Endocrine 4 Flashcards

1
Q

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

A
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2
Q

How does insluin act to lower blood glucose?

A
  • Inhibition of hepoatic gluconeogenesis
  • Promotion of hepatic glycogen synthesis
  • Increased cellular uptake of glucose by muscles + adipose tissue
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3
Q

How does glucagon activity increase blood glucose levels?

A
  • Promotes gluconeogenesis in liver + muscles
  • Promotes glycogenolysis in liver + muscles
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4
Q

How does catecholamine activity increase blood [glucose]?

A
  • Decreases insulin release by pancreatic B-cells
  • Increasing liver glycogenolysis
  • Increasing pituaritary release of GH
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5
Q

How does GH activity increase blood [glucose]?

A

Reduces glucose uptake by myocytes and adipocytes

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6
Q

What is a major consequence of glucose homeostasis?

A
  • Major metabolic consequence of inadequate insulin activity is decreased movement of glucose into insulin-sensitive cells - hepatocytes, adipocytes, skeletal myocytes
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7
Q

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

A
  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
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8
Q

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

A
  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
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9
Q

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

A
  • Autoimmune destruction of B-cells - infiltration of lymphocytes into the islets and antibodies against B-cell + several islet components
  • Genetic susceptibility (breed predisposition)
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10
Q

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

A

Causes insulin resistance

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11
Q

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

A

Obesity

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12
Q

What species of cat is predisposed to insulin resistance?

A

Burmese cat

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13
Q

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

A
  • 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
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14
Q

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

A
  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
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15
Q

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

A
  • Polyuria
  • Polydipsea
  • Polyphagia
  • Weight loss
  • Recurrent cystitis
  • Hepatomegaly
  • +/- ketotic breath
  • Cataracts
  • Neuropathy
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16
Q

How is an insulinoma normally diagnosed?

A

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