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ZA - Endocrine System > Pathology of Diabetes Mellitus > Flashcards

Pathology of Diabetes Mellitus Flashcards

1
Q

What does a normal pancreas look like?

A

Lobules of glandular tissue surrounded by fat

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2
Q

What histological slide is this? How can you tell? And what is the arrow pointing at?

A

Pancreas slide

Can tell by the light pink area the arrow is pointing at

It is the islets of langerhands - the endocrine part of pancreas, the rest of the pancreas is exocrine

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3
Q

What are 2/3s of the islet cells made up of?

A

B-cells

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4
Q

What do B cells do?

A

Secrete insulin

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5
Q

Where in this picture are the B cells?

A

Within the endocrine part/islet area - the small pink circles

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6
Q

What is the white areas within the ednocrine pancreas are?

A

Capillaries for insulin to be secreted to

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7
Q

Is aetiology of type 1 DM known?

A

No

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8
Q

What do the genes that are found so far (that lead to type 1 DM) do?

A

Responsible for Human leukocyte antigen (HLA) molecules that help T cells recognise self from non self

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9
Q

What is the pathology behind type 1?

A

Autoimmune attack on B-cells

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10
Q

What does this slide show? What is arrow pointing at?

A

An autoimmune attack on iselt cells

Arrow points to a lympoid cell

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11
Q

What is insulitis?

A

Lymphoid infiltration of islets

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12
Q

Whats arrow pointing at?

A

A scarred islet

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13
Q

Some hypothosised enviromental triggers of type 1?

A

Chemicals

Viral infection - molecules on infection mimic moleculs on outside of B-cells

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14
Q

Aetiology of type 2?

A

Combination of:

Insulin sensitivity

Inability to secrete high levels of insulin

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15
Q

What is the enviromental factors for type 2?

A

Expanded upper body fat mass due to increase intake of food and lack of diet

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16
Q

What happens if patient has expanded upper body fat mass? Is the patient diabetic at this point?

A

Adipocytes placed under stress and release FFA’s into blood (patient not yet diabetic)

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17
Q

When FFA’s are released into blood - what chain of events does this start?

A

FFAs interfere with insulin receptor sensitivity decreasing it

More insulin needed to get same amount of glucose into cells so pancreas makes more (a patient with central adiposity)

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18
Q

So what does central adiposity cause in regards to insulin?

A

Causes hyperinsulinaemia

19
Q

If patient has hyperinsulinaemia, are they diabetic?

A

Not if the can increase insulin substantially (or increase insulin sensitvity via exercise and diet change)

20
Q

What type of insulin resistance does central adiposity cause?

A

Peripheral insulin resistance

21
Q

Since to stop diabetes if insulin receptor sensitivity is low you need more insulin secreted, what gives certain people an dvantage to do this?

A

Different genes can control if you can secrete a lot of insulin or not

22
Q

Explain the gene stuff?

A

If a patients genes that cause poor B-cell production are abnormal they can make lots of insulin

But if a patient has lots of genes that cause low insulin secretion they cannot make large amounts

23
Q

Can a slim person ever get type 2 diabetes?

A

Yes, if they have a very high number of genes that result in an inability to even modestly raise insulin

24
Q

So what genes are NOT involved in this and what genes are?

A

NOT - HLA genes, adiposity genes

ARE - Genes involving inadequte “high level” insulin secretion by b cells

25
Q

Whats the commenst cause of death for diabetics?

A

MI

26
Q

What does the MI result from?

A

Poor glycemic control

27
Q

What vessels fall under macrocascular catagory? What does hyperglycemia do to these vessels?

A

Arteries - accelerates atheroscerosis

28
Q

What one is a healthy artery and what one isnt? What is wrong with the unhealthy one…

A

Right has atherosclerosis with an occlusive thrombosis

29
Q

How does hyperglyceaemia actually accelerate atheroclerosis?

A
  • Glucose attaches to low densitiy lipoprotein (LDL)
  • LDL can’t then bind onto liver receptors
  • LDL is therefore not removed by the liver
  • Lipoprotein and lipids stay in blood = hyperlipidaemia = atherosclerosis
30
Q

What vessels are affected in microvascular disease? What picture is abnormal and why?

A

Arterioles

Right - arteriole is constricted

31
Q

What cells line arterioles?

A

Endothelial cells

32
Q

What do endothelial cells make to sit on?

A

Basal lamina (collagens)

33
Q

What is between the basal lamina and endothelial cells?

A

Potential space

34
Q

What happens in DM with this potenital space?

A

Molecules flux into the subendothelial space but find it hard to flux back to blood

35
Q

What lies around basal lamina?

A

Smooth muscle cells

36
Q

What do these trapped molecules cause?

A

They build up and cause occlusion by thickening the basal lamina

37
Q

What type of molecules get caught in the subendothelial space?

A

Plasma proteins - albumin

CT - collagens

38
Q

What is arteriolar disease also called?

A

Hyaline change

39
Q

Where does hyaline change affect most?

A

Kidney

Eyes

Arterioles supplying nerves

Peripher tissues - feet

40
Q

State some morbidity risks from hyaline change.

A

Amputation x40

End stage renal disease x25

Blindness x20

41
Q

What vessles are affected in small vessel disease?

A

Capillaries

42
Q

What pathology effects the capillaries? Give and example

A

Increased CT arround capillaries - e.g is glomerulus in kidney

43
Q

How does small vessel disease occur?

A
  • Glucose is added to proteins such as collagen via glycosylation
  • Collagen is normal in basal lamina, and albumin can sometimes enter into the subendothelial space
  • Albumin and collagen do not normally bind but when collagen has glucose on it these proteins cross link = thickening and occlusion
44
Q

Is vessel disease reversible?

A

Not once it is established

ZA - Endocrine System (21 decks)

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