Jan9 M3-Introduction to Renal Pathology Flashcards

(44 cards)

1
Q

4 main compartments of the kidney

A

glomeruli, tubules, interstitium, vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

normal podocytes on EM

A

can distinguish individual podocytes and see the space between them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

2 types of glomerular barriers to proteins

A

size-selective (large proteins and blood)

charge-selective (albumin): BM is negatively charged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

problem in GN nomenclature

A

many types of glomerular diseases have no inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

give 2 immune mediated GNs

A

anti GBM disease

membranous nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

anti GBM disease pathophgy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

membranous nephropathy pathophgy

A

de novo antibodies attack structures near the podocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

type of non immune mechanism of glomerular disease

A

hyperfiltration injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

hyperfiltration injury: 2 main reasons it happens

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
dipstick checks what
blood hemolyzed, non-hemolyzed, protein, glucose, pH, WBCs, ketones, etc.
26
urine sediment checks for what (4)
cells, casts, crystals, organisms
27
nephritic syndrome main features
hematuria, RBC casts, MILD-MODERATE proteinuria, htn
28
RBC casts: how they're formed and sign of what
RBCs pass glomerulus and compact in the tubules. | cast = sign of glomerular injury
29
nephrotic syndrome lab features (5 classical)
``` HEAVY proteinuria (>3g) Hypoalbuminemia Hyperlipidemia Lipiduria Severe edema ```
30
PURE nephrotic syndrome on bx
no cellular proliferation, inflammation, necrosis or crescent formation
31
does finding RBCs in the urine = glomerular problem?
no. casts yes. but blood can come from anywhere in urinary tract until urethra
32
nephrotic syndrome urinary sediment features
fatty and hyaline casts, lipids, oval fat bodies (shedded tubular cells filled with lipids)
33
3 modalities used on renal bx
LM, immunofluorescence(IF), EM
34
what is done in renal bx LM other than usual H&E (2)
other stains to outline GBM and mesengium (silver, PAS, trichrome, ..)
35
3 things that immunofluorescence on renal bx gives us
1. negative or positive for immune complex and Ig presence 2. location (mesengium, capillary wall) 3. patterns: (linear vs granular)
36
3 main things EM tells us on renal bx
- location and appearance of deposits - appearance and thickness of GBM - evaluation of podocytes
37
4 ways a glomerulus can react in GN
- hypercellularity and proliferation of mesengial, epith, inflam cells - necrosis - GBM thickening - sclerosis (scarring)
38
what hypercellularity and proliferation rx of glomerulus shows
there is an inflammatory cell component
39
what's a crescent
proliferation of parietal epithelial cells of Bowman's capsule often associated with glomerular necrosis
40
what crescents show
severe glomerular injury, necrosis, GBM destroyed
41
acute vs chronic crescents
acute: cellular crescent chronic: fibrous crescent
42
4 words in glomerular lesion nomenclature and def
focal: some glomeruli diffuse: most glomeruli segmental: part of glomeruli global: entire glomerulus
43
segmental vs gobal sclerosis or hypercel or wtv: definition
segmental: <50% of glomerular tuft (of the glomerulus) global: >50%
44
exudative injury to the glomeruli meaning
hypercellularity + too many neutrophils