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Endocrinology > Microvascular & Macrovascular complications of diabetes mellitus > Flashcards

Microvascular & Macrovascular complications of diabetes mellitus Flashcards

1
Q

Define microvascular complications and give examples

A

Complications of smaller vessels
e.g:
Retinopathy
Nephropathy
Neuropathy

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2
Q

Define macrovascular complications and give examples

A

Complications of larger vessels
e.g:
Cerebrovascular disease
Ischaemic heart disease
Peripheral vascular disease

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3
Q

What is the relationship b/t glucose levels and microvascular complications?

A
  • Extent of hyperglycaemia (as judged by HbA1c) is strongly associated with the risk of developing microvascular complications
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4
Q

What is the normal levels of HbA1c?

A

48 mmol/mol (6.5%) or below (anything above that is diabetes)
(need to target HbA1c to reduce risk of microvascular complications)

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5
Q

What is the relationship b/t systolic bp and microvascular complication?

A
  • Clear relationship between rising systolic BP (hypertension) and risk of MI and microvascular complications in people with T1DM and T2DM
  • Therefore, prevention of complications requires reduction in HbA1c and BP control
    (not just management of sugars- need to check BP, cholesterol, etc)
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6
Q

What factors increase your risk of the development of microvascular complications

A
  • HbA1c
  • Hypertension
  • Duration of diabetes (cannot be altered/ changed)
  • Smoking – endothelial dysfunction (damages lining of blood vessels)
  • Genetic factors – some people develop complications despite reasonable glycaemic control
  • Hyperlipidaemia (can be modified with medication)
  • Hyperglycaemic memory – inadequate glucose control early on (e.g. having T1DM at young age) can result in higher risk of complications LATER, even if HbA1c improved
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7
Q

Describe the mechanism of damage to the endothelium

A
  1. Hyperglycaemia and hyperlipidemia can result in:
    - Hypoxia
    - Increased formation of mitochondrial superoxide free radicals in the endothelium (oxidative stress)
    - Generation of glycated plasma proteins to form advanced glycation end products (AGEs): the more sugar= more AGEs you have
  2. All 3 of these lead to activation of inflammatory pathways (pro- inflammatory cytokines)
  3. Damaged endothelium results in:
    ‘Leaky’ capillaries
    Ischaemia
    (= Nephropathy, Retinopathy, Neuropathy)
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8
Q

What is diabetic retinopathy?

A
  • Over time, too much sugar in your blood can lead to the blockage of the tiny blood vessels that nourish the retina
  • cutting off its blood supply
  • As a result, the eye attempts to grow new blood vessels
  • But these new blood vessels don’t develop properly and can leak easily.
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9
Q

What would you find on a normal retina scan?

A
  1. Optic disc (bright white spot) the area where specific nerve fibres exit the retina to form the optic nerve
  2. Macula (slightly pink- found centrally) the part responsible for central and fine-detail vision, high resolution and colour vision needed for tasks such as reading.
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10
Q

What is background retinopathy? What would you see on an OCT?

A
  • Earliest stage of retinopathy (no new blood vessels formed yet)
  • The walls of the blood vessels in your retina weaken
  • Tiny bulges protrude from the walls of the smaller vessels, sometimes leaking fluid and slight blood into the retina
  • don’t usually affect your vision – this is known as background retinopathy
    OCT:
  • Hard exudates (yellow bright spots with well defined edges= lipid residues that leak from the impaired blood–retinal barrier)
  • Microaneurysms (dots)
  • Blot haemorrhages (red dots)
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11
Q

What is Pre-proliferative retinopathy? What would you see on an OCT?

A
  • 2nd stage- after background retinopathy (but NO new blood vessels formed yet)
  • More severe and widespread changes affect the blood vessels (more vessels blocked)
  • More significant bleeding into the eye – this is known as pre-proliferative retinopathy
    OCT:
  • Soft exudates (Cotton wool spots- more places with ill- defined edges: hard exudate spots represent leakage, wheras soft exudates represent ischemia and are more serious)
  • Haemorrhage
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12
Q

What is proliferative retinopathy?

A
  • Last stage of retinopathy (new blood vessels form)
  • Damaged blood vessels close off
  • Causing the growth of new, abnormal blood vessels in the retina (esp around the optic disc)
  • These new blood vessels are fragile and can leak
  • Increases the risk of haemorrhage
  • This is known as proliferative retinopathy and it can result in some loss of vision
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13
Q

What is Maculopathy? What would you see on an OCT?

