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ENI > Physiology of diabetes mellitus and insulin resistance > Flashcards

Physiology of diabetes mellitus and insulin resistance Flashcards

1
Q

A

A

Insulin

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2
Q

B

A

Glucagon

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3
Q

Insulin resistance

A

the diminished ability of cells to respond to the action of insulin in transporting glucose from the blood into tissues.

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4
Q

Potential physiological causes of insulin resistance

A
  • Pregnancy
  • Stress
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5
Q

Potential pathological causes of insulin resistance

A
  • Obesity
  • Hereditary predisposition
  • Concurrent diseases
  • Endocrinopathies
    • Hyperadrenocorticism
    • Acromegaly (GH excess)
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6
Q

Outline the pathway from initial insulin resistance to Type 2 diabetic

A

Insulin resistance (compensated) → insulin resistance (uncompensated) → Type 2 diabetic

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7
Q

Compensated insulin resistance

A

‘normal’ concentrations of insulin are unable to remove glucose from the bloodstream; the pancreas then secretes more insulin leading to hyperinsulinaemia (i.e. compensating)

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8
Q

Uncompensated insulin resistance

A

beta cell exhaustion (glucose toxicity): the beta cells can no longer maintain the insulin levels required to overcome the insulin resistance

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9
Q

Diabetes mellitus

A

Relative or absolute insulin deficiency

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10
Q

Of the following processes, explain how they could lead to hyperglycaemia:

  • Reduced tissue utilisation of glucose
  • Increased tissue utilisation of amino acids and fatty acids
  • Increased hepatic glycogenolysis
  • Increased hepatic gluconeogenesis
A
  • Reduced tissue utilisation of glucose → increased circulating glucose
  • Increased tissue utilisation of amino acids and fatty acids → ???
  • Increased hepatic glycogenolysis → increased circulating glucose
  • Increased hepatic gluconeogenesis → increased circulating glucose
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11
Q

Type 1 diabetes

A

beta cell destruction, usually leading to absolute insulin deficiency. May be idiopathic or immune-mediated.

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12
Q

Type 2 diabetes

A

May range from predominantly insulin resistance with relative insulin deficiency to predominantly secretory defect with or without insulin resistance.

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13
Q

Reasons why diabetes could arise - issues with insulin production

A
  • Pancreatectomy
  • Pancreatitis
  • Autoimmunity
  • Islet cell hypoplasia
  • Chemical toxicity
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14
Q

Changes to which hormones could lead to diabetes

A
  • Progesterone/progestagens
  • Growth hormone
  • Glucocorticoids
  • Glucagon
  • Catecholamines
  • Thyroid hormones
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15
Q

What are some potential sites of dysfunction in obesity-induced insulin resistance?

A
  • Inadequate number of insulin receptors
  • Defective insulin receptor structure
  • Cell signalling pathway
  • Defective GLUT4 transport proteins
  • Problems with translocation of GLUT4 to the membrane
  • Interference with the function of GLUT4
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16
Q

What is IDDM and which species is it common in?

A

Insulin-dependent diabetes mellitus

  • Most common form of diabetes
  • The animal has a permanent insulin deficiency and requires exogenous insulin
  • Almost 100% of dogs, 50-70% of cats
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17
Q

What is NIDDM and which species is it common in?

A

Non-insulin dependent diabetes mellitus

  • Obesity-induced insulin resistance
  • The animal can produce some insulin but there is resistance to it/perhaps it is being antagonised by something
  • Common in cats but rare in dogs
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18
Q

True/false: IDDM is the same as Type 1 diabetes mellitus.

A

True, but it’s complicated.

In small animals:

IDDM = consistent with Type 1 diabetes mellitus

IDDM or NIDDM = consistent with Type 2 diabetes mellitus

19
Q

What are the potential causes of canine diabetes mellitus? (common causes in bold)

A
  • Immune-mediated (T cell) destruction of beta cells (may have genetic susceptibility to this)
  • Pancreatitis with beta cell destruction
  • Obesity-induced insulin resistance
  • Insulin-antagonistic disease/conditions
  • Insulin-antagonistic drugs e.g. glucocorticoids
20
Q

Describe how immune-mediated destruction of beta cells could lead to canine diabetes mellitus

A
  • Autoantibodies against insulin and/or beta cells
  • Progressive decrease in glucose-stimulated insulin secretion
  • Breed predisposition does exist
21
Q

Describe how pancreatitis with beta cell destruction could lead to canine diabetes mellitus

A
  • Spontaneous inflammation of pancreas with damage to islets and beta cells
  • May take one severe bout or several over time
22
Q

Describe how insulin-antagonists disease/conditions could lead to canine diabetes mellitus

A
  • e.g. hyperadrenocorticism, met/dioestrus
  • Specific hormones e.g. cortisol and growth hormone can antagonise the action of insulin and induce peripheral insulin resistance
  • These are the counter-regulatory hormones usually evoked in hypoglycaemia → excessive amounts of any of them can promote diabetes
23
Q

Excessive amounts of which hormones (and what disease processes) can lead to diabetes mellitus?

