microvascular complications Flashcards
What blood vessels are the one damaged in DM? What determines how damaged they get?
Retinal arteries. glomerular arterioles, Vasa nervosum (nerve blood supply)
The hyperglycemia is the main reason (HbA1c)-as it rise, the worse it gets (also will increase macrovascular)
The combinations with common high blood pressure doesnt help
What determines how damaged small vasculature gets in t2DM?
The hyperglycemia is the main reason (HbA1c)-as it rise, the worse it gets (also will increase macrovascular)
The combinations with common high blood pressure doesnt help
Also some genetic disposition-not that large but exists
hyperglycemic memory-if glucose controlled well from onset, then better overall. If have a bit of bad control, then good control-less good
(as T2DM is asymptomatic, dont realise they have it and damage has already been done)
What are the 3 main pathways of damage to microvascular?
AGE-RAGE, oxidative stress and hypoxie
All cause high cytokine and inflammation-cause generally all the damage
How common is diabetic retinopathy in DM?
very common-main cause of visual issues in people of working age
How does a normal retina look like? How about a diseased one?
Normal-strong yellow and highlighted optic disc-nice vessels coming out of it-center macular darker spot
in disease-retinopathy-earliest: background changes
Hard exudates (lipids and protiens-yellow color around vessels), Microaneurysms-red spots around, blot hemmorghages-
After a bit: Pre-proliferative retinopathy-
Cotton wool spots (soft exudates)-represents retinal ischemia (leaking a lot)-lighter spot on background
Then proliferative retimopathy
New vessels being made-but less organised, and can get in the way of vision-not smooth/organised/straight
How can hard exudates impact vision?
normally just background changes
But if happen at macula-maculopathy-damages vision
how do you manage someone with retinopathy?
Manage glucose-keeping it down
Warn patient about signs and what to look for (like maculopathy or proliferative retinopathy)
Screening after 12 months (increase if anything abnormal seen)
IN pre-proliferative -if cotton wool spots, prevent new vessels with PAN RETINAL PHOTOCOAGULATION
If new vessels being made, also use pan retinal photocoagulatio
how do you manage someone with maculopathy?
Target photocoagulation to maacula to prevent retinal spread
What are the main signs of diabetic nephropathy?
Hypertension, glycouria, increase proteiuria, progressive loss of kidney function (GFR DOWN), classical histological features
Why is diabetic nephropathy important?
CKD kills a lot, and makes patients near death easier
CKD kills a lot more than diabetic
also costs a lot for dialysis, and kidney transplant v hard
so want to prevent it a lot (tighter control, lose weiight, stop smoking, etc)
What is the main cause of CKD?
Diabetes is the leading cause
then hypertension
and CKD really increase risk of death-
What are the classical histological features found in diabetic patients with diabetic nephropathy?
Mesangial cell expansion
basement membrane thickening-v important-cells become rigid
glomerulosclerosis
only seen in biopsies, which is rarely done
What is the prevalence of nephropathy in T1 and T2 DM?
About 20-40% get it after 30/40 years of diagnoses
t1 40 y/o olds get it
Which means much earlier in t1DM, and later in t2-meaning t2DM patients might die of CVD problems before CKD (or even eyes/nerves)
What are the main clinical features of diabetic nephropathy? How do you check the first one of them
Increasing proteinuria-urine dipstick-but can need labs for tiny proteins, increased BP, impaired renal function
What are the strategies for management of diabetic nephrophathy?
Glucose control
BP control
Inhbition of the activity of the RAS (RENIN ANGIO TENSION) system–ace inhbitors (like captopril, irbesatan)
Stoping smoking (as CVD is very dangerous in CKD)
