Long Term Complications Flashcards

1
Q

What is the natural history of T2D?

A
  • Insulin resistance due to increased adipose tissue = increased FA’s
  • Creates inflam. reaction = cytokines = blocks secondary mechanism system necessary for transport of glucose into cell
    = Increase glucose outside cell so B cells start to produce more & more insulin to compensate
  • After long period of time = hyperinsulinemia
  • B cells eventually burn out & insulin production decreases so fasting glucose increases
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2
Q

What are the risk factors for diabetes?

A
  1. Duration
  2. Age of onset
  3. High HbA1c
  4. Hypertension
  5. Micro albuminuria
  6. Dyslipidaemia
  7. Obesity
  8. Smoking
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3
Q

What is the pathophysiology of chronic glycaemia?

A

Increased glucose = toxic to endothelial cells = inflammatory cascade = increased permeability of endothelial = atheroma = cholesterol deposition in basement membrane = thickening + narrowing of BV + stiffening = ischemia = thrombus formation = infarction

Proximal to blockage vessels can widen = aneurysms

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4
Q

What are the signs of peripheral vascular disease?

A
  • Claudication
  • Rest pain
  • Tissue lost
  • Gangrene
  • High risk amputations

PVD = if femoral arteries involved

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5
Q

What is seen in non proliferative diabetic retinopathy?

A
  • Cotton wool spots
  • Intra retinal haemorrhages
  • Hard exudates
  • Micro aneurysms
  • Visual loss due to macular oedema
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6
Q

What is seen in proliferative diabetic retinopathy?

A

Neovascularization

Pre retinal + vitreous haemorrhages = fibrosis = traction retinal detachment

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7
Q

What is diabetic nephropathy?

A
  • Defined as proteinuria/ micro albuminuria = leaking of protein (albumin) through nephrons
  • BM thickening in glomerular capillaries = reduces blood flow = sclerosis = ischemia
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8
Q

How is diabetes managed?

A
  • Annual albumin/creatinine ratio screening
  • ACE inhibitor/angiotensin receptor blocker (blocks breakdown of bradykinin = vessel dilator so reduced protein leak)
  • Intense glycemic control
  • Control of other RF’s
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9
Q

What is diabetic neuropathy?

A

Decreased sensation + reduction/loss of vibration due to degeneration of schwann cells

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10
Q

What are the types of diabetic nephropathy?

A
  • Distal symmetrical polyneuropathy
  • Autonomic neuropathy
  • Diabetic amyotrophy
  • Mononeuropathy
  • Mononeuropathy multiplex
  • Treatment induced neuropathy
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11
Q

What are the types of diabetic nephropathy?

A
  • Distal symmetrical polyneuropathy: progressive loss of distal sensation followed by motor weakness
  • Autonomic neuropathy: postural hypotension, gastro paresis, enteropathy with constipation or diarrhoea
  • Diabetic amyotrophy: acute asymmetric focal pain followed by weakness in proximal leg, onset of muscle weakness followed by pain
  • Mononeuropathy: median nerve
  • Mononeuropathy multiplex: more than 1 nerve involved in different places
  • Treatment induced neuropathy: metformin (can interfere with B12 absorption)
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12
Q

How do you perform examination of feet?

A
  • Inspection - cracks, deformities, callus formation
  • palpate - dorsalis + posterior tibial artery
  • Vibration sense
  • Monofilament - touch sensation
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13
Q

Why is there a risk of developing infection in diabetes?

A

Reduced blood supply + neuropathy = risk of developing ulcer = inlam. response = reduces in diabetes & phagocytes in diabetics have reduces mobility = infection gets worse = sepsis + amputations

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