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Y2 LCRS Endocrinology > diabetes > Flashcards

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

1
Q

3 sites of microvascular complications, and names of complications

A

retinal arteries (retinopathy), glomerular arterioles in kidney (nephropathy), vasa nervorum supplying nerves (neuropathy)

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2
Q

what 4 things does microvascular complication risk depend on

A

severity of hyperglycaemia (HbA1c), hypertension, genetic, hyperglycaemic memory

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3
Q

microvascular complication relative risk vs HbA1c; MI (macrovascular complication) relative risk in this

A

as HbA1c increases, microvascular complication relative risk increases, as does MI up to point

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4
Q

microvascular complication relative risk vs mean systolic BP; MI (macrovascular complication) relative risk in this

A

as SBP increases, microvascular complication relative risk increases, as does MI

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5
Q

what is hyperglycaemic memory (important in early stage of diabetes)

A

consequence of tissue damage through originally reversible and later irreverstible alterations in proteins (original poor control of glucose will have permanent impact)

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6
Q

mechanism of glucose damage causing microvascular complications

A

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

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7
Q

diabetic retinopathy prevalence

A

main cause of visual loss in people with diabetes, and main cause of blindness in working age people

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8
Q

4 stages of diabetic retinopathy

A

background, pre-proliferative, proliferative, maculopathy

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9
Q

what are the first changes to be seen in background diabetic retinopathy

A

hard exudates (cheese colour, lipid) when proteins leave vessel, followed by microaneurysms (dots) and blot haemorrhages

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10
Q

what changes are seen in pre-proliferative diabetic retinopathy

A

vessels change from leaking out protein to being more ischaemia, with cotton wool spots (soft exudates)

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11
Q

what changes are seen in proliferative diabetic retinopathy

A

visible unorganised new vessels form on optic disk or elsewhere in retina to go around areas of ischaemia

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12
Q

what changes are seen in maculopathy diabetic retinopathy, and what does this threaten

A

similar to 1st stage but at macula, with hard exudates forming near the macula, threatening direct and colour vision

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13
Q

management of background diabetic retinopathy

A

improve control of blood glucose, warn patient that warning signs are present; retinal screen annually, but increase frequency if significant changes

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14
Q

management of pre-proliferative and proliferative diabetic retinopathy

A

general ischamemia, so needs pan retinal photocoagulation (laser therapy to remove new vessels that will bleed and threaten vision)

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15
Q

management of maculopathy diabetic retinopathy

A

only problem around macula, so only needs a grid of photocoagulation, not pan retinal photocoagulation

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16
Q

glomerular histological changes in diabetic nephropathy

A

prolonged hyperglycaemia and hypertension (angiotensin) causes overproduction of matrix leading to mesangial expansion, basement membrane thickening (increasing rigidity) glomerulosclerosis

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17
Q

when is a renal biospy conducted

A

if other tests appear normal

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18
Q

epidemiology of kidney disease in T1DM vs T2DM

A

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

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19
Q

nephropathy epidemiology in T2DM: why maybe not seen

A

loss due to cardiovascular morbiditity e.g. so dies of heart attack before microvascular complications seen

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20
Q

3 clinical features of diabetic nephropathy

A

hypertension, progressively increasing proteinuria, progressively deteriorating kidney function

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21
Q

how is proteinuria measured

A

urine dipstick to quantify amount of microalbumin in lab; nephtroic range >3000mg/24hr

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22
Q

4 stategies for intervention of nephropathy

A

diabetic control (decreasing HbA1c), blood pressure control (antihypertensives reduce BP, GFR and microalbuminuria), inhibition of RAAS (ACE inhibitors and angiotensin II blockers), stopping smoking

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23
Q

example of angiotensin II blocker

A

irbesartan

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24
Q

diabetic neuropathy prevalence

A

most common cause of neuropathy and limb amputation

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25
Q

mechanism of diabetic neuropathy

A

initiating genetic event -> glycation and neuronal injury -> epigenetic -> functional changes causing blockage of vasa nervorum; consistant oxidative stress causing inflammation

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26
Q

6 types of diabetic neuropathy

A

peripheral polyneuropathy (most common, affecting hands and feet), mononeuropathy, mononeuritis multiplex, radiculopathy, autonomic neuropathy, diabtic amyotrophy

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27
Q

5 features of peripheral neuropathy

A

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

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28
Q

describe monofilament examination for feet sensation

A

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

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29
Q

describe Charcot’s joint in diabetics and treatment

A

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

30
Q

4 features of mononeuropathy

A

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)

31
Q

why is 3rd nerve palsy usually pupil sparing in mononeuropathy

A

PSNS fibres on outside so don’t easily lose blood supply in diabetes, so can cause pupil constriction

32
Q

when might the 3rd nerve palsy not be pupil sparing in mononeuropathy

A

space occupying lesion (aneurysm), which presses on PSNS fibres causing fixed dilated pupil

33
Q

what is mononeuritis multiplex

A

random combination of peripheral nerve lesions

34
Q

what is radiculopathy (rare)

