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BVetMed4 - Urinary > Renal Pathology > Flashcards

Renal Pathology Flashcards

1
Q

Describe the gross appearance of kidneys in chronic renal failure.

A

Pale and shrunken with irregular depressions of the capsular surface

  • contraction of scar tissue causes irregularity
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2
Q

What features on histology may be observed in chronic renal failure?

A

Glomerulosclerosis

Periglomerular fibrosis

Degeneration and loss of tubules

Interstitial fibrosis

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3
Q

Define glomerulosclerosis

A

The glomerular tuft can become damaged and replaced by fibrous connective tissue

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4
Q

What is periglomerular fibrosis?

When in disease progression is this seen?

A

Fibrosis just around the glomerulus

Earlier than glomerulosclerosis

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5
Q

What occurs when tubules have degenerated?

A

Scar tissue fills the space where tubules are lost

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6
Q

What occurs as a result of interstitial fibrosis?

A

Presses on tubules causing atrophy

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7
Q

Describe some potential biochemical/clinical features of uraemia

A

Azotaemia + clinical signs :

  • metabolic acidosis,
  • other electrolyte imbalances
  • oedema (plasma protein loss)
  • mild non-regenerative anaemia
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8
Q

Outline secondary renal hyperparathyroidism

A

-When GFR low, phosphate no longer removed by kidneys enough
-Phosphate binds free calcium + precipitates in the serum - METASTATIC MINERALISATION
-Decrease 1 a-hydroxylase activity and subsequent D3 activation
- reduced calcium absorption and ionised serum calcium
PTH secretion -> chief cell hyperplasia

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9
Q

What occurs as a result of secondary renal hyperparathyroidism?

How does this occur

A

Fibrous osteodystrophy
Osteoclastic resorption of bone and replacement by fibrous connective tissue

Nephrocalcinosis - deposition of Ca in the kidney

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10
Q

What causes nephrocalcinosis?

A

Secondary renal hyperparathyroidism
Primary hyperparathyroidism
Vitamin D intoxication
Hypercalcaemia of malignancy

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11
Q

What neoplasias are associated with hypercalcaemia of malignancy?

A

Lymphomas

Anal sac adenocarcinomas

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12
Q

How does hypercalcaemia of malignancy occur?

A

Paraneoplastic effect where PTH-rap is mimicking the effect of PTH in the body

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13
Q

What non-renal mechanisms of pathology are associated with uraemia?

A

VASCULITIS
- endothelial degeneration and necrosis - thrombosis and infarction

Caustic injury to ORAL cavity and STOMACH - ammonia after urea breakdown by bacteria

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14
Q

Describe oral lesions associated with uraemia

A

Ventral surface on edge of tongue
Often bilateral

Ulcerative glossitis and stomatitis

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15
Q

What gastrointestinal lesions can be attributed to uraemia?

A

Ulcerative glossitis and stomatitis

Ulcerative and haemorrhagic gastritis/colitis

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16
Q

What CNS lesion is associated with uraemia?

A

Uraemic encephalopathy (degredation of White matter)

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17
Q

What lesions in the thoracic cavity are associated with uraemia ?

A

Fibrinous pericarditis
Uraemic pneumonitis and pulmonary calcification
Intercostal mineralisation

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18
Q

What is the underlying pathogenesis behind fibrinous pericarditis, arteritis and uraemic pneumonitis and pulmonary calcification?

A

Vasculitis

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19
Q

How is acute renal failure defined and what are the consequences?

A

> 75% loss of function

Oliguria or anuria
Azotaemia 
Hyperkalaemia 
Hypocalcaemia 
Metabolic Acidosis 
Hypertension
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20
Q

How can pathological agents access the kidney?

A

Haematogenous

Glomerular infiltrate

Ascending from the ureter

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21
Q

What haematogenous agents can cause renal pathology?

A

Septic embolic nephritis

Ischaemic necrosis post infarction

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22
Q

What glomerular infiltrate can cause pathology?

A

Substance secreted into the filtrate causing trauma to tubular lining OXYLATE CRYSTALS - ethylene glycol

Filtered preformed toxins or substances processed by tubular lining epithelium

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23
Q

What conditions may predispose a patient to developing an ascending infection from the ureter?

A

GIT contamination - diarrhoea
Genital tract contamination - pyometra
Dermal contamination - perivulval dermatitis

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24
Q

Name some developmental disorders of the kidney

A

Renal aplasia/hypoplasia/dysplasia

Ectopic kidneys

Fused kidneys

Progressive juvenile nephropathy

Polycystic kidney disease

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25
Q

When is renal aplasia/hypoplasia/dysplasia a problem?

A

When it is bilateral

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26
Q

What can be an issue with ectopic kidneys?

A

Secondary Hydronephrosis due to kinking of ureters

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27
Q

What is the presentation seen with progressive juvenile nephropathy?

What species?

