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Renal > Pathology of the kidneys and LUT > Flashcards

Pathology of the kidneys and LUT Flashcards

1
Q

3 functional causes of renal failure

A
  • PRE-RENAL; compromised renal perfusion –> reduced RBF –> renal ischaemia secondary to circulatory collar or local obstruction of BVs
  • INTRA-RENAL: compromised kidney function: tubular necrosis, embolic dz or ascending pyelonephritis
  • POST-RENAL: obstruction of urine outflow: ascending ingection, urolithaisis , neoplasms
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2
Q

When does acute renal failure (ARF) occur?

A

when >75% renal functional capacity abruptly impaired

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3
Q

What happens in ARF?

A
  • abrupt azotaemia
  • retained K+ –> rapid cardiac dysryhthmias and arrest
  • rentained phosphates –> binds ionised Ca (hypocalcaemia) –> mm tremors and coma
  • disturbed electrolytes and reduced pH –> metabolic acidosis
  • hypertension
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4
Q

CS - ARF

A
  • oliguria

- anuria

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5
Q

Hx and CS - CRF

A
  • PU/PD
  • isothenuria
  • dehydration
  • wt loss
  • poor coat condition
  • V and inappetance
  • halitosis with dribbling and oral ulceration
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6
Q

Gross appearance - CRF

A
  • pale and shrunken with irregular depression of capsular surface
  • excessive adhesion of capsule of capsule to underlying cortex
  • thin cortex
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7
Q

Gross appearance - ARF

A
  • enlarged
  • softer
  • redder
  • smooth
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8
Q

Histology - CRF

A
  • increased interstitial CT
  • renal tubules absent, atrophic or compressed
  • hyperplastic and hypertrophic tubules
  • intraluminal protein
  • thick hyalinised BM
  • calcification of BVs and BM
  • multiple acquired cysts
  • glomerulosclerosis
  • foci of interstitial lymphocytes and plasma cells
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9
Q

Features - endstage renal failure

A
  • renal fibrosis is replaceent of renal parenchyma with mature fibrous tissue
  • endpoint of all reparative processes. when conditions aren’t conducive for healing by regeneration
  • severity = intensity of primary renal dz
  • firm and distorted (contraction of fibrous scar)
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10
Q

Define uraemia

A

toxic syndrome associated with renal failure –> multisystemic CS and lesions

  • ARF: rapid onset precludes renal compensation of electrolyte imbalance –> few non-renal lesions
  • CRF: characteristic non-renal lesions
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11
Q

Outline systemic effects of uraemia

A
  • insufficient glomerular filtration –> azotaemia –> progressive retention of nitrogenous metabolites
  • concomitant tubular function failure
  • plasma protein loss –> oedema
  • hyperphosphataemia + secondary renal hyperparathyroidism
  • reduced EPO production –> decreased stimulation of EPO maturation –> non-regenerative anaemia
  • hypertension
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12
Q

Describe how uraemia leads to secondary renal hyperparathyroidism

A

When GFR hyperphosphataemia precipitates ionised calcium concentrated in serum –> decreased calcitriol activation –> decreased GIT Ca absorbed –> decreased ionised serum Ca –> PTH secretion –> Ca release by osteoclastic bone resorption –> increase renal excretion of phosphate and reabsorption of Ca –> parathyroid chief cell hyperplasia –> renal secondary hyperparathyroidism

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13
Q

How does nephrocalcinosis affect renal dz?

A

nephrocalcinosis perpetuates renal dz –> calcification of tubualr BMs, Bowman’s capsules, necrotic tubular epithelium –> gritty when cut

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14
Q

How does secondary renal hyperparathyroidism affect soft tissues?

A

causes fibrous osteodystrophy and mineralisation of soft tissues (e.g. rubber jaw)

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15
Q

Causes of hypercalcaemia

A
  • secondary renal hyperparathyroidism
  • primary hyperparathyroidism
  • vitamin D intoxication
  • hypercalcaemia of malignancy (paraneoplastic syndrome, PTHrp –> bone resorption, lymphoma or anal sac apocrine gland carcinomas or multiple myelomas)
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16
Q

Name 2 non-renal lesions of uraemia

A
  1. Endothelial degeneration + necrosis –> VASCULITIS with secondary thrombosis and infarction in various tissues
  2. CAUSTIC INJURY to epithelium of oral cavity and stomach (ulcers) consequent to production of large concentrations of ammonia after splitting of salivary gastric urea by bacteria
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17
Q

Describe ulcerative glossitis and stomatitis d/t uraemia

A
  • brown foul smelling mucoid material adherent to eroded and ulcerated lingual and oral mucosa
  • often bilaterally symmetrical ulceration present under tongue
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18
Q

Describe ulcerative and haemorrhagic colitis d/t ureamia

A
  • horses and cattke

- large areas of colonic mucosa are often oedematous and dark-red d/t haemorrhage

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19
Q

List non-renal lesions of uraemia

A
  • ulcerative glossitis and stomatitis
  • ulcerative and haemorrhagic colitis
  • ulcerative and haemorrhagic gastritis
  • uraemic encephalopathy
  • uraemic pneumonitis
  • intercostal mineralisation
  • fibrinous pericarditis
  • arterits
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20
Q

Outline ulcerative and haemorrhagic gastritis d/t uraemia

A
  • dogs, cats
  • also secondary to mineralisation of gastric mucosa and submucosal arterioles
  • V (black tarry stomach contents)
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21
Q

What is uraemic encephalopathy?

