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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
what actions does prostacyclin 1 have on vasculature
vasodilator and platelet inhibitor produced in platelets and vascular endothelium
26
how does Dipyridamole work?
reversibly binds to platelet phosphodiesterase | this increases cAMP and decreases platelet activity
27
how does clopidogrel work?
irreversibly blocks ADP P2Y12 receptors on platelets which inhibits ADP dependant platelet activation
28
which inherited trait is associated with an increased risk of atherothromotic complications in clopidogrel patients
the CYP2C19 allele as clopidogrel is a prodrug requiring conversion via p450 cytochromes
29
how does prasugrel work
same as clopidogrel, but more potent and faster onset
30
how does ticagrelor work
by reversibly blocking the ADP P2Y12 receptor | antiplatlet
31
what do glycoprotein IIb-IIIa antagonists such as abcximab and eptifibatide bind to
fibrinogen and vWF
32
what are the contraindications of ACE inhibitor use
severe AS/MS/LVOT obstruction bilateral renal artery stenosis pregnancy angioedema
33
which drug is first line for the primary and secondary preventino of cardiac disease
statins
34
how do statins work
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
which group of drugs are most effective at lowering LDLs
statins
36
which group of drugs are most effective at lowering triglycerides
fibrates
37
why must vibrates be avoided in gallstone disease
increases the amount of cholesterol excreted in bile
38
how does ezetimibe work
decreases intestinal absorption of cholesterol | increased risk of rhabdomyolysis when combined with statin
39
which conditions are cautions for the use of statin
hypothyroidism liver disease those at risk of myopathy/rhabdomyolysis pregnancy - adequate contraception and 1 month after
40
how do bile acid sequestrates work
bind bile acids, therefore preventing their reabsorption | can interfere with fat sol vitamins (ADKE)
41
which stage of the eicosanoid pathway is interrupted by lipcortin 1 from steroids
phospholipase A2 preventing the production of arachidonic acid
42
what is the inheritance pattern of familial hypercholesterolaemia
autosomal dominant | disorder of gene coding for LDL receptor
43
which sign is present in over 70% of patients with familial hypercholesterolaemia over the age of 20
tendon xanthomata
44
what is the definite diagnostic criteria for familial hypercholesterolaemia
total cholesterol > 7.5 or LDL > 4.9 | plus tendon xanthomata in pt or 1st/2nd degree relative
45
what is the diagnostic criteria for possible familial hyper cholesterolaemia
``` total cholesterol >7.5 or LDL >4.9 FHx of: - prem MI - hypercholesterolaemia - raised fasting LDL ```
46
where are atheromas found
elastic arteries and large/medium sized arteries
47
what is the hallmark of atheromatous disease
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
in what conditions is endothelial dysfunction also seen
hypertension diabetes hypercholesterolaemia cigarette smoking
49
what are the potential anti-atherogenic actions of NO
``` inhibits smooth muscle proliferation inhibition of monocyte adhesion anti-platelet effect promotion of macrophage apoptosis inhibition of lipid oxidation ```
50
what happens in endothelium dysfunction
reduced NO production in response to shear stresses
51
what are the characteristics of early atherosclerotic lesions
foam cells | smooth muscles cells surrounded by extracellular connective tissue and lipid
52
what are the characteristics of advanced atherosclerotic lesions
lipid accumulation with necrotic core and fibrous cap formation eccentric vascular remodelling vasa vasorum neovascularisation
53
what are the characteristics of plaques vulnerable to rupture
``` large lipid cores thin caps high densities of macrophages low densities of smooth muscle cells large numbers of vasa vasorum ```
54
what does depression of the ST segment imply
partial thickness ischaemia
55
what do pathological q waves signify
dead myocardium following full thickness ischaemia as is electrically silent and therefore acts as a window

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