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Clinical Reproduction & Urology > Pathology of the Urinary Tract 2 > Flashcards

Pathology of the Urinary Tract 2 Flashcards

1
Q

Renal infarction

A
  • common lesions of localised coagulative necrosis
  • produced by embolic/thrombotic occlusion of renal a. or one of its branches
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2
Q

Renal infarction emboli originate from

A
  • endocardial thrombosis
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3
Q

Renal infarction thrombosis results from

A

vascular dz

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4
Q

Sterile thrombi is an

A

infarct

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5
Q

Sterile emboli is an

A

abscess

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6
Q

What is the morphogenesis of renal infarction?

A
  • form/size related to site of occlusion involving cortex or cotex w/ medulla
  • wedge-shaped to bigger ischameic coagulation necrosis
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7
Q

Describe the morphogenesis of a renal infarct

A
  • initially, infarct is swollen, dark red, cyanotic, congested
  • In 2-3 d, becomes pale, surrounded by red zone of re-established circulation –> macrophages/inflammatory cells present, no more blood supply, kdiney trying to heal area, angiogenesis, fibroblast infiltration, starts around border
  • chronic infarcts –> pale, shrunken, fibrotic –> distortion & depression of renal contour
  • necrotic zone replaced by fibrous tissue & healed infarcts persist as pale grey white indented scars
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8
Q

Describe the form & size related to an infarct at each artery labeled

A
  • Interlobular artery: cortex, small & superficial; due to small embolus
  • Arcuate artery: cortex & wedge-shaped
  • Interlobar artery: cortex & medulla involved; large occlusion, blood supply impacted
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9
Q

Neoplastic emboli will dvlp proliferative

A

lesions/mets

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10
Q

What do kidneys with hyperaemia & congestion look like on gross inspection?

A
  • uniformly dark red & swollen, oedematous
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11
Q

Active hyperaemia

A
  • assoc’d w/ septicaemia, bacterial toxaemias, acute nephritis
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12
Q

Acute nephritis

A
  • Hyperaemia restricted to medulla, esp in dehydration
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13
Q

Passive hyperaemia (congestion)

A
  • due to: cardiovascular insufficiency
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14
Q

When might you find reneal petechial/ecchymotic haemorrhages?

A
  • incidental PM in slaughtered animals
  • piglets dead from anything
  • Classical swine fever, african swine fever, streptococcosis, salmonellosis, porcine dermatitis & nephropathy syndrome, mulberry heart dz
  • lamb kidneys w/ clostridial enterotoxaemia (pulpy kidney dz), porcine erysipelas, juvi canine kidney in CHV-1 infection
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15
Q

When would renal cortical haemorrhages assoc’d with vasculitis, septicaemias, and DIC be seen?

A
  • incidental PM finding
  • acute Pb poisoning in calves
  • ruminal bloat: severe subcapsular haemorrhage in L kidney
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16
Q

Pulpy Kidney is caused by what organism?

A
  • Clostridium perfringens type D
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17
Q

Clostridium perfringens Type D is a normal

A

gut inhabitant that proliferates in high carb diet

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18
Q

Pulpy kidney dz is seen mainly in

A

lambs around 3 mos, growing well

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19
Q

What toxin is released from Clostridium perfringens type D in pulpy kidney dz?

A

Epsilon toxin –> absorbed in blood stream causing vascular damage; lot of gas involved

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20
Q

Pulpy kidney dz has what toxic effects distant to the gut?

A
  • vascular damage - severe pulm oedema
  • neuronal damage - brain necrosis
  • renal tubular damage secondary to endothelial necrosis
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21
Q

What does pulpy kidney dz look like on PM

A
  • fibrin in pericardial sac
  • pulmonary oedema
  • malacia in brain if survives multiple days
  • glucosuria
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22
Q

What is the pathognomonic sign of CHV-1?