A

= non-renal lesion of uraemia

- white-matter spongiform degeneration

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22
Q

What is uraemic pneumonitis?

A

= non-renal lesion of uraemia

  • underlying lesion –> vasculitis affecting alveolar apillaries –> increased vascular permeability
  • pulmonary oedema, fibrin exudation and a mild infiltrate (macrophages, neutrophils)
  • Also, patchy or diffuse pulmonary calcification –> failure to collapse, pale and gritty areas
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23
Q

What is intercostal mineralisaiton?

A

= non-renal lesion of uraemia

- clacification of subpleural CT of ICSs

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24
Q

WHat is fibrious pericarditis?

A

= non-renal lesion of uraemia

- fine granular deposits of Ca in epicardium

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25
Q

What is arteritis?

A

= non-renal lesion of uraemia

  • finely granular plaques within left atrial endocardium and proximal aorta and pulmonary trunk
  • arteritis in conjunction with loss of anticoagulant antithrombin 3 by glomerular leakage is conducive to formation of large mural thrombi at these sites.
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26
Q

How is the renal parenchyma divided proportionally?

A

into cortex and medulla (1:2)

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27
Q

T/F: porcine and bovine kidneys are multilobar but only bovine kideys have external lobation

A

True

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28
Q

Describe spp differences of renal medulla

A
  • CAT: single renal papilla
  • DOG, SHEEP, HORSES: fused crest-like papilla (renal medullary crest)
  • PIG, CATTLE: multiple renal papillae
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29
Q

What are papillae surrounded by?

A

minor calyces that coalesce to form major calyces that empty into renal pelvis where urine collects before it enters the ureters

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30
Q

Define urineferous tubule

A

nephron and CD

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31
Q

T/F: damage to any component of the nephron –> diminished function and progressive damage to the kidney

A

True

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32
Q

In the early stages of disease, specific anatmonic components may be targeted by specific insults

A

True (e.g. glomeruli in IMD)

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33
Q

What are the portals of entry for kidney infections

A
  • HAEMATOGENOUS: septic embolic nephritis or non-septic nephritis with infarction
  • GLOMERILAR INFILTRAT
  • ASCENDING FROM URETER
  • DIRECT PENETRATION
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34
Q

Outline glomerular filtrate as a portal of entry to the kidney

A
  • substances secreted into glomerular filtrate can produce localised trauma to tubular lining cells such as oxalate crystals
  • filtered preformed toxins or metabolised substances processed by the tubular lining epithelium exert their effect principally on PCT epithelium
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35
Q

Outline ascrending form ureter

A

CONTAMINATION d/t:

  • GIT content
  • genital tract contamination
  • dermal contamination (perivulval dermatitis)
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36
Q

Outline direct penetration as a portal of entry

A
  • activation of products in PCT
  • heavy metals
  • crystalline oversaturation
  • direct toxin action
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37
Q

What is the commonest kidney developmental disorder?

A

renal aplasia (uni or bilateral; unilateral cases can be asymptomatic)

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38
Q

List developmental disorders of kidneys

A
  • RENAL APLASIA
  • HYPOPLASIA
  • ECTOPIC KIDNEYS
  • FUSED KIDNEYS
  • DYSPLASIA
  • PROGRESSIVE JUVENILE NEPHROPATHY
  • RENAL CYSTS
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39
Q

Define renal hypoplasia

A

incomplete development of one/both kidney (fewer than normal nephrons)

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40
Q

Define ectopic kidneys

A

pelivc canal or inguinal position –> histological structure and function usually normal byt malposition of ureters predisposes them to obstruction –> secondary hydronephrosis

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41
Q

What are fused kidneys

A

fusion of cr or cd poles –> horseshoe shape –> S+F normal

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42
Q

What is dysplasia?

A

abnormal differentiation in one/both kidneys

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43
Q

What is progressive juvenile nephropathy?

A
  • familial renal dz
  • Llasa apso, Shih Tzu and golden retrievers
  • severe bilateral renal fibrosis
  • shrunken pale kidneys, pitted surface
  • foetal glomeruli, interstitial inflammation, fibrosis and tubular dilation
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44
Q

What are renal cysts?

A

= developmental disorders of kidney

  • spherical thin-walled distensions of cortical or medullary tubules filled with clear fluid
  • congenital secondary to renal dysplasia or acquired d/t renal interstitial fibrosis or other renal dz causing intratubular obstruction
  • genetics, exposure to toxic chemicals
  • as cysts enlarge, adjacent parenchyma compressed –> renal function impaired if extensive
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45
Q

Breeds- polycystic kidney dz

A

Persian cats and bull terriers

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46
Q

List 4 dz of glomeruli

A
  • immune-mediated glomerulonephritis
  • glomerular amyloidosis
  • acute suppurative glomerulitis
  • glomerulosclerosis
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47
Q

What does the glomerular filtration barrier consist of?

