Microvascular Complications of Diabetes Mellitus Flashcards

1
Q

State the three main sites of microvascular complications.

A
Retinal arteries (retinopathy) 
Glomerular arterioles (nephropathy) 
Vasa vasorum (neuropathy)
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2
Q

What factors correlate with risk of microvascular and macrovascular complications?

A

Glycaemic control (HbA1c)
Hypertension
Other factors such as glycaemic memory and genetics can contribute

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3
Q

Describe the mechanism of glucose damage to blood vessels.

A

Hyperglycaemia leads to oxidative stress and hypoxia

This triggers an inflammatory cascade, which leads to damage

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4
Q

What instrument is used to look into the eye?

A

Fundoscope

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5
Q

Where is the optic disc relative to the macula on the back of the eye?

A

The optic disc is nasal to the macula

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6
Q

What are the 4 types of diabetic retinopathy?

A

Background
Pre-proliferative
Proliferative
Maculopathy

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7
Q

What three features do you see in background diabetic retinopathy?

A

Hard exudates
Microaneurysms
Blot haemorrhages

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8
Q

What are hard exudates caused by?

A

Leakage of lipid contents makes the back of the eye look a cheesy colour

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9
Q

Describe pre-proliferative diabetic retinopathy.

A
Soft exudates (cotton wool spots)  
There will be some haemorrhages
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10
Q

What do soft exudates indicate?

A

Retinal ischaemia

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11
Q

Describe proliferative diabetic retinopathy.

A

Involves the formation of new vessels (in response to retinal ischaemia)
The new vessels are generally more fragile and can bleed at any time

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12
Q

Describe maculopathy.

A

Presence of hard exudates in the macula
This is the same disease as background diabetic retinopathy, it’s just that the hard exudates are in the macula
This can threaten direct vision

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13
Q

What are the steps taken in managing background diabetic retinopathy?

A

Improve blood glucose control

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14
Q

What is the treatment for pre-proliferative and proliferative diabetic retinopathy?

A

Pan-retinal photocoagulation

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15
Q

Describe the treatment of maculopathy.

A

You need a grid of photocoagulation in the affected area (aim to limit damage to the macula so you don’t do pan-retinal photo coagulation)

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16
Q

State some histological features of diabetic nephropathy.

A

Mesangial expansion
Basement membrane thickening
Glomerulosclerosis (hardening of the capillaries)

17
Q

In diabetic nephropathy you get over production of matrix. Whatcan this be caused by?

A

Effects of prolonged exposure to high glucose or glycosylated proteins
A rise in pressure within the glomerular capillaries
Angiotensin II

18
Q

State 3 clinical features of diabetic nephropathy.

A

Progressive proteinuria
Increased blood pressure
Deranged renal function

19
Q

What is the normal range for proteinuria?

A

< 30 mg/24hr

20
Q

Why do patients with diabetic nephropathy get oedematous?

A

Increased proteinuria means that they are losing albumin through their urine
This decreases serum albumin hence decreases the osmotic potential of the plasma so less fluid is drawn back into the circulation

21
Q

Describe some strategies for intervention of patients with diabetic nephropathy.

A

Improve blood glucose control
Blood pressure control
Inhibition of the activity of the renin-angiotensin system
Stopping smoking

22
Q

What effect does angiotensin II have on endothelial cells?

A

It makes endothelial cells more rigid

23
Q

Where is renin produced?

A

Juxtaglomerular apparatus

24
Q

What can stimulate renin release?

A

Low renal perfusion (i.e. low blood pressure)

25
Q

Where is ACE found?

A

Lungs

26
Q

State some drug target sites in the renin-angiotensin system.

A

Drugs blocking renin activity
ACE inhibitors
Angiotensin II receptor blockers (ARBs)

27
Q

What causes diabetic neuropathy?

A

Occlusion of the vasa vasorum

28
Q

State 6 different types of diabetic neuropathy.

A
Peripheral polyneuropathy 
Mononeuropathy 
Mononeuritis multiplex 
Radiculopathy 
Autonomic neuropathy 
Diabetic amyotrophy
29
Q

What can peripheral neuropathy lead to and how can it be tested?

A

Loss of sensation can lead to damage going unnoticed
It also leads to loss of ankle jerks and loss of vibrational sense
Inappropriate use of joints can lead to Charcot joints
Test – monofilament examination

30
Q

What is mononeuropathy?

A

Usually sudden motor loss e.g. wrist drop or foot drop

Can also cause cranial nerve palsy

31
Q

Why is the pupil spared in pupil sparing third nerve palsy?

A

The parasympathetic fibres, that are responsible for the diameter of the pupil, run on the outside of the main nerve so they don’t lose their blood supply in diabetes

32
Q

How would an aneurysm causing third nerve palsy present differently to third nerve palsy caused by diabetes?

A

There would be fixed pupil dilation

This is because the parasympathetic fibres would also be affected

33
Q

What is mononeuritis multiplex?

A

A random combination of peripheral nerve lesions

34
Q

What is radiculopathy?

A

Pain over SPINAL nerves

Usually affecting a dermatome on the abdomen or chest wall

35
Q

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

A

Difficulty swallowing
Delayed gastric emptying
Constipation/nocturnal diarrhoea
NOTE: it can also lead to bladder dysfunction

36
Q

What are the effects of autonomic neuropathy on the CVS?

A

Postural hypotension

There have been reports of sudden cardiac death

37
Q

How can you check for autonomic neuropathy?

A

Measure changes in heart rate due to Valsalva manoeuvre

Look at an ECG and compare the R-R intervals