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Flashcards in Myocardial Infarction Deck (55):
1

what is ischaemia

reversible hypoxia

2

what is infarction

non-reversible hypoxia

3

what are the modifiable risk factors for MI

smoking
HTN
diabetes
hyperlipidarmia
obesity
sendentary lifestyle

4

what are the non-modifiable risk factors for MI

age
gender (being male)
Fhx

5

what factors may predispose towards MI

stress
type A personality
LVH
cocaine use
raised fibrinogen

6

in which patients might a silent MI occur

diabetic/elderly patients

7

how might a silent MI present

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

8

what must be present to diagnose MI

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

9

what might suggest excess sympathetic tone following MI

HTN
tachycardia

10

what might suggest excess parasympathetic tone following MI

bradycardia
hypotension
nausea
belching

11

what signs might be suggestive of impaired left ventricular function

hypotension
crackles in the lung
3rd heart sound
murmurs

12

which ECG change is an indication for reperfusion therapy

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

13

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

change in ST segment
Tall pointed T waves

14

what changes would you see on an ECG minutes after MI

pathological Q waves
inversion of the T waves

15

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

normal ST segments

16

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

pathological Q waves
T waves may become upright

17

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

18

which interventions are aimed at prevention of further coronary thrombosis

anticoagulants
antiplatelet treatment

19

which intervention post MI aims to stabilise coronary arteries

statins

20

which intervention post MI aims to optimise healing

ACE inhibitors

21

which interventions aim to restore coronary flow post MI

reperfusion (PCI/thrombolysis)
nitrates
CABG

22

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

streptokinase
TPA

23

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

24

what actions does thromboxane have on vasculature

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