A

DOG

Present usually less than 2 years with end stage kidney disease typical of what you would see in an older animal

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28
Q

What is polycystic kidney disease?

What is it seen in?

A

Persian Cats and Bull Terriers

Problem with the tubular epithelium which allows large cystic cavities to form within the kidney

Pressure atrophy and necrosis of normal surrounding tissue

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29
Q

When does immune mediated glomerulonephritis occur?

A

Persistent infections or prolonged antigenaemias which enhances formation of soluble immune complexes (+complement fixation and damage by leukocytes)

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30
Q

Describe the pathogenesis of immune mediated glomerulonephritis

A

Soluble immune complexes circulating can be deposited in the capillaries of the glomerular tufts or the basement membrane -> interferes with filtration

When deposited, bind with complement releasing chemo tactic substances

Attract leukocytes which release reactive oxygen species causing more damage

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31
Q

What is glomerular amyloidosis?

When does it occur?

A

Deposition of extracellular protein

Chronic inflammatory disorders,
Systemic infectious disease,
Neoplasia

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32
Q

What causes acute suppurative glomerulitis?

A

BACTERAEMIA

Bacteria lodge in glomerular and interstitial capillaries and form microabscesses in the cortex.

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33
Q

What bacteria are associated with acute suppurative glomerulitis in:

Foals
Cows
Pigs
Sheep+goats

A

Foals - actinobacillus equuli

Cows - Trueperella pyogenes

Pigs - Erisipelothrix rheusiopathiae

Sheep+Goats - Corynebacterium pseudotuberculosis

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34
Q

What is Nephrotic syndrome?

A

PLN -> NS

Decrease in plasma osmotic pressure and loss of antithrombin III

Oedema and effusions, hypercoagulability and hupercoagulability

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35
Q

What does nephrotic syndrome occur as a result of?

A

Glomerular damage - PLN

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36
Q

What is the most important cause of acute renal failure?

A

Acute tubular necrosis

37
Q

When does acute tubular necrosis occur?

A

After nephrotoxic or ischaemic injury to the proximal tubular epithelium

38
Q

Why is oliguria/anuria associated with acute tubular necrosis?

A

Leakage of tubular filtrate into interstitium

Intratubular obstruction from sloughed epithelium

39
Q

Why do toxins in blood preferentially damage the kidney?

A

Kidney recieves 25% of CO

40
Q

How does nephrotoxin associated ischaemia occur?

A

Reactive metabolites are produced as they’re being processed by the cells

Stimulate vasoconstriction -> ischaemia

41
Q

After which insult is the tubular basement membrane more likely to be retained?

How does this relate to prognosis?

A

TOXIC

Improved - allows for regeneration

42
Q

What agents can cause acute tubular necrosis?

A

NSAIDS
Fungal and plant toxins
Ethylene glycol
Bacterial toxins

43
Q

How do NSAIDs cause acute tubular necrosis?

A

Decreased PG synthesis (which usually causes vasodilation)

Afferent arteriolar constriction

Decreased renal perfusion

Acute tubular and papillary necrosis

44
Q

What makes ATN from NSAIDs more likely?

A

Excessive doses,
Underlying dehydration,
CHF
CRD

45
Q

What fungal and plant toxins cause ATN?

A

Mycotoxins - Aspergillus
Lily plants cats
Grapes and raisins dogs
Oak poisoning in cows

46
Q

How does Ethylene glycol cause ATN?

A

Dogs cats pigs -> readily absorbed from GIT

Oxidised by the liver to toxic glycolic acid and oxalate

Filtered by glomeruli - direct toxin to tubules

Calcium oxylate crystals precipitate into tubular lumen -> obstruction and damage epithelium

47
Q

What nephrotoxin is produced by C. Perfringens type D?

What does it cause?

A

Epsilon

PULPY KIDNEY

48
Q

How does a small ruminant get pulpy kidney?

A

Overeating esp. well conditioned lambs

Proliferation of clostridium type D

Epsilon toxin

Pulpy kidney

49
Q

Describe the pathology of Pulpy Kidney

A

Acute tubular degeneration and/or necrosis

Interstitial oedema and haemorrhage

50
Q

What changes in the urine are associated with pulpy kidney?

A

Glycosuria

51
Q

What causes disease of the interstitium?

A

Ascending infection - pyelonephritis

Haematogenous - E.Coli and Leptospira, Canine adenovirus

Secondary to injury of tubules/glomeruli (infectious, toxic, IMD)

52
Q

Describe the appearance of a kidney with E.coli

A

White spotted kidney disease

53
Q

Describe the kidney pathology associated with FIP

A

Granulomatous necrotising vasculitis

54
Q

Outline the difference between hyperaemia and congestion

A

Hyperaemia - increased arterial blood flow e.g. acute inflammation

Congestion - venous blood pooling (cardiac insufficiency, hypovolaemic shock, agonal)

55
Q

What kidney changes are seen in septicaemia?

