Flashcards in Week 206 - Myocardial Infarction Deck (58):
1
Week 206 - Myocardial Infarction: What ECG changes would you expect minutes after an MI?
• Elevated ST segments, Tall pointed T waves, in the leads facing the affected area.
2
Week 206 - Myocardial Infarction: What ECG changes would you expect hours after an MI?
• Pathological Q Waves, T-waves invert.
3
Week 206 - Myocardial Infarction: What effect does partial thickness ischaemia have on an ECG?
• ST depression in leads facing the ischaemia.
4
Week 206 - Myocardial Infarction: What effect does full thickness ischaemia have on an ECG?
• ST elevation in leads facing the affected area.
5
Week 206 - Myocardial Infarction: When myocardium dies after iscahemia what effect does the have on an ECG?
• The dead tissue becomes 'silent', forming a window through the heart so leads opposite the injured area begin to see pathological q waves and inverted t-waves.
6
Week 206 - Myocardial Infarction: What is the GRACE scoring system?
Using a series of parameters it is able to predict the likely hood of an individual suffering from Death or MI either in hospital or within 6 months.
7
Week 206 - Myocardial Infarction: Which ECG leads look at the inferior part of the heart?
II, III, aVF.
8
Week 206 - Myocardial Infarction: Which ECG leads look at the lateral aspects of the heart?
I, aVL (Left side)
V5,V6 (Right side)
9
Week 206 - Myocardial Infarction: Which ECG leads look at the anterior aspects of the heart?
V3, V4
10
Week 206 - Myocardial Infarction: Which ECG leads look at the septal part of the heart?
V1, V2
11
Week 206 - Myocardial Infarction: What is the blood concentration of blood lipids dependant on?
• Intake or excretion from the intestine.
• Uptake and secretion from cells.
12
Week 206 - Myocardial Infarction: What is the pathway for the poductions of LDLs?
• The liver converts unused food metabolites into very-low density lipoproteins (VLDL) and secretes them into plasma.
• In the plasma they are converted into intermediate density lipoproteins (IDLs) then into LDLs.
13
Week 206 - Myocardial Infarction: Which particles carry fats from the intestine to the liver?
Chylomicrons.
14
Week 206 - Myocardial Infarction: What is the role of HDLs?
• 'Good Cholesterol'
• Transport cholesterol back to the liver for excretion.
15
Week 206 - Myocardial Infarction: What is the classification of primary lipid disorders called?
Frederickson.
16
Week 206 - Myocardial Infarction: An increase in chylomicrons or VLDLs, would lead to elevated serum levels of what particle?
Triglyceride
17
Week 206 - Myocardial Infarction: An increase in LDLs or IDLs, would lead to elevated levels of what particle?
Cholesterol
18
Week 206 - Myocardial Infarction: What is familial hypercholesterolaemia? What is the pathology behind it?
• Autosomal dominant disorder, defined as a type IIa hyperlipidaemia.
• It occurs due to a mutation with the LDL receptors which prevents efficient uptake of LDLs, there are various types of mutation.
19
Week 206 - Myocardial Infarction: Which clinical sign is virtually diagnostic for familial hypercholesterolaemia?
Tendon xanthomata.
(Corneal arcs and xanthelasma are also common findings but are less specific.)
20
Week 206 - Myocardial Infarction: What is the diagnostic criteria for definite familial hypercholesterolaemia?
• Total cholesterol above 7.5mmol/L or LDL cholesterol above 4.9mmol/L
AND
• Tendon xanthomata in patient or 1/2nd degree relative.
21
Week 206 - Myocardial Infarction: How should familial hypercholesterolaemia be treated relative to sporadic hypercholesterolaemia?
More aggressively, since there is a much greater risk of coronary heart disease.
22
Week 206 - Myocardial Infarction: What is the medical treatment of familial hypercholesterolaemia?
Statins (high dose)
23
Week 206 - Myocardial Infarction: What is the mechanism of action of statins?
• Inhibition of HMG CoA in the liver, this is a rate limiting step of endogenous cholesterol production.
• Reduction in plasma cholesterol and LDL.
• Increase in LDL receptors
• Small decrease in plasma triglyceride and VLDLs.