(because they are insulin-antagonistic in action)

A
  • Cortisol e.g. may be due to HAC or iatrogenic
  • Growth hormone e.g. in acromegaly
  • Catecholamines e.g. phaeochromocytoma
  • Glucagon e.g. glucagonoma
  • Progesterone e.g. diestrus/gestation
24
Q

Give the possible causes of feline diabetes mellitus

A
  • Obesity-induced insulin resistance
  • Islet amyloidosis
  • Pancreatitis
  • Insulin-antagonistic drug e.g. glucocorticoids
  • Insulin-antagonistic disease e.g. acromegaly
  • Genetics
25
Q

Describe how islet amyloidosis can lead to feline diabetes mellitus

A
  • The cat is obese and becomes insulin resistant
  • Amylin (a.k.a. islet amyloid polypeptide) is secreted in greater amounts in obese/insulin-resistant states
  • This may be a consequence of chronic hyperglycaemia/glucose toxicity
  • Amylin is deposited in the islets as amyloid
  • Amyloid fibrils are cytotoxic and cause apoptosis of the islet cells
  • This leads to defective insulin secretion
  • If the deposition is progressive → diabetes mellitus
26
Q

What disease, previously known as Peripheral Cushing’s, shows high levels of insulin and glucose in affected ponies?

A

Equine Metabolic Syndrome

27
Q

Describe the difference between these two images

A

Left: normal islet

Right: beta cell vacuolation (=pathology)

28
Q

What is the primary disorder in Equine Metabolic Syndrome (EMS)?

A

Insulin resistance

29
Q

Which animals is EMS most commonly seen in?

A
  • Ponies
  • Associated with obesity/ regional adiposity
30
Q

What is the most common clinical sign associated with EMS?

A

Laminitis

31
Q

Describe how insulin resistance/diabetes mellitus leads to PUPD

A
  • Normally, glucose is filtered by the kidney into urine and then reabsorbed
  • When blood glucose is too high, it exceeds the renal threshold.
  • Glucose remains in the urine and acts as an osmotic particle, drawing water into the renal tubule
  • This dilutes the urine and increases urine volume (osmotic diuresis)
  • There is polyuria and compensatory polydipsia
32
Q

Describe how insulin resistance/diabetes mellitus leads to polyphagia

A
  • Relates to hypothalamic satiety centre
  • Glucose entry into the centre → decreased hunger.
  • Glucose entry into cells here is via GLUT4 receptors, therefore it requires some insulin to be present also.
  • Diabetes mellitus (esp. type 1/IDDM) = lack of insulin
  • There is thus a failure to inhibit the appetite centre and polyphagia despite hyperglycaemia.
33
Q

Describe how insulin resistance/diabetes mellitus leads to weight loss

A
  • Entry of glucose into cells is mediated by insulin. In DM there is a lack of insulin.
  • The insulin:glucagon ratio falls and promotes the starvation processes
  • Amino acids are used for gluconeogenesis and increased protein breakdown required for this leads to muscle wasting.
  • This is ‘starvation in the midst of plenty’
34
Q

Describe how insulin resistance/diabetes mellitus leads to cataracts

A
  • There is excess circulating glucose due to absence/ineffectiveness of insulin
  • There is therefore glucose uptake into the lens; at normal levels, this can be metabolised to lactate which diffuses out. However, excess glucose is converted to fructose and sorbitol that do not diffuse out.
  • Trapped fructose and orbital draw water into the lens.
35
Q

How does diabetic ketoacidosis develop?

A
  • In the animal with diabetes mellitus, there is a lack of insulin. This means glucose does not enter cells easily, and the disturbed insulin:glucagon ratio favours catabolism.
  • There is thus a shift to fat metabolism for energy.
  • Mobilisation of fatty acids → excessive fatty acids levels → ketones
  • Buildup of ketone → metabolic acidosis
36
Q

What clinical signs will an animal with diabetic ketoacidosis present with?

A
  • Vomiting
  • Diarrhoea
  • Anorexia
  • All the above contributing to dehydration
37
Q

What are some diagnostic tests for diabetes mellitus?

A
  • Blood glucose levels
  • Blood liver enzyme levels (shows hepatic lipidosis)
  • Blood markers that indicate hypercholesterolaemia/hypertrigyceridaemia/visible lipid in serum plasma (=mobilisation of fatty acids from adipose tissue)
  • Urinanalysis
  • Fructosamine levels
38
Q

How could blood glucose be used to diagnose an animal with diabetes mellitus?

A
  • Persistent fasting hyperglycaemia
    • Normal glucose = 3.5-5.5 mmol/L
    • Diabetic = >10 mmol/L
39
Q

What are the issues with diagnosing diabetes mellitus from glucosuria?

A
  • Feline stress-induced hyperglycaemia can occur
  • Stress induces catecholamines and cortisol, and therefore can cause hyperglycaemia
  • Usually there is not glucosuria unless the animal has been previously stressed; recheck in a non-stressed environment
40
Q

How can fructosamine levels be used to diagnose an animal with diabetes mellitus?

A
  • Fructosamine = glycolated serum proteins
  • Non-enzymatic reaction occurs and is proportional to blood glucose concentration
  • Fructosamine reflects the previous 2-3 weeks of blood glucose concentration
  • Abnormal = >400µmol/L
41
Q

What findings might you see in the urinalysis from an animal with diabetes mellitus?

A
  • USG increased by glucosuria; often >1.025
  • May find glucose and potentially ketones in urine
  • May see UTI (WBCs, bacteria, protein) attracted by high glucose levels
42
Q

A

A

Diabetes mellitus

43
Q

B

A

Stress

ENI (11 decks)

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