A

Pinpoint petechial haemorrhages

56
Q

A puppy presents with sudden death and cortical ecchymotic haemorrhage on PM. DDx?

A

Canine HERPESVIRUS

Causes direct endothelial damage

57
Q

What area of the kidney will be affected if the interlobular artery is blocked?

A

CORTEX

58
Q

What area of the kidney will be affected if the arcuate artery is blocked?

A

CORTEX+ MEDULLA

59
Q

What are the sources of renal emboli?

A

Cardiac mural or valvular
Endarteritis in pancreatic dz - angiostrongylus, strongylus vulgaris
Neoplastic cell emboli
Bacterial or septic emboli

60
Q

Describe the appearance of an acute embolism in the kidney

A

Discrete dark wedge

61
Q

Describe the appearance of a sub-acute embolism in the kidney

A

Lighter in colour as cells have undergone necrosis

62
Q

Describe the appearance of chronic embolism in the kidney

A

Fibrous tissue laid down which contracts - depression

63
Q

When would a patient with hydronephrosis tend to present clinically?

A

If bilateral

64
Q

What predisposes a patient to hydronephrosis?

A

Congenital malformation
Urethral or urethral blockage (calculi, neoplasia, inflammation)
Neurogenic functional disorders
Iatrogenic (accidentally tying off ureter)

65
Q

What is pyelonephritis ?

What is the most common cause?

A

Bacterial infection of the pelvis with extension into tubules and interstitium

Ascending infection

66
Q

What bacteria can cause pyelonephritis?

A 
Corynebacteria 
E. coli 
Staph and Strep
Pseudomonas 
Trueperella
67
Q

What type of infarction is associated with pyelonephritis?

A

POLAR

68
Q

What can cause primary papillary necrosis?

A

NSAIDs

Ischaemic necrosis of inner medulla

69
Q

What can cause secondary papillary necrosis?

A

Decreased blood flow to vasa recta

- glomerular dz, interstitial dz, compression of papilla e.g. stones

70
Q

What is the most common primary renal neoplasm?

Metastatic?

A

Renal carcinoma

Highly metastatic

71
Q

What paraneoplastic effect is associated with renal carcinoma?

A

Polycythaemia - EPO

72
Q

What developmental anomalies affect the LUT?

A

Ureteral aplasia and hypoplasia

Ectopic ureters

Patent Urachus (FOALS)

73
Q

How can ureteral aplasia/hypoplasia affect the kidneys?

A

Obstruction -> hydronephrosis

74
Q

How do patients with ectopic ureters tend to present?

Why?

What problems can they cause?

A

Urinary incontinence

Empty into urethra, vagina, or bladder neck

Prone to obstruction or infection

75
Q

What is a patent urachus?

A

Foetal urachus fails to close -> direct channel between the bladder and umbilicus

76
Q

What can cause a patent urachus?

A

Underlying omphalitis or congenital urethral obstruction creating backward pressure.

Increased bladder pressure forces urine out into the urachus therefore dribbles urine from umbilicus

77
Q

What Uroliths form at alkaline pH?

A

Struvites and carbonates

78
Q

What uroliths form at acidic pH?

A

Oxalates

79
Q

What stones are Dalmatians predisposed to?

Why?

A

Urate stones

Uric acid unusually metabolised

80
Q

How can vitamin A deficiency result in Urolithiasis?

A

Causes metaplasia of urinary tract epithelium from transitional to keratinised stratified -> DESQUAMATION

This provides a nidus for calculus formation

81
Q

What factors predispose calculus formation?

A

Urinary pH
Reduced water intake - mineral supersaturation
Bacterial infection LUT
Abnormal metabolism e.g. dalmations
High dietary levels of substances e.g. Mg
VitA deficiency

82
Q

What bacteria causes cystitis in many species?

A

Uropathogenic E. coli

83
Q

What causes cystitis in cattle?

A

Corynebacterium renale

84
Q

What causes cystitis in pigs?

A

Eubacterium suis

85
Q

Describe the pathogenesis of cystitis

A

Hydrolysis of urea by urease producing bacteria

Excessive ammonia

Mucosal damage and increased urine pH

86
Q

What causes emphysematous cystitis?

A

E.g DIABETICS

Glycosuria enhances bacteria
E.coli/C.perfringens metabolise and release CO2

CO2 released into bladder Lumen

Absorption of gas into lymphatics ->emphysema

87
Q

What causes toxic cystitis

A

Bracken fern -> enzootic haematuria

Cyclophosphamide

88
Q

What causes Enzootic haematuria?

A

Chronic ingestion of Bracken fern

Haemorrhage, chronic cystitis, bladder neoplasia

89
Q

Bladder neoplasia is uncommon but what are the main types?

A

Epithelial - transitional cell carcinoma

Mesenchymal - rhabdomyosarcoma

BVetMed4 - Urinary (15 decks)

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