Microvascular complications of diabetes Flashcards

1
Q

What are the three major sites of damage from hyperglycemia?

A
  • retinal arteries
  • renal glomerular arterioles
  • Vasa nervorum - tiny blood vessels that supply nerve
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2
Q

what’s the biggest factor that is associated with development of microvascular complications?

A

high blood pressure

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3
Q

hyperglycaemia and hyperlipidaemia cause beta cells to die due to what?

A

oxidative stress

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4
Q

what does AGE stand for in diabetes?

A

advanced glycated end products

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5
Q

what happens with advanced glycated end products in diabetes?

A

disrupts how proteins function eg. proteins in blood vessel wall get glycated

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6
Q

hypoxia caused by hyperglycaemia and hyperlipidaemia activates what?

A

pro-inflammatory cytokines resulting in microvascular damage

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7
Q

the Polyol pathway is involved with?

A

neuropathy formation

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8
Q

what is the mechanism of diabetic retinopathy?

A
  • Activation of various pathways in the presence of hyperglycaemia
  • Leads to dysfunction of the endothelium
  • which leads to retinal ischaemia
  • which leads to vascular permeability which is also worsened by hypertension
  • this can lead to diabetic macular oedema
  • ischaemia can also increase the production of haemoglobin, resulting in neovascularisation
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9
Q

what are the four stages of retinopathy?

A
  1. background retinopathy
  2. pre-proliferative retinopathy
  3. proliferative retinopathy
  4. maculopathy (can occur at any stage)
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10
Q

what is background retinopathy?

A

hard exudates (bit of fluid and associated proteins have leaked out of the vessel and settled in the retina

microaneurysms

blot haemorrhages

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11
Q

what is pre-proliferative retinopathy?

A

‘cotton wool’ spots which look less crisp than hard exudates, called soft exudates - they represent retinal ischaemia

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12
Q

proliferative retinopathy is what?

A

visible new vessels on disc or elsewhere in retina (neovascularization)

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13
Q

what is maculopathy?

A

hard exudates/ oedema / soft exudates near the macula, can threaten vision

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14
Q

what is the treatment for retinopathy?

A

Improve HbA1c and blood pressure

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15
Q

what sort of reviews would someone with background retinopathy have?

A

continued annual surveillance

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16
Q

what specific treatment would someone with pre-proliferative or proliferative retinopathy receive?

A

pan-retinal photocoagulation (burning vessels off to stop new vessel formation which will compromise vision)

17
Q

What treatment would someone with new vessel formation around the macula receive?

A

grid laser therapy/ photocoagulation

and

anti-VEGF intra-ocular injections to reduce oedema in macula

18
Q
A
19
Q

how is diabetic nephropathy diagnosed?

A

take a spot urine sample and take a creatinine: urine albumin ratio

normal range is <2.5mg/mmol in men

<3.5mg/mmol in women

(microalbuminuria)

if greater than 30mg/mmol you would do a proper proteinuria assessment

20
Q

progressively increasing proteinuria

progressively deteriorating kidney function

classic histological features

are linked with?

A

diabetic retinopathy

21
Q

what are the classic histological features of diabetic nephropathy?

A
  • mesangial expansion
  • basement membrane thickening
  • glomerulosclerosis
22
Q

what are risk factors for diabetic nephropathy in T2DM?

A
  • age at development of disease
  • ethnic differences
  • age at presentation
  • loss due to cardiovascular morbidity
23
Q

what do you look for when diagnosing diabetic nephropathy?

A
  • progressive proteinuria (urine albumin:creatinine ratio)
  • increased BP
  • deranged eGFR
  • advanced: peripheral oedema
24
Q

what are the strategies for intervention for diabetic nephropathy?

A
  • decrease HbA1c
  • manage blood pressure with anti-hypertensive treatment
  • Inhibit renal-angiogtensin-aldosterone system (ACE inhibitor)
  • SGLT-2 inhibition
  • stop smoking
25
Q

what is the mechanism of renal failure in diabetes?

A
  1. hyperglycaemia and hypertension
  2. glomerular hypertension
  3. proteinuria
  4. glomerular and interstitial fibrosis
  5. glomerular filtration rate decline
  6. renal failure
26
Q

what does diabetic neuropathy result from?

A

blockage of small vessels supplying nerves called vasa nervorum

27
Q

how do ACE inhibitors affect diabetic nephropathy?

A
  • inhibit angiotensin 2 formation
  • therefore inhibiting inflammation
28
Q
  • loss of sensation
  • loss of vibration sense
  • loss of temperature sensation
  • loss of proprioception
  • loss of ankle jerks

in the feet, are all signs of?

A

peripheral neuropathy

29
Q

why does peripheral neuropathy happen first in the feet, and why is it higher in tall people?

A

the nerves going to the feet are the longest in the body

30
Q

how do you manage peripheral neuropathy?

A
  1. regular inspection of feet by affected individual
  2. good footwear
  3. avoid barefoot walking
  4. podiatry and chiropody if needed
31
Q

how would you manage peripheral neuropathy with ulceration?

A
  1. admit to hospital and multidisciplinary diabetes foot clinic
  2. offloading
  3. revascularisation if concomitant PVD
  4. antibiotics if needed
  5. orthotic footwear
  6. amputation if all else fails
32
Q

what is an example of mononeuropathy and what are the symptoms?

A

3rd nerve palsy with pupil sparing as parasympathetic fibres are not compromised

33
Q

what is mononeuritis multiplex?

A

random combination of peripheral nerve lesions

34
Q

what is radiculopathy?

A

pain over spinal nerves, usually affecting a dermatome on the abdomen or chest wall

35
Q

autonomic neuropathy

A

loss of sympathetic and parasympathetic nerves to GI tract, bladder, cardiovascular system

36
Q
  • difficulty swallowing
  • delayed gastric emptying: nausea and vomiting
  • constipation/nocturnal diarrhoea
  • bladder dysfunction
  • postural hypotension - collapsing on standing
  • cardiac autonomic supply effects - case reports of sudden cardiac death

these symptoms are due to what?

A

autonomic neuropathy - a complication of diabetes