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Transport > Myocardial Infarction > Flashcards

Myocardial Infarction Flashcards

1
Q

what is ischaemia

A

reversible hypoxia

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2
Q

what is infarction

A

non-reversible hypoxia

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3
Q

what are the modifiable risk factors for MI

A 
smoking
HTN
diabetes
hyperlipidarmia
obesity
sendentary lifestyle
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4
Q

what are the non-modifiable risk factors for MI

A

age
gender (being male)
Fhx

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5
Q

what factors may predispose towards MI

A 
stress
type A personality
LVH
cocaine use
raised fibrinogen
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6
Q

in which patients might a silent MI occur

A

diabetic/elderly patients

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7
Q

how might a silent MI present

A 
syncope
pulmonary oedema
epigastric pain
vomiting
acute confusional state
stroke
diabetic hyperglycaemia
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8
Q

what must be present to diagnose MI

A

symptoms of chest pain
ECG changes suggested of ischaemia
Evidence of myocyte necrosis

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9
Q

what might suggest excess sympathetic tone following MI

A

HTN

tachycardia

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10
Q

what might suggest excess parasympathetic tone following MI

A

bradycardia
hypotension
nausea
belching

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11
Q

what signs might be suggestive of impaired left ventricular function

A

hypotension
crackles in the lung
3rd heart sound
murmurs

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12
Q

which ECG change is an indication for reperfusion therapy

A

ST elevation as it indicates complete coronary occlusion and therefore full thickness ischaemia

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13
Q

what are the immediate changes you would see on an ECG (with in minutes)

A

change in ST segment

Tall pointed T waves

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14
Q

what changes would you see on an ECG minutes after MI

A

pathological Q waves

inversion of the T waves

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15
Q

what changes would you see on an ECG days after an MI

A

normal ST segments

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16
Q

what changes would you see on an ECG weeks after an MI

A

pathological Q waves

T waves may become upright

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17
Q

what are the non-ACS causes of troponin elevation

A 
chronic/acute renal dysfunction
severe congestive heart failure
hypertensive crisis
tachy/brady arrhythmias
PE/pulmonary hypertension
inflammatory diseases 
etc etc etc there are LOADS
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18
Q

which interventions are aimed at prevention of further coronary thrombosis

A

anticoagulants

antiplatelet treatment

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19
Q

which intervention post MI aims to stabilise coronary arteries

A

statins

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20
Q

which intervention post MI aims to optimise healing

A

ACE inhibitors

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21
Q

which interventions aim to restore coronary flow post MI

A

reperfusion (PCI/thrombolysis)
nitrates
CABG

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22
Q

which thrombolytic drugs are used when PCI is not available within 90 minutes of MI

A

streptokinase

TPA

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23
Q

how does aspirin exert its anti-platelet effect

A

it permentantly acetylates COX 1 in platelets and therefore halts thromboxane A2 for the life span of the platelet (10days)
it also increases the prostacyclin1: thromboxane as this is produced by COX2 which is unaffected by aspirin

24
Q

what actions does thromboxane have on vasculature

A

potent vasoconstrictor and platelet agonist

25
Q

what actions does prostacyclin 1 have on vasculature

A

vasodilator and platelet inhibitor

produced in platelets and vascular endothelium

26
Q

how does Dipyridamole work?

A

reversibly binds to platelet phosphodiesterase

this increases cAMP and decreases platelet activity

27
Q

how does clopidogrel work?

