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Y3 Urinary pathology > Urinary system pathology 3 > Flashcards

Urinary system pathology 3 Flashcards

1
Q

Why is the kidney highly susceptible to toxic damage?

A
  • High exposure
  • High sensitivity
  • PCT has a high level of metabolic activity
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2
Q

Explain different proposed mechanisms of the pathogenesis of toxic disease => acute tubular necrosis

A
  • Toxins later the ion pump in the tubular epithelium membrane causing reduced sodium absorption, Na loss leads to vasoconstriction and ischaemia through the RAAS
  • Obstruction of tubular flow by cell debris + interstitial oedema.
  • Tubular fluid leakage into interstitium
  • Impaired glomerular permeability
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3
Q

How does ethylene glycol toxicity occur?

A

Found in car antifreeze, it can be ingested by an animal and is multistage metabolised into oxalates – calcium oxalate crystals form in the renal tubules

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4
Q

What are the initial effects of ethylene glycol toxicity?

A

Initial dulling effects on the CNS

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5
Q

What are the effects of ethylene glycol following GI absorption and liver metabolism breakdown?

A
  • insoluble Ca oxalate crystals form in the PCT tubules => obstruction
  • Leads to metabolic acidosis
  • Azotaemia, hypocalcaemia, hyperkalaemia, renal failure
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6
Q

How do the kidneys appear grossly with ethylene glycol toxicity?

A
  • Red
  • Swollen
  • Fine yellow/white striated cortex
  • Damage to vessels, leakage of fluid
  • pulmonary oedema in the lung
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7
Q

How will ethylene glycol toxicity appear histologically?

A
  • Glomeruli visible
  • Some tubules will appear normal
  • Other tubules will be dilated and filled with calcium oxalate crystals which block the flow of filtrate through the tubules
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8
Q

Which bacteria causes Enterotoxaemia pulpy kidney disease?

A

Clostridium perfringens type D

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9
Q

What are the consequences of pulpy kidney disease?

A

Acute, infectious, non-contagious disease of lambs: convulsions + sudden death

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10
Q

Where is clostridium perfringens found?

A

Soil
Manure
Intestinal commensal flora of ruminants

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11
Q

What ages of animal are most commonly affected by C.perfringens?

A

All ages susceptible, but 3-10 week-old fast - growers on high nutritional plane/a sudden change in feed, are commonly affected

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12
Q

What signs of C.perfringens are shown in:

  • lambs
  • older sheep
A

Lambs: die peracutely without clinical signs, or after brief neurological signs
Older: few days of mild GI signs. Others survive longer + develop CNS signs: blindness, ataxia + head-pressing

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13
Q

Describe how clostridium perfringens type D is ingested and multiplies in the body

A
  • Ingestion of C.perfringens spores
  • Normal peristalsis prevents high concentration of bacteria/toxin accumulating
  • Consumption of lush grasses/concentrated grain/large quantities of milk => undigested starches in SI providing substrate for Clostridial overgrowth
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14
Q

Describe how clostridium perfringens type D, now in the SI, causes enterotoxaemia

A
  • Multiplying bacteria in the SI produce toxin
  • Toxin decreases intestinal mobility and allows uptake into circulation via portal capillaries
  • Toxin acts on endothelium producing widespread oedema, haemorrhages + acute tubular necrosis
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15
Q

Describe the gross appearance of kidneys affected by clostridium perfringens type D enterotoxaemia

A

From an infected lamb – soft, very friable and break apart easily. Can be confused with autolysis so animals need to get to PM quickly for diagnosis.
We know this toxin damages endothelium and blood vessels so there will be multi-focal, haemorrhages on the serosa of a variety of tissues.

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16
Q

Describe the type of neoplasia that most commonly occurs in the kidneys

A
  • Primary renal neoplasia uncommon

- Metastasis most common: Melanoma, Carcinoma, Lymphoma

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17
Q

What features of the kidney make it susceptible to metastasis?

A

Fine capillary network

Good blood supply – embolic tumour fragments can pass through the bloodstream and lodge in the kidney

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18
Q

What is an adenoma?

A
  • a type of non-cancerous tumour: benign
  • well circumscribed
  • cortical mass
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19
Q

Adenocarcinomas form from which cells?

A

Tubular epithelial cells

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20
Q

How can an adenocarcinoma in the kidneys lead to polycythaemia and hypertension?

A
  • Erythropoietin is the hormone that dictates the speed of RBC production: more erythropoietin production
  • Hypertension is caused by the increase in HR due to trying to pump the more viscous blood around the body
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21
Q

Where would a transitional cell carcinoma in the kidneys develop?

