diabetes Flashcards
complications of diabetes: explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention
3 sites of microvascular complications, and names of complications
retinal arteries (retinopathy), glomerular arterioles in kidney (nephropathy), vasa nervorum supplying nerves (neuropathy)
what 4 things does microvascular complication risk depend on
severity of hyperglycaemia (HbA1c), hypertension, genetic, hyperglycaemic memory
microvascular complication relative risk vs HbA1c; MI (macrovascular complication) relative risk in this
as HbA1c increases, microvascular complication relative risk increases, as does MI up to point
microvascular complication relative risk vs mean systolic BP; MI (macrovascular complication) relative risk in this
as SBP increases, microvascular complication relative risk increases, as does MI
what is hyperglycaemic memory (important in early stage of diabetes)
consequence of tissue damage through originally reversible and later irreverstible alterations in proteins (original poor control of glucose will have permanent impact)
mechanism of glucose damage causing microvascular complications
hyperglycaemia and hyperlipidaemia -> advanced glycation end products, oxidative stress and hypoxia (polyol pathway, protein kinase C, hexosamine) -> inflammatory signalling cascades -> local activation of pro-inflammatory cytokines -> inflammation -> microvascular complications
diabetic retinopathy prevalence
main cause of visual loss in people with diabetes, and main cause of blindness in working age people
4 stages of diabetic retinopathy
background, pre-proliferative, proliferative, maculopathy
what are the first changes to be seen in background diabetic retinopathy
hard exudates (cheese colour, lipid) when proteins leave vessel, followed by microaneurysms (dots) and blot haemorrhages
what changes are seen in pre-proliferative diabetic retinopathy
vessels change from leaking out protein to being more ischaemia, with cotton wool spots (soft exudates)
what changes are seen in proliferative diabetic retinopathy
visible unorganised new vessels form on optic disk or elsewhere in retina to go around areas of ischaemia
what changes are seen in maculopathy diabetic retinopathy, and what does this threaten
similar to 1st stage but at macula, with hard exudates forming near the macula, threatening direct and colour vision
management of background diabetic retinopathy
improve control of blood glucose, warn patient that warning signs are present; retinal screen annually, but increase frequency if significant changes
management of pre-proliferative and proliferative diabetic retinopathy
general ischamemia, so needs pan retinal photocoagulation (laser therapy to remove new vessels that will bleed and threaten vision)
management of maculopathy diabetic retinopathy
only problem around macula, so only needs a grid of photocoagulation, not pan retinal photocoagulation
glomerular histological changes in diabetic nephropathy
prolonged hyperglycaemia and hypertension (angiotensin) causes overproduction of matrix leading to mesangial expansion, basement membrane thickening (increasing rigidity) glomerulosclerosis
when is a renal biospy conducted
if other tests appear normal
epidemiology of kidney disease in T1DM vs T2DM
T1DM: 20-40% will have kidney disease after 30-40 years after earlier diagnosis, with T2DM similar but with later diagnosis, so won’t get microvascular disease until later on in life
nephropathy epidemiology in T2DM: why maybe not seen
loss due to cardiovascular morbiditity e.g. so dies of heart attack before microvascular complications seen
3 clinical features of diabetic nephropathy
hypertension, progressively increasing proteinuria, progressively deteriorating kidney function
how is proteinuria measured
urine dipstick to quantify amount of microalbumin in lab; nephtroic range >3000mg/24hr
4 stategies for intervention of nephropathy
diabetic control (decreasing HbA1c), blood pressure control (antihypertensives reduce BP, GFR and microalbuminuria), inhibition of RAAS (ACE inhibitors and angiotensin II blockers), stopping smoking
example of angiotensin II blocker
irbesartan
diabetic neuropathy prevalence
most common cause of neuropathy and limb amputation
mechanism of diabetic neuropathy