A

irreversibly blocks ADP P2Y12 receptors on platelets which inhibits ADP dependant platelet activation

28
Q

which inherited trait is associated with an increased risk of atherothromotic complications in clopidogrel patients

A

the CYP2C19 allele as clopidogrel is a prodrug requiring conversion via p450 cytochromes

29
Q

how does prasugrel work

A

same as clopidogrel, but more potent and faster onset

30
Q

how does ticagrelor work

A

by reversibly blocking the ADP P2Y12 receptor

antiplatlet

31
Q

what do glycoprotein IIb-IIIa antagonists such as abcximab and eptifibatide bind to

A

fibrinogen and vWF

32
Q

what are the contraindications of ACE inhibitor use

A

severe AS/MS/LVOT obstruction
bilateral renal artery stenosis
pregnancy
angioedema

33
Q

which drug is first line for the primary and secondary preventino of cardiac disease

A

statins

34
Q

how do statins work

A

inhibit HMG CoA reductase which is the rate limiting enzyme in cholesterol synthesis

as 50% of cholesterol is endogenously produced circulating cholesterol is reduced (esp LDL)

the numbers of LDL -Rs are increased - increased uptake out of the circulation

35
Q

which group of drugs are most effective at lowering LDLs

A

statins

36
Q

which group of drugs are most effective at lowering triglycerides

A

fibrates

37
Q

why must vibrates be avoided in gallstone disease

A

increases the amount of cholesterol excreted in bile

38
Q

how does ezetimibe work

A

decreases intestinal absorption of cholesterol

increased risk of rhabdomyolysis when combined with statin

39
Q

which conditions are cautions for the use of statin

A

hypothyroidism
liver disease
those at risk of myopathy/rhabdomyolysis
pregnancy - adequate contraception and 1 month after

40
Q

how do bile acid sequestrates work

A

bind bile acids, therefore preventing their reabsorption

can interfere with fat sol vitamins (ADKE)

41
Q

which stage of the eicosanoid pathway is interrupted by lipcortin 1 from steroids

A

phospholipase A2 preventing the production of arachidonic acid

42
Q

what is the inheritance pattern of familial hypercholesterolaemia

A

autosomal dominant

disorder of gene coding for LDL receptor

43
Q

which sign is present in over 70% of patients with familial hypercholesterolaemia over the age of 20

A

tendon xanthomata

44
Q

what is the definite diagnostic criteria for familial hypercholesterolaemia

A

total cholesterol > 7.5 or LDL > 4.9

plus tendon xanthomata in pt or 1st/2nd degree relative

45
Q

what is the diagnostic criteria for possible familial hyper cholesterolaemia

A 
total cholesterol >7.5 or LDL >4.9
FHx of:
- prem MI
- hypercholesterolaemia
- raised fasting LDL
46
Q

where are atheromas found

A

elastic arteries and large/medium sized arteries

47
Q

what is the hallmark of atheromatous disease

A

endothelial dysfunction
this leads to adherence of platelets and WBCs
this allows the passage of inflammatory cells into the sub endothelium and the accumulation of lipid rich cells, smooth muscle and new blood vessel growth

48
Q

in what conditions is endothelial dysfunction also seen

A

hypertension
diabetes
hypercholesterolaemia
cigarette smoking

49
Q

what are the potential anti-atherogenic actions of NO

A 
inhibits smooth muscle proliferation
inhibition of monocyte adhesion
anti-platelet effect
promotion of macrophage apoptosis
inhibition of lipid oxidation
50
Q

what happens in endothelium dysfunction

A

reduced NO production in response to shear stresses

51
Q

what are the characteristics of early atherosclerotic lesions

A

foam cells

smooth muscles cells surrounded by extracellular connective tissue and lipid

52
Q

what are the characteristics of advanced atherosclerotic lesions

A

lipid accumulation with necrotic core and fibrous cap formation

eccentric vascular remodelling

vasa vasorum neovascularisation

53
Q

what are the characteristics of plaques vulnerable to rupture

A 
large lipid cores
thin caps
high densities of macrophages
low densities of smooth muscle cells
large numbers of vasa vasorum
54
Q

what does depression of the ST segment imply

A

partial thickness ischaemia

55
Q

what do pathological q waves signify

A

dead myocardium following full thickness ischaemia as is electrically silent and therefore acts as a window

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