macrovascular complications of dm Flashcards

1
Q

what are the main macrovascualr complications *

A

early widespread aterosclerosis

ischemic hheart disease

CVD

PVD

renal artery stenosis

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2
Q

describe the development of an atheroma *

A

initatial lesion - histophatologically normal, macrophage infiltration, foam cells

fatty streak - symptomless and harmless, intracellular lipid accumulation

intermediate lesion - visible to naked eye, intracellular lipid accumulation and extracellular lipid pools

atheroma - intracellular lipid accumulation and core of extracellular lipid - symptoms late because earlier stages are silent

fibroatheroma - single or multiple lipid cores, fibrotic/calcific layers (ca stores measured on CT to assess extent of atheroma)

complicated lesion - surface defect, haematoma/haemorrhage, thrombosis - lining of te artery is lost, fat is in contact with blood = thrombosis = blocked artery = pump failiure or ellectrical arrhythmia - block heart. this is rare <50yrs age. partial blcokage of artery = TIA or angina, full block = MI or stroke

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3
Q

what are te risk factors for ischemic heart disease *

A

fasting glucose >6mmol/L - elevated sugar

HDL - men <1, women <1.3

hypertension >135/80 = damage to arteries

insulin resistance, inflammation CRP, adipocytokines, urine microalbumin - these are important in macrovascualr risk but not measured in clinical practice

waist circumference - men >102, women 88

metabolic syndrome is a combination of conditions that increases risk of IHD and dm

all processes important in insuil resistance, dm and atheroma (before even have dm/raised sugar - is non-diabetic macrovascualr disease)

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4
Q

wat are te risk factors for different stages of atheroma development *

A

initial lesion, fatty streak and intermediate - hig lipids, bp, insulin resistance

atheroma - sm hypertrophy and insulin resistance

complicated lesion - thrombosis (associated with insulin resistance)

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5
Q

wy does hyperglycaemia reduce lidfe expectancy *

A

macrovascular disease

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6
Q

how does life expecancy relate to the age of diagnosis

A

younger diagnosed = more loss of life

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7
Q

what is a surrogate marker for insulin resistance *

A

measuring insulin

more insulin = more resistant

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8
Q

is insulin resistance important to CHD, ow do we now *

A

yes

more insuilin (and so resistance) means iger cance of developing CHD

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9
Q

what is the risk of CHD in diabetes *

A

it is increased

and is higher in women than men

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10
Q

what does it mean that dm is a progressive disease

A

even with intensive treatment, HbA1c gets worse as patients age

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11
Q

effect of HbA1c on microvascular and microvascular complications *

A

complications increase wit HbA1c increases

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12
Q

what is te difference between the micro and macrovascular correlation wit HbA1c *

A

microvascualr increase is much sharper - only get it wit dm

macro is more linear - have risk even if dont have dm

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13
Q

why is there a higer deat rate from CVD in diabetics tan in the normal population *

A

people with dm have a higher chance of getting CVD than general population

teh CVD kills people with dm before they can develop malignancies

in normal population atheroma kill 1/2 pop under 70years

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14
Q

how does the survival in diabeteic relate to people who have or havent had previous MI *

A

general pop who have never had MI - high survival

general pop with prior MI = reduced survival

dm without prior mi = similar survival to general WITH prior mi

dm with prior mi - very low survival

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15
Q

compare the response after mi of people with dm and general pop *

A

people with dm haave worse outcomes - dm interfers with the response to treatment and so mi is less suseptible to correction

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16
Q

is the risk for cHD the same in all ethnic groups *

A

no

south asians have a higer risk

17
Q

what does it mean that macrovascular disease is a systemic disease *

A

that it is present inb lots of arterial beds eg coronary, in brain, in peripheries, in kidneys

18
Q

what is the major cause of morbidity and mortality in dm 8

19
Q

are the mechanisms of ihd similar or diff in dm to general pop 8

20
Q

what is the difference in cerebrovascular disease in dm than in general pop *

A

earlier in dm

more widespread in dm

when otehr parts of brain try to compensate for lost parts - dont do it as well

occur younger

more likely to have more small infarcts as well

21
Q

consequence of peripheral vascular disease in dm *

A

contribute to diabetic foot problems wit neuropathy

arteries are narrowed because of atheroma

this blocks off arteries/showers emboli and blocks arteries further down

this causes gangrene and so lose toes

attempts made to recover blood flow and bypass blockage but very hard to recover when a bit of tissue has died

22
Q

what is the effect of renal artery stenosis *

A

artery blocked = restricted flow = hypertension = progression to renal failure

this is common

23
Q

is good glucose control effective agaibst the increased risk of cardiovascular disease in dm *

A

not really

it does reduce the risk of chd

but doesnt affect mortality

need to address the lipid and blood pressure too

24
Q

what are the risk factors for macrovascular disease *

A

modifiable: dyslipidaemia, hypertension, smoking, dm, insulin resistance before dm - can adjust these to reduce death risk

nonpmodifiable - age, sex (male higehr risk), birth weight (light at birth predict ihd)

25
what is the effect of treating cholesterol (eg with atorvastatin) on macrovascular end points \*
significant reduction in primary endpoints
26
what is necessary for the prevention of macrovascular disease \*
aggressive management of multiple risk factors
27
what is the effect of bp in macrovascular disease \*
the higher the bp, the higher the risk
28
effect of treating high bp on macrovascular risk \*
reduced risk as lower bp
29
what is the effect of multifactoral therapy of risk factors for macrovascular conditions descriibe the intensive multifactoral therapy \*
multifactoral therapy - medication, dietician, personal trainer reduces the chance of death and dignificant reduction in incidence of cardiovascular events
30
what is the problem with intensive treatment of risk factors \*
massive ask for pts - reduce compliance
31
what is the treatment for dm and macrovascualr disease \*
there are complex algorythms as drugs have different benefits in different circumstances we dont know the casue of dm so treat the risk factors as new drug is found to be useflul algorhithms change
32
describe the mechanism of canakinumab \*
reduces inflammation (which is probably a cause fof damage to arteries) without reducing the lipid levels by targeting inl-1b lowers hba1c and reduces teh risk of recurrent cardiovascualr events but increases risk of infection - so probably not going to be used.