initiating genetic event -> glycation and neuronal injury -> epigenetic -> functional changes causing blockage of vasa nervorum; consistant oxidative stress causing inflammation
6 types of diabetic neuropathy
peripheral polyneuropathy (most common, affecting hands and feet), mononeuropathy, mononeuritis multiplex, radiculopathy, autonomic neuropathy, diabtic amyotrophy
5 features of peripheral neuropathy
loss of sensation by longest nerves supplying feet, so more common in tall people (or those with poor glucose control); loss of ankle jerks and vibration sense; multiple fractures on foot x-ray (Charcot’s joint); danger of not sensing foot injury
describe monofilament examination for feet sensation
nylon wire with specific weight of touch, applying consistent certain pressure on key areas of foot; if can’t feel it, warn that they should check feet consistently to ensure no injury, and to wear comfortable shoes
describe Charcot’s joint in diabetics and treatment
may step on one part of foot more than others, so at risk of multiple fractures (e.g. if walk on side), causing changes in bone (Charcot’s joint) and tender red areas not felt as no sensation -> if left untreated can cause severe deformities; treat with not walking for a bit
4 features of mononeuropathy
usually sudden motor loss; wrist drop, foor drop; cranial nerve palsy; double vision due to pupil sparing 3rd nerve palsy (affected eye pulled down and out, with pupil response to light)
why is 3rd nerve palsy usually pupil sparing in mononeuropathy
PSNS fibres on outside so don’t easily lose blood supply in diabetes, so can cause pupil constriction
when might the 3rd nerve palsy not be pupil sparing in mononeuropathy
space occupying lesion (aneurysm), which presses on PSNS fibres causing fixed dilated pupil
what is mononeuritis multiplex
random combination of peripheral nerve lesions
what is radiculopathy (rare)
pain over spinal nerves, usually affecting a dermatome on abdomen or chest wall
what is autonomic neuropathy, when does it occur and what does it lead to
loss of SNS and PSNS nerves to GI tract, bladder and CVS, when diabetes has been occuring for a long time; leads to dysphagia, incontinence, bladder dysfunction, postural hypotension and arrhythmias (also sudden cardiac death)
technique for monitoring autonomic neuropathy
measure changes in heart rate in response to Valsalva manoevre (blow into syringe to build up pressure and increase heart rate; look at ECG and compare R-R intervals
4 microvascular diseases related to DM and early widespread atherosclerosis
ischaemic heart disease, cerebrovascular disease, renal artery stenosis, peripheral vascular disease
process of atherosclerosis
initial lesion -> fatty streak -> IC collections and small EC collections of lipid (intermediate lesion) -> atheroma with core of IC lipid inside -> fibroatheroma with fibrous surface with Ca2+ in it (measured on CT) -> complicated lesion (surface defect as lining of artery lost, with fat coming into contact with blood), causing blockage to artery and ischaemia (MI in heart)
4 measurable risk factors for metabolic syndrome, which contribute to macrovascular disease
high fasting glucose (>6mmol/l), high waist circumference (easiest to measure), low HDL (less takes cholesterol back to liver), hypertension
4 contributors to macrovascular complications that are not usually measured in clinical practice
insulin resistance, inflammation CRP, adipocytokines, urine microalbumin
macrovascular disease and metabolic syndrome: stages of atherosclerosis where insulin resistance is associated
initial lesion, fatty streak, intermediate lesion, atheroma (smooth muscle)
macrovascular disease and metabolic syndrome: stages where lipids involved, and importance
initial lesion, fatty streak, intermediate lesion; important in blood and wall of artery (fat accumulates in cells then exits, with wall of plaque ulcerating and blocking artery, as well as sending emboli further down)
macrovascular disease and metabolic syndrome: stage where thrombosis associated with insulin resistance occurs
complicated lesion
relationship between expected life expectancy and age at diagnosis of diabetes in years
diabetics still die prematurely, but those diagnosed at an earlier age will lose significantly more years due to hyperglycaemic association with macrovascular disease
