Week 206 - Myocardial Infarction

Question 1

Week 206 - Myocardial Infarction: What ECG changes would you expect minutes after an MI?

Answer 1

• Elevated ST segments, Tall pointed T waves, in the leads facing the affected area.

Question 2

Week 206 - Myocardial Infarction: What ECG changes would you expect hours after an MI?

Answer 2

• Pathological Q Waves, T-waves invert.

Question 3

Week 206 - Myocardial Infarction: What effect does partial thickness ischaemia have on an ECG?

Answer 3

• ST depression in leads facing the ischaemia.

Question 4

Week 206 - Myocardial Infarction: What effect does full thickness ischaemia have on an ECG?

Answer 4

• ST elevation in leads facing the affected area.

Question 5

Week 206 - Myocardial Infarction: When myocardium dies after iscahemia what effect does the have on an ECG?

Answer 5

• 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.

Question 6

Week 206 - Myocardial Infarction: What is the GRACE scoring system?

Answer 6

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.

Question 7

Week 206 - Myocardial Infarction: Which ECG leads look at the inferior part of the heart?

Answer 7

II, III, aVF.

Question 8

Week 206 - Myocardial Infarction: Which ECG leads look at the lateral aspects of the heart?

Answer 8

I, aVL (Left side)

V5,V6 (Right side)

Question 9

Week 206 - Myocardial Infarction: Which ECG leads look at the anterior aspects of the heart?

Answer 9

V3, V4

Question 10

Week 206 - Myocardial Infarction: Which ECG leads look at the septal part of the heart?

Answer 10

V1, V2

Question 11

Week 206 - Myocardial Infarction: What is the blood concentration of blood lipids dependant on?

Answer 11

• Intake or excretion from the intestine.

* Uptake and secretion from cells.

Question 12

Week 206 - Myocardial Infarction: What is the pathway for the poductions of LDLs?

Answer 12

• 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.

Question 13

Week 206 - Myocardial Infarction: Which particles carry fats from the intestine to the liver?

Answer 13

Chylomicrons.

Question 14

Week 206 - Myocardial Infarction: What is the role of HDLs?

Answer 14

• ‘Good Cholesterol’

* Transport cholesterol back to the liver for excretion.

Question 15

Week 206 - Myocardial Infarction: What is the classification of primary lipid disorders called?

Answer 15

Frederickson.

Question 16

Week 206 - Myocardial Infarction: An increase in chylomicrons or VLDLs, would lead to elevated serum levels of what particle?

Answer 16

Triglyceride

Question 17

Week 206 - Myocardial Infarction: An increase in LDLs or IDLs, would lead to elevated levels of what particle?

Answer 17

Cholesterol

Question 18

Week 206 - Myocardial Infarction: What is familial hypercholesterolaemia? What is the pathology behind it?

Answer 18

• 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.

Question 19

Week 206 - Myocardial Infarction: Which clinical sign is virtually diagnostic for familial hypercholesterolaemia?

Answer 19

Tendon xanthomata.

Corneal arcs and xanthelasma are also common findings but are less specific.

Question 20

Week 206 - Myocardial Infarction: What is the diagnostic criteria for definite familial hypercholesterolaemia?

Answer 20

• Total cholesterol above 7.5mmol/L or LDL cholesterol above 4.9mmol/L
AND
• Tendon xanthomata in patient or 1/2nd degree relative.

Question 21

Week 206 - Myocardial Infarction: How should familial hypercholesterolaemia be treated relative to sporadic hypercholesterolaemia?

Answer 21

More aggressively, since there is a much greater risk of coronary heart disease.

Question 22

Week 206 - Myocardial Infarction: What is the medical treatment of familial hypercholesterolaemia?

Answer 22

Statins (high dose)

Question 23

Week 206 - Myocardial Infarction: What is the mechanism of action of statins?

Answer 23

• 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.

Question 24

Week 206 - Myocardial Infarction: What layer of the arterial wall do atheromas form?

Answer 24

Intima

Question 25

Week 206 - Myocardial Infarction: What are the two basic components of an atheromatous plaque?

Answer 25

* Connective tissue cap | * Core - Extracellular lipid with surrounding macrophages.

Question 26

Week 206 - Myocardial Infarction: What is the basic mechanism behind the formation of an atheromatous plaque?

Answer 26

* 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.

Question 27

Week 206 - Myocardial Infarction: What is the potential anti-atherogenic role played by NO?

Answer 27

• 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.

Question 28

Week 206 - Myocardial Infarction: What are foam cells?

