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Australasian Veterinary Examination, formerly the National Veterinary Examination General Veterinary Pathology: practice questions

Australasian Veterinary Examination (AVE), formerly the National Veterinary Examination (NVE) · Australia / New Zealand · Australasian Veterinary Boards Council (AVBC)

Original practice questions written to the published syllabus · not past papers
7worked here, free
40written to this exam in this subject
11syllabus units

What this subject covers

The general responses of tissue to injury: circulatory disturbances, degeneration and necrosis, inflammation and repair, immunopathology and neoplasia.

In the exams: ICAR AICE-JRF core group 06; ICAR AIEEA-PG 13 (Pathology); PRC 10%; Nepal NLEV 6; China basic paper 20; BCSE 20-23 items; AVE Paper 1 at least 8 (with clinical pathology); SAVC diagnostic pathology 25

Where the 40 questions fall

How our questions for Australasian Veterinary Examination, formerly the National Veterinary Examination spread across the units of General Veterinary Pathology. Difficulty: 1 easy, 31 medium, 8 hard.

Oncology: benign and malignant tumours7
Haemodynamic derangements6
Inflammation5
Degeneration4
Genetic diseases4
Necrosis and gangrene3
Pathological calcification3
Immunopathology3
Healing and repair2
Disturbances of growth2
Aetiology of disease1

7 practice questions, worked

Choose an answer, then open the working. Each explanation says why the right answer is right and why the others are not.

1 · Haemodynamic derangements · medium

At necropsy you find a rubbery, shiny intravascular mass that is not attached to the vessel wall, with a dark red lower part and a yellow upper part. It is most likely:

  1. A mixed arterial thrombus
  2. A septic thromboembolus
  3. A post-mortem clot
  4. A mural thrombus in the atrium
Answer and working

C. A post-mortem clot

Post-mortem clots separate into 'currant jelly' and 'chicken fat' layers because red cells settle before clotting; they are moist, elastic and unattached. Ante-mortem thrombi are dry, friable, attached and may show lines of Zahn.

Further reading: Zachary JF, Pathologic Basis of Veterinary Disease, 7th ed.

2 · Haemodynamic derangements · hard

A 20 kg dog loses 540 mL of blood acutely. Taking the canine blood volume as about 90 mL/kg (a teaching value that varies with body condition), what fraction of its blood volume has it lost?

  1. About 45 per cent
  2. About 2.7 per cent
  3. About 30 per cent
  4. About 3 per cent
Answer and working

C. About 30 per cent

Blood volume = 20 kg x 90 mL/kg = 1,800 mL; 540 / 1,800 = 0.30, or 30 per cent, enough to produce hypovolaemic shock. Using the feline value of about 60 mL/kg gives 1,200 mL and 45 per cent; dividing 540 mL by body weight in grams (20,000) gives 2.7 per cent, a unit slip; 3 per cent takes the blood volume as 900 mL/kg.

Further reading: Zachary JF, Pathologic Basis of Veterinary Disease, 7th ed.

3 · Degeneration · hard

A 4-year-old Shar-Pei with a history of recurrent fever and swollen hocks develops proteinuria and azotaemia. The most likely renal lesion is:

  1. Familial AA amyloidosis, predominantly in the renal medulla
  2. AL amyloidosis from multiple myeloma
  3. Membranous glomerulonephritis secondary to an unnoticed pyometra
  4. Renal lymphoma
Answer and working

A. Familial AA amyloidosis, predominantly in the renal medulla

Shar-Pei dogs have a familial autoinflammatory syndrome with episodic fever and hock swelling that leads to AA amyloid, often mainly medullary. AL amyloid requires a plasma cell tumour, and the history does not suggest pyometra.

Further reading: Zachary JF, Pathologic Basis of Veterinary Disease, 7th ed.

4 · Degeneration · medium

A 9-year-old horse is anorexic for three days and has mildly yellow sclerae, but liver enzymes and bile acids are normal. The best explanation is:

  1. Acute hepatic failure
  2. Biliary obstruction by a cholelith in the common bile duct
  3. Fasting hyperbilirubinaemia, a normal response in horses
  4. Neonatal isoerythrolysis
Answer and working

C. Fasting hyperbilirubinaemia, a normal response in horses

Horses develop a rise in unconjugated bilirubin during anorexia without liver disease. Normal liver enzymes and bile acids argue against hepatic failure or obstruction; neonatal isoerythrolysis affects foals.

Further reading: Zachary JF, Pathologic Basis of Veterinary Disease, 7th ed.

5 · Necrosis and gangrene · medium

A necropsy on a cow dead for 18 hours in hot weather shows green-black discolouration of the kidneys and intestinal serosa. This is most likely:

  1. Melanosis, a congenital pigment deposit
  2. Haemosiderosis from chronic haemorrhage in the weeks before death
  3. Pseudomelanosis, a post-mortem change from iron sulphide
  4. Gangrenous enteritis during life
Answer and working

C. Pseudomelanosis, a post-mortem change from iron sulphide

Bacterial hydrogen sulphide combines with iron from haemoglobin after death to form iron sulphide. Ruminants autolyse rapidly in heat. Melanosis is congenital, black and focal, and haemosiderin is golden brown.

Further reading: Zachary JF, Pathologic Basis of Veterinary Disease, 7th ed.

6 · Inflammation · medium

Sulphur granules with club-shaped colonies surrounded by eosinophilic material (Splendore-Hoeppli reaction) in a hard swelling of the bovine mandible indicate:

  1. Wooden tongue (actinobacillosis) caused by Actinobacillus lignieresii only in soft tissue
  2. Tuberculosis caused by Mycobacterium bovis
  3. Osteosarcoma of the mandible
  4. Actinomycosis (lumpy jaw) caused by Actinomyces bovis
Answer and working

D. Actinomycosis (lumpy jaw) caused by Actinomyces bovis

Lumpy jaw is a pyogranulomatous osteomyelitis of the mandible with sulphur granules. Actinobacillus lignieresii also forms granules but typically affects soft tissues such as the tongue; tuberculosis lacks sulphur granules.

Further reading: Maxie MG, Jubb, Kennedy and Palmer's Pathology of Domestic Animals, 6th ed.

7 · Immunopathology · medium

Acquired myasthenia gravis in dogs is caused by:

  1. Autoantibodies against thyroglobulin and thyroid peroxidase in the gland
  2. Autoantibodies to acetylcholine receptors of the neuromuscular junction
  3. Immune complexes in glomeruli
  4. T-cell destruction of the adrenal cortex
Answer and working

B. Autoantibodies to acetylcholine receptors of the neuromuscular junction

Antibodies block and destroy acetylcholine receptors, causing fatigable weakness and often megaoesophagus; a thymoma is sometimes associated. Thyroglobulin antibodies mark lymphocytic thyroiditis.

Further reading: Zachary JF, Pathologic Basis of Veterinary Disease, 7th ed.

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Read the subject

General Veterinary PathologyThe full study manual, free Australasian Veterinary Examination, formerly the National Veterinary ExaminationFormat, sections and how it has changed

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