A
  • Maculopathy occurs when the leaked fluid builds up at the macula,
  • leaking into the retina causing swelling
  • Occasionally, the blood vessels in the macula become so constricted that the macula is starved of oxygen and nutrition causing your sight to get worse
    OCT:
    *Hard exudates/ oedema near the macula
  • Cotton wool spots (soft exudates)
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14
Q

How would you treat Background retinopathy?

A

General retinopathy treated with:
- Improve HbA1c
- stop smoking
- lipid lowering
- good blood pressure control <130/80 mmHg
BR specifically:
Continued annual surveillance

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15
Q

How would you treat pre-proliferative retinopathy?

A

General retinopathy treated with:
- Improve HbA1c
- stop smoking
- lipid lowering
- good blood pressure control <130/80 mmHg
PPR specifically:
(If left alone will progress to new vessel growth) so, early panretinal photocoagulation

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16
Q

What is panretinal photocoagulation?

A

Thermal burns in the peripheral retina leading to tissue coagulation, the overall consequence of which is improved retinal oxygenation
- prevents formation of new blood vessels BUT can cause peripheral vision damage

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17
Q

How would you treat Proliferative retinopathy?

A

General retinopathy treated with:
- Improve HbA1c
- stop smoking
- lipid lowering
- good blood pressure control <130/80 mmHg
PR specifically:
Panretinal photocoagulation

18
Q

How would you treat diabetic maculopathy?

A

General retinopathy treated with:
- Improve HbA1c
- stop smoking
- lipid lowering
- good blood pressure control <130/80 mmHg
Maculopathy specifically:
- Oedema: Anti-VEGF injections directly into the eye (VEGF: vascular endothelial growth factor)
- Grid photocoagulation

19
Q

What is diabetic nephropathy?

A

kidney damage caused by diabetes

20
Q

Why is diabetic nephropathy important?

A
  1. Associated with progression to end-stage renal failure requiring haemodialysis
  2. Healthcare burden
  3. Associated with increased risk of cardiovascular events
21
Q

How would you diagnose diabetic nephropathy?

A
  1. Progressive proteinuria (urine albumin:creatinine ratio - ACR): urine dipstick not accurate enough, annually screened/ tested
    * Microalbuminuria >2.5 mg/mmol can be used as a v. early sign where most patients still have kidney function
    * Proteinuria = ACR > 30mg/mmol
    * Nephrotic Range > 3000mg/24hr
  2. Increased blood pressure
  3. Deranged renal function (eGFR)
  4. Advanced: peripheral oedema (occurs in later stages
22
Q

Describe the mechanism for diabetic nephropathy

A
  • Hyperglycemia and hypertension leads to glomerular hypertension (pressure builds up in the glomerulus)
  • Proteins are, therefore, forced/ leak out
  • = proteinuria
  • Causes damage to the glomerulus (decreased function)
  • Leads to Glomerular and intersitial fibrosis and glomerular filtration rate decline
    = RENAL FAILURE
23
Q

What is the reltionship b/t nephropathy and the Renin- Angiotensin System?

A

System is more activated in patients with nephropathy
(treatment targets the RAS system)

24
Q

How/ what parts of the RAS system are targeted in the treatment of nephropathy?

A

RAS system:
1. Liver releases Angiotensinogen
2. Kidney releases renin which converts the Angiotensinogen into Angiotensin I
3. ACE coverts Angiotensin I into Angiotensin II
4. Angiotensin II causes vasoconstriction and binds to Angiotensin receptors to promote the rlease of aldosterone (increasing salt/ water retention to increase bp/ hypertension)

Targets:
a. ACE inhibitors [ACEi] (antihypertensives which block ACE)
b. Angiotensin receptor blockers [ARBs] (antihypertensives which block the receptors)
DO NOT GIVE BOTH TOGETHER: EITHER OR

Blocking RAS with an ACE inhibitor (‘-pril) or angiotensin 2 receptor blocker (ARB, ‘-sartan’) reduces blood pressure & progression of diabetic nephropathy
All diabetes patients with microalbuminuria/proteinuria should have an ACEi/ARB even if normotensive (give max dose tolerated by bp)
No benefit to having both ACEi/ARB simultaneously

25
Q

Describe the relationship of microalbuminuria on the heart

A

Microalbuminuria is a risk factor for cardiovascular disease

26
Q

How would you manage diabetic nephropathy?

