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Systems PATH > Urinary > Flashcards

Urinary Flashcards

1
Q

A horseshoe kidney is caused by what?

Can they be functional?

A

Fusion of the cranial or caudal poles of the kidneys

Yesm if no urethral obstruction is present

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2
Q

Ectopic kidney

A

Abnormal kidney migration - may be found in the inguinal ring or pelvic cavity (urethral obstruction may occur)

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3
Q

Name seven congenital abnormalities of the kidneys.

A
  1. Ectopic kidney (fused
  2. Aplasia
  3. Hypoplasia
  4. Dysplasia
  5. Familial renal disease
  6. Cystic renal disease
  7. Tubular function abnormalities (genetic)
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4
Q

What features of the kidney should be examined at necropsy?

A
  • Examine shape, position + size of kidneys.
  • Contours / adherence of capsule.
  • Cortex is finely radially striated + dark red / brown (except cats). Medulla pale brown.
  • Cortex ratio of approx 1:2 to 1:3 with medulla of domestic spp (smaller in desert species which have larger medulla).
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5
Q

Familial renal disease

Which breeds are predisposed?

A

Renal disease often presenting under the age of 2, proteinuria is common, kidneys appear small, pale with loss of nephrons and fibrosis

Breeds: Cocker, Doberman, Samoyed, Shih Tzu

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6
Q

Describe this histo slide of a 2yo cocker with familial renal disease.

A
  • Clumps of inflammatory cells
  • Dilated tubules
  • Dense proteinaceous fluid within the tubules - protein
  • Marked fibrosis
  • Nephron loss
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7
Q

What pathological finding is often found alongside renal dysplasia?

What can be the cause of this phenomenon?

A

Hydroureter

  • Familial
  • Viral
    • CHV
    • FPV
    • BVDV
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8
Q

Describe this lesion.

What can these lesions result in?

Which breeds are prone?

A

The cortex of the kidney contains multifocal raised round fluid filled nodules of varying sizes (from 2mm to 10mm in diameter). Some of the nodules extend into the medulla.

May lead to pressure atrophy of adjacent renal tissue

Persian and WHW terriers.

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9
Q

Describe three types of tubular functional abnormalities and their breed specific signs.

A
  1. Cystinuria - cysteine stones in the bladder - X-linked
  2. Primary renal glycosuria - reduced ability to reabsorb glucose - Elkhounds
  3. Fanconi syndrome - multiple defects = aa/glycos/protein/phosphuria - Basenjis
  4. Urate metabolism - urate crystal preone - Dalmatians
  5. DI
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10
Q

Describe the response to injury of the glomerulus.

A

Fibrosis and loss

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11
Q

Describe the response to injury of the tubular epithelium

A

Repair if the basement membrane remains intact

Compensatory hypertrophy and atrophy if basement membrane is damaged

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12
Q

Describe this lesion

A

Multifocal to coelescing, round, dark red-black 1x1mm lesions. Coelescing to two large areas (affecting 70% of the tissue).

Acute multifocal to coelescing severe haemorrhage of the kidney

Disseminated intravascular coagulation

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13
Q

Describe this lesion

A

Multifocal to coelescing round 2x2mm red lesions found on the kidney surface and penetrating the cut surface (cortex). The kidney appears firm (no-oozing of fluid).

Acute multifocal to coelescing moderate haemorrhagic nephritis

CHV, salmonella, CSF, erysipelas

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14
Q

Describe this lesion.

A

Focal area of dark red to black fluid found on the surface of this kidney. 5x5cm. Irregular demarcation.

Acute focally extensive severe traumatic haemorrhage of the kidney

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15
Q

Describe these lesions

A

Interlobular and interlobar acute infarcts.

Pale tan wedged shaped lesions.

Peripheral haemorrhage

Indented cortical surface

Caused by microthrombi in renal blood supply

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16
Q

Outline the difference between interlobular and interlobar infarcts.

A

Differences in blood supply

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17
Q
A

Chronic infarct leading to wedge shaped necrosis and consolidation of tissue

Leaves a deep cortical depression visible on the renal surface

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18
Q

Describe

A

Papillary necrosis (where collecting ducts empty into the pelvis)

Reduced renal blood flow secondary to NSAIDs (bute!)

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19
Q
A

Renal cortical necrosis - kidney is diffusely damaged due to microthromi.

Hypereosinophilic cells

Tubular structures are filled with degenerate necrotic debris

Inflammatory cells have infiltrated interstitium

Gram-ve microthrombi

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20
Q
A

Fibrin and cell debris within tubular lumen. Hypereosinophilic cells w/out nuclei.

