Renal Flashcards

1
Q

Pre-renal and post-renal diseases can cause renal changes.

T/F?

A

True

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2
Q

oseodystrophy associated with renal diseases

A

jaw - rubber jaw

flat bones

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3
Q

soft tissue calcification metastatic v. dystrophic

A

meta - inc. calcium -> deposits

dystrophic - damage -> calcification

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4
Q

how to know if ulceration is chronic or acute?

A

redness - active hemorrhage

chronic - raised rounded edge (trying to epithelialize)

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5
Q

mineralization of aorta/endocardium

A
  • uremia
  • dystrophic
  • metastatic (hyper PTism, granulomatous, lymphoma)
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6
Q

nodular, small, pale kidneys (fatty looking) differentials

A
  • fibrosis (think anything small and pale)
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7
Q

fibrosis

A

small and pale

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8
Q

uremic pneumonitis

A
affects alveoli (not full pneumonia)
mineralization
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9
Q

small kidney
big kidney
not there

A

hypoplasia
renomegally (hyperplasia)
aplasia

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10
Q

pale streaks in renal medula

A

fibrosis
mineralization
inflammation (nephritis)

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11
Q

progressive juvenile nephropathy

A

progressive renal fibrosis in young dogs, hereditary

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12
Q

polycystic kidney disease, pathogenesis?

A

related to PKD1 gene

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13
Q

Polycystic kidneys vs. renal cyst

A

widespread numerous - poly

a couple cysts - incidental in cats

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14
Q

Multifocal hemorrhages of cortex kidney

pathogenesis?

A
  1. septic emboli
  2. DIC
  3. congenital disorder
  4. toxins causes vasculitis (herpes virus)

trauma (unlikely to be multifocal)

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15
Q

Mitral valve endocarditis ->

friable mass in heart -> kidney consequences

A

bacterial emboli
->glomerulonephritis

Also some infarcts

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16
Q

typical infarct

A

dark red triangle
acute - red (unless ischemic)
chronic - pale, raised, edges CONTRACTED in (cavitated)

17
Q

acute hemorrhagic vs. acute ischemic infarct

A

red vs.

pale with red line around it

18
Q

how long does fibrosis take

A

2 weeks (10-14days)

19
Q

part of kidney is pale/enlarged

& part is normal red

A

fluid accumulation (tubule blockage) edema

20
Q

renal cortical necrosis

A

bilateral
g neg septicemia/endotoxemia
severe hypovolemia /renal shutown

21
Q

renal papillary necrosis

A

= medullary crest necrosis - ischemic lesion

  • medullary amylloidosis
  • pyelitis
  • renal calculi
  • obstructive pressure
  • NSAIDs
22
Q

tubular necrosis

A
  1. Ischemic - basement membrane destroyed - SCARRING -> fibrosis
  2. toxic - may leave BM intact - may heal
23
Q

signs of tubular necrosis

A

uremic, oliguric, anuric renal failure

24
Q

tubular necrosis lesions

A

acute

- swollen, pale

25
Q

pale swollen kidney

A

tubular necrosis
glomerular nephritis
hydronephrosis
toxins

26
Q

streaking in cortex

A

inflammation

mineralization

27
Q

hemoglobinuric nephrosis mechanism?

looks like?

A

intravasular necrosis

whole kidney is black

28
Q

glomerular damage leads to what?

A

proteinuria

- basement membrane damaged

29
Q

immune complex glomerular nephritis

net result?

A

chronic infections/antigen

basement membrane compromised!

30
Q

little red dots multifocal/miliary on cortex surface

vs. larger raised tan

A

acute glomerular nephritis (swollen smooth pale)

vs. chronic (shrunken granular thin)

31
Q

what is a cyst?

A

tubule got blocked, got bigger

32
Q

put iodine on kidney

A

to see glomeruli

for renal amyloidosis

33
Q

renal amyloidosis also causes

A

PLN
papillary necrosis due to ischemia
uremia
tubular atrophy

34
Q

hematogenous changes

vs. ascending infection

A

random multifocal

radial changes

35
Q

multifocal nodules differentials

A
  • neoplasia

- nephritis (granulomatous, fungal, FIP)

36
Q

pyelonephritis

A

exudate!

can lead to necrosis/radial streaks

37
Q

hydronephrosis

A

dilated pelvis, medulla gone

38
Q

primary renal neoplasia

A

SINGLE nodules

vs. metastatic can be multiple nodules

39
Q

types of cystitis

A
  1. polypoid cystitis - calculi, chronic trauma
  2. follicular - bacterial infection
  3. empysemitous cystitis - diabetes