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LCRS Year 2 - Endocrinology > Microvascular Complications of Diabetes Mellitus > Flashcards

Microvascular Complications of Diabetes Mellitus Flashcards

1
Q

How does poor control of diabetes affect blood vessels and risk of vascular complications?

A

Diabetes damages blood vessels

- poor control of diabetes causes a higher risk of both micro and macrovascular complications

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2
Q

What are the sites of microvascular complications?

A 
Retinal arteries (retinopathy)
Glomerular arterioles (nephropathy)
Vasa nervorum (tiny blood vessels that supply the nerves, neuropathy)
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3
Q

What is the normal range of HbA1c (in terms of %)?

A

<6%

  • above 6.5% is type 2 diabetes
  • 6-6.5% is pre-diabetes
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4
Q

What do study results show about the relationship between the quality of glycaemic control (measured as HbA1c levels) and the risk of microvascular complications developing?

A

Shows a strong positive correlation between worsening quality of glycaemic control and increasing risk of developing microvascular complications

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5
Q

How does hypertension contribute to microvascular complications?

A

Hypertension
- the higher a patient’s blood pressure, the more likely the patient will develop microvascular complications and increases severity of said complications (shown very clearly in the UKPDS study)

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6
Q

What is hyperglycaemic memory?

A

Concept explained by this

  • a patient who had poor glucose control over a decade and then had ideal glucose control for the following decade (20 years split between the two) will have worse microvascular complications or microvascular risk than a patient who had ideal glucose control for all 20 years
  • important because many patients don’t control their glucose well when they’re not experiencing any symptoms but there is evidence to suggest that this early control of glucose is more impactful on microvascular complication risk than their current quality of glycaemic control
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7
Q

What are the factors that contribute to assessing a patient’s risk of microvascular complications?

A
  • Severity of hyperglycaemia
  • Hypertension
  • Genetic
  • Hyperglycaemic memory
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8
Q

What is the general process by which hyperglycaemia and hyperlipidaemia cause microvascular complications (nephropathy, neuropathy, retinopathy)?

A

Hyperglycaemia + Hyperlipidaemia

  • cause AGE-RAGE + oxidative stress + hypoxia
  • these stimulate inflammatory signalling cascades
  • these cascades lead to local activation (in specific tissues) of pro-inflammatory cytokines
  • these cytokines cause inflammation
  • this inflammation leads to retinopathy, neuropathy, and nephropathy
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9
Q

What is diabetic retinopathy and what is it the main cause of?

A

Diabetic retinopathy is the main cause of visual loss in people with diabetes
Also the main cause of blindness in patients of working age

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10
Q

What do diabetic patients have every year to check for retinopathy?

A

Retinal screen

- ophthalmologists take photos of the back of the eye to check for signs of retinopathy

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11
Q

What are the features of the back of a normal eye?

A

Pale/white circle - healthy optic disc
Smooth, clear blood vessels extending outward from optic disc
Dark, dense circle in the middle is the fovea (aka the macula)

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12
Q

What are some background changes of diabetic retinopathy?

A

These changes occur in most patients no matter how tight their glucose control is

  • Hard exudates (protein-like structures which go past the eye, cheese colour, lipid)
  • Microaneurysms (endothelial lining of the vessels bulge outward, ‘dots’)
  • Blot haemorrhages (where these small vessels bleed)
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13
Q

What is pre-proliferate diabetic retinopathy and what is seen on the retina at this stage?

A

Next stage of diabetic retinopathy after background diabetic retinopathy

  • Cotton wool spots (also called soft exudates)
  • Markers of retinal ischaemia (loss of oxygen to some regions of the retina)
  • Can see pre-retinal haemorrhage as well
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14
Q

What is proliferative retinopathy and what is seen on the retina at this stage?

A

3rd stage of diabetic retinopathy changes

  • visible new vessels (hence proliferative)
  • on the optic disk or elsewhere in the retina
  • don’t just extend outward across the eye, go everywhere
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15
Q

What is maculopathy and what are features of it?

A

Maculopathy is a variant of diabetic retinopathy

  • occurs when there are hard exudates near the macula
  • same disease as background DRpathy but happens to be near macula
  • this can threaten direct vision
  • yearly retinal screening program attempts to detect this before vision loss starts to occur
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16
Q

What is the management of background diabetic retinopathy?

A

Background DR

  • improve control of blood glucose
  • warn patient that warning signs are present and they must enter the yearly retinal screening program and must alert a physician if they start to experience vision problems
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17
Q

What is the management of pre-proliferative diabetic retinopathy?

