Renal Flashcards
1
Q
Crescentic GN depositions
A
- RPGN crescents:
- glomerular parietal cells
- monocytes and macrophages
- FIBRIN on deckkk
2
Q
type 1 RPGN (Goodpasture syndrome) deposits
A
C3 and IgG-linear depositis seen on IF microscopy
3
Q
Acute PSGN depositions
A
- IF:
- IgG, IgM, C3: lumpy bumpy
- (will have DEC serum C3 levels)
- EM: subepithelial IC
4
Q
DPGN deposits
A
- EM: (subendothelial, sometimes intramembranous)
- IgG based IC + C3
5
Q
MPGN deposits
A
- Type 1: subendothelial IC +granular IF
- Type 2: intramembranous IC (dense deposits)
6
Q
FSGS deposits
A
- IF: focal IgM, C1, C3
7
Q
ACE inhibitors and bradykinin
A
- ACE metabolizes brady=LESS brady
- ACE inhibitors=less brady metab=MORE brady
8
Q
TWO main causes of overflow incontinence
A
- impaired detrusor contractility
- bladder outlet obstruction (BOO)
- tumor obstructing the urethra
CP: involuntary+continuous urinary leakage when bladder is full
-incomplete emptying
9
Q
what is the differential diagnosis for urinary incontinence
A
- stress
- loss of urethral support and abdo pressure>urethral sphincter pressure
- s/s: leaking with cough, sneeze,laugh, lift
- urge
- detrusor overactivity (PT with MS)
- s/s: sudden overwhelming or freq need to empty bladder
- overflow
- impaired detrusor contractility, BOO
- s/s: involuntry dribbling of urine, incomplete emptying
10
Q
classifications for RP(crescentic)GN
A
- anti-GBM RPGN
- linear GBM of IgG and C3
- some: antiGBM in lungs (Goodpasture)
- immune-complex RPGN
- lumpy bumpy d/t IgA + IgG + complement
- d/t:
- PSGN
- SLE (serum anti-PHOSPHOLIPID Ab)
- IgA nepropathy
- HSP
- pauci-immune RPGN
- nada on BM
- ANCA in serum=
- granulomatosis with polyangiitis
- microscopic polyangiitis
- idiopathic
11
Q
nephrotic syndrome and aldosterone
A
- plasma oncotic pressure is DEC
- net plasma filtration into interstitium
- DEC effective circulating intravascular volume
- compensatory INC in RAAS
- elevated circulating aldosterone
12
Q
CP MCD
A
- 5yo boy w/ generalized edema after mild URI
- UA: proteinuria, albumin + trace IgG
- PP: loss of GBM anions=can no longer repell albumin=SELECTIVE albuminuria
- d/t immune dysregulation, systemic T cell dysfunction= overproduce glomerular permeability factor (GPF)
- GPF:
- causes podocyte foot process fusion
- DEC anionic properties of the glomerular basement membrane
**INC SELECTIVE FILTRATION OF PROTEINS**
13
Q
Thrombotic microangiopathy
A
- PENTAD for TTP (thrombocytopenic thrombotic purpura-HUS is a thrombotic microangiopathy-TMA)…all in the setting of a GI illness
- fever
- neuro symptoms (progressive lethargy)
- renal failure
- anemia
- thrombocytopenia
14
Q
what are the shared common clinical and pathologic features of TMA syndromes (thrombotic microangiopathy)
A
- platelet activation in arterioles and capillaries
- diffuse micro-vascular thrombosis (most commonly affect: brain, kidneys, heart)
- microangiopathic hemolytic anemia with schistocytes
- thrombocytopenia
15
Q
FSGS CP
A
- (has a collapsing variant)
- CP: heavy proteinuria
- “collapse and sclerosis of glomerular tufts”