A
  • fenestrated endothelium
  • basal lamina
  • pedicles of podocytes (visceral epithelium of Bowman’s capsule)
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48
Q

List causes of glomerular damage

A
  • damage to filtration barrier by deposition of immune complexes
  • entrapment of thromboemboli and bacterial emboli
  • direct viral or bacterial infxn of glomerular components
  • damage to other parts of nephron
  • reduced BF
  • chronic loss of tubular function
  • amyloid deposition
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49
Q

What functions of the glomerulus might be affected in disease?

A
  • plasma ultrafiltration
  • BP regulation
  • peritubular BF regulation
  • tubular metabolism regulation
  • circulating macromolecule removal
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50
Q

What is a consequence of protein losing nephropathy?

A
  • albumin leaks into glomerular filtrate and overwhelms reabsorptibe capabilities of PCT
  • protein rich glomerular filtrate accumulates in dilated tubular lumina –> proteinuria and hypoproteinaemia
  • prolonged –> reduced plasma COP and loss of AT3 –> nephrotic syndrome
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51
Q

Characteristics - nephrotic syndrome

A
  • generalised oedema
  • ascites
  • pleural effusion
  • hypercoagulability
  • hypercholesterolaemia
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52
Q

What are the responses of the glomeruli to injury?

A
  • necrosis
  • proliferation (cells and membranes)
  • infiltration (leukocyte)
  • reduced vascular perfusion
  • increased vascular permeability (protein leakage)
  • continued/ severe injury –> atrophy and fibrosis of glomerular tuft (sclerosis) and secondarily atrophy of renal tubules
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53
Q

Outline I-M glomerulonephritis

A
  • criculating immune complexes may be depositied in subepithelial, subendothelial or mesangial locations
  • formation of Abs against entrapped non-specific Ags or Ags within the GBM
  • stimulates complement fixation –> chemotactic (neutrophils, macrophages) –>release of proteinases and O2 derived free radicals –> BM damage
  • activation (glomerular epithelial and mesangial cells) to produce damaging mediators (oxidants, proteases)
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54
Q

What does I-M glomerulonephritis (GN) occur in association with?

A
  • with persistent infections or other diseases with prolonged antigenaemia that enhances the formation of soluble immune complexes
  • specific viruses (FeLV, FIP)
  • chronic basteria (pyometra, pyoderma)
  • chronic parasitism
  • autoimmune dz (SLE)
  • neoplasia
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55
Q

Effect of continual exposure of glomeruli to soluble immune complexes

A

Persistent infections –> progressive glomerular injury

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56
Q

Dx - I-M glomerulonephritis

A
  • IF or IHC (Ig and complement in glomerular tufts)
  • specific causative Ag usually undeterminable
  • demonstration of electron dense deposits in mesangial, subepithelial or subendothelial locations by EM is supportive of IM-GN
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57
Q

Gross appearance - I-M glomerulonephritis

A
  • glomeruli visible as pinpoint red/pale dots on cut surface of cortex
  • fine granularity to cortical surface
  • capsule may be adherent
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58
Q

Histopathology - IM-GN

A
  • increased cellularity and proliferation (glomerular cells)
  • thickening of glomerular BM and Bowman’s capsule
  • deposition of fibrinous thrombi in glomerular capillaries
  • dilated renal tubules filled with homegenous proteinaceous fluid
  • interstitial and periglomerular fibrosis
  • foci of interstitial lymphocytes and plasma cells
  • glomerulosclerosis
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59
Q

Outline glomerular amyloidosis

A
  • reactive amyloidosis (often associated with chronic inflammatory disorders, systemic infectious dz, neoplasia)
  • amyloid deposits composed of fragments of serum APP
  • glomeruli commonest renal site for deposition
  • idiopathic
  • Abyssinian cats and shar peis (medullary interstitium) hereditary
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60
Q

Consequences - glomerular amyloidosis

A
  • PLN and nephrotic syndrome –> proteinaemia and uraemia
  • decreased RBF through glomeruli and vasa recta –> tubular atrophy, degeneration, fibrosis. Severe –> renal papillary necrosis
  • medullary amyloidosis usually asymptomatic unless results in papillary necrosis
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61
Q

Gross appearance - glomerular acidosis

A
  • enlarged, pale, smooth to finely granular capsular surface
  • amyloid laden glomeruli may be visible as fine glistening dots on cut cortex
  • brown staining of glomeruli after I2 tx
  • medullary amyloidosis not grossly visible
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62
Q

Histopathology - glomerular acidosis

A
  • glomerular amyloid is deposited in mesangium and subendothelium
  • acellular eosinophilic homogenous to fibrillar material
  • secondary changes in tubules –> dilated + contain proteinaceous and cellular casts
  • stains with congo red and the amyloid deposits have apple-green birefringence when viewed under polarised light
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63
Q

Other names - acute suppurative glomerulitis

A

bacterial or embolic nephritis

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64
Q

Describe acute suppurative glomerulitis

A
  • Bacteraemia –> bacteria lodge in glomerular and interstitial capillaries –> microabscesses form throughout cortex.
  • although glomeruli targeted –> manifestation of renal vascular dz
  • bacteria produce toxic by-products –> damage endothelium –> localised vasculitis and colonisation –> embolic nephritis
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65
Q

CAuses - acute suppurative glomerulitis

A
  • Actinobacillus equuli (foals)
  • E. rhusiopathie (pigs)
  • Corynebacterium pseudotuberculosis (sheep/goats)
  • Arcanobacteirum pyogenes (cattle)
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66
Q

