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FD6 > Pathology of the urinary system > Flashcards

Pathology of the urinary system Flashcards

1
Q

Name the features of a nephron

A
  • renal corpuscle
    • glomerulus with Bowmans capsule
  • Tubular system
    • prox convoluted tubule
    • L of H
    • distal convoluted tubule
    • collecting duct
  • intersititium (conn tissue)
  • vasculature
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2
Q

What occurs if 1 kidney is lost?

A
  • compensatory hypertrophy of other kidney- nephrons increase in size
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3
Q

What happens if you lose above 60% of functional nephrons?

A
  • start to see signs of renal disease
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4
Q

What id the nephron loss is more than 75%?

A
  • renal failure
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5
Q

What are the most common anomalies of renal development in domestic animals and describe their main features

A

Anomalies in the amount of renal tissue

  • Agenesis (unilateral or bilateral) - kidney does not develop
  • Renal hypoplasia- does not fully develop (reduced number of nephrons)

Anomalies of position, form and orientation

  • malposition = renal ectopia, pevlic or inguinal location
  • fusion e.g. horseshoe kidney
  • fetal lobulation

Renal dysplasia

Renal cysts

  • simple renal cysts
  • polycystic kidney disease
  • obstructive cysts
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6
Q

What anomalie is this?

A
  • unilateral renal agenesis
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7
Q

What anomalie is this?

A
  • horseshoe kidney
  • fusion at the cranial poles
  • not fatal as long as theres no blockage
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8
Q

What anomalie is this?

A
  • renal dysplasia
  • bilateral asymmetric development
  • small size and fibrous tissue strands
    • disorganised development of renal parenchyma
    • usually congenital
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9
Q

What anomalie is this and which species would you expect to find it?

A
  • simple renal cysts
  • (pig + calves-common)
  • no functional problems
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10
Q

What anomalie is this and what species does it normally affect?

A
  • feline PKD
  • Persian cats and Bull terriers
  • defects in polycistin gene
  • concurrent cysts in liver, pancreas
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11
Q

What are the circulatory disturbances of the kidney?

A
  • renal hyperaemia
  • renal haemorrhages
  • renal infarction
  • renal cortical necrosis
  • renal medullary necrosis
  • hydronephrosis
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12
Q

What is Infarction?

A
  • focal lesions of coagulative necrosis produced by embolic or thrombotic occlusion of the renal artery or one of its branches
    • trunk of artery- subtotal infarction
    • arcuate a. - wedge of cortex = medulla
    • radiate vessel - just a wedge of cortex
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13
Q

What is wrong with these kidneys?

A
  • infarction
    • well defined borders
    • cortex not shiny
    • lower pic = obstruction at apex
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14
Q

Describe the sequelae of events from acute infarction to scarring

A
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15
Q

What are Renal cortical necrosis and Acute tubular necrosis usually the result of?

A
  • hypoperfusion or shock
  • during hypotension
    • perfusion of outer cortical nephrons is reduced
    • perfusion of the deeper cortical nephrons is maintained
    • = intrarenal blood flow is redistributed towards the inner cortex and medulla
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16
Q
A
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17
Q

Name the glomerular diseases

A
  • multifocal/ embolic glomerulonephritis - inflammation of the glomerulus, also implies tubule-interstitial and vascular disease
  • glomerulitis- inflammation restricted to the glomerulus
  • glomerulopathy - glomerular disease with no inflammatory cell/ unknown aetiology
  • diffuse glomerular disease
    • membrano-proliferative
    • membranous
  • glomerulosclerosis - fibrosis of the glomeruli
  • glomerular amyloidosis
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18
Q

How does embolic/ multifocal glomerulitis occur?

A
  • embolic through circulation
  • bacteriaemia/ embolism -> lodges in glomeruli -> suppurative inflammation
  • often induced directly by agent
  • foals and calves
  • Pigs - erysepelothrix rhuspathies
  • foals - actinobacillae equi
  • can cause septicaemia
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19
Q

What is this showing?

A
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20
Q

What is diffuse glomerulonephritis?

A
  • 2 mechanisms:
  • IC deposition on GBM - (non-glomerulus IC) - immune response
  • Anti -GBM granulonephritis - immune response
  • always immune responses in subep area or BM
  • activation of the complement system
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21
Q

What is membrano-proliferative glomerulonephritis?

A
  • most common in dogs
  • soluble IC deposit
    • subendo
    • intramembranous
  • attracts leukocytes/ fixes complement
  • neutrophils damage glomerulus
  • proliferation of mesengial cells, accumulation of inflam cells, hypertrophy of endothelial cells
  • thickening of the BM
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22
Q

What is membranous glomerulonephritis?

