Endocrine 4

Question 1

What are the four major types of cells in the endocrine pancreas?

Answer 1

Question 2

How does insluin act to lower blood glucose?

Answer 2

• Inhibition of hepoatic gluconeogenesis
• Promotion of hepatic glycogen synthesis
• Increased cellular uptake of glucose by muscles + adipose tissue

Question 3

How does glucagon activity increase blood glucose levels?

Answer 3

• Promotes gluconeogenesis in liver + muscles
• Promotes glycogenolysis in liver + muscles

Question 4

How does catecholamine activity increase blood [glucose]?

Answer 4

• Decreases insulin release by pancreatic B-cells
• Increasing liver glycogenolysis
• Increasing pituaritary release of GH

Question 5

How does GH activity increase blood [glucose]?

Answer 5

Reduces glucose uptake by myocytes and adipocytes

Question 6

What is a major consequence of glucose homeostasis?

Answer 6

• Major metabolic consequence of inadequate insulin activity is decreased movement of glucose into insulin-sensitive cells - hepatocytes, adipocytes, skeletal myocytes

Question 7

1) What is diabeties mellitus?
2) How does the pathogenesis of it vary between cats and dogs?

Answer 7

1. Diabeties mellitus = a group of metabolic disorders characterised by hyperglycaemia from from defects in insulin secretion and/or action
2. Dogs get type 1 - Beta cell destruction leads to insulin deficiency, cats get Type 2 - impaired insulin secretion/insulin resistance

Question 8

What are the clinicopathologic changes seen as a result of diabetes mellitus?

Answer 8

1. Hyperglycaemia - absence of insulin (type 1) or impaired insulin action (insulinresistance - type 2)
2. Glycosuria - hyperglycaemia is higher than renal tubular transport maximum
3. Hyperlipemia - defective lipoprotein lipase activity due to decreased insulin = defective processing of chylomicrons - increased lipomobilisation
4. Ketonemia - ketogenesis occurs in liver - promoted by glucagone + inhibited by insulin
5. Increased fructosamine - irreversible non-enzymatic linking of glucose + albumin
6. Stress leukogram
7. Increased ALP and ALT - hepatic lipidosis
8. Hyponatremia + hypcholoraemia - shifiting of H20 from ICF to ECF due to gradient established by hyperglycaemia - osmotic diuresis due to glycosuria
9. Proteinuria - associated with urinary tract infections - USG is generally high despite the polyuria because glucose increases it

Question 9

Descirbe the pathogenesis of the two main ways that diabeties mellitus can arise:

Answer 9

• Autoimmune destruction of B-cells - infiltration of lymphocytes into the islets and antibodies against B-cell + several islet components
• Genetic susceptibility (breed predisposition)

Question 10

How does hypercortisolism (hyperadrenocorticism) in the dog result in diabeties mellitus?

Answer 10

Causes insulin resistance

Question 11

What is an example of predipsosing factor for diabeties mellitus type 2 in cats?

Answer 11

Obesity

Question 12

What species of cat is predisposed to insulin resistance?

Answer 12

Burmese cat

Question 13

Briefly explain the pathogenesis of diabeties mellitus type 2 within cats:

Answer 13

• Decreased adiponectin: Adiponectin functions to enhance insulin sensitivity and also has antiinflammatory properties
• Leptin resistance: Appetitie supression + modulation of insulin sensitivity
• Increased TNF-a: pro-inflammatory cytokine + has negative influence on insulin singalling

Question 14

Briefly explain the pathogenesis of B-cell destruction as a result of amyloid deposition:

Answer 14

1. Amyloid is normal product of B-cells and is co-secreted with insulin
2. Amyloid levels are elevated in conditions associated with insulin resistance
3. Amyloid deposits in the islets of the pancreas

Question 15

What are the main clinical signs that are associated with diabeties mellitus?

Answer 15

• Polyuria
• Polydipsea
• Polyphagia
• Weight loss
• Recurrent cystitis
• Hepatomegaly
• +/- ketotic breath
• Cataracts
• Neuropathy

Question 16

How is an insulinoma normally diagnosed?

Answer 16

Diagnosis of insulinoma - persistent hypoglycaemai + inappropriately high plasma insulin concentration