Renal

Question 1

What are the 4 comparetments of renal disease?

Answer 1

glomeruli
tubules
interstitial
blood vessels

chronic renal disease eventually gets all 4

Question 2

what is azotemia?

Answer 2

elevation of BUN and creatinine due to decreased GFR

Question 3

what is prerenal azotemia?

Answer 3

azotemia due to hypoperfusion , CHF, volume depletion, shock

Question 4

what is postrenal azotemia?

Answer 4

azotemia due to outflow obstruction

Question 5

what is uremia?

Answer 5

the symptoms of azotemia

Question 6

what is nephritic syndrome?

Answer 6

hematuria and some proteinuria and hypertension due to glomerular injury

Question 7

what is nephrotic syndrome?

Answer 7

> 3.5 g/day proteinuria, hypoalbuminemia, edema, hyperlipidemia due to glomerular injury

Question 8

what is rapidly progressive glomerulonephritis?

Answer 8

nephritic with rapid decline in GFR

Question 9

what if hematuria or proteinuria is asymptomatic?

Answer 9

mild glomerular injury

Question 10

what is acute tubular injury?

Answer 10

rapid decline in GFR resulting in azotemia, injury to any compartment

Question 11

what is CKD?

Answer 11

chronic kidney disease significant GFR reduction lasting >3 months
this is the end stage

Question 12

what is ESRD?

Answer 12

end stage renal disease

<5% GFR

Question 13

what are renal tubular defects?

Answer 13

tubule disorders that show up as polyuria and electrolyte abnormalities

Question 14

what is the difference between primary and secondary glomerulonephritis?

Answer 14

primary-glomeruli are the guy

secondary-other systemic disease

Question 15

what are the pathologic responses to glomerulus injury?

Answer 15

hypercellularity
basement membrane thickening
hyalinosis and sclerosis
diffuse/focal/global lesions

Question 16

why does glom injury have hypercellularity?

Answer 16

proliferation of mesangials/endothelials
infiltration of leukocytes
glomerular epithelial prolif

Question 17

why does glom injury have BM thickening?

Answer 17

depositiion of immune complexes, fibirin, amyloid, etc

Question 18

why does glom injury have hylainosis and sclerosis?

Answer 18

hyalinosis-endothelial inury –> plasma proteins come in

sclerosis –> damage –> deposition of collagen

Question 19

what causes most glomerulonephritis?

Answer 19

immune compexes, Ig deposition

Question 20

what is the antigen in renal epithelium that causes lots of GN? what happens when antibodies bind?

Answer 20

M-type phospholipase A2 (PLA2r)

immune complexes cause basement thickeing and a granular pattern (heymann nephritis)

Question 21

what occurs in antibodies against planted antigens?

Answer 21

basically antigens from other stuff get stuck in kidney then antibodies come and do damage

discrete granular pattern

Question 22

what is antibody induced GN?

Answer 22

autoimmune disease, antibodies directed against normal components of the GBM

example: goodpasture syndrome

Question 23

what is goodpasture syndrome? staining pattern?

Answer 23

auto abs bind to a3 chain of type IV collagen in glomerular basement membrane–> linear staining pattern –> leads to nephritic syndrome, azotemia, oliguria, HTN

Question 24

how does gGN result from deposition of immune complexes? stain?

Answer 24

complexes get trapped –> Fc receptors activate complement –> damage to subendothelial, subeithelial, mesangial

granular pattern

Question 25

where do immune complexes normally deposit and what determines that?

Answer 25

determined by size/charge

cationic –> crosses GBM and forms sub-epithelial complexes
-non inflammatory

anionic –> trapped in sub-endothelium
-inflammatory
neutral –> mesangium

large –> get eaten by macros before they can do damge

sm

Question 26

how does cell mediated GN work?

Answer 26

T cells do stuff

Question 27

how does complement do damage?

Answer 27

C3 directed GN

Question 28

what are the mediators of glomerular injury?

Answer 28

cells
-neutros, monos, 
-macros 
-plateletes
-resident glomerular cells (mesangial) 
soluble mediators
-complement 5b-9 MAC
-eicosanoids, NO, AT, endothelin
-cytokines, IL1, TNF
-chemokines-PDGF and TGFb
-coag proteins-fibirin

Question 29

what cell type is injured in glomerular disease that cant regenerate?

Answer 29

podocytes –> causes them to detach from BM

neprin and podocin mutations can also do this w/o inflammation

Question 30

what occurs in focal segmental glomerulosclerosis? (also in FA)

Answer 30

usually via systemic HTN –> increase GBF/filtration/pressure –> endothelial injury –> protein accumulation –> macros come –> increase matrix synthesis

rest of good glomeruli compensate by hypertrophying to make up for the ones that suck –> then they eventually undergo same fate