Gross appearance - acute suppurative glomerulitis

A

Multifocal random raised tan pinpoint foci –> subcapsular and cut surface or renal cortex

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67
Q

Histopathology - acute suppurative glomerulitis

A
  • glomerular capillaries contain numerous bacterial colonies admixed with necrotic debris + neutrophils
  • glomerular or interstitial haemorrhage
  • can persist as focal residual abscesses or progressively replaced by chronic inflammation and coalescing scars
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68
Q

Define glomerulosclerosis

A
  • decreased # functional glomeruli
  • loss of glomerular capillaries and replacement of mesangial matrix and Bowman’s space by FCT
  • decreased BF through vasa recta derived from glomerular efferent arteriole
  • resulting hypoxia –> tubular epthelial degeneration adn loss
  • chronic proteinuria
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69
Q

Name 2 diseases of tubules

A
  • inherited

- acute tubular necrosis

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70
Q

Function - tubular BM

A
  • prevent intraluminal organisms gaining easy access to interstitium
  • scaffold for reepithelialisation of tubule which follows tubular necrosis
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71
Q

Causes - tubular disease

A
  • blood borne infections
  • ascending infections (intratubular pathogens)
  • direct damage from toxins (intratubular effects)
  • ischaemia
  • infarction
  • tubular obstruction
  • interstitial fibrosis
  • external compression
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72
Q

T/F: toxic and hypoxic insults to the kidney can be synergistic

A

True - can be hard to differentiate the two

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73
Q

Responses of tubules to injury

A
  • degeneration, necrosis, apoptosis +/or atrophy –> PCT most vulnerable
  • cells slough into lumen to form cellular casts
  • remaining tubules undergo compensatory hypertrophy in attempt to maintain overall renal function
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74
Q

T/F: there is no regeneration of nephrons

A

True

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75
Q

Are tubular BMs retained more after toxic or ischaemic insults?

A

toxic

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76
Q

What happens in tubular injury if BM remains intact?

A

Repair by proliferation of remaining epithelial cells

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77
Q

What happens in tubular injury if BM doesn’t remain intact?

A

Necrosis, failure of functional repair and replacement by fibrosis

78
Q

Name 3 inherited abnormalities in renal tubular function

A
  • primary renal glycosuria
  • fanconi syndrome
  • cystinuria
79
Q

Describe primary renal glycosuria

A
  • Norwegian elkhounds, sporadically in other breeds
  • functional disorder 00> capacity of tubular epithelial cells to reabsorb glucose is reduced –> no gross /histo findings
  • predisposes LUT bacterial infection
80
Q

Describe Fanconi syndrome

A
  • Basenji (hereditary defect in tubular protein reabsorption, glucose, phosphate, aa)
  • can develop progressive renal unsufficiency and associated renal fibrosis
81
Q

Describe cytinuria

A
  • sex linked

- tubular defect in male dogs –> predisposes calculus formation and obstruction of LUT

82
Q

Most important cause - acute renal fualure

A

Acute tubular necrosis

- it is nephrotoxic or ischaemic injury to renal tubular epithelium

83
Q

CS - acute tubular necrosis –> ARF

A
  • oliguria or anuria:
  • leakage of tubular filtrate across disrupted BM –> intersitium
  • intratubular obstruction –> sloughed necrotic epithelium
84
Q

Describe toxins causing acute tubular necrosis

A
  • from vasculature or tubular lumen
  • preferentially damage kidney
  • direct damage + reactive metabolites
  • stimulate vasoconstriction –> nephrotoxin asscoiated ischaemia
  • decreased renal perfusion –> decreased GFR and activation of arteriolar vasoconstriction –> prolonged ischaemia
85
Q

Causes - haemogloninuric nephrosis

A
  • chronic Cu toxicity (sheep)
  • babesiosis (cattle)
  • red male toxicity (horses)
  • AIHA (dogs)
86
Q

Describe myoglobinurix nephrosis

A

–> extensive mm necrosis –> azoturia of horses, capture myopathy of exotic or wild animals and severe trauma

87
Q

How do heavy metals cause acute tubular necrosis?

A
  • lead –> membrane or mitochondrial damage in PCT cells
  • acid fast IN inclusions (PCT epithelium)
  • in general, the specific metal in toxic tubular injury cannot be ID by renal lesions alone
88
Q

What causes acute tubular necrosis?

A
  • nephrotoxic pigments
  • heavy metals
  • pharmaceutical agents
  • fungal and plant toxins
  • ethylene glycol (antifreeze)
  • vitamin D
  • pet food contaminants
  • bacterial toxins
89
Q

How do pharmaceutical agents cause acute tubular necrosis?

A
  • NSAIDs –> decreased synthesis of PG –> afferent arteriolar constriction –> decreased renal perfusion –> acute tubular degeneration and papillary necrosis
  • excessive amounts or concomitant disorder e.g. dehydration, CHF or CRD
90
Q

Name 4 fungal/ plant toxins that can cause acute tubular necrosis

A
  • mycotoxins produced by Aspergillus spp.
  • lily plant - cats
  • grapes and raisins -dogs
  • oak - cattle
  • oxalate - cattle and sheep
91
Q

Outline oak poisoning of cattle

A
  • ingestion of leaves, buds or acrons
  • toxic substances are metabolites of tannins
  • target endothelial cells –> vascular damage
  • perirenal oedema
92
Q

How do oxalate containing plants cause acute tubular necrosis in cattle/sheep?

