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BRS Year 2 > Microvascular Diabetic Complications > Flashcards

Microvascular Diabetic Complications Flashcards

1
Q

What are the 3 major sites of damage from hyperglycaemia?

A

Retinal arteries
Renal glomerular arterioles
Vasa nervorum - tiny blood vessels that supply nerves

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2
Q

Which of the following is associated with the development of microvascular complications?

Lower HbA1c
High cholesterol level
Hypertension
Shorter duration of diabetes

A

Hypertension

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3
Q

What is the relationship between risk of developing microvascular complications and HbA1c?

A

Rising HbA1c = increasing risk of microvascular complications

Exponential curve, normal HbA1c = still slight risk of microvascular complications

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4
Q

How does increased microvascular complications relate to development of MI?

A

Increased microvascular complications = increased risk of MI

So increased HbA1c = increased microvascular complications = increased risk of MI

Exponential curve

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5
Q

Using what increases microvascular complications, what else would you control in T2DM patients?

A

HbA1c

BP (particularly hypertension)

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6
Q

What other factors contribute to the development of microvascular complications?

A

Severity of hyperglycaemia
Hypertension

Genetic factors - some people develop the complications despite reasonable control

Hyperglycaemic memory - inadequate glucose control early on can result in higher risk of complications later, even is HbA1c has improved

Longer duration of high HbA1c = higher risk of microvascular complications

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7
Q

What is the mechanism of damage to the rising of the microvascular complications?

A

There is oxidative stress due to hyperglycaemia and hyperlipidemia

Advanced glycated end-products (i.e. glucose combined with lipids or proteins) - affects proteins

Then leads to activation of pro-inflammatory cytokines = causes inflammation

Leads to the 3 microvascular complications

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8
Q

What are the 3 microvascular complications?

A

The 3 pathies:

Nephropathy
Retinopathy
Neuropathy

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9
Q

What is diabetic retinopathy?

A

Main cause of visual loss in people with diabetes
Early stages of retinopathy are all asymptomatic, therefore screening is needed to detect retinopathy at a stage which can be treated before visual loss

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10
Q

How does diabetic retinopathy develop?

A

Activation of multiple factors that should not be activated
Leads to vascular endothelial dysfunction - can lead to retinal ischaemia

This can increase leakiness (vascular permeability) of vessels

Factors can leak out of the vessels, including erythropoeitin (stuff RBCs are made out of)

This can lead to formation of new blood vessels on the retina - retinal neovascularisation

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11
Q

What are the stages of retinopathy?

What do they look like on retina screens / images?

A

Background retinopathy - present on the retina as: hard exudates (yellow dots), microaneurysms (red dots), blot haemmorhages

Pre-proliferative retinopathy - present on the retina as: soft exudates (fuzzy, cotton wool spots) - represent retinal ischaemia

Proliferative retinopathy - present on the retina as: neovascularisation (formation of new vessels) due to ischaemia - squiggly vessels as they are fragile

Maculopathy can attack at any of these stages - present on the retina specifically over the macula

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12
Q

What is the treatment of retinopathy?

A

For all stages: improve HbA1c and BP control

Background: Annual checks, feedback to person with diabetes

Pre-proliferative and proliferative:
Pan-retinal photocoagulation - burn off new vessel formation using laser (across the retina)
Grid laser therapy - treat new blood vessel formation (across macula)

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13
Q

What is diabetic nephropathy? How is it diagnosed?

A

Due to hypertension
Progressively increasing proteinuria
Progressively deteriorating kidney function
Actively screened for

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14
Q

How is it diagnosed?

A

Random urine sample

Measure albumin and creatinine and look at the ratio between them

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15
Q

Why is nephropathy important?

A

Diabetic kidney disease = biggest reason for dialysis in the UK
Associated with increased risk of CVD events

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16
Q

How do microvascular complications in diabetics influence macrovascular complications?

A

Microvascular complications from diabetes e.g. CKD = increases the risk of macrovascular complications e.g. ischemic heart disease, peripheral vascular disease, cerebrovascular disease etc.

17
Q

How do the glomeruli change with diabetic nephropathy?

