

nephritis

A

mild proteinuria
HEMATURIA (RBCs, RBC casts, dysmoprhic RBCs)
HTN
edema

9
Q

nephrotic glomerular diseases

A

minimal change disease
focal segmental glomerulosclerosis
membranous nephropathy
IgA neprhopathy

10
Q

nephritic glomerular diseases

A

membranoproliferative GN
acute post infec GN
crescentic (ANCA) GN
IgA nephropathy

11
Q

acute glomerulonephritis causes

A
IgA nephropathy
post infec GN
anti GBM disease/Goodpasture's
small vessel vasculitis
lupus nephritis
membranoproliferative GN
12
Q

what is the most common GN?

A

IgA nephropathy

13
Q

in what disease does hematuria frequently occur with an URI? (synpharyngitic hematuria)

A

IgA nephropathy

14
Q

what is a histologic feature of IgA nephropathy?

A

IF: mesangial IgA deposition

15
Q

HSP

A

systemic disorder with IgA deposition in multiple organs (skin, joints, GI, kidney)

16
Q

oliguria

A

low urine output

17
Q

histology findings for post Strep GN

A

EM: mesangial and large subepithelial hump-like deposits of immune complexes

18
Q

rapidly progressive GN

A

nephritic syndrome with rapid progression (in days to weeks) to renal failure

19
Q

causes of rapidly progressive GN

A

anti-GBM/Goodpasture’s
immune complex GN
ANCA associated GN (pauci immune)

20
Q

how do you diagnose anti GBM/Goodpasture’s?

A

anti GBM Ig in blood

LINEAR IgG and C3 on kidney biopsy IF

21
Q

pauci immune GN

A

crescenteric GN with little deposition of immune reactants (as opposed to anti-GBM disease, IgA nephropathy, lupus nephritis)

idiopathic or associated with ANCA vasculitis

22
Q

what do RPGNs look like under light microscopy?

A

crescenteric GN

23
Q

IF microscopy of immune complex mediated RPGN?

A

variable deposition of immune complex and complement

24
Q

IF microscopy of pauci immune RPGN?

A

negative

25
Q

nephrotic syndrome from primary renal disease ex

A

membranous nephropathy
focal segmental glomerulosclerosis
minimal change disease

in children, 80% have minimal change disease

26
Q

secondary causes of nephrotic syndrome include

A

systemic diseases-diabetes mellitus, SLE, amyloidosis
infections
drugs-NSAIDs

27
Q

what is the most common cause of nephrotic syndrome in children

A

minimal change disease

28
Q

minimal change disease in adults can be caused by

A

idiopathic or

drugs-NSAIDs
neoplasms-Hodgkin’s lymphoma
infections

29
Q

minimal change disease histology

A

LM: glomeruli, interstitium and tubules look NORMAL
EM: podocyte foot process effacement (fusion)

30
Q

membranous nephropathy-what secondary causes are responsible for it?

A

infections-HBV

connecive tissue diseases-SLE

neoplasms-carcinoma of lung, colon, stomach, breast. Non-Hodgkin’s lymphoma

drugs

31
Q

membranous nephropathy histology

A

LM: diffuse thickening of GBM. GBM spikes on silver stain

32
Q

membranous nephropathy

A

immune deposits form on subepithelial aspect of glomerular basement membrane

33
Q

forms of focal segmental glomerulosclerosis

A

primary (acute onset nephrotic syndrome)
secondary
hereditary

34
Q

causes of secondary FSGS

A

drugs-NSAIDs
infections-HIV
etc

35
Q

FSGS histology

A

LM: focal and segmental glomerular sclerosis with capillary collapse

36
Q

in terms of glomerular diseases, SLE can cause

A

a number of different ones