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Urinary Flashcards

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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
Hypercalcaemic nephropathy A secondary lesion (hpth etc) Mineralisation of tubular basement membrane
26
What can cause glomerulitis?
Viral - EVA, CSF, newcastle disease virs Bacterial emboli - Actinobacillosis Septicaemic endothelial damage
27
Glomerulonephritis
Damage to the glomerulus leading to inflammation downstream
28
Outline the mechanism of glomerulonephritis. Name three causes.
Type three hypersensitivity (immune complexes) causing inflammation. Causes: FIP, FeLV, AIHA, neoplasia, CSF, PRRS, BVDV
29
Glomerulonephritis - chronic leading to fibrosis
30
Pale tan cortex and petechial haemorrhage Acute glomerulonephritis with PDNS
31
Fibrin deposits within the glomerulus and tubular lumen Acute glomerulonephritis - PDNS
32
PDNS chronic glomerulonephritis - fibrosis and fibroblasts present
33
Tubulointerstitial nephritis can occur how?
* 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
34
This brachyspira is a cause of acute tubulonephritis in the dog..
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
35
Marked atrophy of the microvillous border of the PCT and DCT Inflammatory debris within the tubular lumen Caused by canine leptospirosis
36
This Leptospire species causes a drop in a cows milk yield.
L. harjo
37
Describe this lesion
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
What type of interstitial nephritis is caused by FIP?
Suppurative/ granulomatous
39
Granulomatous inflammation found in a badger - Tubercules
40
Pyelonephritis
Affects renal parenchyma and pelvis
41
Why are females predisposed to pyelonephritis?
Shorter ureter
42
What makes the medulla of the kidney prone to infection?
Hypertonicity which inhibits n# NH3 inhibits complement
43
Bacteria which can cause pyelonephritis?
Actinobacillus equili Corynebacterium renale Eubacterium suis
44
Pyelonephritis - degenerate neutrophils
45
Name three parasitic causes of renal inflammation.
* Toxocara - dogs * Migration of ascarid larvae producing granulomatous nephritis * Dioctophyma renale * Stephanurus dentatus – pig subtropics * Capillaria plica – bladder
46
What mechanisms of pathology have been proposed of toxic acute tubular necrosis?
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
Ethylene glycol
Causes: Metabolic acidosis Calcium oxalate crystal formation (insoluble) Azotaemia, hyperkalaemia, renal failure, hypocalcaemia
48
Stages of Ethylene Glycol related disease..
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
Describe this lesion
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
Calcium oxalate crystals blocking renal tubules. Crystals form during ethylene glycol toxicity
51
Describe this lesion
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
Describe this lesion
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
Describe this lesion
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
Intranuclear inclusions in the PCT of the kidney Caused by heavy metals - lead, arsenic Coupled with acute tubular necrosis
55
These classes of antibiotic can cause acute tubular necrosis.
Aminoglycosides Tetracyclines Sulphonamides
56
Describe the lesion Outline the pathogenesis
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
Describe this lesion
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
Describe this lesion
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
Name four congenital defects associated with the lower urinary tract
* 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
Describe this lesion
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
What can cause bladder haemorrhage?
* Septicaemia * Viraemia (classical swine fever) * Trauma * Cyclophosphamide – Sterile haemorrhagic cystitis
62
Describe this lesion
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
Cystorrhexis
Bladder rupture Can lead to fibrinosuppurative peritonitis and ascities
64
Urolith
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
What factors can predispose an animal to development of urolithiasis?
* 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
Describe this lesion.
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
Describe feline urological syndrome.
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
Polypoid hyperplasia of the bladder wall which occurs with chronic cystitis
69
Oedematous bladder wall
70
What types of organisms usually cause cystitis?
Intestinal bacteria - makes sense! Ecoli etc
71
Enzootic haematuria Cause Pathogenesis
Chronic bracken ingestion (ptaquiloside) or BPV2 * Hyperplastic/hyperaemic cystitis * Recurrent haemorrhage * Squamous/ mucous metaplasia * Epithelial tumours
72
Streams of myocytes + disorganised mesh of cells Rhabdomyosarcoma
73
Describe this lesion
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
Dysuria
Painful urination
75
Haematuria
Blood in urine
76
Anuria
No urination
77
Oligouria
Small amount of urine
78
Polyuria/ dypsia
Excessive urination/ drinking
79
Hyposthenuria
Decreased specific gravity of urine
80
Azotaemia
Increased nitrogenous products & urea (BUN)
81
Uraemia
Clinical syndrome of renal failure Malaise and toxic effects * PUPD * Anorexia * Weakness/ muscle wastage * Hypothermia * Ataxia/ coma/ seizure * V+ * Renal pain
82
Isosthenuria
SG the same as protein free plasma - 1.010
83
What factors predispose an animal to development of cystitis?
* Urine stasis * Incomplete bladder emptying * Bladder trauma * Glycosurine * Increased pH/ dilution of urine * Short and wide ureter (female)
84
Hypoperfusion of the kidney causes prerenal renal failure. What mechanisms can cause this?
Hypobolaemia Iatrogenic - NSAIDs Dehydration Shock Cardiac failure Trauma
85
Increased repair and compensatory hypertrophy can lead to intrinsic renal failure. What can cause this?
Infection Inflammation Toxin Fibrosis Congenital abnormalities
86
Reduced urine clearance can lead to post-renal renal failure. What can cause this?
LUT obstruction/ inflammation bladder dysfunction bladder rupture
87
Renal insufficiency
30-50% of renal capacity remains
88
Renal failure
\< 30% of renal capacity remains
89
Acute renal failure
Peracute loss of 70-100% of renal function * Ischemia * Blocked outflow * Toxins Characterised by anuria/oligouria, isosthenuria and swollen painful kidneys on palpation
90
Chronic renal failure
Progressive nephron loss Caused by chronic inflammatory processes/ amyloidosis Characterised by hypothenurea, PUPD, diffuse fibrosis and tubular destruction
91
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?
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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