A
  • most common in cats
  • soluble IC deposite
    • subepithelial
  • little inflammation
  • little prolif of mesengial cells
  • thickened BM (wire loop)
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23
Q

Name the diseases associated with IC deposition

A
  • dogs
    • neoplasia
    • pyometra
    • Leishmania spp
    • acute pancreatitis
    • SLE
    • canine adenovirus
  • cats
    • SLE
    • FeLV
  • Horses
    • equine infectious anaemia
    • streptococcus
  • Pigs
    • African and classical swine fever
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24
Q

What is IC deposition normally associated with?

A
  • diseases with prolonged antigenaemia
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25
Q

What is glomerulosclerosis?

A
  • end result - not revesible
  • sequel to chronic glomerular disease
    • increase in fibrous tissue
    • increase in mesengial matrix
    • loss of capillaries
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26
Q

What is glomerular amyloidosis?

A
  • amyloidosis = deposition of insoluble amyloid fibrils in extracellular spaces, disrupting normal function
  • amyloid - from acute phase protein serum amyloid A (SAA)
  • from liver (chronic inflam)
  • familial disease - Abyssinian cat and Shar Pei dog = excess
  • most animals - in glomeruli
  • CATS EXCEPTION - in medulla (interstitium, vessel walls, tubular BM)
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27
Q

What is this?

A
  • Glomerular amyloidosis
    • enlarged, pale, firm kidney
    • waxy consistency
    • prominent glomeruli on cut edge = grains of salt
    • small, irregular ‘emd-stage- kidneys if blood supply affected
    • can have secondary necrosis
    • Lugols iodine and dilure sulfuric acid - red/ brown staining of amyloid
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28
Q

What is shown?

A
  • Glomerular amyloidosis
  • glomeruli are enlarged by amorphous, pale eosinophilic deposits (amyloid)
  • acellular
  • same material deposited in medulla
  • stains orange-red/ peach with Congo red
  • apple green birefringence under polarised lught
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29
Q

How would you describe this kidney?

A
  • end stage
  • small
  • hard
  • irregular
  • finely granulated surface
  • pale
  • lost most of parenchyma
  • fibrous tissue
  • chronic kidney disease
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30
Q

What is proteinuria?

A
  • = hallmark of glomerular pathology and increased glomerular permeability (absence of haematuria and inflam)
  • low - small proteins
  • then damage increases - globulins + albumins
  • weight loss, lethargy, decreased muscle mass
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31
Q

What is Nephrotic syndrome?

A
  • characterised by:
    • hypoalbuminaemia
    • hypercholestrolaemia
    • ascites
    • anasarca
  • systemic oedema - reflects hypoalbuminaemia and activation of RAAS + independent intrarenal mechanisms (retains Na and water)
  • liver responds to hypoalbuminaemia - by producing more protein and also LDLs - large so not lost through leaky glomerulus = hypercholestrolaemia
  • animals with this = hypercoagulability
    • hypoalbuminaemia promotes sticky platelet aggregation
    • antithrombin only 6,500 daltons - so lost
    • increased hepatic synthesis of large clotting factors
32
Q

How does renal failure occur from glomerular disease?

A
  • decreased glomerular capillary blood flow
  • decreased GFR
  • decreased formation of ultrafiltrate
  • decreased perfusion of peritubular capillaries
  • decreased blood suppl to tubules and renal intersitium
  • loss of entire nephron
  • lead to acute or chronic renal failure
33
Q

What is a difference between toxic and ischaemic injury (ATI)?

A
  • toxic - lose an area involving several nephrons
  • ischaemic - lose segments (lack of O2)
34
Q
A
35
Q

What are the causes of ischaemic ATI?

A
  • prolonged hypotension (shock - haemorrhagic, post-op)
  • ischaemia - severe dehydration, heat stroke, anaemia, burns
  • necrosis of tubular ep and BM
36
Q

What are the causes of Nephrotoxic ATI?

A
  • drugs
    • aminoglycosides e.g. gentamycin
    • cisplatin
    • tetracyclines
    • amphotericin
  • oxalate
    • ethylene glycol
    • plants containign oxalate - halogeton, rhubarb
  • melamine and cyanuric acid
  • plants
    • amaranthus
    • quercus spp
    • lilium
    • grapes and raisins
  • pigments
    • haemoglobin
    • myoglobin
  • bacterial toxins
    • C.perfringens type D
37
Q

What are the mechanisms of action of the toxic renal drugs?

A
  • aminoglyocides - direct tubular toxicity and vasoconstriction
  • cisplatin - direct tubular damage and RAAS system vasoconstriction
  • tetracyclines - direct tubular toxicity
  • amphotericin B - direct tubular toxicity
38
Q

What is this?