A

Mesangial expansion
Basement membrane thickening
Glomerulosclerosis

18
Q

How common is diabetic nephropathy in T1DM and T2DM?

A

T1DM: 20-40% after 30-40 years

T2DM: Probably equivalent but many other factors modifying the risk: age at development of disease, ethnic differences, age at presentation

19
Q

How is diabetic nephropathy diagnosed?

A

Progressive proteinuria - urine ACR
Increased BP
Deranged renal function (eGFR)
Advanced: peripheral oedema

20
Q

What are the boundaries for microalbuminuria?

A

> 2.5 mg/mmol (men)
3.5 mg/mmol (women)

Proteinuria = ACR >30mg/mmol

21
Q

What is the mechanism for the development of diabetic nephropathy?

A 
Hypertension and hyperglycaemia from diabetes lead to 
Increased glomerular hypertension
Leads to proteinuria 
Glomerular and interstitial fibrosis
eGFR decline 
Eventually renal failure

Ask Anouk

22
Q

What are the strategies for intervention of diabetic nephropathy?

A
  1. Decreasing HbA1c reduces risk of microvasclar complications
  2. Managing BP (anti-hypertensive treatment) allows for slower decrease in eGFR and reduces albuminuria
  3. Inhibit renal-angiotensin-aldosterone system (RAS) - reduces creatinine levels
  4. SGLT-2 inhibition reduces degree of microalbuminuria and slower decrease in eGFR
23
Q

Why do RAS blockades work?

A

Angiotensin 2 involved in inflammatory factors that affect the glomerulus
So RAS blockades reduce incidence of nephropathy

24
Q

Give a summary for nephropathy treatment:

A 
Aim for tighter glycaemic control
Reduce BP as much as tolerated
RAS blockading agent 
Stop smoking 
Start SGLT-2 inhibitors
25
Q

What is diabetic neuropathy?

A

Small blood vessels called vasa nervorum supply nerves

Neuropathy = results from blockage of these vessels

26
Q

Why are feet affected first in diabetic neuropathy?

A

Longest nerves supply feet - most peripheral
Manifests as loss of sensation
More common in tall people
Danger is that patients will not sense injury to the foot

Can lead to lower limb amputation

27
Q

How is this (peripheral neuropathy) screened for?

A

All diabetics have foot checks annually

Assessed for using a 10g monofilament (tests for loss of sensation)

28
Q

What are the clinical features of peripheral neuropathy?

A 
Loss of sensation 
Loss of vibration sense
Loss of temperature sensation 
Loss of propioception 
Loss of ankle jerks
29
Q

How can peripheral neuropathy be managed?

A
  1. Good glycaemic control
  2. Regular inspection of feet - at least once a week
  3. Good footwear - without can lead to calluses and ulcerations
  4. Avoid barefoot walking
  5. For severe neuropathy - refer to podiatry and chiropody
30
Q

What happens if a patient has an ulcer in their foot?

A 
Medical emergency 
MDT diabetes foot clinic 
Offload pressure - give them good footwear
Revascularisation to improve blood flow
Antibiotics if infected 
Amputation if all else fails
31
Q

What are some other neuropathies?

A

Mononeuropathy - CN palsy

Mononeurotis multiplex - a random combination of nerve lesions

Radiculopathy - pain over spinal nerves, usually affects dermatome on abdo or chest wall

Autonomic neuropathy - loss of sympathetic and parasympathetic nerves to GI tract, bladder, CVS

32
Q

What is mononeuropathy?

A

Usually sudden motor loss: wrist drop, foot drop, CN palsy; double vision due to 3rd nerve palsy

33
Q

What is autonomic neuropathy?

A

Loss of sympathetic and parasympathetic nerves to GI tract, bladder, CVS

GI tract: difficulty swallowing, delayed gastric emptying leads to nausea and vomiting, constipation, diarrhoea, bladder dysfunction

CV (cardiovascular): postural hypotension - can be disabling, lead to collapsing on standing; cardiac autonomic supply affected - case reports of sudden cardiac deaths

BRS Year 2 (110 decks)

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