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D&E Pathology > Pathology of Diabetes Mellitus > Flashcards

Pathology of Diabetes Mellitus Flashcards

1
Q

What is the normal macroscopic structure of the pancreas?

A

Lobules of glandular tissue surrounded by fat

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2
Q

Insulin is secreted by what?

A

Beta cells (islet of langerhans)

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3
Q

Insulin is secreted into what?

A

Blood via capillaries

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4
Q

What is the function of Human Leukocyte Antigen?

A

Helps T-cells recognise self from non-self

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5
Q

What is insulitis?

A

Lymphocyte infiltration of islets (autoimmune mediated)

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6
Q

What is the result of insulitis?

A

Destruction of B cells

Reduced insulin

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7
Q

What is believed to be a cause of T1DM?

A 
Environmental triggers:
- Chemicals
- Gut flora changed in infancy
- Viral infection
GENES
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8
Q

How are viruses suspected to cause T1DM?

A

Molecular mimicry

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9
Q

What is the cause of T2DM?

A

Reduced tissue sensitivity to insulin

Inability to secrete hight levels of insulin

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10
Q

What is T2DM?

A

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

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11
Q

What is the environmental cause of T2DM?

A

Upper body fat mass
Increased intake of food
Lack of exercise

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12
Q

What is the effect of increased upper body fat mass? Why?

A

Increased free fatty acids in blood

Overweight adipocytes stressed to release FAs

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13
Q

Increased free fatty acids in blood leads to what?

A

Decreased insulin receptor sensitivity to insulin

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14
Q

How is the role of the pancreas changed in a patient with central adiposity?

A

More insulin is needed to move in the same amount of glucose

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15
Q

Decreased insulin receptor sensitivity to insulin causes what?

A

Decreased removal of glucose from the blood

So MORE insulin is secreted

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16
Q

What is peripheral insulin resistance?

A

Increased insulin needed to cope with decreased tissue sensitivity to insulin

17
Q

No diabetes will occur in peripheral insulin resistance when?

A

When the individual can substantially increase insulin secretion

18
Q

How is the amount of insulin secreted by the pancreas controlled?

A

GENES

Cant produce HIGH levels of insulin

19
Q

Which genes are implicated for T2DM?

A

Genes for Beta cell high end insulin secretion

20
Q

What factors do genes not appear to be for in T2DM?

A

Peripheral insulin resistance

Increased central adiposity

21
Q

What is the ONLY genetic factor of T2DM?

A

Whether or not Beta cells can secrete insulin bigly

22
Q

What is the annual mortality of T2DM?

A

5.4%

23
Q

What is the LE of someone with T2DM?

A

Reduced by 5-10 years

24
Q

What is the most common CoD in T2DM patients?

A

MI

25
Q

Long term complications of T2DM are a result of what?

A

Prolonged poor glycaemic control

26
Q

What is the main complication of T2DM?

A

Large vessel disease

Small vessel disease

27
Q

What are the macrovascular complications of T2DM?

A

Acceleration of atherosclerosis

28
Q

What are the increases in risk of CHD, MI and Stroke?

A

CHD - 2-20x
MI - 2-5x
Stroke 2-3x

29
Q

What mechanisms are proposed for poor glycaemic control causing accelerated atherosclerosis in large vessels?

A

Glucose attaches to LDLs,
this stops LDLs binding to liver cell receptors
LDLs not removed by liver
–> Hyperlipidaemia

30
Q

What mechanisms are proposed for poor glycaemic control causing accelerated atherosclerosis in small vessels?

A

DM causes molecules to flux into subendothelial space but not flux back out
Molecules trapped under endothelial cells
Thickening of the basal lamina

31
Q

What is hyaline change?

A

Body-wide arteriolar disease causing ischaemia

32
Q

What are the increased risks of amputation, end stage renal disease and blindness?

A

Amputation - 40x
ESRD - 25x
Blindness - 20x

33
Q

What is a Kimmelstiel-Wilson lesion?

A

Nodule of connective tissue in the glomerulus caused by DM

34
Q

How does glycosylation cause small vessel disease?

A

Non-enzymatic binding of glucoses to proteins which starts reversible and progresses

35
Q

When does glycosylation cause irreversible damage in DM?

A

Covalent bonding of glucose to proteins

AGEs (advanced glycosylation end-product) formation

36
Q

How is the activity of glycosylated collagen in arteriole walls changed in DM?

A

Glycosylated collagen binds to albumin causing albumin to accumulate in the subendothelial space of arterioles

37
Q

Why do arteriolar basal lamina proteins become irremovable in DM?

A

GLYCOSYLATION proteins cross link to their neighbours

38
Q

What is the net effect of glycosylation of proteins in the basal lamina of arterioles?

A

Small arteriolar disease
Accumulation of trapped plasma proteins
Accumulation of cross-linked basal lamina proteins
These persist in basal lamina even in normoglycaemia

D&E Pathology (18 decks)

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