Myocardial Infarction Flashcards
what is ischaemia
reversible hypoxia
what is infarction
non-reversible hypoxia
what are the modifiable risk factors for MI
smoking HTN diabetes hyperlipidarmia obesity sendentary lifestyle
what are the non-modifiable risk factors for MI
age
gender (being male)
Fhx
what factors may predispose towards MI
stress type A personality LVH cocaine use raised fibrinogen
in which patients might a silent MI occur
diabetic/elderly patients
how might a silent MI present
syncope pulmonary oedema epigastric pain vomiting acute confusional state stroke diabetic hyperglycaemia
what must be present to diagnose MI
symptoms of chest pain
ECG changes suggested of ischaemia
Evidence of myocyte necrosis
what might suggest excess sympathetic tone following MI
HTN
tachycardia
what might suggest excess parasympathetic tone following MI
bradycardia
hypotension
nausea
belching
what signs might be suggestive of impaired left ventricular function
hypotension
crackles in the lung
3rd heart sound
murmurs
which ECG change is an indication for reperfusion therapy
ST elevation as it indicates complete coronary occlusion and therefore full thickness ischaemia
what are the immediate changes you would see on an ECG (with in minutes)
change in ST segment
Tall pointed T waves
what changes would you see on an ECG minutes after MI
pathological Q waves
inversion of the T waves
what changes would you see on an ECG days after an MI
normal ST segments
what changes would you see on an ECG weeks after an MI
pathological Q waves
T waves may become upright
what are the non-ACS causes of troponin elevation
chronic/acute renal dysfunction severe congestive heart failure hypertensive crisis tachy/brady arrhythmias PE/pulmonary hypertension inflammatory diseases etc etc etc there are LOADS
which interventions are aimed at prevention of further coronary thrombosis
anticoagulants
antiplatelet treatment
which intervention post MI aims to stabilise coronary arteries
statins
which intervention post MI aims to optimise healing
ACE inhibitors
which interventions aim to restore coronary flow post MI
reperfusion (PCI/thrombolysis)
nitrates
CABG
which thrombolytic drugs are used when PCI is not available within 90 minutes of MI
streptokinase
TPA
how does aspirin exert its anti-platelet effect
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
what actions does thromboxane have on vasculature
potent vasoconstrictor and platelet agonist
what actions does prostacyclin 1 have on vasculature
vasodilator and platelet inhibitor
produced in platelets and vascular endothelium
how does Dipyridamole work?
reversibly binds to platelet phosphodiesterase
this increases cAMP and decreases platelet activity
how does clopidogrel work?
irreversibly blocks ADP P2Y12 receptors on platelets which inhibits ADP dependant platelet activation
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
how does prasugrel work
same as clopidogrel, but more potent and faster onset
how does ticagrelor work
by reversibly blocking the ADP P2Y12 receptor
antiplatlet
what do glycoprotein IIb-IIIa antagonists such as abcximab and eptifibatide bind to
fibrinogen and vWF
what are the contraindications of ACE inhibitor use
severe AS/MS/LVOT obstruction
bilateral renal artery stenosis
pregnancy
angioedema
which drug is first line for the primary and secondary preventino of cardiac disease
statins
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
which group of drugs are most effective at lowering LDLs
statins
which group of drugs are most effective at lowering triglycerides
fibrates
why must vibrates be avoided in gallstone disease
increases the amount of cholesterol excreted in bile
how does ezetimibe work
decreases intestinal absorption of cholesterol
increased risk of rhabdomyolysis when combined with statin
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
how do bile acid sequestrates work
bind bile acids, therefore preventing their reabsorption
can interfere with fat sol vitamins (ADKE)
which stage of the eicosanoid pathway is interrupted by lipcortin 1 from steroids
phospholipase A2 preventing the production of arachidonic acid
what is the inheritance pattern of familial hypercholesterolaemia
autosomal dominant
disorder of gene coding for LDL receptor
which sign is present in over 70% of patients with familial hypercholesterolaemia over the age of 20
tendon xanthomata
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
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
where are atheromas found
elastic arteries and large/medium sized arteries
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
in what conditions is endothelial dysfunction also seen
hypertension
diabetes
hypercholesterolaemia
cigarette smoking
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
what happens in endothelium dysfunction
reduced NO production in response to shear stresses
what are the characteristics of early atherosclerotic lesions
foam cells
smooth muscles cells surrounded by extracellular connective tissue and lipid
what are the characteristics of advanced atherosclerotic lesions
lipid accumulation with necrotic core and fibrous cap formation
eccentric vascular remodelling
vasa vasorum neovascularisation
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
what does depression of the ST segment imply
partial thickness ischaemia
what do pathological q waves signify
dead myocardium following full thickness ischaemia as is electrically silent and therefore acts as a window
