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!!!!! BRS YR2 !!!!! > Endo - Micro/Macrovascular Risk of DM > Flashcards

Endo - Micro/Macrovascular Risk of DM Flashcards

1
Q

What are the microvascular complications of DM?

A

→ retinopathy
→ nephropathy
→ neuropathy

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2
Q

What is the relationship between Hb1Ac and risk of microvascular complications?

A

→ increasing Hb1Ac = increasing risk

→ Hb1Ac < 53 mmol/mol

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3
Q

What is the relationship between BP and risk of microvascular complications?

A

→ increasing BP = increasing risk

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4
Q

What factors influence risk of MicroV complications in DM?

A 
→ Hb1Ac > 53 mmol/mol
→ elevated BP
→ duration of diabetes 
→ smoking - endothelial dysfunction
→ genetic factors
→ hyperlipidaemia
→ hyperglycaemic memory
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5
Q

What is the mechanism of damage in hyperglycaemia + hyperlipidemia?

A

→ Increased formation of mitochondrial superoxide free radicals in the endothelium
→ Generation of glycated plasma proteins to form advanced glycation end products (AGEs)
→ Activation of inflammatory pathways
→ Damaged endothelium results in ‘Leaky’ capillaries + Ischaemia

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6
Q

What is the main cause of visual loss in DM + blindness in people of working age?

A

diabetic retinopathy

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7
Q

Why is screening very important in diabetic retinopathy?

A

→ early stages of retinopathy are all asymptomatic

→ detect retinopathy early when it can be treated before visual loss + disturbances occur

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8
Q

How often do people with diabetes get screened for diabetic retinopathy?

A

annually

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9
Q

What does a normal retina without retinopathy look like?

A

→ macula : central high resolution, colour vision

→ optic disc

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10
Q

What are the stages of progression of diabetic retinopathy?

A

→ background retinopathy
→ pre-proliferative retinopathy
→ proliferative retinopathy
→ maculopathy

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11
Q

What are the characteristics of background retinopathy?

A

→ hard exudates (cheese colour, lipid)
→ micro-aneurysms (‘dots”)
→ blot haemorrhages

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12
Q

What are the characteristics of pre-proliferative retinopathy?

A

→ Cotton wool spots also called soft exudates

→ Represent retinal ischaemia

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13
Q

What are the characteristics of proliferative retinopathy?

A

Visible new vessels on disc or elsewhere in retina

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14
Q

What are the characteristics of maculopathy?

A

→ Hard exudates / oedema near the macula
→ Same disease as background, but happens to be near macula
→ This can threaten vision

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15
Q

How is background retinopathy treated?

A

→ continued annual surveillance

→ improve Hb1Ac, stop smoking, lipid lowering, good BP control

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16
Q

How is pre-proliferative retinopathy treated?

A

start early pan-retinal photocoagulation

→ if left alone, will progress to new vessel growth

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17
Q

How is proliferative retinopathy treated?

A

pan-retinal photocoagulation

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18
Q

How is maculopathy treated?

A

→ grid photocoagulation

→ oedema treated with anti-VEGF injections directly into the eye

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19
Q

What is VEGF?

A

vascular endothelial growth factor

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20
Q

What is pan-retinal photocoagulation?

A

burn the new growth of blood vessels to reduce risk of haemorrhaging and therefore reduce risk of visual disturbances, etc.

21
Q

What is diabetic nephropathy is important?

A

→ associated with progression to end-stage renal failure requiring haemodialysis
→ healthcare burden
→ associated with increased risk of cardiovascular events

22
Q

What are signs of diabetic nephropathy clinically + phsyically?

A 
→ progressive proteinuria (albumin: creatinine ration > 30mg/mmol)
→ increased blood pressure
→ deranged renal function (eGFR)
→ microalbuminuria > 2.5 mg/mmol
→ advanced: peripheral oedema
23
Q

What is a side effect of pan-retinal photocoagulation?

A

causes loss of peripheral vision

24
Q

What is the mechanism of diabetic nephropathy?

A 
→ hyperglycaemia + hypertension from diabetes
→ glomerular hypertension
→ proteinuria
→ glomerular + interstitial fibrosis
→ GFR decline
→ renal failure
25
Q

How can diabetic nephropathy be treated?

A

→ ACE inhibitors

→ Angiotensin Receptor Blockers (ARBs)

26
Q

How do ACE inhibitors work?

A

→ antihypertensives
→ blocks ACE from catalysing angiotensin I to angiotensin II
→ inhibits aldosterone production in zona glomerulosa of adrenal cortex
→ reduces BP + progression of diabetic nephropathy

27
Q

How do ARBs work?

