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Endocrinology > Endo 16 - Microvascular and Macrovascular Complications of DM > Flashcards

Endo 16 - Microvascular and Macrovascular Complications of DM Flashcards

1
Q

State the three main sites of microvascular complications.

A

Retinal artiers
Glomerular arteries
Vasa Vasorum

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2
Q

What factors correlate with the risk of microvascular and macro complications?

A

HbA1c - glycaemic control

hypertension

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3
Q

Describe the mechanism of glucose damage to blood vessels

A

Hyperglycaemia leads to oxidative stress and hypoxia

triggers inflammatory cascade which leads to damage

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4
Q

What are the 4 types of diabetic retinopathy?

A

Background
Pre-proliferative
Proliferative
Maculopathy

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5
Q

What 3 things do you see in background retinopathy?

A

hard exudates
microaneurysms
blot haemiorrhages

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6
Q

What are hard exudates caused by?

A

leakage of lipid contents - looks cheesy

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7
Q

Describe pre-proliferative diabetic retinopathy.

A

soft exudates - cotton wool

haemorrhages

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8
Q

What do soft exudates indicated?

A

Retinal ischaemia

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9
Q

Describe proliferative retinopathy.

A

formation of new blood vessels in response to retinal ischaemia

new blood vessels are fragile and can bleed easily

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10
Q

Describe maculopathy

A

presence of hard exudates in the macula

threatens direct vision

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11
Q

How would you manage background retinopathy?

A

control blood glucose

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12
Q

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

A

pan-retinal photocoagulation

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13
Q

Describe the treatment of maculopathy.

A

grid of photocoagulation

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14
Q

What is the overproduction of matrix in diabetic nephropathy caused by?

A

prolonged exposure to high glucose

angiotensin II

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15
Q

State 3 clinical features of diabetic nephropathy.

A

Progressive proteinuria
increased blood pressure
deranged renal function

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16
Q

Whatis the normal range for proteinuria?

A

<30mg/24 hours

17
Q

Why do patients with diabetic nephropathy get oedematous?

A

increased proteinuria = decreased serum albumin = decreased osmotic potential = less fluid drawn back in

18
Q

Describe some strategies for intervention for patients with diabetic nephropathy.

A

Better blood glucose control
blood pressure control
inhibition of RAAS system

19
Q

What effect does angiotensin II have on endothelial cells?

A

makes endothelial cells more rigid

20
Q

Where is renin produced?

A

Juxtoglomerular cells

21
Q

What can stimulate renin release?

A

low renal perfusion e.g. low blood pressure

22
Q

Where is ACE found?

A

Lungs

23
Q

State some drug target sites in the RAAS.

A

ACE inhibitors

ARB

24
Q

What causes diabetic neuropathy?

A

occlusion of vasa vasorum

25
Q

State 6 different types of diabetic neuropathy.

A 
Peripheral polyneuropathy
Mononeuropathy
Mononeuritis multiplex
Radiculopathy
Autonomic neuropathy
Diabetic amyotrophy
26
Q

What can peripheral neuropathy lead to?

A

loss of sensation can lead to damage not being noticed

loss of ankle verks and vibrational sense

27
Q

How would you test for peripheral neuropathy?

A

Monofilament examination - produces a certain amount of force, see if patient can feel

28
Q

What is mononeuropathy?

A

Sudden motor loss .e.g wrist drop

29
Q

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

A

parasympathetic fibres that are responsible for the diameter of the pupil run on the outside of the main nerve so don’t lose blood supply

30
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

31
Q

What is mononeuritis multiplex?

A

random combination of peripheral nerve lesions

32
Q

What is radiculopathy?

A

pain over spinal nerves

33
Q

What are the effects of autonomic neuropathy on the GI?

A

difficulty swallowing
late gastric emptying
constipation

34
Q

What are the effects of autonomic neuropathy on the CVS?

A

Postural hypotension

Endocrinology (18 decks)

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