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Systems: Endocrine AB > Pathology of Diabetes Mellitus > Flashcards

Pathology of Diabetes Mellitus Flashcards

1
Q

What is the normal macroscopic appearance of the pancreas?

A

Lobules of glandular tissue surrounded by fat

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2
Q

How does a normal pancreas appear histologically?

A
  • Endocrine part: Islets of Langerhans

- Exocrine part

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3
Q

What cells make up 2/3rd of the islets of Langerhans?

A

B cells

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4
Q

What do B cells secrete?

A

Insulin

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5
Q

What stimulates insulin release?

A

Intake of food which is converted to glucose

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6
Q

What is insulin secreted into?

A

Blood capillaries

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7
Q

How does insulin act on various tissues?

A

Binds to its receptor and drives glucose into the cells

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8
Q

What does the glucose metabolism pathway require?

A
  • Increase in glucose
  • Increase in insulin
  • Increase glucose uptake by cells
  • Decrease of glucose in serum
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9
Q

What is the aetiology of T1DM?

A
  • Not entirely known
  • Genes found so far are molecules that help T cells recognise self from non-self = Human Leukocyte Antigen (HLA) molecules
  • Environmental triggers?
    1. Chemicals
    2. Viral infection? Molecules on viral surface mimic molecules on outside of B cells
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10
Q

How are the B cells destroyed in T1DM?

A
  • In type 1 DM, cannot distinguish own cells from other cells> autoimmune attack on pancreatic B cells
  • Autoimmune attack on islet cells > lymphocyte infiltration of islets (insulitis)> destruction of B cells> decreased insulin
  • Genes+ environment leads to destruction of B cells
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11
Q

What is the aetiology of T2DM?

A
  • Not entirely known
  • Combination of:
    1. Reduced tissue sensitivity to insulin (insulin resistance)
    2. Inability to secrete very high levels of insulin
  • Environment
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12
Q

What environmental factors contribute to T2DM?

A

Expanded upper body visceral fat mass

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13
Q

What doe expanded upper body visceral fat mass result in?

A

Results in increased free fatty acids in blood (NOTE, the patient is not yet diabetic) because overweight adipocytes are probably stressed and release fatty acids which leads to decreased insulin receptor sensitivity

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14
Q

Why do increased free fatty acids decrease insulin sensitivity?

A

It is not clear why the increase in fatty acids leads to a decrease in insulin receptor sensitivity

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15
Q

What does the decreased insulin sensitivity caused by central obesity result in?

A
  • Now have insulin receptors that do not work very efficiently. Some glucose gets into cells but some does not
  • Now need more insulin to get same amount of glucose into cells, so pancreas needs to secrete more insulin to move glucose into cells in person with central adiposity
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16
Q

When will diabetes not occur with central obesity?

A

If the individual can increase their insulin substantially

17
Q

If peripheral insulin resistance is present, how are glucose levels kept normal?

A

Needs a pancreas that will produce larger quantities of insulin

18
Q

Which genes control insulin secretion in pancreas?

A
  • Many different genes
  • Some of these genes control whether you can secrete very large amounts of insulin or not
  • If a gene is a variant it may promote insulin production at low levels but not high levels
19
Q

What are the genes involved in T2DM?

A
  • Multiple genes involved in causing inadequate ‘high level’ insulin secretion by B cells
  • NOT HLA genes
  • NOT adiposity genes
  • So if you have only a few genes abnormal you will be able to secrete lots of insulin
  • Some patients have many gene variants for lower insulin secretion and cannot produce large amounts of insulin
20
Q

When will T2DM occur?

A

When there are numerous defective genes for high end insulin secretion and central adiposity which means there is insufficient insulin for the volume of glucose in the plasma

21
Q

What is the essential mechanism of T2DM?

A

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

22
Q

When may a slim person develop T2DM?

A

Slim person who puts on a small amount of weight may get type 1 diabetes if they have very high dosage of genes resulting in inability to even modestly raise insulin

23
Q

What is T2DM?

A

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

24
Q

What are 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
  • Vessel disease
25
Q

What is the main complication of DM?

A

Damage to vessels

26
Q

What large vessel disease can DM play a part in?

A

Atherosclerosis

27
Q

How does DM accelerate atherosclerosis?

A
  • There are many mechanisms proposed
  • Glucose attach to low density lipoprotein
  • Glucose molecules stop low density lipoprotein from binding its receptor (on liver cells) tightly
  • Low density lipoprotein is not removed by liver cells> lipoprotein and lipid stay in blood> hyperlipidaemia
  • Hyperlipidaemia leads to atherosclerosis
28
Q

How does DM cause small vessel disease?

A
  • Several endothelial cells line lumen of arterioles making basal lamina
  • Between basal lamina and endothelial cells is a potential space which molecules flux in and out of.
  • In DM molecules flux into subendothelial space but find it hard to flux back to blood
  • Build-up of trapped molecules under endothelial cells
  • Basal lamina also becomes thickened
  • Subendothelial accumulation of plasma proteins (e.g. albumin) and connective tissue (e.g. collagens)
29
Q

What is arteriolar disease also known as?

A

Hyaline change

30
Q

What does arteriolar disease lead to?

A
  • Process occurs throughout the body

- Narrow arteriole leads to poor blow flow and ischaemia

31
Q

Where is arteriolar disease especially damaging?

A

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

32
Q

How does small vessel disease occur?

A

Via glycosylation in a non-enzymatic mechanism

33
Q

When does small and large vessel disease occur in DM?

A

It occurs in settings of prolonged, poor diabetic control

34
Q

How is small and large vessel disease cured?

A

It is irreversible and so cannot be cured

35
Q

How does expanded upper body visceral fat lead to hyperinsulinaemia?

A
  • Expanded upper body visceral fat mass leads to decreased insulin receptor sensitivity which then causes decreased removal of glucose from blood
  • Decreased removal of glucose from blood leads to raised glucose and insulin levels then have to markedly increase to make glucose go back to normal levels
  • So in summary, central adiposity leads to hyperinsulinemia
36
Q

Describe the mechanism of glycosylation leading to small vessel disease.

A
  • Collagen=normal basal lamina is glycosylated
  • Glycosylated collagen binds to albumin which enters the sub endothelial space of arterioles leading to an accumulation of trapped albumin
  • Glycosylated proteins will also bind to neighbouring proteins via cross-links which cannot be easily removed.
  • This leads to further persistence of proteins in vessels walls.
37
Q

What does glycosylation of collagen in arterioles lead to?

A
  • Accumulation of trapped plasma proteins

- Accumulation of cross-linked basal lamina

Systems: Endocrine AB (25 decks)

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