Renal Flashcards

1
Q

What are the 4 comparetments of renal disease?

A

glomeruli
tubules
interstitial
blood vessels

chronic renal disease eventually gets all 4

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2
Q

what is azotemia?

A

elevation of BUN and creatinine due to decreased GFR

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3
Q

what is prerenal azotemia?

A

azotemia due to hypoperfusion , CHF, volume depletion, shock

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4
Q

what is postrenal azotemia?

A

azotemia due to outflow obstruction

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5
Q

what is uremia?

A

the symptoms of azotemia

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6
Q

what is nephritic syndrome?

A

hematuria and some proteinuria and hypertension due to glomerular injury

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7
Q

what is nephrotic syndrome?

A

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

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8
Q

what is rapidly progressive glomerulonephritis?

A

nephritic with rapid decline in GFR

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9
Q

what if hematuria or proteinuria is asymptomatic?

A

mild glomerular injury

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10
Q

what is acute tubular injury?

A

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

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11
Q

what is CKD?

A

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

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12
Q

what is ESRD?

A

end stage renal disease

<5% GFR

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13
Q

what are renal tubular defects?

A

tubule disorders that show up as polyuria and electrolyte abnormalities

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14
Q

what is the difference between primary and secondary glomerulonephritis?

A

primary-glomeruli are the guy

secondary-other systemic disease

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15
Q

what are the pathologic responses to glomerulus injury?

A

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

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16
Q

why does glom injury have hypercellularity?

A

proliferation of mesangials/endothelials
infiltration of leukocytes
glomerular epithelial prolif

17
Q

why does glom injury have BM thickening?

A

depositiion of immune complexes, fibirin, amyloid, etc

18
Q

why does glom injury have hylainosis and sclerosis?

A

hyalinosis-endothelial inury –> plasma proteins come in

sclerosis –> damage –> deposition of collagen

19
Q

what causes most glomerulonephritis?

A

immune compexes, Ig deposition

20
Q

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

A

M-type phospholipase A2 (PLA2r)

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

21
Q

what occurs in antibodies against planted antigens?

A

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

discrete granular pattern

22
Q

what is antibody induced GN?

A

autoimmune disease, antibodies directed against normal components of the GBM

example: goodpasture syndrome

23
Q

what is goodpasture syndrome? staining pattern?

A

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

24
Q

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

A

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

granular pattern

25
where do immune complexes normally deposit and what determines that?
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
26
how does cell mediated GN work?
T cells do stuff
27
how does complement do damage?
C3 directed GN
28
what are the mediators of glomerular injury?
``` 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 ```
29
what cell type is injured in glomerular disease that cant regenerate?
podocytes --> causes them to detach from BM | neprin and podocin mutations can also do this w/o inflammation
30
what occurs in focal segmental glomerulosclerosis? (also in FA)
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