Pathology of the Urinary Tract 2 Flashcards
(61 cards)
1
Q
Renal infarction
A
- common lesions of localised coagulative necrosis
- produced by embolic/thrombotic occlusion of renal a. or one of its branches
2
Q
Renal infarction emboli originate from
A
- endocardial thrombosis
3
Q
Renal infarction thrombosis results from
A
vascular dz
4
Q
Sterile thrombi is an
A
infarct
5
Q
Sterile emboli is an
A
abscess
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
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
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
9
Q
Neoplastic emboli will dvlp proliferative
A
lesions/mets
10
Q
What do kidneys with hyperaemia & congestion look like on gross inspection?
A
- uniformly dark red & swollen, oedematous
11
Q
Active hyperaemia
A
- assoc’d w/ septicaemia, bacterial toxaemias, acute nephritis
12
Q
Acute nephritis
A
- Hyperaemia restricted to medulla, esp in dehydration
13
Q
Passive hyperaemia (congestion)
A
- due to: cardiovascular insufficiency
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
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
16
Q
Pulpy Kidney is caused by what organism?
A
- Clostridium perfringens type D
17
Q
Clostridium perfringens Type D is a normal
A
gut inhabitant that proliferates in high carb diet
18
Q
Pulpy kidney dz is seen mainly in
A
lambs around 3 mos, growing well
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
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
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
22
Q
What is the pathognomonic sign of CHV-1?
A
Diffuse petechial & ecchymotic haemorrhages in kidneys, adrenals, liver, lungs, GIT
23
Q
CHV-1 can be characteried by
A
- tubular necrosis
- diffuse petechial/ecchymotic haemorrhages
- causing necrotizing vasculitis –> vascular damge & leakage –> necrosis & haemorrhage
24
Q
When are renal haemorrhages found in pigs?
A
- piglets that die of any causes
25
Renal cortical necrosis develops hypoperfusion resulting from:
* DIC
* Endotoxic shock
* Other types of shock/thrombosis of renal a.
26
Describe the process of renal cortical necrosis
* 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
Renal medullary necrosis is caused by...
* Prolonged ischaemia damaging medullary vessels --> necrosis
* restricted to the papillary structures
28
List the medulla protective factors
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
Papillary necrosis can be a non-specific
lesion in chronic, progressive renal dz
30
Specific causes of renal papillary necrosis
* 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
Amyloid
fibrillar glycoprotein w/ Beta-pleated sheet structure that cannot be removed, is resistant to proteolysis & insoluble
32
ECM components always associated w/ amyloid include
* proteins of pentraxin family
* glycosaminoglycans
* proteoglycans
33
Glomerular amyloidosis causes...
proteinuria in dogs & cattle
34
interstitial fibrosis & lymphoplasmacytic interstitial nephritis may follow
interstitial amyloidis (esp in cats) leading to chronic renal failure
35
Other organs affected by interstitial fibrosis & lymphoplasmacytic interstital nephritis
* liver, spleen
* possible in any organ
36
Dogs w/ renal amyloidosis may present w/
W/ thrombosis of pulm. a. due to renal loss of low molecular proteins
37
Renal amyloidosis gross
enlarged, pale, increase in consistency, capsule easily peels off, cortical surface has finely stippled appearance
38
Sources of amyloid
* reactive systemic amyloidosis (most common) --> Serum amyloid A (SAA), chronic antigenic stimulation
* Immunoglobulin-derived
* Familial amyloidosis (AA)
* Islet amyloid polypeptide (IAPP)
39
Where would amyloid deposition occur in the following species: cattle, dog, cats, horse, sheep/pig?
* cattle: glomeruli, tubules, gut wall
* dog: glomeruli, tubules
* cats: medulla
* horse: liver
* sheep/pig: uncommon
40
amyloid affecting glomeruli primarily?
nephrotic syndrome
41
amyloid primarily affecting medulla
uraemic syndrome
42
Glomerular fxn
* produces ultrafiltrate (albumin & high molecular wt plasma proteins excludd from filtrate)
43
What are the 3 layers of the glomerular filtration membrane?
* 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
Damage to basement membrane leads to the leakage of...
albumin
45
What are the 3 resident cell types within the renal corpuscle
* Podocytes
* capillary endothelial cells
* mesangial cells
46
Primary glomerular dz's
* glomerulonephritis
* minimal-change nephropathy
* IgA-nephropathy
* focal segmental glomerulosclerosis
47
Systemic dz's assoc'd w/ glomerulopathies
* amyloidosis
* systemic lupus erythematosus (SLE)
* DM
48
hereditary disorders of the glomeruli
* familial glomerulopathies in dogs
* breed specific dz in other species (sheep, pigs)
49
Glomerulonephritis is a primary glomerular dz is accompanied by
secondary tubulointerstitial & vascular changes
50
glomerulonephritis is usually
immune-mediated
51
glomerulitis
inflammation restricted to glomeruli
52
glomerulopathy
glomerular dz w/o cellular inflammatory components
53
Pathogenesis of Immune-complex glomerulonephritis
* 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
Diseases associated w/ immune complex glomerulonephritis in dogs
CAV-1, chronic bacterial infections, valvular endocarditis, pyometra, borreliosis, SLE, neoplasia, Dirofilaria immitis, Leishmania, IMHA, hereditary complement deficiency, idiopathic
55
Diseases associated w/ immune complex glomerulonephritis in horses
* Strep spp.
* EIA virus
56
Diseases associated w/ immune complex glomerulonephritis in cows
* BVDV
* trypanosomiasis
57
Diseases associated w/ immune complex glomerulonephritis in cats
* FeLV
* FIP
* FIV
* neoplasia
* idiopathic
58
Diseases associated w/ immune complex glomerulonephritis in sheep
* herediatry complement deficiency (Finnish Landrace sheep)
59
Diseases associated w/ immune complex glomerulonephritis in pigs
* classical swine fever
* african swine fever
* PCV-2
* hereditary complement deficiency
60
Pathogenesis of immune-mediated glomerular injury
* 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
Membranous glomerulonephritis
* 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