A

Pre-proliferative DR (cotton wool spots/soft exudates)

  • suggests ischaemia
  • if left alone, new vessels WILL grow
  • treated with pan retinal photocoagulation (laser beam therapy)
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18
Q

What is the management of proliferative (visible new vessels) diabetic retinopathy?

A 
Also needs (more urgently) laser therapy
(pan retinal photocoagulation)
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19
Q

What is involved in the management of maculopathy?

A

Problem is only around the macula
- needs only a GRID of photocoagulation (targeted laser beams on the spots near the macula, this is NOT pan retinal photocoagulation as it is only partial)

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20
Q

What would you normally see in a patient with diabetic nephropathy?

A
  • Hypertension
  • Progressively increasing proteinuria (protein measured)
  • Progressively deteriorating kidney function (creatinine/GFR measured)
  • Classical histological features in a biopsy
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21
Q

Why is it important to know about diabetic nephropathy?

A

Diabetes is one of the biggest causes of kidney disease

  • Associated morbidity and mortality
  • Healthcare burden including intense cost
  • Treatment options present
22
Q

What is the aim of treatment in those with kidney disease, particularly diabetic nephropathy?

A

Improved cardiovascular health and good glucose control

23
Q

What are the 3 areas of the body that are biopsied in patients with diabetic nephropathy?

A

Glomerular tissue
Vascular tissue
Tubulointerstitial tissue

24
Q

What are the classical histological features of a glomerular tissue biopsy in a patient with diabetic nephropathy?

A

Glomerular changes visible include:

  • mesangial cell expansion
  • basement membrane thickening
  • glomerulosclerosis (hardening and thickening of the renal cells)

These changes can also contribute to the hypertension found in patients with diabetic nephropathy

25
Q

What is the outline of the processes by which CKD/diabetic nephropathy is caused?

A

There are multiple stimuli for these processes but they include prolonged exposure to high glucose or glycosylated proteins. In addition, rise in the pressure within the glomerular arterioles can stimulate these processes

  • The main process at work is overproduction of matrix leading to mesangial cell expansion and basement membrane thickening. As this progresses, you get sclerosis of the glomerulus and secondary effects on the tubulointerstitium
  • one common measurable loss of function is albuminuria, the level of albumin in the urine can be measured as a metric of how bad kidney function has become
26
Q

What is the occurrence of diabetic nephropathy in T1DM and T2DMN?

A

T1DM - 20-40% of patients after 30-40 years

T2DM - Probably equivalent but may never occur because the patient might die of macrovascular disease (MI, ischaemic heart disease) before DN presents

27
Q

What is the epidemiology of diabetic nephropathy influenced by in T2DM patients?

A

Age at development of T2D
Racial factors
Age at presentation
Loss due to cardiovascular morbidity (macrovascular disease is what kills these individuals, not microvascular)

28
Q

What are the clinical features of diabetic nephropathy?

A

Progressive proteinuria
Increased BP
Deranged renal function (progressively worse renal function)

29
Q

What are the protein ranges for normal, microalbuminuric, assymptomatic, and nephrotic proteinuria?

A

Normal - <30mg/24hrs
Microalbuminuric - 30-300mg/24hrs
Assymptomatic - 300-3000mg/24hrs
Nephrotic - >3000mg/24hrs

30
Q

What are the strategies for intervention in patients with diabetic nephropathy?

A

Diabetic control
Blood pressure control (amazing evidence showing antihypertensive treatment slowing and stopping renal deterioration)
Inhibition of the activity of RAS (renin-angiotensin system)
Stopping smoking - increases general cardiovascular disease risk which compounds on diabetic nephropathy’s effects

31
Q

What is the beneficial effect of ACE inhibitors on diabetic nephropathy?

A

Very good for blood pressure regulation in diabetic nephropathy, slows renal function deterioration significantly

  • ACE inhibitors dilate efferent arterioles to relieve the increased glomerular pressure due to high systemic BP
  • reduction in progression of proteinuria
32
Q

What is diabetic neuropathy the most common cause of and what else results from this?

A

Diabetes is the most common cause of neuropathy

- diabetic neuropathy is therefore the most common cause of amputation in the UK

33
Q

What are the small blood vessels that supply the nerves called and what results when they get blocked?

A

Vasa nervorum

- when these get blocked neuropathy develops

34
Q

What are the different types of diabetic neuropathy?