A
  • calcium oxalates precipitate in BVs or within renal tubules
  • cause obstruction and epithelial cell necrosis
  • neuromuscular dysfunction –> hypocalcaemia
93
Q

Outline ethylene glycol –> acute tubular necrosis

A
  • dogs, cats, occasionally pigs
  • readily absorbed from GIT
  • oxidised by hepatic alcohol dehydrogenase to toxic metabolites including glycolic acid and oxalate
  • filtered by glomeruli
  • directly toxic to tubules
  • calcium oxalate crystals precipitate in renal tubular lumens –> intrarenal obstruction
94
Q

How does vitamin D –> acute tubular necrosis?

A
  • multiple excessive doses
  • accidental ingestion of calciferol containing rodenticides
  • chronic ingestion of plants which contain a chemical with vit D like biologic activity (Cestrum diurnum)
  • increased GIT Ca absorption –> hypercalcaemia –> progressive mineralisation of tubular and GBMs
95
Q

Which pet food contaminants can cause acute tubular necrosis?

A

melamine and cyanuric acid

96
Q

Outline bacterial toxin induced acute tubular necrosis

A
  • enteric proliferation of C.perfringens type D –> epsilon toxin produced (small ruminants)
  • pulpy kidney –> acute tubular degeneration and/or necrosis, intersitital oedema and haemorrhage
  • autolysis can produce similar changes
97
Q

Name a disease of renal interstitium

A

Interstitial nephritis

98
Q

What is renal interstitium?

A

the fibrovascular stroma that surrounds the nephron

99
Q

What can primary interstitial dz or subsequent to tubular damage lead to?

A

tubulointerstitial disease

100
Q

Causes - dz of renal interstitium

A
  • ascending infection (pyelonephritis)
  • haematogenous infection of tubules and interstitium –> E.coli, leptospira, canine adenovirus
  • secondary to injury of vasculature, tubules or glomeruli
101
Q

Responses of interstitium to injury

A
  • oedema
  • haemorrhage
  • inflammation
  • fibrosis
102
Q

Gross appearance - diseases of interstitium

A

coalescing grey foci on the capsular and cut surface

103
Q

Histopathology - interstitial diseases

A
  • initially oedema, haemorrhage and neutrophilic infiltration
  • tubular epithelial degeneration
  • vascular compromise
  • fibrosis
104
Q

List some diseases of renal interstitium

A
  • E.coli septicaemia
  • equine arteritis virus and PRRS
  • canine adenovirus
  • leptospirosis
  • FIP
105
Q

Effect of E.coli septicaemia on renal interstitiu,

A
  • ‘white spotted kidney’
  • embolic nephritis or nonsuppurative interstitial nephritis
  • microabscesses replaced by lymphocytes, plasma cells and macrophages
106
Q

Effect of EAV or PRRS on interstitium

A
  • multifocal lymphohistiocytic tubulointersitial nephritis with interstitial oedema
  • vasculitis –> fibrinoid necrosis and lymphohistiocytic infiltrates
  • virus in the endothelium and macrophages
107
Q

Effect of canine adenovirus on renal interstitium

A
  • viraemia –> localisation in glomeruli (viral glomerulitis)
  • transient immune complex GN
  • recovery from acute dz
  • disappearance of virus from glomeruli only to reappear in tubular epithelial cells
  • basophilic IN viral inclusions
  • persistence of virus in tubular epithelium (wks-months)
  • viral induced cytolysis –> tubular epithelial necrosis –> production of chronic lymphoplasmacytic and less commonly histiocytic interstitial nephritis
108
Q

Effect of leptopspirosis on renal interstitium

A
  • bacterial tubulointerstitial nephritis
  • leptospiraemia –> organsisms localise in renal interstitial capillaries
  • migrate through vascular endothelium –> persist in interstitial spaces
  • migrate into renal tubular lumina
  • degeneration and necrosis of tubular epithelial cells
  • infiltrate of macrophages, lymphocytes and plasma cells in interstitium and neutrophils can be present in tubular lumina
109
Q

Effect of FIP on renal interstitium

A
  • granulomatous necrotising vasculitis
  • interstitial pyogranulomas
  • other causes of granulomatous interstitial nephritis: mycobacteria, fungi, parasites
110
Q

Name 3 dz of renal vascular system

A
  • hyperaemia and congestion
  • haemorrhage and thrombosis
  • infarction
111
Q

What gives rise to vasa recta?

A

efferent glomerular arteriole (as close to juxtamedullary region)

112
Q

What gives rise to the peritubular capillary network?

A

efferent GA as close to the subcapsular region

113
Q

T/F: the arterial BS to cortex is terminal

A

True

114
Q

Name defence mechanisms of vascular intact epithelium

A
  • prevents access by intravascular pathogens

- prevents activation of clotting cascade and formation of thrombi

115
Q

List responses of the vasculature to injury

A
  • hyperaemia and congestion
  • haemorrhage and thrombosis
  • infarction
  • papillary (medullary crest) necrosis
  • embolic nephritis
116
Q

Differnetiate hyperaemia and congestion

A
  • HYPERAEMIA: active process in which arterial dilation increases BF
  • CONGESTION: passive process in which venous blood accumulates within vasculature secondary to hypovolaemic shock, cardiac insufficiency or hypostatic
117
Q

When/why might you get haemorrhages in the renal vascular system?