A

Diffuse petechial & ecchymotic haemorrhages in kidneys, adrenals, liver, lungs, GIT

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23
Q

CHV-1 can be characteried by

A
  • tubular necrosis
  • diffuse petechial/ecchymotic haemorrhages
  • causing necrotizing vasculitis –> vascular damge & leakage –> necrosis & haemorrhage
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24
Q

When are renal haemorrhages found in pigs?

A
  • piglets that die of any causes
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25
Q

Renal cortical necrosis develops hypoperfusion resulting from:

A
  • DIC
  • Endotoxic shock
  • Other types of shock/thrombosis of renal a.
26
Q

Describe the process of renal cortical necrosis

A
  • intrarenal blood flow redistributed to inner cortex & medulla leading to decreased perfusion of outer cortex & maintenance of perfusion of inner cortical nephrons leading to RAAS activation
  • Causes vasoconstriction in cortical vessels, affects opposed in inner cortex by PGE2 produced in medulla that causes localised vasodilation
  • if cortical ischaemia prolonged, swelling of endothelial cells of glomeruli, vasa recta, capillaries, & parenchymal cells occurs which inhibits reflow of blood
  • Gross changes det’d by severity, distribution & duration of ischaemia
  • Renal cortical tissue pale, resembling multple confluent infarcts
    * most severe manifesttion of ischaemia
27
Q

Renal medullary necrosis is caused by…

A
  • Prolonged ischaemia damaging medullary vessels –> necrosis
  • restricted to the papillary structures
28
Q

List the medulla protective factors

A
  1. renin/angiotensin-induced (by reduced glomerular blood flow) vasoconstriction is inhibited in medulla by release of PGE2 –> vasodilation
  2. reduced renal blood flow cauases selective redistribution of blood to the juxtamedullary nephrons
29
Q

Papillary necrosis can be a non-specific

A

lesion in chronic, progressive renal dz

30
Q

Specific causes of renal papillary necrosis

A
  • prolonged txt w/ NSAIDs (esp in horse, cat, dog)
  • dehydration
  • amyloidosis & vessels (esp cat) impinging on bv’s (cattle) when amyloid is deposited in renal medulla
  • urinary obstruction & pyelonephritis could be caused by oedema of papillary interstitium alone, collapse of venous outflow
31
Q

Amyloid

A

fibrillar glycoprotein w/ Beta-pleated sheet structure that cannot be removed, is resistant to proteolysis & insoluble

32
Q

ECM components always associated w/ amyloid include

A
  • proteins of pentraxin family
  • glycosaminoglycans
  • proteoglycans
33
Q

Glomerular amyloidosis causes…

A

proteinuria in dogs & cattle

34
Q

interstitial fibrosis & lymphoplasmacytic interstitial nephritis may follow

A

interstitial amyloidis (esp in cats) leading to chronic renal failure

35
Q

Other organs affected by interstitial fibrosis & lymphoplasmacytic interstital nephritis

A
  • liver, spleen
  • possible in any organ
36
Q

Dogs w/ renal amyloidosis may present w/

A

W/ thrombosis of pulm. a. due to renal loss of low molecular proteins

37
Q

Renal amyloidosis gross

A

enlarged, pale, increase in consistency, capsule easily peels off, cortical surface has finely stippled appearance

38
Q

Sources of amyloid

A
  • reactive systemic amyloidosis (most common) –> Serum amyloid A (SAA), chronic antigenic stimulation
  • Immunoglobulin-derived
  • Familial amyloidosis (AA)
  • Islet amyloid polypeptide (IAPP)
39
Q

Where would amyloid deposition occur in the following species: cattle, dog, cats, horse, sheep/pig?

A
  • cattle: glomeruli, tubules, gut wall
  • dog: glomeruli, tubules
  • cats: medulla
  • horse: liver
  • sheep/pig: uncommon
40
Q

amyloid affecting glomeruli primarily?

