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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

Week 206 - Myocardial Infarction: Briefly describe the renin-angiotensin-aldosterone system.

• Renin is released from the kidney in response to reduced GFR / reduced Na in distal tubule. Renin catalyses Angiotensinogen into Angiotensin I.
• Angiotensin I is converted to Angiotensin II by ACE.
• Angiotensin II has a number of effects including vasoconstriction.