Jan9 M3-Introduction to Renal Pathology Flashcards

1
Q

4 main compartments of the kidney

A

glomeruli, tubules, interstitium, vasculature

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2
Q

arterial-venous system in the kidney

A

arteries: renal, interlobar, arcuate, lobular, afferent, efferent
capillaries: network under capsule + peritub drain in stellate veins. vasa recta drain in arcuate vein
veins: stellate veins-lobular veins-arcuate veins-interlobar-renal

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3
Q

normal podocytes on EM

A

can distinguish individual podocytes and see the space between them

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4
Q

2 types of glomerular barriers to proteins

A

size-selective (large proteins and blood)

charge-selective (albumin): BM is negatively charged

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5
Q

selective vs non selective proteinuria + indicates what + particular thing in non-selective

A
  • selective = albumin only = alteration of negative charge

- non selective = not albumin only = anomaly to endoth or GBM or podocytes. can see hematuria

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6
Q

pathological consequence of the glomerulus being part of our (micro)vasculature

A

anything that injures small blood vessels affects it (diabetes, htn, vasculitis, thrombosis)

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7
Q

glomerulus is a site of predilection for the deposition of ________ and this is the major form of ________

A

immune complexes. major form of GN

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8
Q

problem in GN nomenclature

A

many types of glomerular diseases have no inflammatory cells

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9
Q

immune vs non immune glomerular injury

A

immune: often bx, antibody mediated, in situ complex formation or deposition of preformed complexes
non-immune: nephron loss, injury to podocytes, no bx

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10
Q

give 2 immune mediated GNs

A

anti GBM disease

membranous nephropathy

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11
Q

anti GBM disease pathophgy

A

CIRCULATING antibodies attack type IV collagen in GBM: leads to inflam rx

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12
Q

membranous nephropathy pathophgy

A

de novo antibodies attack structures near the podocytes

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13
Q

2 types of diseases where deposition of preformed circulating immune complexes exists + where they deposit

A

-endocarditis and post infection rheumatic
-lupus (SLE)
Deposit on glomerulus

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14
Q

what determines the location where preformed circulating immune complexes deposit (2) + where do they deposit

A
  1. their size and their charge
  2. the balance of Ag to Ab
    Deposit on the glomerulus
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15
Q

type of non immune mechanism of glomerular disease

A

hyperfiltration injury

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16
Q

hyperfiltration injury: 2 main reasons it happens

A

adaptive changes in glomeruli (hypertrophy + GC htn) and systemic htn

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17
Q

pathophgy of hyperfiltration injury and how disease detected

A

GC htn, G hypertrophy and systemic htn lead to epithelial and endo injury and proteinuria

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18
Q

what is the glomerulus’ reponse in hyperfiltration injury and what is typically seen

A

glomerulosclerosis (mesengial cells prolif, ECM prod, intraglom coagulation, vessels obliterated, tubules and interstitium disappear and become fibrotic)

19
Q

what happens to tubules and interstitium in hyperfiltration injury

A

they disappear and become fibrotic

20
Q

why is there a vicious circle in hyperfiltration injury

A

glomeruli that aren’t injured try to compensate so they become hypertrophic and hyperfiltrate so buildup of GC pressure

21
Q

to what extent is hyperfiltration injury reversible

A

to some extent until too much fibrosis

22
Q

causes of hyperfiltration injury

A

htn, diabetes, GN, cystic kidney disease

23
Q

9 major renal syndromes

A
  1. asymptomatic proteinuria
  2. nephrotic syndrome
  3. asymptomatic hematuria
  4. nephritic syndrome
  5. rapidly progressive GN
  6. AKI
  7. CKD
  8. UTI
  9. nephrolithiasis (stones)
24
Q

first test performed on nephro patient and when to check urine sediment

A

dipstick. when dipstick positive for anything

25
Q

dipstick checks what

A

blood hemolyzed, non-hemolyzed, protein, glucose, pH, WBCs, ketones, etc.

26
Q

urine sediment checks for what (4)

A

cells, casts, crystals, organisms

27
Q

nephritic syndrome main features

A

hematuria, RBC casts, MILD-MODERATE proteinuria, htn

28
Q

RBC casts: how they’re formed and sign of what

A

RBCs pass glomerulus and compact in the tubules.

cast = sign of glomerular injury

29
Q

nephrotic syndrome lab features (5 classical)

A
HEAVY proteinuria (>3g)
Hypoalbuminemia
Hyperlipidemia
Lipiduria
Severe edema
30
Q

PURE nephrotic syndrome on bx

A

no cellular proliferation, inflammation, necrosis or crescent formation

31
Q

does finding RBCs in the urine = glomerular problem?

A

no. casts yes. but blood can come from anywhere in urinary tract until urethra

32
Q

nephrotic syndrome urinary sediment features

A

fatty and hyaline casts, lipids, oval fat bodies (shedded tubular cells filled with lipids)

33
Q

3 modalities used on renal bx

A

LM, immunofluorescence(IF), EM

34
Q

what is done in renal bx LM other than usual H&E (2)

A

other stains to outline GBM and mesengium (silver, PAS, trichrome, ..)

35
Q

3 things that immunofluorescence on renal bx gives us

A
  1. negative or positive for immune complex and Ig presence
  2. location (mesengium, capillary wall)
  3. patterns: (linear vs granular)
36
Q

3 main things EM tells us on renal bx

A
  • location and appearance of deposits
  • appearance and thickness of GBM
  • evaluation of podocytes
37
Q

4 ways a glomerulus can react in GN

A
  • hypercellularity and proliferation of mesengial, epith, inflam cells
  • necrosis
  • GBM thickening
  • sclerosis (scarring)
38
Q

what hypercellularity and proliferation rx of glomerulus shows

A

there is an inflammatory cell component

39
Q

what’s a crescent

A

proliferation of parietal epithelial cells of Bowman’s capsule often associated with glomerular necrosis

40
Q

what crescents show

A

severe glomerular injury, necrosis, GBM destroyed

41
Q

acute vs chronic crescents

A

acute: cellular crescent
chronic: fibrous crescent

42
Q

4 words in glomerular lesion nomenclature and def

A

focal: some glomeruli
diffuse: most glomeruli
segmental: part of glomeruli
global: entire glomerulus

43
Q

segmental vs gobal sclerosis or hypercel or wtv: definition

A

segmental: <50% of glomerular tuft (of the glomerulus)
global: >50%

44
Q

exudative injury to the glomeruli meaning

A

hypercellularity + too many neutrophils