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*Diabetes & Endocrinology > Pathology of Diabetes Mellitus > Flashcards

Pathology of Diabetes Mellitus Flashcards

1
Q

What is the main property of exocrine pancreatic tissue?

A

Acinus

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2
Q

What is the main property of endocrine pancreatic tissue?

A

Islets of Langerhans

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3
Q

What type of cells are found in the Islets of Langerhans?

A

B cells (2/3 of cells in I of L)

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4
Q

What is the function of the B cells in the I of L?

A

Secrete insulin into blood in capillaries

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5
Q

Give a v basic summary of the effect of insulin on fat tissue

A

Insulin binds to its receptor and drives glucose from plasma into adipocytes (same with muscle cells etc)

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6
Q

Increased glucose =

A

increased insulin = increased glucose uptake by cells = decreased glucose in serum

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7
Q

Is there a definite aetiology of type 1 diabetes?

A

No, not entirely known

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8
Q

Give a gene complex found so far to be a possible aetiology of type 1 DM

A

HUMAN LEUKOCYTE ANTIGEN (HLA)

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9
Q

What is the normal function of the HLA gene complex?

A

Encodes the major histocompatibility complex (MHC) proteins in humans = cell-surface proteins responsible for regulation of immune system

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10
Q

What does P Brown say is the function of HLA molecules?

A

‘Molecules that help T cells recognise self from non-self’

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11
Q

How do HLA molecules malfunction to cause type 1 DM?

A

Cant distinguish own cells form other cells = autoimmune attack on islet cells in pancreas = lymphocyte infiltration of islets (insulitis) = DESTRUCTION OF B CELLS

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12
Q

Name 3 possible environmental triggers for type 1 DM

A

Chemicals (pollutants e.g. PCBs, toxicants, air pollutants)
Bacteria altered in gut in infancy
Viral infection (molecules on viral surface mimic molecules on outside of B cells)

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13
Q

What is the general ‘equation’ for aetiology of type 1 DM?

A

Genes + Environment = Destruction of B cells = Decreased Insulin + increased blood Glc

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14
Q

Is there a definite known aetiology for type 2 DM?

A

No, not entirely known

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15
Q

What 2 things are the aetiology of type 2 DM thought to be a result of?

A
  1. Reduced tissue sensitivity to insulin (insulin resistance)
  2. Inability to secrete very high levels of insulin
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16
Q

What simple way does P Brown put the aetiology of type 2 DM?

A

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

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17
Q

What is an important ‘environmental’ factor in the aetiology of type 2 DM? (I dont rly think this is ‘environmental’ ??)

A

Expanded upper body visceral fat mass (‘pot belly’)

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18
Q

Are genes associated with expanded upper body visceral fat mass?

A

No, genes are relatively unimportant - usually due to increased intake of food and lack of exercise

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19
Q

How does expanded upper body visceral fat mass affect blood content?

A

Results in increased free fatty acids in blood

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20
Q

Why does pot belly increase free fatty acids in blood?

A

Overweight adipocytes are ‘stressed’ and so release fatty acids

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21
Q

What effect do increased free fatty acids have on insulin receptors?

A

They decrease insulin receptor sensitivity

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22
Q

Why do free fatty acids decrease insulin receptor sensitivity?

A

Unclear

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23
Q

Describe how the body copes with peripheral insulin resistance caused by central adiposity

A

Decreased insulin receptor sensitivity, so pancreas now needs to secrete more insulin to get normal amount of glucose into cells = hyperinsulinaemia

24
Q

Does the fact that central adiposity causes hyperinsulinaemia and peripheral insulin resistance mean that these people have diabetes?

A

No, people might not yet be diabetic; diabetes will occur if insulin increases substantially

25
Q

So if central adiposity does not necessarily cause type 2 DM, what factor when added to the central adiposity can cause it?

A

Genetics

26
Q

Describe how some genes can lead to type 2 DM

A

Gene variants which can control whether you secrete large amounts of insulin or not

27
Q

How do these gene variants impact insulin levels?

A

Gene may promote insulin production at low levels but NOT high levels; implicated genes are for poor B cell ‘high end’ insulin secretion

28
Q

What is the difference between having a few of these abnormal gene variants and having many of these gene variants?