A
  • tetracyclin toxicity, cattle
  • tubular necrosis = pink
39
Q

Explain the pathogenesis of aminoglycosides

A
  • aminoglycosides filtered by the glomerulus
  • stick to the phospholipids in the brush border of proximal convulted tubular ep cells
  • enter via pinocytosis
  • fuse with lysosomes
  • inhibit lysosomal enzymes e.g. phospholipase, sphingomyelinase
  • the lysosomal enzymes cannot degrade the phospolipid rich cell membranes (phosphlipidosis)
  • membranes accumulate in phagolysosome
  • formation of myeloid bodies - lamellar structures that contain undegraded phospholipid)
  • lysosomes enlarge and rupture
  • enzyme leakafe causes cellular degradation and necrosis
  • also inhibit Na-K-ATPase
  • influx of Hydrogen and sodium
  • influx of water
  • cellular swelling
  • cell death
40
Q
A
  • aminoglyoside toxicity
  • accumulation of lamellar bodies which eventually cause necrosis of tubular ep cells
  • blue = myelin body
41
Q

Why is ethylene glycol toxic?

A
  • antifreeze
  • young dogs - 6.6 ml/kg
  • cats - 1.5 ml/kg
  • cattle
  • small amount oxidised by alcohol dehydrogenase in the liver
  • glycoaldehyde
  • glycolic acid
  • glycoxylate
  • oxalate binds to Ca - filtered by glomeruli
  • as water is reabsorbed by tubules and pH of the filtrate decreases, calcium oxalates precipitate to form crystals
  • renal tubular blockage
  • degeneration and necrosis
  • nephrosis
  • hypocalcaemia, uraemia
  • renal failure, death
42
Q

What would be seen in ethylene glycol poisoning?

A
  • large numbers of crystals in the tubules is nearly pathognomonic for EG
  • tubular estasia, renal ep cell degeneration and necrosis , with a PRESERVED tubular BM
  • the calcium oxalate crystals - found in the intersitium, tubular ep cells and prox tubule lamina
  • light yellow
  • arranged in sheaves, rosettes and prisms
43
Q

WHat is seen here?

A
  • calcium oxalate crystals sticking to ep membrane
44
Q

What are these?

A
  • rhubarb
  • halogeton
  • contain oxalate at toxic levels
45
Q

What is melamine nephrosis?

A
  • melamine - pet food contaminant
  • falsely increases protein content
  • china, 2007
  • used to make plastic, fertilizer, dyes
  • it sticks in the tubules
  • big brown crystals
  • causes massive tubular ep necrosis
  • clinical signs in a couple of days
46
Q

What is this?

A
  • melamine nephrosis
47
Q

What is this showing? which animal does it effect?

A
  • lily toxicity
  • cats - very small amounts
  • acute tubular necrosis
48
Q

Is nephrotoxicosis reversible?

A
  • in absence of renal failure - yes
  • proximal convoluted tubule ep cells will regenerate - BM preserved
49
Q

What is haemoglobinuria?

A
  • intravascular haemolysis - rupture of erythrocytes
    • chronic copper toxicity in sheep
    • red maple leaf toxicity
    • leptospirosis
    • babesiosis
  • Haemoglobin binds to haptoglobin - transport (HG = 65)
  • it is not secreted in urine if bound to haptoglobin - but if haptoglobin is saturated then it is - haemoglobinuria
  • the tubular ep reabsorb some of it and stored as ferritin and haemosiderin
  • TOXIC
50
Q
A
51
Q

WHat is this?

A
  • foal, haemoglobinuric nephrosis due to Babesia equi
  • would also have red urine due to haemoglobin in urine
52
Q

What is this?

A
  • myoglobinuria
    • rhabomyolysis - rupture of skeletal muscle
      • azoturia - monday morning disease - horses
      • capture myopathy - exotic/ wild
      • direct trauma to muscle
    • release of myoglobin from muscles -> go through glomerular filtration system
    • passed out in urine
    • renal ischaemia secondary to hypovolaemic shock
    • (myoglobin increases tubular toxicity)
    • myoglobinuric nephrosis
53
Q

What are the tubulo-interstitial diseases?

A
  • interstitial nephritis
    • suppurative
    • non-suppurative
  • pyelonephritis - inflam of renal pelvis
54
Q

What is intersitial nephritis?

A
  • accumulation of inflam cells in interstitium
  • interference with transport between tubules and capillaries
  • can affect resoption
55
Q

WHat is non-suppurative interstitial nephritis?

A
  • inflammation against arteries, veins, lymohatics, connective tissue
  • usually non-consequential
  • non-specific
  • granulomatous / lymphoplasmatic
  • duration - chronic more common - fibrosis and atrophy
56
Q

What is supurative interstitial nephritis?

A
  • haematogenous (embolic)
  • ascending from lower urinary tract
57
Q

What is the difference between primary and secondary intersitial nephritis?

