Endo 16 - Microvascular and Macrovascular Complications of DM Flashcards

(34 cards)

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?

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
State 6 different types of diabetic neuropathy.
``` Peripheral polyneuropathy Mononeuropathy Mononeuritis multiplex Radiculopathy Autonomic neuropathy Diabetic amyotrophy ```
26
What can peripheral neuropathy lead to?
loss of sensation can lead to damage not being noticed loss of ankle verks and vibrational sense
27
How would you test for peripheral neuropathy?
Monofilament examination - produces a certain amount of force, see if patient can feel
28
What is mononeuropathy?
Sudden motor loss .e.g wrist drop
29
Why is the pupil spared in pupil sparing third nerve palsy?
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
How would an aneurysm causing third nerve palsy present | differently to third nerve palsy caused by diabetes?
There would be fixed pupil dilation | This is because the parasympathetic fibres would also be affected
31
What is mononeuritis multiplex?
random combination of peripheral nerve lesions
32
What is radiculopathy?
pain over spinal nerves
33
What are the effects of autonomic neuropathy on the GI?
difficulty swallowing late gastric emptying constipation
34
What are the effects of autonomic neuropathy on the CVS?
Postural hypotension