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Endocrine System > Pathology of Diabetes Mellitus > Flashcards

Pathology of Diabetes Mellitus Flashcards

1
Q

Describe the pancreas

A

Lobules of glandular tissue surrounded by fat

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2
Q

Describe the normal insulin formation and secretion

A
  • Islet of langerhans = endocrine pancreas
  • 2/3 of the Islet cells are B cells
  • B cells secrete insulin into the capillaries
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3
Q

What is the effect of the intake of food on insulin?

A

Food converted to glucose –> stimulates insulin

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4
Q

How is the action of insulin?

A

Insulin binds its receptor and drives glucose into adipocytes (= fat cells)

  1. Increase Glc
  2. Increase insulin
  3. Increase Glc uptake by cells
  4. Decrease Glc in serum
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5
Q

What is the aetiology of Type I DM?

A

• Not entirely known
• Genes found so far:
Molecules that help T cells recognise self from non-self = Human Leukocyte Antigen (HLA) molecules
• Autoimmune attack on islet cells
• Environment: ?chemical, viral infection, bacteria in gut

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6
Q

Why does Human Leukocyte Antigen (HLA) molecules increase risk of Type I DM?

A

Cannot distinguish own cells from other cells –> autoimmune attack on pancreatic B cells (therefore cannot produce insulin)

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7
Q

Why does autoimmune attack on islet cells increase risk of Type I DM?

A

Lymphocyte infiltration of islets (insulitis) – destruction of B cells (-> decreased insulin)

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8
Q

What is the effect of destruction of islet?

A

Decreased insulin

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9
Q

How do genes and environment increase risk of Type I DM?

A

Destruction of B cells and scarred islet

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10
Q

What is the effect of the destruction of B cells in Type I DM?

A

Decrease insulin –> increase Glc

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11
Q

What is the aetiology of Type II DM?

A

Combination of:
• Reduced tissue sensitivity to insulin (insulin resistance)
• Inability to secrete very high levels of insulin

A failure of B cells to meet an increased demand for insulin in the body

• Environment: expanded upper body visceral fat mass (pot belly)

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12
Q

What are the causes of expanded upper body fat?

A

Increased intake of food + lack of exercise (genes relatively unimportant)

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13
Q

What is the result of expanded upper body visceral fat mass (pot belly)?

A

Increase free fatty acids in blood, because ‘overweight’ adipocytes are ‘stressed’ and release FA

This causes decreased insulin receptor sensitivity to insulin (peripheral insulin resistance)

But patient is not necessarily diabetic as could be able to produce increased levels of endogenous insulin

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14
Q

Why does increase plasma free FA decrease insulin receptor sensitivity?

A

Not clear why the FA interfere with the insulin receptor pathway

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15
Q

What is the effect of inefficient insulin receptors?

A

Some Glc gets into cells but some does not (increase Glc in blood)

In order for Glc to be taken up, more insulin is required to get the same amount of glucose into cells

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16
Q

What is a requirement in a person with central adiposity?

A

Pancreas needs to secrete more insulin to move glucose into cells

17
Q

What does central adiposity lead to?

A

Hyperinsulinaemia

18
Q

When does diabetes occur in central adiposity?

A

If the pancreas cannot increase insulin substantially to overcome peripheral insulin resistance

19
Q

Are there genes which control insulin secretion in the pancreas?

A
  • Many different genes

* Some of these genes control whether you can secrete very large amounts of insulin or not

20
Q

What type of genes are involved in Type II DM?

A

Implicated genes are for poor B cell ‘high end’ insulin secretion, not for person increasing their central adiposity

So if you have only a few genes abnormal you will be able to secrete lots of insulin

21
Q

What occurs in Type II DM?

A

Insulin secretion does not increase enough to counteract insulin resistance caused by central adiposity

22
Q

What are the oddities in Type II DM?

A

Slim person who puts on a small amount of weight may get type II diabetes if they have very high dosage of genes resulting in inability to even modestly raise insulin

23
Q

Is Type II DM reversible?

A

Yes, if you slim back down to normal weight

A multiple gene defect of pancreatic B cell insulin production which is unmasked by central adiposity

24
Q

What is the long-term complications of DM?

A
  • Annual mortality is 5.4% - double the rate of non-diabetics
  • Life expectancy is decreased by 5-10 years
  • Myocardial infarction is the commonest cause of death
  • Result from prolonged poor glycaemic control
25
Q

What are the main complication of DM?

A

Damage to vessels
• Large vessel disease
• Small vessel disease

26
Q

What are the large vessel (‘macrovascular’) complications

A

DM accelerates atherosclerosis

Can lead to CHD, MI, atherothrombotic stroke

27
Q

How is atherosclerosis accelerated?

A
  1. Glc attach to low density lipoprotein
  2. Glc stop LDL from binding its receptor (on liver cells) highly
  3. LDL is not removed by liver cells –> lipoprotein and lipid stay in blood
  4. Hyperlipidaemia -> atherosclerosis
28
Q

Describe the small vessel (‘microvascular’) disease - arterioles

A
  1. Molecules flux into and out from this subendothelial space bu find it hard to flux back into blood
  2. Build up of ‘trapped’ molecules under endothelial cell - accumulation of plasma proteins (i.e. albumin) and connective tissue (i.e. collagen)
  3. Basal lamina also becomes thickened
29
Q

What is another name for arteriolar disease?

A

Hyaline change

30
Q

How is arteriolar disease damaging?

A

Narrow arteriole –> poor blood flow –> ischaemia

Very damaging in kidney, peripheral tissues (foot), eyes and in arterioles supplying nerves

31
Q

What are the possible outcomes of DM pathology?

A
  • Amputation
  • End stage renal disease
  • Blindness
32
Q

Describe the small vessel disease - capillaries

A

Increased connective tissue around capillaries – eg. Glomerulus in kidney

33
Q

How does small vessel disease occur?

A

Glucoses added to proteins = glycosylation
• Non-enzymatic
• Reversible
• Irreversible if covalent bonds = advanced glycosylation end-products = AGE’s

34
Q

Give an example of small vessel disease occur?

A

Collagen normal in basal lamina

  1. Albumin can get into subendothelial space, but fluxes out as cannot bind -> no accumulation of albumin
  2. Glycosylated collagen does bind albumin –> accumulation of albumin in subendothelial space of arterioles
  3. Albumin trapped in subendothelial space
35
Q

Give example of advanced glycosylation products in small vessels

A

Proteins are cross-linked

  1. Many normal basal lamina proteins do not crosslink and can be removed easily - but glycosylated proteins bind their neighbouring proteins
  2. Rigid, cross-linked protein cannot easily be removed
36
Q

What is glycosylation?

A

Accumulation of trapped plasma proteins and accumulation of cross-linked basal lamina proteins

37
Q

Describe large and small vessel disease in DM

A
  • Typically irreversible when established

* Occurs in setting of prolonged, poor diabetic control

Endocrine System (29 decks)

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