A
  • primary - specifically target kidneys
    • leptospira
    • encephalitozoon cuniculi - rabbits
    • white spotted kidneys
  • secondary (involvement as part of systemic disease)
    • feline infectious peritonitis
    • embolic nephritis
    • larva migrans in dogs (toxocara )
58
Q

What is leptospirosis?

A
  • specifically targets kidneys
  • septicaemia
  • nephritis
  • hepatitis
  • meningitis
  • abortion
  • stillbirth
  • natural reservoir = proximal convoluted tubules
  • dogs
    • leptispira interrogans var canicola, icterohaemorrhagiae and others
  • pigs/ cattle
    • leptospira interrogans var pomona
59
Q

Describe the lesions of leptospirosis?

A
  • acute renal injury
    • leptospira reaches renal capillaries
    • persists to intersitium (interisitial inflam)
    • migrates through tubular ep and into lumen
    • associates with ep microvilli
    • degeneration and necrosis of tubular ep
  • septicaemia/ bacteraemia -> haemolysis -> haemoglobinuria
  • acute liver disease
  • placentitis (pig and cattle) -> abortion
60
Q

What is this?

A
  • pig, intersitial nephritis - white flat coalescing spots in cortex
  • multifocal white lesions - accumualtion of lymphocytes and plasma cells in interstitium
61
Q

What is this?

A
  • dog, chronic intersitial nephritis
  • fibrosis
  • scarring
  • atrophy
  • parenchyma lost - end stage
62
Q

What is white spotted kidneys?

A
  • best known as non-suppurative interstitial nephritis
  • early lesions - suppurative / chronic - non
  • incidental finding - calves
  • multifactoral - E.coli, salmonella, leptospira, brucella
63
Q
A
  • white spotted kidneys
  • radial or wedge-shaped inflam infiltrate expands the intersitium
64
Q

What is this showing?

A
  • encephalitozoon cuniculi
    • obligate, intracellular microsporidiam parasite
    • commonly results in latent infection of lab rabbits
    • wide range of hosts
    • immunosupression - clinical disease - lesions in brain and kidneys
    • macrophages cannot clear infection - persistent
65
Q

What would be seen in kidneys and brain with encephalitozoon cuniculi?

A
  • kidneys - granulomatous/ nonsuppurative inflam - organisms present in ep and lumina of tubules, glomerular caps, in intersitium
  • brain - granulomatous meningoencephalilitis, foci of malacia
66
Q

What is this?

A
  • feline infectious peritonitis
    • round lesions
    • granulomatous inflam
    • white coalescing nodules
    • differential = renal lymphoma
67
Q

WHat is suppurative intersitial nephritis?

A
  • analogous to abscess formation in any organ
  • seeding of bacteria in bacteraemia or thromboembolism
  • usually start from glomeruli
  • agents
    • horses
      • actinobacillus equuli
    • swine
      • erysipelothrix rhusiopathiae
    • cattle
      • trueperella pyogenes
    • sheep and goats
      • corynebacterium pseudotuberculosis
68
Q

What is pyelonephritis?

A
  • inflam of the renal pelvis and renal parenchyma
  • infections ascending from lower urinary tract
  • E.coli, strept, staph, enterobacter, proteus, pseudomonas
  • mechanism: vesico-ureteral reflux
    • during micturition
    • manual compression of bladder
  • medulla - most susceptible
69
Q

WHat is this?

A
70
Q

What causes renal gout?

A
  • result of impaired excretion by kidneys and overproduction of uric acid
  • increased plasma conc of uric acid - hyperuricaemia
  • precipitation of monosodium urate crystals (tophi) on visceral and articular surfaces
  • inflam and fibrosis
  • causes of impaired excretion
    • severe dehydration
    • renal disease
    • postrenal obstruction
    • nephrotoxic drugs
71
Q

What causes gout in birds?

A
  • cold/ damp
  • vit A/ B12 def
  • type A influenza
  • high protein diets
  • dehydration
72
Q

What is this?

A
  • gout
73
Q
A
  • numerous tophi expand the tubular lumen and cause degen and necrosis of the tubular ep
  • granulmatous inflam surrounding tophi
74
Q

What is gout?

A
  • characterised by urate crystal deposition on articular/ synovial surfaces of joints and serous surfaces of viscera in birds, reptiles, humans
  • catabolism of purines (nucleotides and dietary)
    • adenine -> inosine -> hypoxanthine -> xanthine -> uric acid -> allantoin
    • guanine -> xanthine -> uric acid -> allantoin
  • humans and higher apes, birds and reptiles - no uricase (uric acid -> allantoin)
  • uric acuid normally eliminated by glomerular filtration, secretion, reabsorption, post-secretory reabsorb
  • 8-12% - excreted
  • 90% reabsorbed
75
Q

What is renal neoplasia?

A
  • renal adenoma - benign
  • renal carcinoma - malignant
  • nephroblastoma
76
Q
A

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