GI clin path

Question 1

When would a clin path work up be required?

Answer 1

Where disease is severe or persistent - otherwise it may be self-limiting or resolve with symptomatic treatment

Question 2

Neutrophilia in GI disease

Answer 2

Non specific

Physiologic (adrenaline)

Inflammatory (esp if left shift and toxic change)

Stress related (stress leukogram)

Question 3

Lymphocytosis in GI disease

Answer 3

Non-specific

Physiologic (young animals, hyperthyroid cats)

Reactive (inflammation)

Neoplastic (lymphoid neoplsia e.g. lymphoma)

Hypoadrenocorticism

Question 4

Eosinophilia in GI disease

Answer 4

Hypersensitivity and eosinophilic inflammmatory disorders

Parasitism

Paraneoplastic (esp. T cell lymphoma and mast cell tumour)

Hypoadrenocorticism

Question 5

Erythrocytosis in GI disease

Answer 5

Haemoconcentration (dehydration)

Question 6

Anaemia in GI disease

Answer 6

Acute blood loss (haemorrhagic vomiting/diarrhoea)

Anaemia of chronic inflammatory disease (reduced RBC production)

Chronic blood loss (chronic GI bleeding, typically microcytic, hypochromic, and non-regenerative)

Question 7

Most common electrolyte changes in GI disease

Answer 7

Hypokalaemia (loss of K+ in vomit/diarrhoea, reduced food intake)

Hypochloraemia (vomiting, due to loss of HCl)

Metabolic alkalosis (loss of HCl in vomit)

Question 8

Less common electrolytes changes in GI disease

Answer 8

Hyponatraemia (loss of Na+ in vomit/diarrhoea),

Hypernatremia/hyperchloremia (hypotonic fluid loss, e.g. osmotic diarrhoea),

Hyperchloremic metabolic acidosis (vomiting that includes loss of bicarbonate-rich intestinal content),

Lactic acidosis (increased blood lactate concentration secondary to hypovolemia),

Hyperkalaemia (hypoadrenocorticism)

Question 9

Non-electrolyte biochemical changes in GI disease

Answer 9

Urea increased by GI bleeding and in dehydration (pre-renal
azotaemia)

Decreases in albumin and globulin with PLE and GI blood loss

Hypocalcaemia (due to hypoalbuminaemia) or maybe hypercalcaemia with hypoadrenocorticism)

Increased liver enzymes - mild

Mild increase in lipase (even without pancreatitis)

Cholesterol often decreased with PLE, especially if lymphangiectasia

Question 10

Markers of intestinal function

Answer 10

Cobalamin (B12) and folate

Both absorbed in SI

Question 11

Where is cobalamin absorbed?

Answer 11

Absorbed exclusively in distal SI (ileum)

Question 12

Where is folate absorbed?

Answer 12

Proximal SI (duodenum and jejunum)

Question 13

Both cobalamin and folate decreased:

Answer 13

Diffuse SI malabsorption e.g. secondary to chronic inflammatory enteropathies

Question 14

Reduced cobalamin

Answer 14

Small intestinal dysbiosis (e.g. secondary to an inflammatory enteropathy) - increased use by bacteria

Secondary to exocrine pancreatic insufficiency and congenital deficiencies (e.g. Border collies)

Question 15

Increased folate:

Answer 15

Small intestinal dysbiosis - synthesis by some bacteria

Non-specific

Could also be sample haemolysis as stored in RBCs

Question 16

Types of faecal testing

Answer 16

Antigen detection (PCR)
Bacterial culture (e.g. salmonella and Campylobacter)
Parasitology

Question 17

Examples of indications for faecal testing

Answer 17

Exclusion of parvovirus (CPV2) in a dog with acute haemorrhagic diarrhoea (especially if not fully vaccinated)

Detection of Giardia in a young animal with small intestinal diarrhoea

Detection of Tritrichomonas in a young cat with foul-smelling diarrhoea

Question 18

Potential indications for cytology in GI disease

Answer 18

Presence of a focal mass or thickening within the GI tract, of sufficient size for sampling

Presence of lymphadenopathy (aspiration of the enlarged node)

Suspected or possible hepatic or splenic infiltrative disease (easier to sample)

Question 19

Potential risks of US guided FNA

Answer 19

Bleeding

Seeding of neoplastic cells

Rupture of the content

Anaphylaxis