HbA1c and T2DM: intensive treatment impact on HbA1c
intensive treatment will have lower HbA1c vs conventional treatment, but diabetes is progressive so will still get worse
HbA1c association with macrovascular complications
more linear with HbA1c than microvascular complications, so affects everyone not just diabetics, although hyperglycaemia is a risk factor for arterial disease
impact of macrovascular complications on morbidity and mortality vs microvascular complications
macrovascular causes morbidity and mortality, whereas microvascular just causes morbidity
impact of ethnicity on mortality from macrovascular complications in diabetes
South Asians more likely to die from coronary heart disease than white caucasians
location of macrovascular disease
systemic disease commonly present in multiple arterial beds
what is the major cause of morbidity and mortality in diabetes
ischaemic heart disease
mechanism difference of ischaemic heart disease with diabetics and non-diabetics
similar
cerebrovascular disease prevalence in diabetics vs non-diabetics
earlier than without diabetes, more widespread
what does peripheral vascular disease contribute to alongside neuropathy
diabetic foot problems
what does renal artery stenosis contribute to
hypertension, renal failure
problem with treatment specifically targeted to hyperglycaemia alone in DM with regard to CVD, and impact on treatment
minor effect on increased CVD risk, so must have aggressive management (intensive so big ask of patient) of multiple risk factors (treating cholesterol in diabetes using statins to prevent macrovascular complications is much more successful than controlling sugar alone, as is controlling BP)
4 non-modifiable risk factors for macrovascular disease
age, sex, birth weight, family hypercholesterolaemia/genes
4 modifiable risk factors for macrovascular disease
dyslipidaemia, hypertension, smoking, diabetes
complications of both diabetes predisposing to foot disease: 2 types
neuropathy (most important; sensory, motor, autonomic), peripheral vascular disease
8 pathways to foot ulceration
sensory neuropathy, motor neuropathy, limited joint mobility, autonomic neuropathy, peripheral vascular disease, trauma, reduced resistance to infection, other diaebtic complications e.g. retinopathy so have injury as can’t see where going
presentation of motor neuropathy
clawing of toes as imbalance of long extensors and short plantar flexors, causing loss of foot shape (direct harm as toe knuckles scratch; indirect harm as greatest pressure on big toe metatarsal head so difficulty balancing)
why is there limited joint mobility in diabetes
e.g. “glycosylated hands”; can’t put tgether as sugar sticks to proteins and stops them working properly, like in hands with collagen -> feet don’t bend properly when walking
why does autonomic neuropathy lead to loss of strength and integridity of foot skin
lose control of sweat glands
how is peripheral vascular disease treated
angioplasty or sew in vein around blocked artery to improve blood flow further down
describe neuropathic foot
numb, warm, dry, palpable foot pulses, ulcers at points of high pressure loading
describe ischaemic foot
cold, pulseless, ulcers at the foot margins
describe neuro-ischaemic foot (worst)
numb, cold, dry, pulseless, ulcers at points of high pressure loading and at foot margins, with thick skin around ulcers preventing healing
4 things to asses when assessing diabetic feet
appearance (deformity, callus), feel (hot/cold, dry), pulses, neuropathy (vibration, temperature, ankle jerk reflex, fine touch - best way to predict foot problems later)
2 pulses when assessing diabetic feet
dorsalis pedis, posterior tibial pulse
6 preventative managements for diabetic feet
control diabetes, inspect feet daily, comfortable shoes (laces and square toe box), cut nails straight across, care with heat, never walk barefoot
7 MDT members when assessing and treating diabetic feet
diabetes nurse, diabetologist, chropodist, orthotist, vascular surgeon, orthopaedic surgeon, limb fitting centre
5 managements of foot ulceration
relief of pressure (bed rest, redistribution of pressure), antibiotics, debridement (get rid of dead tissue), revascularisation (angioplasty or arterial bypass surgery), amputation