• Modest increase in HDL.
24
Week 206 - Myocardial Infarction: What layer of the arterial wall do atheromas form?
Intima
25
Week 206 - Myocardial Infarction: What are the two basic components of an atheromatous plaque?
• Connective tissue cap
• Core - Extracellular lipid with surrounding macrophages.
26
Week 206 - Myocardial Infarction: What is the basic mechanism behind the formation of an atheromatous plaque?
• Endothelial dysfunction leads to platelet and WBC adhesion.
• Passage of inflammatory cells into the subepithileum space.
• Accumulation of lipid-rich cells, smooth muscle and new blood vessel growth.
27
Week 206 - Myocardial Infarction: What is the potential anti-atherogenic role played by NO?
• NO is produced by endothelial cells.
- Inhibits smooth muscle proliferation.
- Inhibits monocyte adhesion and migration through endothelium.
- Anti-platelet effects.
- Promotion of macrophage apoptosis.
- Inhibition of lipid oxidation.
28
Week 206 - Myocardial Infarction: What are foam cells?
These are macrophages that have ingested modified lipids that occupy the sub-epithelial space.
29
Week 206 - Myocardial Infarction: When vascular smooth muscles are in the intima that take on a different phenotype from the contractile phenotype they normally express?
• 'Synthetic phenotype'
• Produces growth factors, proteases, collagen and elastin.
30
Week 206 - Myocardial Infarction: What are the characteristics of an unstable plaque?
• Large lipid cores.
• Unstable cap, in which structure is disorganised.
• High densities of macrophages.
• Low densities of smooth muscle cells.
31
Week 206 - Myocardial Infarction: In clinical practice what is required to confirm an acute myocardial infarction?
Evidence of cardiac myocyte necrosis (i.e. Troponin T)
32
Week 206 - Myocardial Infarction: What are the signs of acute myocardial infarction?
• Pale, Sweaty, Anxious
• Excess sympathetic tone / Excess parasympathetic tone.
• Impaired LV function - hypotension, crackles, 3rd heart sound, murmurs.
33
Week 206 - Myocardial Infarction: Which type of ECG change is an indication for reperfusion therapy?
ST-Elevation, since this is generally an indicator of complete coronary occlusion.
34
Week 206 - Myocardial Infarction: Incomplete occlusion of a coronary vessel, leading to an MI, is associated with which ECG changes?
• ST-depression
• Variable T wave abnormalities
35
Week 206 - Myocardial Infarction: Troponin is used for confirmation of a AMI, but it can be raised due to other causes. Give examples.
• PE, septicaemia, Renal failure.
• Myocarditis, trauma, hypertensive crisis.
36
Week 206 - Myocardial Infarction: What is a Type 1 acute myocardial infarction?
An MI related to ischaemia due to a primary coronary event, such as plaque erosion/rupture, fissuring or dissection.
37
Week 206 - Myocardial Infarction: What is a Type 2 acute myocardial infarction?
An MI secondary to ischaemia due to an imbalance of 02 supply and demand.
- E.g. coronary embolism, anaemia, hypotension, arrhythmia's, hypertension.
38
Week 206 - Myocardial Infarction: What is a type 3 acute myocardial infarction?
• Sudden cardiac death with ischaemia, accompanied by new st-elevation or Lbbb or pathological or angiographic evidence of fresh coronary thrombus.
- In the absence of reliable biochemical bindings.
39
Week 206 - Myocardial Infarction: Type 4a,4b and 5 acute myocardial infarctions are due to iatrogenic causes, what are they?
• 4a - MI associated with PCI.
• 4b - MI associated with verified stent thrombosis.
• 5 - MI associated with CABG.
40
Week 206 - Myocardial Infarction: What are the four criteria for diagnosing Types 1 and 2 myocardial infarction?
• Detection of rise/fall of cardiac markers above 99th centile.
• Symptoms of ischaemia.
• ECG changes of new ischaemia.
• Imaging evidence.
41
Week 206 - Myocardial Infarction: What is the medical treatment for a nSTEMI?