A

Only a few genes abnormal means will be able to secrete lots of insulin to compensate whereas having many gene variants for lower insulin production means you CANT produce large amounts of insulin

29
Q

So summarise in concise, simple terms what occurs to cause type 2 DM

A

In type 2 diabetes, insulin secretion does not increase enough to counteract insulin resistance caused by central adiposity

30
Q

Are there oddities in the development of type 2 diabetes?

A

Yes, a slim person who puts on small amount of weight may get type 2 if they have v high dosage of lower insulin genes; vice versa with an overweight person with v good genes

31
Q

Are HLA genes or adiposity genes involved in development of type 2 DM?

A

NO

32
Q

Define type 2 diabetes (according to Paul)

A

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

33
Q

By how much is life expectancy reduced for diabetics?

A

5-10 yrs

34
Q

What is the most common cause of death for diabetics?

A

Myocardial infarction

35
Q

Are the long term complications of DM dependent on the cause?

A

no, occur regardless of cause

36
Q

What do long term complications of DM result from?

A

prolonged poor glycaemic control (5-10 yrs)

37
Q

What is the main complication of DM

A

Vessel disease (large - arteries; small - arterioles/capillaries)

38
Q

What does DM cause in large vessels?

A

Acceleration of atherosclerosis

39
Q

Describe one proposed mechanism of how DM causes atherosclerosis

A

Glucose molecules attach to LDL; stop it binding to its receptors tightly; LDL is therefore not removed by e.g. liver cells and stays in the blood = hyperlipidaemia = atherosclerosis

40
Q

Describe the structure of arterioles (3 ‘layers’)

A

Endothelial lining cells make basal lamina (collagens) so sit on and creates a potential subendothelial space between endothelial cells and lamina; around lamina are smooth muscle cells

41
Q

Describe the movement of molecules in and out of the subendothelial space in arterioles in DM

A

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

42
Q

In DM arterioles, molecules have difficulty fluxing back into blood, what does this result in?

A

Build up of ‘trapped’ molecules under endothelial cell and thickening of basal lamina

43
Q

What type of molecules accumulate in subendothelial space of arterioles?

A 
Plasma proteins (e.g. albumin)
Connective tissue (e.g. collagens)
44
Q

What is arteriolar disease also called?

A

Hyaline change

45
Q

What does this thickening of lamina result in in arterioles?

A 
Narrow arteriole
=
Poor blood flow
=
Ischaemia
46
Q

Where does arteriolar disease/hylaine change particularly damage in the body?

A

Kidney
Peripheral tissues (foot)
Eyes
Arterioles supplying nerves

47
Q

What is there an increased morbidity for as a result of arteriolar disease in DM?

A

Amputation 40x
End stage renal disease 25x
Blindness 20x

48
Q

What is there a higher risk of developing as a result of atherosclerosis as a result of DM?

A

Coronary heart disease 2-20x
Myocardial infarction 2-5x
Atherothrombotic stroke 2-3x

49
Q

What change occurs in small vessels (capillaries) as a result of DM?

A

Increased connective tissue around capillaries e.g. glomerulus in kidney

50
Q

What is the name for a nodule of connective tissue in capillary?

A

Kimmelstiel-Wilson

51
Q

Give one mechanism for how small vessel disease occurs in DM

A

Glucose added to proteins (= glycosylation)

52
Q

Give some properties of glycosylation in small vessel disease

A

Non-enzymatic
Reversible at first
Irreversible if covalent bonds = Advanced Glycosylation End-products (AGEs)

53
Q

Give an example of glycosylation products in small vessels

A

Collagen is glycosylated; albumin fluxing out of cell will bind to glycosylated collagen (will not bind to it when not glycosylated); results in accumulation of albumin subendothelial space

54
Q

Give another example of glycosylation products in small vessels

A

Normal basal lamina proteins dont crosslink and can be removed easily, but glycosylated proteins bind to their neighbours and become rigid (cant be easily removed), and persist even in normoglycaemia

55
Q

Glycosylation in capillaries =

A

accumulation of TRAPPED plasma proteins + accumulation of CROSS-LINKED basal lamina proteins

56
Q

Is large + small vessel disease in DM typically reversible or irreversible?

A

Irreversible when established

57
Q

What setting does large + small vessel disease in DM usually occur?

A

Prolonged, poor diabetic control

*Diabetes & Endocrinology (24 decks)

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