Causes:

  • Toxic/ ischemic insult
  • Myoglobinuria
  • Increase in serum Hb
  • AIHA
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21
Q

With amyloidosis of the kidney which areas are most commonly affected?

A

Glomerulus

In cats the medulla

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22
Q

What effect does amyloid have on the glomerulus?

A

Pressure atrophy - protein uria - hypoproteinaemia

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23
Q

Describe

A

Cortex is diffusely affected, appears pale tan and waxy, firm.

Amyloidosis - protein depositation (stained red with congo red)

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24
Q

Urine blockage can lead to hydronephrosis. What characteristic lesions would be found in this case?

A

Pressure atrophy

Dilation of the pelvis

Medulla ischemia (vascular occlusion)

Cortical atrophy

Causes: ureteral anomalies/ obstruction, LUT inflammation, neoplasia, bladder paralysis

Leads to secondary infection

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25
Q
A

Hypercalcaemic nephropathy

A secondary lesion (hpth etc)

Mineralisation of tubular basement membrane

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26
Q

What can cause glomerulitis?

A

Viral - EVA, CSF, newcastle disease virs

Bacterial emboli - Actinobacillosis

Septicaemic endothelial damage

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27
Q

Glomerulonephritis

A

Damage to the glomerulus leading to inflammation downstream

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28
Q

Outline the mechanism of glomerulonephritis.

Name three causes.

A

Type three hypersensitivity (immune complexes) causing inflammation.

Causes: FIP, FeLV, AIHA, neoplasia, CSF, PRRS, BVDV

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29
Q
A

Glomerulonephritis - chronic leading to fibrosis

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30
Q
A

Pale tan cortex and petechial haemorrhage

Acute glomerulonephritis with PDNS

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31
Q
A

Fibrin deposits within the glomerulus and tubular lumen

Acute glomerulonephritis - PDNS

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32
Q
A

PDNS chronic glomerulonephritis - fibrosis and fibroblasts present

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33
Q

Tubulointerstitial nephritis can occur how?

A
  • Interstitial inflammation/ fibrosis results in tubular atrophy and degeneration with 2o damage to glomeruli ana vessels.
  • Tubular damage stimulates inflammation, which spills over into interstitium
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34
Q

This brachyspira is a cause of acute tubulonephritis in the dog..

A

Leptospira - from rat urine/ bite wounds

  1. Leads to microvilli destruction in the tubules
  2. Large volume of inflammatory cells within the interstitium
  3. Chronicity and regeneration lead to marked fibrosis
  4. Subclinical shedding can occur
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35
Q
A

Marked atrophy of the microvillous border of the PCT and DCT

Inflammatory debris within the tubular lumen

Caused by canine leptospirosis

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36
Q

This Leptospire species causes a drop in a cows milk yield.

A

L. harjo

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37
Q

Describe this lesion

A

Disseminated white to red round raised lesions. They are soft to firm and about 3x3mm.

Subacute disseminated moderate to severe pyogranulomatous interstitial nephritis

White spot kidney - E. coli

38
Q

What type of interstitial nephritis is caused by FIP?

A

Suppurative/ granulomatous

39
Q
A

Granulomatous inflammation found in a badger - Tubercules

40
Q

Pyelonephritis

A

Affects renal parenchyma and pelvis

41
Q

Why are females predisposed to pyelonephritis?

A

Shorter ureter

42
Q

What makes the medulla of the kidney prone to infection?

A

Hypertonicity which inhibits n#

NH3 inhibits complement

43
Q

Bacteria which can cause pyelonephritis?

A

Actinobacillus equili

Corynebacterium renale

Eubacterium suis

44
Q
A

Pyelonephritis - degenerate neutrophils

45
Q

Name three parasitic causes of renal inflammation.

A
  • Toxocara - dogs
    • Migration of ascarid larvae producing granulomatous nephritis
  • Dioctophyma renale
  • Stephanurus dentatus – pig subtropics
  • Capillaria plica – bladder
46
Q

What mechanisms of pathology have been proposed of toxic acute tubular necrosis?

A
  1. Toxins alter tubular ion pumps
    1. Reducing Na+ reabsorption or excretion
  2. Interstitial oedema
    1. Cell debris and tubular fluid leakage
  3. Altered glomerular permeability
47
Q

Ethylene glycol

A

Causes:

Metabolic acidosis

Calcium oxalate crystal formation (insoluble)

Azotaemia, hyperkalaemia, renal failure, hypocalcaemia

48
Q

Stages of Ethylene Glycol related disease..

