microvascular complications of dm Flashcards
what are the blood vessels that are damaged in microvascular complications *
retinal arteries - retinopathy
glomerular arteries - kidney
vasa nephorum (tiny bv that supply the nerves) - neuropathy
list the microvascular complications that happen in dm *
retinopathy
neuropathy
nephropathy
how are microvascular complications related to hyperglycaemia *
more severe the hyperglycaemia = more likely to have microvasc disease
ie higher hba1c = higher relative risk
how does bp affect microvascular disease *
hypertension puts you at risk of microvascular disease
higher bp = more risk
what factors in dm contribute to microvascular disease *
severity of hyperglycaemia
hypertension
genetic
hyperglycaemic memory - if have good control from outset better outcomes compared to someone who had bad control and now has good control
why do you wnat to screen people with risk factors for dm *
might have pre-dm - and so could have the mcirovascular conditions
microvascular conditions begin reversible but of you waited until dm diagnosis - might not be reversible
what is the mechanism for microvascular damage *
high glucose causes release of inflammatory signalling cytokines
causes inflammation
this damages the microvessels
what is the problem with diabetic retinopathy *
main cause of visual loss in people with dm
and main cause of blindness in people of working age
how does dm cause retinopathy 8
glucose cause retinal ischemia
cause retinopathy
what are the stages in diabetic retinopathy *
background diabetic retinopathy
pre-proliferative diabetic retinopathy
preoliferative diabetic retinopathy
maculopathy
describe background diabetic retinopathy *
hard exudates - protein come out of vessels, lipid rich = yellow
microaneurysms ‘dots’ - outsprouting of the vessels buldging out
blot haemorrhages - bleeding from the vessels
describe preproliferative retinopathy *
cotton wool spots called soft exudates
represent retinal ischemia - vessel is ischemic
occurs if dont treat background retinopathy
describe proliferative retinopathy *
visible new vessels - not organised or smooth - go around the area of ischemia
they are on disk or elsewhere in retina
bleed = effect vision
describe maculopathy *
hard exudates near the macula
same disease as background retinopathy - but near the macula
this can threaten direct vision
how to you manage background diabetic retinopathy *
lower blood glucose = less likely that it will progress
warn the pt that there are warning signs - explain why they could get loss of vision (maculopathy or new vessels)
screen everyone every year - if signs are present screen more regualy
how do you manage pre-proliferative retinopathy *
pre-proliferative suggests general ischemia so if left alone more vessels will grow
so you need pan retinal photooagulation - laser beam fired into retina - prevent the vessel forming
how do you manage proliferative diabetic retinopathy *
pan retinal photocoagulation
how do you manage maculopathy *
only have problem around the macula so only need a grid of photocoagulation - targeted
when dont you need to give lasor therapy for hard exudates *
when at the pperiphery of the retina
what are the signs of diabetic nephropathy *
hypertension
progressively increasing proteinuria
progressively deteriorating kidney func - reducing GFR
classical histological features
why is nephronopathy important *
associated high morbidity and mortality - if you abve CKD and dm - much higher risk of dying from macrovascular disease
health care burden - expensive if get onto dialysis or transplant, drugs for transplant are expensive
treatment options present - BP, glucose and smoking control
if ypou have dm - much higher chance of getting CKD
what are the classical histological features of nephronopathy *
glomerular changes - mesangial expansion, basememt membrane thickening (cells become rigid - affect changes in the kidneys), glomerulosclerosis
descrieb the mechanism of how dm causes nephronopathy *
high glucose causes inflammation because of high cytokines adn growth factors
causes extracellular matrix accumulation
causes protein to be lost in urine
describe the difference in epi of nephronopathy in T1 and T2 *
t1 - 20-40% have it after 30-40 yrs