A
  • direct trauma
  • coagulopathies
  • septicaemia –> erysipelas, streptococcal infections
  • embolic bacterial diseases –> actinobacillus equuli
  • vasculitis –> FIP
  • vascular necrosis –> canine herpesvirus
  • DIC
118
Q

Define thrombosis

A

formation of an inappropriate blood clot on the wall of a blood or lymphatic vessel

119
Q

What is Virchow’s triad?

A

major determinants of thrombosis

120
Q

What are the parts of Virchow’s triad?

A
  1. ENDOTHELIAL INJURY (canine adenovirus, FIP, endotoxin)
  2. DYNAMICS OF BF –> stasis or turbulent BF –> cardiac dz or hypovolaemia
  3. HYPERCOAGULABILITY: inflammation, DIC, glomerulonephritis and glomerular amyloidosis, AT3 deficiency
121
Q

What is DIC?

A
  • serious manifestation f abnormal coagulation –> generation of excess thrombin
  • diffuse vascular damage –> endotoxin induced –> exposure of tissue factor –> induced activation of extrinsic coagulation to produce thrombin
  • formation of widespread fibrin thrombi in renal microcirculation –> PLT and coagulation factor consumption –> widespread haemorrhages
  • not a primary dz but possible complication of any condition associated with widespread thrombin activation
  • results in cortical infarction if ischaemic (coagulative) necrosis)
122
Q

Result - renal infarcts

A

areas of peracute ischaemia that undergo coagulative necrosis

123
Q

How does infarction cause occlusion of either arterial supply or venous drainage?

A
  • emboli (thromboembolic most common)
  • vasospasm
  • extrinsic compression of vessel
  • traumatic rupture
124
Q

What region is affected if the interlobular artery is blocjed?

A

only the cortex

125
Q

What region is affected if the arcuate artery is blocked?

A

both cortex and medulla

126
Q

Sources of renal emboli

A
  • cardiac mural or valvular thrombi
  • endarteritis in parasitic dz (equine strongylosis)
  • neoplastic cell emboli
  • bacterial or septic emboli (A. pyogenes in cattle, E.rhusiopathie in pigs. S.aureus in dogs)
127
Q

Appearance - infarct

A
  • soon after: dark-red
  • Later: some become paler and defined by a narrow rm of congestion
  • as cells undergo necrosis and swell in the affected area blood is forced out of the infarcted region
  • lysis and phagocytosis of necrotic tissue and replacement by FCT –> matures to discrete scar
128
Q

Name different kidney neoplasias

A
  • tumours of embryological origin
  • mesenchymal tumours
  • epithelial tumours
129
Q

How common are renal neoplasias?

A

Not very -

130
Q

How malignant are primary renal tumours?

A

highly malignant - metastatic dz common

131
Q

Outline renal tumours of embryological origin

A
  • nephroblastomas (pigs, chickens, common)
  • usually incidental finding at slaughter
  • arise from primitive pluripotential tissue (young animals)
132
Q

Name different renal epithelial tumours

A
  • renal adenomas
  • renal carcinomas
  • transitional cell papillomas and carcinomas
133
Q

Feature - renal adenoma

A

usually incidental at necropsy

134
Q

Outline renal carcinomas

A
  • large with foci of haemorrhage, necrosis and cystic degeneration
  • usually occupy and obliterate one pole of kidney
  • paraneoplastic condition –> polycythemia –> EPO overexpression
135
Q

Describe TC papillomas and carcinomas

A
  • arise in renal pelvis and LUT
  • can obstruct urinary outflow
  • can invade into kdiney
136
Q

Outline metastitic tumours of the kidney

A
  • carcinomas and sarcomas arising in other organs can metastasise to kidneys
  • randomly scattered multiple nodules
  • usually involves both kidneys
  • renal lymphoma –> cats and cattle
  • neoplastic cells form sheets of cells within renal parenchyma
137
Q

Name 3 diseases of the renal pelvis

A
  • hydronephrosis
  • pyelonephrosis
  • papillary (medullary crest) necrosis
138
Q

What is EBL?

A

= Enzootic bovine leukosis

  • causes lymphocyte transformation –> lymphoma
  • all bovine tumours are notifiable (except papillomas and HSA)
139
Q

Describe hydronephrosis

A
  • dilation of renal pelvis because obstruction in urine outflow –> increased pelvic pressure –> atrophy of renal parenchyma
  • as pressure increases –> interstitial vessels collapse and renal BF is decreased –> hypoxia and ischaemic necrosis –> tubular atrophy and interstitial fibrosis
  • thin walled fluid filled sac lined by flattened transitional epitheliumm
  • if contaminated by blood bacteri lodging in hydronephrosis kideny –> filled with pus (pyonephrosis)
140
Q

Causes - hydronephrosis

A
  • congenital malformation
  • ureteral or urethral blockage d/t urinary calculi
  • chronic inflammation
  • ureteral or urethral neoplasia
  • neurogenic functional disorders
141
Q

