microvascular complications of dm

Question 1

what are the blood vessels that are damaged in microvascular complications *

Answer 1

retinal arteries - retinopathy

glomerular arteries - kidney

vasa nephorum (tiny bv that supply the nerves) - neuropathy

Question 2

list the microvascular complications that happen in dm *

Answer 2

retinopathy

neuropathy

nephropathy

Question 3

how are microvascular complications related to hyperglycaemia *

Answer 3

more severe the hyperglycaemia = more likely to have microvasc disease

ie higher hba1c = higher relative risk

Question 4

how does bp affect microvascular disease *

Answer 4

hypertension puts you at risk of microvascular disease

higher bp = more risk

Question 5

what factors in dm contribute to microvascular disease *

Answer 5

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

Question 6

why do you wnat to screen people with risk factors for dm *

Answer 6

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

Question 7

what is the mechanism for microvascular damage *

Answer 7

high glucose causes release of inflammatory signalling cytokines

causes inflammation

this damages the microvessels

Question 8

what is the problem with diabetic retinopathy *

Answer 8

main cause of visual loss in people with dm

and main cause of blindness in people of working age

Question 9

how does dm cause retinopathy 8

Answer 9

glucose cause retinal ischemia

cause retinopathy

Question 10

what are the stages in diabetic retinopathy *

Answer 10

background diabetic retinopathy

pre-proliferative diabetic retinopathy

preoliferative diabetic retinopathy

maculopathy

Question 11

describe background diabetic retinopathy *

Answer 11

hard exudates - protein come out of vessels, lipid rich = yellow

microaneurysms ‘dots’ - outsprouting of the vessels buldging out

blot haemorrhages - bleeding from the vessels

Question 12

describe preproliferative retinopathy *

Answer 12

cotton wool spots called soft exudates

represent retinal ischemia - vessel is ischemic

occurs if dont treat background retinopathy

Question 13

describe proliferative retinopathy *

Answer 13

visible new vessels - not organised or smooth - go around the area of ischemia

they are on disk or elsewhere in retina

bleed = effect vision

Question 14

describe maculopathy *

Answer 14

hard exudates near the macula

same disease as background retinopathy - but near the macula

this can threaten direct vision

Question 15

how to you manage background diabetic retinopathy *

Answer 15

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

Question 16

how do you manage pre-proliferative retinopathy *

Answer 16

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

Question 17

how do you manage proliferative diabetic retinopathy *

Answer 17

pan retinal photocoagulation

Question 18

how do you manage maculopathy *

Answer 18

only have problem around the macula so only need a grid of photocoagulation - targeted

Question 19

when dont you need to give lasor therapy for hard exudates *

Answer 19

when at the pperiphery of the retina

Question 20

what are the signs of diabetic nephropathy *

Answer 20

hypertension

progressively increasing proteinuria

progressively deteriorating kidney func - reducing GFR

classical histological features

Question 21

why is nephronopathy important *

Answer 21

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

Question 22

what are the classical histological features of nephronopathy *

Answer 22

glomerular changes - mesangial expansion, basememt membrane thickening (cells become rigid - affect changes in the kidneys), glomerulosclerosis

Question 23

descrieb the mechanism of how dm causes nephronopathy *

Answer 23

high glucose causes inflammation because of high cytokines adn growth factors

causes extracellular matrix accumulation

causes protein to be lost in urine

Question 24

describe the difference in epi of nephronopathy in T1 and T2 *

Answer 24

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

Question 25

what is proteinuria and how do you test it \*

Answer 25

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

Question 26

what are the strategies for intervention for diabetic nepronopathy \*

Answer 26

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

Question 27

what are the negative effects of angiotensin

Answer 27

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

Question 28

problem of smoking and having CKD \*

Answer 28

high cance of MI

Question 29

are all patients affected by nepronopathy \*

Answer 29

no people with good bp control and non-smokers dont get it

Question 30

what is the problem with diabetic neuropathy \*

Answer 30

diabetes most common cause of neuropathy and hence lower limb amputation

Question 31

what causes neuropathy \*

Answer 31

vasa nervorum (small vessels supplying the nerves are blocked)

Question 32

what are the different forms of diabetic neuropathy \*

Answer 32

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

Question 33

who is peripheral nepropathy more likely to occur in \*

Answer 33

tall pts pts with poor glucose control

Question 34

describe the monofilament examination \*

Answer 34

use monofilament and give pressure to key areas of foot - see if they can feel it make sure the pts check feet

Question 35

what are the consequences of peripheral neuropathy \*

Answer 35

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

Question 36

describe mononeuropathy \*

Answer 36

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

Question 37

how can you get pupil sparing 3rd nerve palsy \*

Answer 37

parasympathetic fibres are on the outside of area that controls the pupil - they dont lose blood supply in diabetes

Question 38

what causes a 3rd nerve palsy with pupil that will not respond to light \*

Answer 38

aneurysm or tumour - space occupying lesion - press on parasymp fibres causing a fixed dilated pupil

Question 39

describe mononeuritis multiplex \*

Answer 39

random combination of peripheral nerve lesions = pain

Question 40

describe radiculopathy \*

Answer 40

pain over spinal nerves just affecting 1 dermatome eg abdo or chest wall

Question 41

describe autonomic neuropathy \*

Answer 41

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

Question 42

how do you examine autonomic neuropathy \*

Answer 42

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

Question 43

what do you screen for every year in people with dm \*

Answer 43

retinal screening feet microalbumin