A

pain over spinal nerves, usually affecting a dermatome on abdomen or chest wall

35
Q

what is autonomic neuropathy, when does it occur and what does it lead to

A

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)

36
Q

technique for monitoring autonomic neuropathy

A

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

37
Q

4 microvascular diseases related to DM and early widespread atherosclerosis

A

ischaemic heart disease, cerebrovascular disease, renal artery stenosis, peripheral vascular disease

38
Q

process of atherosclerosis

A

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)

39
Q

4 measurable risk factors for metabolic syndrome, which contribute to macrovascular disease

A

high fasting glucose (>6mmol/l), high waist circumference (easiest to measure), low HDL (less takes cholesterol back to liver), hypertension

40
Q

4 contributors to macrovascular complications that are not usually measured in clinical practice

A

insulin resistance, inflammation CRP, adipocytokines, urine microalbumin

41
Q

macrovascular disease and metabolic syndrome: stages of atherosclerosis where insulin resistance is associated

A

initial lesion, fatty streak, intermediate lesion, atheroma (smooth muscle)

42
Q

macrovascular disease and metabolic syndrome: stages where lipids involved, and importance

A

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)

43
Q

macrovascular disease and metabolic syndrome: stage where thrombosis associated with insulin resistance occurs

A

complicated lesion

44
Q

relationship between expected life expectancy and age at diagnosis of diabetes in years

A

diabetics still die prematurely, but those diagnosed at an earlier age will lose significantly more years due to hyperglycaemic association with macrovascular disease

45
Q

HbA1c and T2DM: intensive treatment impact on HbA1c

A

intensive treatment will have lower HbA1c vs conventional treatment, but diabetes is progressive so will still get worse

46
Q

HbA1c association with macrovascular complications

A

more linear with HbA1c than microvascular complications, so affects everyone not just diabetics, although hyperglycaemia is a risk factor for arterial disease

47
Q

impact of macrovascular complications on morbidity and mortality vs microvascular complications

A

macrovascular causes morbidity and mortality, whereas microvascular just causes morbidity

48
Q

impact of ethnicity on mortality from macrovascular complications in diabetes

A

South Asians more likely to die from coronary heart disease than white caucasians

49
Q

location of macrovascular disease

A

systemic disease commonly present in multiple arterial beds

50
Q

what is the major cause of morbidity and mortality in diabetes

A

ischaemic heart disease

51
Q

mechanism difference of ischaemic heart disease with diabetics and non-diabetics

A

similar

52
Q

cerebrovascular disease prevalence in diabetics vs non-diabetics

A

earlier than without diabetes, more widespread

53
Q

what does peripheral vascular disease contribute to alongside neuropathy

A

diabetic foot problems

54
Q

what does renal artery stenosis contribute to

A

hypertension, renal failure

55
Q

problem with treatment specifically targeted to hyperglycaemia alone in DM with regard to CVD, and impact on treatment

A

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)

56
Q

4 non-modifiable risk factors for macrovascular disease

A

age, sex, birth weight, family hypercholesterolaemia/genes

57
Q

4 modifiable risk factors for macrovascular disease

A

dyslipidaemia, hypertension, smoking, diabetes

58
Q

complications of both diabetes predisposing to foot disease: 2 types

A

neuropathy (most important; sensory, motor, autonomic), peripheral vascular disease

59
Q

8 pathways to foot ulceration

A

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

60
Q

presentation of motor neuropathy

A

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)

61
Q

why is there limited joint mobility in diabetes

A

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

62
Q

why does autonomic neuropathy lead to loss of strength and integridity of foot skin

A

lose control of sweat glands

63
Q

how is peripheral vascular disease treated

A

angioplasty or sew in vein around blocked artery to improve blood flow further down

64
Q

describe neuropathic foot

A

numb, warm, dry, palpable foot pulses, ulcers at points of high pressure loading

65
Q

describe ischaemic foot

A

cold, pulseless, ulcers at the foot margins

66
Q

describe neuro-ischaemic foot (worst)

A

numb, cold, dry, pulseless, ulcers at points of high pressure loading and at foot margins, with thick skin around ulcers preventing healing

67
Q

4 things to asses when assessing diabetic feet

A

appearance (deformity, callus), feel (hot/cold, dry), pulses, neuropathy (vibration, temperature, ankle jerk reflex, fine touch - best way to predict foot problems later)

68
Q

2 pulses when assessing diabetic feet

A

dorsalis pedis, posterior tibial pulse

69
Q

6 preventative managements for diabetic feet

A

control diabetes, inspect feet daily, comfortable shoes (laces and square toe box), cut nails straight across, care with heat, never walk barefoot

70
Q

7 MDT members when assessing and treating diabetic feet

A

diabetes nurse, diabetologist, chropodist, orthotist, vascular surgeon, orthopaedic surgeon, limb fitting centre

71
Q

5 managements of foot ulceration

A

relief of pressure (bed rest, redistribution of pressure), antibiotics, debridement (get rid of dead tissue), revascularisation (angioplasty or arterial bypass surgery), amputation

Y2 LCRS Endocrinology (37 decks)

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