Differentiate unilateral and bilateral hydronephrosis

A
  • UNILATERAL: hydronephrosis can become notable –> continual urine production adn pooling of urine into expanding pelvis
  • BILATERAL: uraemia before pelvic enlargement becomes extensive
142
Q

Describe pyelonephritis

A
  • bacterial infxn of pelvis extending into renal tubules and concomitant interstitial inflammation
  • form of suppurative tubulointerstitial dz
  • pyelonephritis frequently bilateral and recurrent infxn common
  • BACTERIA: Corynebacterium spp, E coli, Staph spp, Strep spp, Pseudomonas aeruginosa and Arcanobacterium pyogenes
  • cows and sows
  • associated with parturition, service, catheter use
  • renal medullar v susceptible to effects of pressure and bacterial infection
143
Q

Contrast cow and sow pyelonephritis

A
  • COW: cases sporadic, most likely chronic

- SOW: 2-3wks pp, acute cases

144
Q

Is pyelonephritis usually uni or bilateral?

A

bilateral

145
Q

Mechanisms - pyelonephritis

A
  • ascending bacterial infection from LUT via ureter –> vesicoureteral reflux during micturition of bacteria contaminated urine
  • competency of vesicoureteral valve is compromised –> increased reflux
  • descending bacterial infxn/ haematogenous –> extension from embolic nephritis (rare)
146
Q

Common descending infection –> pyelonephritis

A
  • Staph

- E.coli

147
Q

Common ascending infection –> pyelonephritis

A
  • E.coli
  • Proteus
  • Enterobacter
148
Q

Effects - increased vesicoureteral reflux

A
  • when pressure is increased in urinary bladder –> urethral obstruction
  • bladder wall inflammation –> cystitis
  • endotoxin from gram negative bacteria –> inhibit ureteral peristalsis
149
Q

Gross appearance - pyelonephritis

A
  • ureters distended with suppurative exudate
  • exudate in pelvis and medulla
  • may extend into cortex –> radially orientated red or grey streaks
  • polar scars
  • inflammation can extend through kidney surface –> peritonitis
150
Q

Histopatholgy - pyelonephritis

A
  • transitional epithelium necrotic and sloughed
  • necrotic debris, fibrin, neutrophils, bacteria adhere to denuded surface and accumulate in tubules
  • interstitial inflammation, haemorrhage and oedema
  • if vasa recta are obstructed –> papillary necrosis
  • extend radially into cortical tubules
  • lymphocytes, plasma cells, macrophages and fibrosis
151
Q

T/F: most of the medullary blood supply comes from teh cortex after passing through the glomeruli and entering the vasa recta

A

True

152
Q

Types of papillary necrosis

A

Primary and secondary

153
Q

Outline primary papillary necrosis

A
  • prolonged tx/ overdose of NSAIDs –> damages medullary interstitial cells
  • decreased PG synthesis (vasodilator) –> decreased normal blood flow –> ischaemic necrosis of inner medulla
154
Q

Causes - secondary papillary necrosis

A
  1. decreased vasa recta BF –> glomerular amyloidosis or glomerulosclerosis
  2. compression of vasa recta within medulla –> interstitial oedema or fibrosis
  3. compression of renal papilla –> pelvic calculi, LUT obstruction, pyelonepritis and vesiculoureteral reflux
155
Q

Progression of papillary necrosis

A
  • sharply delineated coagulative necrosis of inner medulla
  • eventually sloughs –> detached fragment in pelvis –> large fragments could obstruct ureter –> hydronephrosis
  • or nidus for formation of calculi
  • rarely lead to progressive renal damage/failure
156
Q

List diseases of LUT

A
  • developmental
  • LUT obstruction
  • urolithiasis
  • cystitis
  • neoplasia of LUT
157
Q

What is the vesicoureteral valve?

A
  • a mucosal flap
  • prevents reflux of urine from bladder into ureter and renal pelvis
  • mucosal surface should be smooth and glistening
158
Q

Appearance - urine

A
  • clear (except horses) - cloudy

- mucous and crystalline material produced by mucous glands in submuscosa or renal pelvis and proximal ureter

159
Q

What lines the LUT (epithelium-wise)?

A

pseudostratified transitional epithelium

160
Q

Causes - dz of LUT

A
  • infection (extension from GIT, genitals or skin OR descending infxn - pyelonephritis)
  • neoplasia
  • toxins/poisons
  • congenital defects
  • physical trauma –> urolith
  • obstruction
161
Q

Defence mechanisms - LUT

A
  • flushing of urine minimises risk of ascension of bacteria
  • peristalsis acts to elimiante bacteria with adhesion capabilites
  • inhospitable environment for bacterial growth controlled by urine pH
  • protective urothelial mucus coating
  • innate, humoral, cellular immune responses
162
Q

Responses of LUT to injury

A
  • dilation and pressure necrosis by obstruction
  • inflammation
  • neoplastic transformation
163
Q

List developmental abnormalities of LUT

A
  • ureteral aplasia and hyoplasia
  • ectopic ureters
  • patent urachus
164
Q

Describe ectopic ureters

A
  • empty into urethra, vagina or bladder neck
  • prediposes to infection or obstruction
  • CS = urinary incontinence
165
Q