A
  1. First 12 hours after ingestion. Vomiting, PU/PD + appear intoxicated. Observant owners might bring their pet in for an exam.
  2. 12-24 hours after ingestion. Symptoms are vague - apparent recovery.
  3. 24-72 hours after ingestion. Severe depression, not eating, vomiting and not producing urine. Death is imminent.
    1. ​Renal failure (casts) and pulmonary oedema (acidosis)
49
Q

Describe this lesion

A

Diffusely yellow striated cortex. The kidney is diffusely red and swollen with a soft texture.

Acute diffuse severe necrotising nephritis

Toxic - ethylene glycol toxicity

50
Q
A

Calcium oxalate crystals blocking renal tubules.

Crystals form during ethylene glycol toxicity

51
Q

Describe this lesion

A

Disseminated, round, flat, gritty lesions 2mm in diameter can be found throughout the renal surface.

On histology ca be seen tubular calcinosis - basophilic amorphous (mineral) substance.

Acute disseminated severe necrotising nephrocalcinosis

52
Q

Describe this lesion

A

The cortex of the kidney is diffusely pale tan in colour with perivascular haemorrhage also seen.

Tubular architecture is severely distrupted with amorphous eosinophilic material (necrosis) filling the tubular spaces - coagulative necrosis.

Acute diffuse severe necrotising nephritis

Caused by Acorn/ oaks - tannins

53
Q

Describe this lesion

A

The kidney is diffusely whitened with moderate enlargement. The surface of the kidney is mottled and mildly rough.

Mild pelvic dilation

Chronic diffuse severe fibrosing nephritis

Mycotoxicosis - Aspergillus

54
Q
A

Intranuclear inclusions in the PCT of the kidney

Caused by heavy metals - lead, arsenic

Coupled with acute tubular necrosis

55
Q

These classes of antibiotic can cause acute tubular necrosis.

A

Aminoglycosides

Tetracyclines

Sulphonamides

56
Q

Describe the lesion

Outline the pathogenesis

A

Soft congested kidney, petechial haemorrhage

(will also see pulmonary oedema, CNS malasia)

Pathogenesis: Clostridium perfringens type D enterotoxin causes increased intestinal permeability and vascular damage leading to systemic pathology..

  • Lung - oedema
  • Kidney - tubular damage - glucosuria
  • Liver - glycogen release
  • Brain - oedema
  • Adrenal - catecholamine release
57
Q

Describe this lesion

A

A single unilateral, unencapsulated, creamy white mass with areas of haemorrhage. The mass completely distrupts the normal architecture of the kidney and is highly infiltrative.

Renal carcinoma

58
Q

Describe this lesion

A

Nodular white unencapsulated round to irregular lesions (moderate demarcation, some better than others)

Histologically appears as sheets of round cells which distrupt the normal structure of the tissue and is highly infiltrative.

Renal lymphosarcoma

59
Q

Name four congenital defects associated with the lower urinary tract

A
  • Ureteral aplasia
  • Ectopic ureters - complications common eg hydronephrosis + UTI.
  • Hypospadia, epispadia - Urethra opens on ventral or dorsal penis.
  • Patent urachus
  • Bladder agenesis, hypoplasia, duplication
60
Q

Describe this lesion

A

Diffuse dilation of the ureter can be seen - fluid filled and soft with thin walls

Chronic diffuse severe hydroureter secondary to congenital ectopic ureter placement

61
Q

What can cause bladder haemorrhage?

A
  • Septicaemia
  • Viraemia (classical swine fever)
  • Trauma
  • Cyclophosphamide – Sterile haemorrhagic cystitis
62
Q

Describe this lesion

A

Unilateral dilation of the ureter and renal pelvis (fluid filled renal pelvis)

Subacute focal moderate to severe hydronephrosis and hydroureter

Secondary to obstruction of the urine outflow tract

63
Q

Cystorrhexis

A

Bladder rupture

Can lead to fibrinosuppurative peritonitis and ascities

64
Q

Urolith

A

A sand-like/ large stone of mineral or organic content found within the urinary tract.

Can cause:

  • Obstruction
  • Pressure necrosis / ulceration
  • Acute haemorrhagic inflammation - SBI
  • Possible rupture of bladder or urethra
65
Q

What factors can predispose an animal to development of urolithiasis?

