17 - Microvascular complications of DM 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 are the vasa vasorum?

A

tiny blood vessels that supply nerves

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3
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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4
Q

What is a good indicator of glycemic control?

A

HbA1c

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5
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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6
Q

What instrument is used to look into the eye?

A

Fundoscope

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7
Q

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

A

The optic disc is nasa/medial to the macula

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8
Q

What is the macula involved in?

A

involve in colour vision and acuity

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9
Q

What are the 4 types of diabetic retinopathy?

A

Background
Pre-proliferative
Proliferative
Maculopathy

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10
Q

What three features do you see in background diabetic retinopathy?

A

Hard exudates
Microaneurysms
Blot haemorrhages

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11
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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12
Q

Describe pre-proliferative diabetic retinopathy.

A
Soft exudates (cotton wool spots) 
There will be some haemorrhages
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13
Q

What do soft exudates indicate?

A

retinal ischaemia

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14
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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15
Q

Describe maculopathy.

A

Presence of hard exudates in the macula
same disease as background diabetic retinopathy, but the hard exudates are in the macula
This can threaten direct vision

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16
Q

What are the steps taken in managing background diabetic retinopathy?

A

Improve blood glucose control

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17
Q

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

A

Pan-retinal photocoagulation

18
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

19
Q

State some histological features of diabetic nephropathy.

A

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

20
Q

State 3 clinical features of diabetic nephropathy.

A

Progressive proteinuria
Increased blood pressure
Deranged renal function

21
Q

What is the normal range for proteinuria?

A

< 30 mg/24hr

22
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

23
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

24
Q

What effect does angiotensin II have on endothelial cells?

A

It makes endothelial cells more rigid

25
Q

Where is renin produced?

A

Juxtaglomerular apparatus

26
Q

What can stimulate renin release?

A

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

27
Q

Where is ACE found?

A

Lungs

28
Q

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

A

Drugs blocking renin activity

  • ACE inhibitors
  • Angiotensin II receptor blockers (ARBs)
29
Q

Give an example of an AT1 antagonist

A

irbesartan

30
Q

What causes diabetic neuropathy?

A

Occlusion of the vasa vasorum

31
Q

State 6 different types of diabetic neuropathy.

A
Peripheral polyneuropathy
Mononeuropathy
Mononeuritis multiplex
Radiculopathy
Autonomic neuropathy
Diabetic amyotrophy
32
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

33
Q

What is mononeuropathy?

A

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

Can also cause cranial nerve palsy

34
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

35
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
(aneurysm = space occupying lesion - exerts pressure on the parasympathetic nerve)

36
Q

What is mononeuritis multiplex?

A

A random combination of peripheral nerve lesions

37
Q

What is radiculopathy?

A

Pain over SPINAL nerves

Usually affecting a dermatome on the abdomen or chest wall

38
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

39
Q

What are the effects of autonomic neuropathy on the CVS?

A

Postural hypotension

There have been reports of sudden cardiac death

40
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