Describe patent urachus

A
  • foals
  • foetal urachus fails to close –> direct channel b/w bladder and umbilicus –> urine dribbles from umbilicus
  • underlying omphalitis or congenital urethral obstruction
  • increased bladder pressure d/t obstruction –> forces urine out of urachus
166
Q

CS - LUT obstruction

A
  • stranguria
  • dysuria
    +/- haematuria
167
Q

Causes of obstruction (LUT)

A
  • CONGENITAL: cysts, ureter aplasia, ectopic ureters
  • ACQUIRED: calciuli, neoplasia, trauma/inflammation, circumferential fibrosis, bladder paralysis, vaginal/uterine prolapse, feline urologic syndrome –> fine struvite crystals (sand) in a mucoid protein matrix fill the urethra
168
Q

Consequences - LUT obstruction

A
  • distended/ruptured bladder
  • transmural ecchymotic haemorrhages
  • mucosal ulceration and haemorrhages
  • peritonitis
  • inflammation
169
Q

What is urolithiasis?

A

urinary calculi (uroliths) –> concretions formed from precipitation of excretory metabolites in urine

  • mineral admixed with proteinaceous debris
  • various sites
  • -> obstruction (males)
  • larger calculi in females
  • -> local pressure necrosis, mucosal ulcer, haemorrhage
170
Q

Predisposing factors - urolithiasis

A
  • unusual uric acid metabolism (Dalmations)
  • substances process abnormally by kidney (cystine or xanthine)
  • substances encountered in high levels in diet –> Mg in commercial cat food
  • vitamin A deficiency –> metaplasia of urinary tract epithelium –> desquamation of epithelium –> nidus for calculus formation
171
Q

Factors important for calculus formation in urolithiasis

A
  • urinary pH (struvites and carbonates form in alkaline, oxalates in acidic pH)
  • decreased water intake
  • mineral supersaturation
  • bacterial infection of LUT
  • structural abnormalities
172
Q

Sites of urolithiasis obstruction in different spp

A
  • CATTLE: proximal end of sigmoid flexure
  • SHEEP: urethral process
  • DOGS: proximal to base of os penis
173
Q

CS - acute cystitis

A
  • dysuria
  • stranguira
  • haematuria
174
Q

Cause - acute cystitis

A
  • Bacteria: uropathogenic E coli in many spp, Corynebacterium renale in cattle and Eubacterium suis in pigs
  • hydrolysis of urea by urease producing bacteria –> Crenale and E suis in pigs –> release excessive ammonia –> damage mucosa and increase urine pH
  • denuded oedematous mucosa, adherent neutrophils, bacterial colonies, hyperaemia and haemorrhage
175
Q

Predisposing factors - acute cystitis

A
  • urinary stasis
  • infrequent urination
  • calculi
  • catheterisation
  • prolonged AB use
176
Q

3 types of chronic cystitis

A
  • diffuse
  • follicular
  • polypoid
177
Q

Describe diffuse chronic cystitis

A
  • thickened mucosa infiltrated with mononuclear inflammatory cells
  • submucosal fibrosis
  • muscularis hypertrophy
178
Q

Describe follicular chronic cystitis

A
  • multiple small red nodules on mucosal surace
  • hyperplastic lymphoid cells surrounded hyperaemia and haemorrhage
  • associated with uroliths
179
Q

Describe polypoid chronic cystitis

A
  • multiple masses of proliferative nodules of CT (polyps)

- lymphocytes and neutrophils

180
Q

Describe emphysematous cystitis

A
  • glycosuria enhances bacterial growth
  • glucose molecules split by bacteria (E.coli, C. perfringens)
  • subsequent release of CO2 in bladder lumen. Absorption of gas into bladder lymphatics
181
Q

Describe toxic cystitis of cattle

A
  • chronic ingestion of bracken fern –> enzootic haematuria –> haemorrhage, chronic cystitis or bladder neoplasia
  • active metabolites of cyclophosphamide –> used to tx neoplasia and IMD
182
Q

What can develop after cattle ingest bracken?

A
  • toxic cystitis –> enzootic haematuria if ingestion is chronic
  • TCC and SCC
183
Q

Aetiology - LUT neoplasms

A

retention of urine with longer exposure of the eputhelium to carcinogens

184
Q

List examples of LUT neoplasias

A
  • EPITHELIAL: transitional cell papillomas or carcinomas, SCC and adenocarcinomas
  • MESENCHYMAL: leiomyomas, fibromas, lymphoma, rhabdmyosarcoma
185
Q

Describe transitional cell papillomas/ carcinomas of LUT

A
  • pedunculated
  • trigone
  • can cause obstruction –> hydronephrosis
  • males > females
186
Q

Where can SCC and adenocarcinomas of LUT arise from?

A

transitional epithelium

187
Q

Where do epithelial tumours of LUT metastasise to?

A
  • LN
  • lungs
  • kidneys
188
Q

Describe leiomyomas of LUT

A
  • circumscribed pale firm masses
  • resembles normal smooth mm
  • benign
189
Q

Where do fibromas of LUT arise from?

A

lamina propria

190
Q

Describe rhabdomyosarcomas of LUT

A
  • rare

- bladder and urethra (young

191
Q

Define botryoid

A

having the form of a bunch of grapes

- as in the appearance of rhabdomyosarcoma masses that protrude into bladder lumen

Renal (30 decks)

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