A

Peripheral polyneuropathy (peripheral nerves affected)
Mononeuropathy (one nerve affected)
Mononeuritis multiplex (whole branch of nerves affected)
Radiculopathy
Autonomic neuropathy
Diabetic amyotrophy
- severe pain comes with some of these

35
Q

What is the general process of neuropathy initiation/progression?

A

There is usually an initiating event, either by GENETICS or INFLAMMATION

  • this leads to production of advanced glycation end products (AGEs)
  • these end products cause neuronal injury leading to functional changes (e.g. pain sensation or loss of sensation)
  • these functional changes then lead to progressive pathological changes such as diabetic foot ulcers and autonomic nervous pathologies which then further influence functional changes and this cycle then repeats
36
Q

What happens in peripheral neuropathy?

A

Longest nerves supply the feet

  • loss of sensation is the end result
  • the danger is that patients will not sense an injury to the foot (e.g. stepping on a nail and contracting an infection and ending up in hospital)
37
Q

What advice is given to patients with peripheral neuropathy?

A

Check your feet often

Wear suitable footwear, comfortable not tight etc

38
Q

Who is peripheral neuropathy more likely to occur in?

A 
Tall people (not fully understood)
Patients with poor glucose control
39
Q

What is used to assess a patients peripheral neuropathy stage?

A

Monofilament examination

  • metal filament device used to poke the foot and ask the patient if they can feel it while moving to different areas of the foot
  • this is done long-term to assess the progression of neuropathy as patients can be fully sensitive and gradually lose sensation throughout their foot, region by region until they cant feel their foot at all
  • good chance to examine the foot for ulcers or signs of infection that may have gone unnoticed as well
40
Q

What are the clinical signs of peripheral neuropathy?

A

Loss of ankle jerk (patellar hammer used to test it, usually dorsiflexion (towards you) occurs)
Loss of vibration sense (using tuning fork, no idea when the vibration stops as well)
Multiple fractures on foot X-ray (can produce Charcot’s joint - deformity long-term) - they have no sensation of uneven pressure on their feet and start to develop deformities due to not walking properly

41
Q

What are the clinical features of mononeuropathy?

A
  • Can result in sudden motor loss
  • Wrist drop, foot drop
  • Cranial nerve palsy
  • Double vision due to 3rd nerve palsy
42
Q

What happens in pupil-sparing 3rd nerve palsy?

A

Eye is usually “down and out”
6th nerve pulls eye out and 4th nerve pulls it down while 3rd nerve controls the opposite movements
- Pupil DOES respond to light in this condition (hence pupil-sparing)

43
Q

What does pupil involvement in third nerve palsy mean about diabetes involvement?

A

The parasympathetic fibres are on the outside of the 3rd nerve so do not lose their blood supply easily to diabetes
- however an aneurysm will press on the parsympathetic fibres first (because they’re on the outside) causing fixed dilated pupil, non pupil-sparing 3rd nerve palsy

Overall point is, if they have 3rd nerve palsy but it is pupil-sparing, then the 3rd nerve palsy is due to diabetes and not a tumour or aneurysm
DIABETES = PUPIL SPARING 3RD NERVE PALSY

44
Q

What is mononeuritis multiplex?

A

A random combination of peripheral nerve lesions

45
Q

What is radiculopathy?

A

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

46
Q

What is autonomic neuropathy and where does it affect in the body?

A

Loss of sympathetic and parasympathetic nervous supply to GI tract, bladder, cardiovascular system

47
Q

What are the effects of autonomic neuropathy on the GI tract?

A

GI tract effects:

  • difficulty swallowing
  • delayed gastric emptying
  • constipation/nocturnal diarrhoea
  • bladder dysfunction
48
Q

What effects can autonomic neuropathy have on the cardiovascular system?

A

Postural hypotension
- can be disabling, collapsing on standing

Cardiac autonomic supply
- case reports of sudden cardiac death from autonomic dysfunction

49
Q

What is a test we can do to assess presence or degree of autonomic neuropathy?

A
  • Measure changes in heart rate in response to Valsalva manoeuvre (blow into a very tight instrument, creates a lot of pressure)
  • normally there is a change in heart rate
  • a patient with autonomic neuropathy will have no change in heart rate
  • you can look at ECG and compare R-R intervals between that of the patient and a normal person
50
Q

What is a summary of microvascular complications of diabetes and how to manage these clinically?

A

Glycaemic control central to microvascular complications

  • however other factors may accelerate and worsen these complications
  • major cause of morbidity for patients with diabetes

So when you see someone who is diabetic in a clinical setting, check their eyes, their feet and their kidney function

LCRS Year 2 - Endocrinology (21 decks)

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