A

Renal pelvis

22
Q

Describe the gross appearance of a renal carcinoma

A
  • multinodular mass that is creamy white and red/black in colour. If palpated it would be firm.
  • A degree of hydronephrosis (dilation of the renal pelvis): at some point there would have been partially blocked urine output
23
Q

Describe the histo appearance of a renal carcinoma

A

Formed of tubular epithelial cells so at low power it is very cell dense.
The tubular cells are neoplastic but still want to form tubules – but they are irregular and branching.

24
Q

What is a lymphosarcoma?

A

Tumour of lymphocytes - can have originated in the kidney or spread from another site
- can be nodular or diffused

25
Q

Renal lymphosarcoma may affect cats with what disease?

A

FeLV

26
Q

Describe the cells lining the LUT

A

Stratified transitional epithelial lining which is 8-10 cells thick

27
Q

What are the most common LUT problems in males and females?

A 
Females = infection
Males = obstruction
28
Q

Ectopic ureters can occurs congenitally, what are the outcomes of this?

A
  • Ureters enter the bladder or urethra more caudal than they should, avoiding the urethral sphincter at the neck of the bladder
  • Chronic urinary incontinence
  • UTI and hydronephrosis as secondary complications
29
Q

How can ectopic ureters be diagnosed?

A

Contrast media

allows the urinary tract anatomy to be seen and surgically corrected

30
Q

What are the 3 causes of haemorrhage?

A
  • Trauma
  • Septicaemia
  • Viraemia
31
Q

What is a hydroureter/hydrourethra?

A
  • Dilation of ureter(s) or urethra secondary to partial obstruction
  • Often associated with hydronephrosis (dilation of the renal pelvis)
32
Q

How could a neoplastic mass cause a hydroureter?

A

Neoplastic mass adjacent to the ureter, as the mass enlarges it puts increasing pressure on the ureter which creates a partial blockage to urine flow. The renal pelvis and ureter dilate because of this pressure.

33
Q

How would a kidney with hydronephritis and hydroureter appear?

A
  • kidney has a dilated, reddened pelvis

- the ureter is double the diameter showing there is an obstruction in the ureter, proximal to the bladder.

34
Q

How can the bladder become displaced?

A

Abdominal masses

Pregnancy

35
Q

Give 3 examples of acquired anatomic variations of the bladder

A
  • displacement
  • dilation
  • rupture
36
Q

What factors can cause rupture of the bladder?

A
  • Urethral obstruction
  • Trauma e.g. RTA
  • Parturition
37
Q

How can a ruptured bladder cause peritonitis?

A

Urine is an irritant and if its left chronically within the peritoneal cavity it will produce local inflammation even though for the most part, urine is sterile.

38
Q

What is Urolithiasis?

A

Kidney stones - hard deposits made of minerals and salts that form inside your kidneys

39
Q

What are the effects of urolithiasis?

A
  • Partial/complete obstruction depending on how severe
  • Pressure necrosis/ulceration
  • Acute haemorrhagic inflammation with bacterial overgrowth
  • possible rupture of bladder or urethra
40
Q

Give examples of urolithiasis particles

A

Sand-like particles (or large stones – less common)

- Variable mineral content: “Struvite”, calcium carbonate, silicate, oxalate, urate, cystine

41
Q

Give some examples of urolithiasis predisposing factors

A
  • pH
  • Bacterial infection
  • Diet
  • Sex
  • Species
  • Hereditary
42
Q

Which species most commonly suffers with urolithiasis?

A

Cats - feline urological syndrome

43
Q

Feline urological syndrome is predisposed by?

A
  • neutered males
  • cry diets
  • alkaline urine pH
  • increased intervals between urination
44
Q

How does feline urological syndrome progress?

A
  • Urethral obstruction => dysuria, haematuria + post-renal azotaemia
  • Secondary bacterial infection => severe haemorrhagic, transmural cystitis
45
Q

How would the urinary tract of a cat with feline urological syndrome appear grossly?

A

Multifocal to coalescing, focally extensive.
Affecting the bladder there is a red/black, friable consistency to the mucosa and the urine also has a red/black colour which indicates severe haemorrhage

46
Q

Name the common LUT inflammatory disease

A

Cystitis

47
Q

Give examples of factors that influence the occurrence of cystitis

A
  • urine stasis
  • incomplete voiding of urine
  • trauma
  • glycosuria
  • dilute urine
  • short and wide urethra
48
Q

What is the main bacterial cause of cystitis?

A

E.coli

49
Q

How can acute cystitis appear grossly - bladder?

A

Catarrhal
Haemorrhagic
Necrotic
- brown/grey colour with deeper areas of haemorrhage

50
Q

How can chronic cystitis appear grossly - bladder?

A
  • polypoid
  • follicular
  • metaplastic
    Multifocal to coalescing nodules scattered over the bladder mucosal surface

Y3 Urinary pathology (5 decks)

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