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BRS Year 2 > microvascular comp diabetes > Flashcards

microvascular comp diabetes Flashcards

1
Q

site of microvascular complications

A

retinal arteries
renal glomerular arterioles
vasa nervorum - tiny blood vessels that supply nerves

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2
Q

what can be used to approximate risk of microalbuminuria, neuropathy, nephropathy, retinopathy

A

HbA1c (mmol/mol)

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3
Q

factors relating to development of microvascular complications

A
  • severity of hyperglycemia
  • hypertension
  • genetic factors
  • hyperglycaemia memory
  • duration/glucose variability?
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4
Q

mechanism of damage

A

hyperglycaemia/lipidemia leads to:

  • AGE-RAGE/ oxidative stress/ hypoxia
  • inflammatory signalling cascades
  • local activation of pro-inflammatory cytokines
  • inflammation
  • nephropathy, retinopathway, neuropathy
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5
Q

what is the main cause of visual loss in people with diabetes and the main cause of blindness of people of working age?

A

diabetic retinopathy

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6
Q

what kind of symptoms do you get in the early stages of diabetes?

A

asymptomatic

- visual issues due to osmotic changes in lens early on in diagnosis

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7
Q

increased vascular permeability in diabetic retinopathy causes what?

A
  • retinal neovascularisation

- diabetic macular oedema

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8
Q

where do the blood vessels emerge from in the eye?

A

the optic disc

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9
Q

stages of retinopathy

A
  1. background retinopathy
  2. preproliferative retinopathy
  3. proliferative retinopathy
  4. maculopathy
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10
Q

background retinopathy features

A
  • hard exudates (lipid looks like cheese)
  • microaneurysms (dots)
  • blot haemorrhages
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11
Q

preproliferative retinopathy features

A
  1. cotton wool spots - soft exudates

- > represent retinal ischaemia

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12
Q

proliferative retinopathy features

A
  • visible new vessels over the disc (neovascularisation)
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13
Q

maculopathy features

A
  • hard exudates/ oedema near macula
  • same disease as background but near macula
  • can threaten vision
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14
Q

treatment for retinopathy

A
  • improve HbA1c

- improve BP

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15
Q

pan-retinal photocoagulation

A
  • burning eye vessels to stop neovascularisation (for proliferative nephropathy)
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16
Q

How can we treat diabetic maculopathy?

A

anti-VEGF injections directly into eye (vascular endothelial growth factor)
- grid photocoagulation

17
Q

maculopathy can threaten what?

A

direct vision

18
Q

features of diabetic nephropathy: (4)

A
  • hypertension
  • progressively increasing proteinuria
  • progressive decline in kidney function
  • classic histological features
    anyone with diabetes at risk of it
19
Q

how is albumin recorded

A

expressed as a ratio to creatinine

20
Q

why is nephropathy important?

A
  • assocaited with progression to end stage renal failure requiring haemodialysis
  • healthcare burden
  • associated with increased risk of cardiovasc events
21
Q

histological features of nephropathy

A
  • mesangial expansion (glomerular changes)
  • basement membrane thickening
  • glomerulosclerosis
22
Q

epidemiology of nephropathy

A

20-40% of T1DM have it after 30-40 years

T2DM similar but depends on age at development of disease, ethnic differences, age at presentation,

23
Q

diagnosis of nephropathy

A
  • progressive proteinuria
  • increased blood pressure
  • deranged renal function
  • advanced peripheral oedema
24
Q

managing nephropathy

A
  • manage BP (aim for <130/80 mmHg) with ACEi or ARBs
  • Give ACEi/ARB even if normotensive as soon as they have microalbuminuria
  • Stop smoking
  • tighter glycaemic control
  • SGLT-2 inhibitor if T2DM (not official guidance)
25
Q

why does RAS blockage work?

A

In diabetes the RAS system is in overdrive
Blocking RAS with ACE inhibitors or ARBs (angiotensin 2 receptor blocker) reduces BP and progression of diabetic nephropathy
No benefit of giving ACEi/ARB simultaneously- end up with K problems

26
Q

what makes neuropathy happen?

A
  • vasa nervorum blocked

- nerves don’t get blood supply

27
Q

commonest manifestation of diabetic neuropathy

A
  • in feet (longest nerves supply feet)
  • Glove and sock distribution- peripheral neuropathy
  • loss of sensation (issues with ulceration and DFD)
28
Q

clinical features of peripheral neuropathy

A
  • loss of sensation
  • loss of vibration sense
  • loss of temperature sensation
  • loss of proprioception
  • loss of ankle jerks
  • ## glove and stocking distribution
29
Q

management (prevention) of peripheral neuropathy

A
  1. regular inspection of affected feet
  2. good footwear
  3. avoid barefoot walking
30
Q

management of peripheral neuropathy with ulceration

A
  1. Multidisciplinary diabetic foot clinic
  2. offloading ( a term generally understood as relieving pressure from an ulcerated area. )
  3. revascularisation if concomitant peripheral vascular disease
  4. Antibiotics if infected
  5. orthotic footwear
  6. amputation if all else fails
31
Q

other neuropathies

A
  • mononeuropathy e.g. cranial (III) nerve palsy
  • mononeuritis multiplex
  • radiculopathy (SN)
  • autonomic neuropathy
32
Q

What is autonomic neuropathy?

A

Damage to sympathetic and parasympathetic nerves innervating GI tract, bladder and cardiovascular system

Symptoms:
Delayed gastric emptying causing nausea and vomiting
Constipation / nocturnal diarrhoea 
Postural hypotension
Sudden cardiac death
33
Q

what symtpoms let you know you’re developing diabetic nephropathy?

A
  • asymptomatic
  • detected by screening

Aim of screening is to detect it early when it can be detected- annual retinal screening in UK for diabetic patients

34
Q

How is the endothelium affected in microvascular complications?

A

Increased formation of mitochondrial superoxide free radicals in the endothelium
Generation of glycated plasma proteins to form advanced end products (AGEs)
Damaged endothelium leads to leaky capillaries and ischaemia

35
Q

what does vascular endothelial dysfunction lead to?

A
  • retinal ischaemia

- vascular permeability

36
Q

diabetic mechanism of renal failure?

A
  • hyperglycaemia and hypertension
  • leads to glomerular hypertension
  • followed by proteinuria
  • then glomerular and interstitial fibrosis
  • then GFR decline
  • then renal failure
37
Q

how to disrupt mechanism of renal failure?

A

hyperglycaemic treatments

- ACEi/ARB

BRS Year 2 (110 decks)

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