Pathology of Diabetes Mellitis and its Complications Flashcards

1
Q

what is the aetiology of type 1 diabetes?

A

not entirely known

genes found so far- molecules that help T cells recognise self from non-self= human leukocyte antigen molecules

autoimmune attack on islet cells- lymphocyte infiltration of islets- destruction of B cells

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2
Q

what happens in type 1 diabetes mellitus?

A

Cannot distinguish own cells from other cells –> autoimmune attack on pancreatic B cells

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3
Q

what is the result of destruction of islets?

A

decreased insulin

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4
Q

what are the environmental triggers/aetiology of type 1 diabetes

A

? Chemicals
? Bacteria in gut altered in infancy
? Viral infection - ? Molecules on viral surface mimic molecules on outside of B cells

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5
Q

destruction of B cells causes (insulin) (glucose)

A

decrease insulin and increase in glucose

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6
Q

aetiology of type 2 diabetes mellitus?

A

Combination of:

1) reduced tissue sensitivity to insulin (insulin resistance) and
2) inability to secrete very high levels of insulin

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

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7
Q

what are the environmental triggers of type 2 diabetes?

A

Expanded upper body visceral fat mass - due to increased intake of food and lack of exercise

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8
Q

what does expanded upper body visceral fat mass result in?

A

increased free fatty acids in blood

decreased insulin receptor sensitivity to insulin

which then causes decreased removal of glucose from blood

which then leads to raised glucose, and insulin levels then have to markedly increase to make glucose go back to normal levels

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9
Q

what does central adiposity ultimately lead to?

A

hyperinsulinaemia

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10
Q

what type of genes are involved in type 2 DM?

A

Implicated genes are for poor B cell ‘high end’ insulin secretion- so if you have only a few genes abnormal you will be able to secrete lots of insulin

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11
Q

therefore you can have central adiposity but if you have many genes promoting high end insulin secretion your glucose levels can still be okay

A

:)

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12
Q

if you have central adiposity and numeroous genes defective for high end insulin secretion what does this do?

A

not enough insulin to decrease glucose therefore glucose increases and results in type 2 diabetes

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13
Q

what are the long term complicaations 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

dammage to vessels- most common

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14
Q

how is atherosclerosis accelerated?

A

Glucoses 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

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15
Q

true or false normal collagen binds to albumin

A

false normal collagen does not bind to albumin

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16
Q

does gycosylated collagen bind to albumin?

A

yes

17
Q

where is the albumin trapped in a cell?

A

subendothelial space

18
Q

what does glycosylation lead to?

A

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

19
Q

are the B cells in the pancreas the same as the B cells in autoimmune system?

A

no

20
Q

what do B cells secrete?

A

insulin

21
Q

how much of islet cells are B cells?

A

2/3