t2 - probably same but diagnosed later so dont get nepronopathy until later, also more likely to get macrovascular complications than people with type 1 so die before get nephronopathy
what is proteinuria and how do you test it *
normal level of protein in urine is <30mg/24hrs
urine dipstick to look for protein
small changes not always evident in dipstick - so look for microalbumin in lab - 1st change that occurs in nephronopathy
microalbuminia 30-300mg/24hrs
assymptomatic range 300-3000mg/24rs
nephrotic range >3000mg/24hrs
what are the strategies for intervention for diabetic nepronopathy *
diabetic control to prevent progression - decreasing hba1c reduces microvascular complication risk
blood pressure control - prevent microvascular change getting worse - GFR doesnt change as much if on antiypertensive and have nephronopathy and protein in urine goes down
inhibition of the activity of the RAAS (ace inhibitor or ang 2 receptor blocker) - deteriation of renal func is reduced
smoking cessation
what are the negative effects of angiotensin
vasoactive
mediate glomerular hyperfiltration
increased tubular uptake of proteins
induction of pro fibrotic cytokines
stimulation of glomerular and tuibular growth
podocyte effects
induction of pro-inflamm cytokines
generation of ROS and NF-kB
stimulate fibroblast proliferation
up regulation of adhesion molecules on endothelial cells
up regulation of lipoprotein receptors
problem of smoking and having CKD *
high cance of MI
are all patients affected by nepronopathy *
no people with good bp control and non-smokers dont get it
what is the problem with diabetic neuropathy *
diabetes most common cause of neuropathy and hence lower limb amputation
what causes neuropathy *
vasa nervorum (small vessels supplying the nerves are blocked)
what are the different forms of diabetic neuropathy *
peripheral polyneuropathy - most common - affect hand and feet in glove and stocking distribution
mononeuropathy - just one nerve affected
mononeuritis multiplex - certain areas of the nerves affected
radiculopathy- certain dermatomes affected
autonomic neuropathy
diabetic amyotrophy - affects the thighs, hips, buttocks and legs, causing pain and muscle wasting
who is peripheral nepropathy more likely to occur in *
tall pts
pts with poor glucose control
describe the monofilament examination *
use monofilament and give pressure to key areas of foot - see if they can feel it
make sure the pts check feet
what are the consequences of peripheral neuropathy *
loss of ankle jerks
loss of vibration sense - using tuning fork
multiple fractures on the foot of x ray because step on one part of foot more than other- charcot’s joint - need immobilising in plaster, tender and red area - difficult to treat so = perm abnormalities
describe mononeuropathy *
usually sudden motor loss
you get wrist drop, foot drop and cranial nerve palsy
get double vision due to 3rd nerve palsy - eye cant move medially because lost supply to CN3 - eye down and out because still getting innervation from CN4 and 6 - pupil does respond to light - ligt sparing 3rd nerve palsy
how can you get pupil sparing 3rd nerve palsy *
parasympathetic fibres are on the outside of area that controls the pupil - they dont lose blood supply in diabetes
what causes a 3rd nerve palsy with pupil that will not respond to light *
aneurysm or tumour - space occupying lesion - press on parasymp fibres causing a fixed dilated pupil
describe mononeuritis multiplex *
random combination of peripheral nerve lesions = pain
describe radiculopathy *
pain over spinal nerves just affecting 1 dermatome eg abdo or chest wall
describe autonomic neuropathy *
happen after had dm for a long time
loss of symp and parasymp nerves to GI tract, bladder and CVS
causing:
gastroparesis (nausea, vom and abdo pain), difficulty swallowing, delayed gastric emptying - affecting nerves involved in peristalsis, constipation/nocturnal diarrhoea
incontinence
postural hypotension - can be disabling - collapse on standing
arrythmia, case reports of sudden cardiac death
how do you examine autonomic neuropathy *
measure changes in hr in response to valsalva manoevre - blow syringe and cause build up of pressure
normally change in hr
look at ecg and compare R-R intervals
what do you screen for every year in people with dm *
retinal screening
feet
microalbumin
