Pathology of DM complications Flashcards

1
Q

How much of pancreatic islet cells are B cells?

A

2/3rds

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2
Q

Pathology of T2DM is a combination of….

A
  1. reduced tissue sensitivity to insulin (insulin resistance)
  2. inability to secrete very high levels of insulin
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3
Q

Increase in FFA effect on insulin

A

Leads to decreased insulin receptor sensitivity

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4
Q

What does central adiposity lead to and why?

A

Hyperinsulinaemia
More insulin needs to be produced to make glucose go back to normal levels as decreased removal of glucose from the blood

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5
Q

Annual mortality % of diabetics compared to non diabetics

A

5.4%

double the rate of non diabetics

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6
Q

How much is life expectancy decreased by in DM?

A

5 - 10 years

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7
Q

What does DM accelerate in large vessels and therefore they are at a higher risk of what?

A

Atherosclerosis so at a higher risk of

  • CHD
  • MI
  • atherothrombotic stroke
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8
Q

How does DM accelerate atherosclerosis?

A

Glucose attaches 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

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9
Q

How does DM cause arteriolar disease?

A

Molecules flux into subendothelial but find it hard to flux back to the blood.
Build up of ‘trapped’ molecules under endothelial cell
Basal lamina also becomes thickened
Narrow arteriole - poor blood flow - ischaemia

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10
Q

Risk of amputation in DM

A

40x

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11
Q

`Risk of end stage renal disease in DM

A

25x

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12
Q

Risk of blindness in DM

A

20x

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13
Q

Pathology of small vessel disease in DM

A

Increase connective tissue around capillaries e.g. glomerulus in kidney
Collagen is glycosylated which binds to albumin (doesn’t bind usually) and albumin accumulates in subendothelial spaces of arterioles

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14
Q

Protein structure in DM small vessels and what does this mean?

A

Proteins are cross linked
Rigid, cross-linked proteins cannot easily be removed
They persistent even if return to normoglycaemia

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15
Q

2 results of glycosation

A

Accumulation of trapped plasma proteins

Accumulation of cross linked basal lamina proteins

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16
Q

Treatment of sensory neuropathy

A
Painkillers
Gabapentin 
Duloxetine
Acupunture
More
17
Q

What type of pulse tends to be bounding? Why do we have to beware of this?

A

Neuropathic pulse

As can have good pulse but poor perfusion

18
Q

How are calluses related to ulcers?

A

Pressure causes callus formation

If the callus gets too hard then can break down the tissues underneath it

19
Q

What are involuted nails?

A

Gentle curves to a pincer shape

20
Q

When is there a big ulcer risk under calluses?

A

Neuropathic

21
Q

Presentation of Charcots

A
Rockerbottoms foot
Clawing of toes
Bounding pulses
Possible 3C temperature difference between the feet
Look for infection
22
Q

What is charcots a combination of?

A

Osteopenia
Sensory neuropathy
Trauma

23
Q

What type of condition is charcots?

A

Inflammatory

24
Q

Examples of GI autonomic neuropathies

A

Chronic diarrhoea
GORD
Gastroporesis

25
Q

What is GORD caused by?

A

Reduced LOS pressure

26
Q

When does chronic diarrhoea as a result of autonomic neuropathy often occur?

A

At night

27
Q

Features of gastroparesis

A

Erratic BG control
Bloating
Vomiting

28
Q

Treatment of gastroporesis and what kind of drugs are these?

A

Metoclopramide
Domperidone
Erythromycin
PROKINETIC DRUGS