Flashcards in Week 206 - Myocardial Infarction Deck (58)
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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
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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.
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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.
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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.
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