• Anti-platelet (e.g. Aspirin, Clopidogrel)
• Anticoagulant (e.g. Heparin)
• Anti-ischaemic therapy (Beta-blockers, GTN)
42
Week 206 - Myocardial Infarction: What is the medical treatment for a STEMI?
• Anti-platelet (E.g. Aspiring, Clopidogrel)
• Anticoagulant (Heparin)
• Anti-ischaemic therapy (Beta-blockers, GTN)
• Fibrinolytic therapy
• Immediate PCI
43
Week 206 - Myocardial Infarction: What are the two forms of reperfusion therapy?
• Primary PCI
• IV Thombolytic drugs are used when PCI is not available.
44
Week 206 - Myocardial Infarction: What is the name of the receptor that the pathways of platelet activation converge on?
Fibrinogen receptor, glycoprotein IIbIIIa receptor.
45
Week 206 - Myocardial Infarction: What is the effect of activation of the glycoprotein IIbIIa receptor?
• Also known as the fibrinogen receptor, it is the convergence point of the platelet activation pathway.
• Causes fibrinogen/fibrin binding.
46
Week 206 - Myocardial Infarction: Which two component of the platelet activation cascade causes the recruitment of more platelet activation?
ADP and Thromboxane.
47
Week 206 - Myocardial Infarction: What is the role of COX-1?
This receptor is expressed in most cell types and has a role in tissue homeostasis (e.g. synthesis of mucosal prostaglandins in intestine lining.)
48
Week 206 - Myocardial Infarction: What is the role of COX-2 receptors?
These are induced by the activation of inflammatory cells, in response to IL-1 and TNF-alpha, and is involved in the generation of prostaglandins.
49
Week 206 - Myocardial Infarction: What is the mechanism behind the anti-platelet activity of aspirin?
Aspirin causes the permanent acetylation of COX in platelets, preventing the synthesis of thomboxane and prostacyclin.
50
Week 206 - Myocardial Infarction: What is the mechanism behind the anti-platelet activity of clopidogrel?
Inhibits the ADP receptor on platelets, which inhibits ADP-dependant platelet activation.
51
Week 206 - Myocardial Infarction: The loss of the CYP2C19 allele is associated with increased risk of atherothrombotic complications following treatment with which medication?
Clopidogrel
52
Week 206 - Myocardial Infarction: Which therapy is required for patients who have had a bare metal stent? How long should the regime last?
Anti-platelet therapy (Aspirin and Clopidogrel)
1 month in stable angina.
53
Week 206 - Myocardial Infarction: Dual anti-platelet therapy (Clopidogrel and Aspirin) is indicated in which three groups?
• 1 month and bare metal stent implantation in stable angina.
• 6-12 months after drug-eluting stent implantation.
• 1 year after acute coronary syndrome (irrespective of revascularization).
• Some population groups may benefit from DAPT beyond 1 year.
54
Week 206 - Myocardial Infarction: What is prasugrel indicated for? What is its mechanism of action?
• Anti-platelet therapy.
• Acts in a similar way to clopidogrel but inhibits the ADP P2Y12 receptor more potently.
• Has a rapid activation and more prolonged platelet inhibition.
55
Week 206 - Myocardial Infarction: NICE recommends the use of prasugrel in which three circumstances?
• Immediate primary PCI
• Diabetics
• ACS caused by stent thrombosis while taking clopidogrel.
56
Week 206 - Myocardial Infarction: What is the function of Ticagrelor? What is its mechanism? Why is it better than Clopidogrel and Prasugrel?
• Anti-platelet therapy.
• Reversibly inhibits the ADP P2Y12 receptor, inhibiting ADP-dependant platelet activation.
• When used in combination with aspirin, significantly reduced the primary outcome of death, non-fatal MI and non-fatal stroke when compared with clopidogrel.
57
Week 206 - Myocardial Infarction: What is the role of glycoprotein IIB-IIIa antogonists in anti-platelet therapy? Give examples.
• Receptors are located on megakaryocytes and platelets.
• The GP IIa-IIIb receptors mediate platelet activation through the binding of fibrinogen and von Willebrand factor.
• Eptifibatide and tirofiban/lamifiban and competitive inhibitors of the receptor.
58