A

→ antihypertensives
→ angiotensin receptors are blocked
→ inhibits aldosterone production in zona glomerulosa of adrenal cortex
→ reduces BP + progression of diabetic nephropathy

28
Q

Why aren’t ACEi and ARBs prescribed together?

A

no benefit is using both simultaneously

29
Q

How is diabetic nephropathy managed?

A

→ Aim for tighter glycaemic control
→ ACEi/ARB even if normotensive as soon as patient has microalbuminuria
→ Reduce BP (aim <130/80 mmHg) usually through ACEi or A2RB
→ Stop smoking
→ Start an SGLT-2 inhibitor if T2DM?

30
Q

What is the most common cause of neuropathy + lower limb amputation?

A

diabetes mellitus

31
Q

What is neuropathy?

A

→ Small vessels supplying nerves are called vasa nervorum

→ Neuropathy results when vasa nervorum get blocked

32
Q

What are the risk factors of diabetic neuropathy?

A 
→ Age
→ Duration of diabetes
→ Poor glycaemic control
→ Height (longer nerves in lower limbs of tall people)
→ Smoking
→ Presence of diabetic retinopathy
33
Q

Where is neuropathy most common in the body? Why?

A

→ commonly glove + hand distribution (peripheral neuropathy)

→ longest nerves supply feet, so more common in feet

34
Q

Why is neuropathy dangerous?

A

→ can be painful

→ danger is that patients don’t sense injuries to feet (e.g. stepping on nail)

35
Q

Why do diabetic patients get annual foot checks?

A

high risk of foot ulceration (and foot injuries in general) due to :
→ diabetic neuropathy = reduced sensation in feet
→ peripheral vascular disease = poor vascular supply to feet

36
Q

What is looked for in an annual foot check for DM?

A

→ foot deformity, ulceration
→ Assess sensation (monofilament, ankle jerks)
→ Assess foot pulses (dorsalis pedis + posterior tibial)

37
Q

How is peripheral neuropathy managed?

A

→ Regular inspection of feet by affected individual
→ Good footwear
→ Avoid barefoot walking
→ Podiatry and chiropody if needed

38
Q

How is peripheral neuropathy with ulceration managed?

A 
→ Multidisciplinary diabetes foot clinic (podiatrist, etc.)
→ Offloading (bed rest, etc.)
→ Revascularisation if concomitant PVD
→ Antibiotics if infected
→ Orthotic footwear
→ Amputation if all else fails
39
Q

What are some other types of neuropathy?

A

→ mononeuropathy

→ autonomic neuropathy

40
Q

What are the characteristics of mononeuropathy?

A

→ usually sudden motor loss e.g. wrist drop, foot drop

→ cranial nerve palsy (double vision + 3rd nerve palsy (eyes look down + out))

41
Q

What is autonomic neuropathy?

A

damage to sympathetic + parasympathetic nerves innervating GI tract, bladder, cardiovascular system

42
Q

How does autonomic neuropathy affect the GI tract?

A

→ Delayed gastric emptying: nausea and vomiting (can make prandial short-acting insulin challenging)
→ Constipation / nocturnal diarrhoea

43
Q

How does autonomic neuropathy affect the cardiovascular system?

A

→ Postural hypotension: can be disabling e.g. collapsing on standing.
→ Cardiac autonomic supply: sudden cardiac death

44
Q

What are the macro-vascular complications of DM?

A

→ cerebrovascular disease
→ ischaemic heart disease
→ peripheral vascular disease

45
Q

Why can’t the macro-vascular complications of DM be treated solely by treating the hyperglycaemia?

A

→ treatment targeted to hyperglycaemia alone has minor effect on increased risk of cardiovascular disease
→ prevention of macro-vascular disease requires aggressive management of multiple risk factors

46
Q

What is the trend in males and females and their diabetic cardiovascular mortality?

A

increased mortality compared to no DM

47
Q

What are the non-modifiable risks of macro-vascular disease?

A

→ age
→ sex
→ birth weight
→ genetics

48
Q

What are the modifiable risks of macro-vascular disease?

A 
→ Dyslipidaemia
→ Hypertension 
→ Smoking
→ Diabetes mellitus
→ Central obesity
49
Q

How is cardiovascular risk managed in DM?

A

→ Smoking status – support to quit
→ Blood pressure < 140/80 mmHg, < 130/80 mmHg if microvascular complication (NB often needs multiple agents)
→ Lipid profile – total chol <4, LDL <2
→ Weight – discuss lifestyle intervention with or without pharmacological treatments
→ Annual urine microalbuminuria screen – risk factor for cardiovascular disease

!!!!! BRS YR2 !!!!! (72 decks)

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