A
  • pH – acid (oxalates) alkaline (struvite)
  • Bacterial infection – urea, NH3 by bacterial ureases, elevates pH.
  • Diet – high PO4, oxalate /silicate /oestrogenic plants, dehydration, vit A deficiency
  • Heredity
  • Sex – F infection, M obstruction
  • Species – cats
66
Q

Describe this lesion.

A

Multifocal to coelecing gritty grey material is lightly adhered to the mucosal wall of the bladder. There are also multifocal areas of haemorrhage associated with the sand-like particles. The bladder wall is diffusely thickened.

Chronic diffuse severe necrotising hyperplastic cystitis caused by urolithiasis

67
Q

Describe feline urological syndrome.

A

Obstructive urethra urolithiasis.

Predisposed by…

  • male, neutered cats.
  • dry diets
  • alkaline urine pH
  • increased intervals between urination

Urethral obstruction > post-renal azotemia, dysuria + haematuria. SBI > severe haemorrhagic, transmural cystitis.

Rupture / uroperitoneum may occur.

68
Q
A

Polypoid hyperplasia of the bladder wall which occurs with chronic cystitis

69
Q
A

Oedematous bladder wall

70
Q

What types of organisms usually cause cystitis?

A

Intestinal bacteria - makes sense!

Ecoli etc

71
Q

Enzootic haematuria

Cause

Pathogenesis

A

Chronic bracken ingestion (ptaquiloside) or BPV2

  • Hyperplastic/hyperaemic cystitis
  • Recurrent haemorrhage
  • Squamous/ mucous metaplasia
  • Epithelial tumours
72
Q
A

Streams of myocytes + disorganised mesh of cells

Rhabdomyosarcoma

73
Q

Describe this lesion

A

Transitional cell carcinoma of the bladder wall.

Highly infiltrative and metastatic. Aggregates of large round cells with prominent nucleus/ nucleolus - transitional cells - anisokaryosis and anisocytosis

74
Q

Dysuria

A

Painful urination

75
Q

Haematuria

A

Blood in urine

76
Q

Anuria

A

No urination

77
Q

Oligouria

A

Small amount of urine

78
Q

Polyuria/ dypsia

A

Excessive urination/ drinking

79
Q

Hyposthenuria

A

Decreased specific gravity of urine

80
Q

Azotaemia

A

Increased nitrogenous products & urea (BUN)

81
Q

Uraemia

A

Clinical syndrome of renal failure

Malaise and toxic effects

  • PUPD
  • Anorexia
  • Weakness/ muscle wastage
  • Hypothermia
  • Ataxia/ coma/ seizure
  • V+
  • Renal pain
82
Q

Isosthenuria

A

SG the same as protein free plasma - 1.010

83
Q

What factors predispose an animal to development of cystitis?

A
  • Urine stasis
  • Incomplete bladder emptying
  • Bladder trauma
  • Glycosurine
  • Increased pH/ dilution of urine
  • Short and wide ureter (female)
84
Q

Hypoperfusion of the kidney causes prerenal renal failure.

What mechanisms can cause this?

A

Hypobolaemia

Iatrogenic - NSAIDs

Dehydration

Shock

Cardiac failure

Trauma

85
Q

Increased repair and compensatory hypertrophy can lead to intrinsic renal failure. What can cause this?

A

Infection

Inflammation

Toxin

Fibrosis

Congenital abnormalities

86
Q

Reduced urine clearance can lead to post-renal renal failure.

What can cause this?

A

LUT obstruction/ inflammation

bladder dysfunction

bladder rupture

87
Q

Renal insufficiency

A

30-50% of renal capacity remains

88
Q

Renal failure

A

< 30% of renal capacity remains

89
Q

Acute renal failure

A

Peracute loss of 70-100% of renal function

  • Ischemia
  • Blocked outflow
  • Toxins

Characterised by anuria/oligouria, isosthenuria and swollen painful kidneys on palpation

90
Q

Chronic renal failure

A

Progressive nephron loss

Caused by chronic inflammatory processes/ amyloidosis

Characterised by hypothenurea, PUPD, diffuse fibrosis and tubular destruction

91
Q

A cat with renal failure will likely present with:

  1. Azotaemia
  2. Metabolic acidosis
  3. Odd electrolyte levels
  4. Dehydration - PUPD
  5. And endocrine disturbances

By what mechanisms do these occur?

A
  1. Build up of waste products - urea
  2. No acid-base regulation
  3. Endocrine disturbances
  4. No fluid-volume regulation
  5. EPO, RAAS, VitD3

Systems PATH (13 decks)

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