A

nephrotic syndrome

41
Q

amyloid primarily affecting medulla

A

uraemic syndrome

42
Q

Glomerular fxn

A
  • produces ultrafiltrate (albumin & high molecular wt plasma proteins excludd from filtrate)
43
Q

What are the 3 layers of the glomerular filtration membrane?

A
  • capillary endothelium containing fenestrae of 50-100 nm diameter
  • glomerular basement membrane: 100-300 nm thick central elctron dense lamina densa & peripheral electron-lucent layers
  • visceral epitehelial cells (podocytes), complex itnerdigitating trabeculae whose foot proesses are embedded in lamina rara external of GBM
44
Q

Damage to basement membrane leads to the leakage of…

A

albumin

45
Q

What are the 3 resident cell types within the renal corpuscle

A
  • Podocytes
  • capillary endothelial cells
  • mesangial cells
46
Q

Primary glomerular dz’s

A
  • glomerulonephritis
  • minimal-change nephropathy
  • IgA-nephropathy
  • focal segmental glomerulosclerosis
47
Q

Systemic dz’s assoc’d w/ glomerulopathies

A
  • amyloidosis
  • systemic lupus erythematosus (SLE)
  • DM
48
Q

hereditary disorders of the glomeruli

A
  • familial glomerulopathies in dogs
  • breed specific dz in other species (sheep, pigs)
49
Q

Glomerulonephritis is a primary glomerular dz is accompanied by

A

secondary tubulointerstitial & vascular changes

50
Q

glomerulonephritis is usually

A

immune-mediated

51
Q

glomerulitis

A

inflammation restricted to glomeruli

52
Q

glomerulopathy

A

glomerular dz w/o cellular inflammatory components

53
Q

Pathogenesis of Immune-complex glomerulonephritis

A
  • glomerular damage caused by combo of insoluble, soluble, & in-situ formed immune complexes
  • circulating non-glomerular antigen-antibody complexis localise in/at either side of glomerular basement membrane or in mesangium
  • small soluble antigen-complexes or antigen penetrate basement membrane & localises in subepithelial position
  • deposition of ciculating immune complexes (most common if persistent antigenaemia)
  • in situ immune complexes - nephrotoxic nephritis rare in domestic animals
  • location of immune complexes dependnt on molecular size/charge
  • deposition of immune complexes initiates inflammatory response –> injury
54
Q

Diseases associated w/ immune complex glomerulonephritis in dogs

A

CAV-1, chronic bacterial infections, valvular endocarditis, pyometra, borreliosis, SLE, neoplasia, Dirofilaria immitis, Leishmania, IMHA, hereditary complement deficiency, idiopathic

55
Q

Diseases associated w/ immune complex glomerulonephritis in horses

A
  • Strep spp.
  • EIA virus
56
Q

Diseases associated w/ immune complex glomerulonephritis in cows

A
  • BVDV
  • trypanosomiasis
57
Q

Diseases associated w/ immune complex glomerulonephritis in cats

A
  • FeLV
  • FIP
  • FIV
  • neoplasia
  • idiopathic
58
Q

Diseases associated w/ immune complex glomerulonephritis in sheep

A
  • herediatry complement deficiency (Finnish Landrace sheep)
59
Q

Diseases associated w/ immune complex glomerulonephritis in pigs

A
  • classical swine fever
  • african swine fever
  • PCV-2
  • hereditary complement deficiency
60
Q

Pathogenesis of immune-mediated glomerular injury

A
  • injury –> foot processes effacement, detachment of epithelial cells, protein leakage thru defective GBM & filtration slits
  • lodge in area, inflammatory response which infiltrates GBM –> protein leakage
61
Q

Membranous glomerulonephritis

A
  • assoc’d w/ thickening of basement membrane
  • no or minimal cell inifltration
  • assoc’d w/ severe proteinuria
  • present clinically as nephrotic syndrome
  • most common form of immune complex nephritis in cat

Clinical Reproduction & Urology (29 decks)

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