A
  1. Aim for tighter glycaemic control
  2. ACEi/ARB even if normotensive as soon as patient has microalbuminuria
  3. Reduce BP (aim <130/80 mmHg) usually through ACEi or A2RB
  4. Stop smoking
  5. Start an SGLT-2 inhibitor if T2DM (only used for T2DM, prevents glucose reabsorbtion in kidneys/ delays the progression of T2DM)
27
Q

What is diabetic neuropathy?

A

“when diabetes causes damage to your nerves”
- Diabetes mellitus is the most common cause of neuropathy and therefore lower limb amputation
- Small vessels supplying nerves are called vasa nervorum
- Neuropathy results when vasa nervorum get blocked (ischemia will lead to damage)

28
Q

What are the risk factors of diabetic neuropathy?

A
  • Age (more likely to have prolonged alcohol intake0
  • Duration of diabetes
  • Poor glycaemic control
  • Height (longer nerves in lower limbs of tall people)
  • Smoking
  • Presence of diabetic retinopathy
29
Q

What areas of the body are commonly affected in neuropathy?

A
  • Longest nerves supply feet – so more common in feet
  • Commonly glove & stocking distribution (hands and lower limbs)– peripheral neuropathy
  • Can be painful (worsens at night- can reduce sleep)
  • Danger is that patients will not sense an injury to the foot (eg. stepping on a nail), so more likely to get diabetic foot ulcers
30
Q

How do we track diabetic foot ulcerations?

A

All people with diabetes: annual foot check
- Look for foot deformity, ulceration
- Assess sensation (monofilament, ankle jerks)
- Assess foot pulses (dorsalis pedis and posterior tibial)

31
Q

What can increase the risk of foot ulcerations

A
  • reduced sensation to feet (peripheral neuropathy)
  • poor vascular supply to feet (peripheral vascular disease)
32
Q

How would you manage peripheral neuropathy (with no ulcerations)?

A
  1. Regular inspection of feet by affected individual
  2. Good footwear
  3. Avoid barefoot walking
  4. Podiatry and chiropody if needed (seeing a specialist)
33
Q

How would you manage peripheral neuropathy (with ulcerations)?

A
  1. Multidisciplinary diabetes foot clinic
  2. Offloading
  3. Revascularisation if concomitant PVD
  4. Antibiotics if infected
  5. Orthotic footwear
  6. Amputation if all else fails
34
Q

What is Monoeuropathy?

A

“damage that occurs to a single nerve”:
- Usually, sudden motor loss eg wrist drop, foot drop
- Cranial nerve palsy (palsy= lack of function) = double vision due to 3rd (oculomotor) nerve palsy (eye looks down and out)

35
Q

What is autonomic neuropathy?

A

“Damage to sympathetic and parasympathetic nerves innervating GI tract, bladder, cardiovascular system”
1. GI tract
- Delayed gastric emptying: nausea and vomiting (can make prandial short-acting insulin challenging)
- Constipation / nocturnal diarrhoea (reduced peristalsis/ contractions) V. DIFFICULT TO TREAT
2. Cardiovascular
- Postural hypotension (low bp when standing up): can be disabling - collapsing on standing.
- Cardiac autonomic supply: sudden cardiac death

36
Q

What are some examples of macrovascular complications?

A

Cerebrovascular disease
Ischaemic heart disease
Peripheral vascular disease (lower limb)

37
Q

Why is it difficult to treat macrovascular complications?

A
  • Treatment targeted to hyperglycaemia alone has minor effect on increased risk of cardiovascular disease
  • Prevention of macrovascular disease requires aggressive management of multiple risk factors
38
Q

What are some non modifiable risk factors of macrovascular disease?

A

Age
Sex
Birth weight
FH/Genes

39
Q

What are some modifiable risk factors of macrovascular disease?

A

Dyslipidaemia (imbalance of lipids): statins to decrease cholesterol
Hypertension (ACEi/ ARBs)
Smoking
Diabetes mellitus
Central obesity “weight around the tummy” (produces hormones that antagonise insulin)

40
Q

How would you manage cardiovascular risk in diabetes mellitus?

A
  1. Smoking status – support to quit
  2. Blood pressure < 140/80 mmHg, < 130/80 mmHg if microvascular complication (NB often needs multiple agents)
  3. Lipid profile – total chol <4, LDL <2
  4. Weight – discuss lifestyle intervention +/- pharmacological treatments
  5. Annual urine microalbuminuria screen – risk factor for cardiovascular disease

Endocrinology (14 decks)

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