Answer 28

These are macrophages that have ingested modified lipids that occupy the sub-epithelial space.

Question 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?

Answer 29

* 'Synthetic phenotype' | * Produces growth factors, proteases, collagen and elastin.

Question 30

Week 206 - Myocardial Infarction: What are the characteristics of an unstable plaque?

Answer 30

* Large lipid cores. * Unstable cap, in which structure is disorganised. * High densities of macrophages. * Low densities of smooth muscle cells.

Question 31

Week 206 - Myocardial Infarction: In clinical practice what is required to confirm an acute myocardial infarction?

Answer 31

Evidence of cardiac myocyte necrosis (i.e. Troponin T)

Question 32

Week 206 - Myocardial Infarction: What are the signs of acute myocardial infarction?

Answer 32

* Pale, Sweaty, Anxious * Excess sympathetic tone / Excess parasympathetic tone. * Impaired LV function - hypotension, crackles, 3rd heart sound, murmurs.

Question 33

Week 206 - Myocardial Infarction: Which type of ECG change is an indication for reperfusion therapy?

Answer 33

ST-Elevation, since this is generally an indicator of complete coronary occlusion.

Question 34

Week 206 - Myocardial Infarction: Incomplete occlusion of a coronary vessel, leading to an MI, is associated with which ECG changes?

Answer 34

* ST-depression | * Variable T wave abnormalities

Question 35

Week 206 - Myocardial Infarction: Troponin is used for confirmation of a AMI, but it can be raised due to other causes. Give examples.

Answer 35

* PE, septicaemia, Renal failure. | * Myocarditis, trauma, hypertensive crisis.

Question 36

Week 206 - Myocardial Infarction: What is a Type 1 acute myocardial infarction?

Answer 36

An MI related to ischaemia due to a primary coronary event, such as plaque erosion/rupture, fissuring or dissection.

Question 37

Week 206 - Myocardial Infarction: What is a Type 2 acute myocardial infarction?

Answer 37

An MI secondary to ischaemia due to an imbalance of 02 supply and demand. - E.g. coronary embolism, anaemia, hypotension, arrhythmia's, hypertension.

Question 38

Week 206 - Myocardial Infarction: What is a type 3 acute myocardial infarction?

Answer 38

• 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.

Question 39

Week 206 - Myocardial Infarction: Type 4a,4b and 5 acute myocardial infarctions are due to iatrogenic causes, what are they?

Answer 39

* 4a - MI associated with PCI. * 4b - MI associated with verified stent thrombosis. * 5 - MI associated with CABG.

Question 40

Week 206 - Myocardial Infarction: What are the four criteria for diagnosing Types 1 and 2 myocardial infarction?

Answer 40

* Detection of rise/fall of cardiac markers above 99th centile. * Symptoms of ischaemia. * ECG changes of new ischaemia. * Imaging evidence.

Question 41

Week 206 - Myocardial Infarction: What is the medical treatment for a nSTEMI?

Answer 41

* Anti-platelet (e.g. Aspirin, Clopidogrel) * Anticoagulant (e.g. Heparin) * Anti-ischaemic therapy (Beta-blockers, GTN)

Question 42

Week 206 - Myocardial Infarction: What is the medical treatment for a STEMI?

Answer 42

* Anti-platelet (E.g. Aspiring, Clopidogrel) * Anticoagulant (Heparin) * Anti-ischaemic therapy (Beta-blockers, GTN) * Fibrinolytic therapy * Immediate PCI

Question 43

Week 206 - Myocardial Infarction: What are the two forms of reperfusion therapy?

Answer 43

* Primary PCI | * IV Thombolytic drugs are used when PCI is not available.

Question 44

Week 206 - Myocardial Infarction: What is the name of the receptor that the pathways of platelet activation converge on?

Answer 44

Fibrinogen receptor, glycoprotein IIbIIIa receptor.

Question 45

Week 206 - Myocardial Infarction: What is the effect of activation of the glycoprotein IIbIIa receptor?

Answer 45

* Also known as the fibrinogen receptor, it is the convergence point of the platelet activation pathway. * Causes fibrinogen/fibrin binding.

Question 46

Week 206 - Myocardial Infarction: Which two component of the platelet activation cascade causes the recruitment of more platelet activation?

Answer 46

ADP and Thromboxane.

Question 47

Week 206 - Myocardial Infarction: What is the role of COX-1?

Answer 47

This receptor is expressed in most cell types and has a role in tissue homeostasis (e.g. synthesis of mucosal prostaglandins in intestine lining.)

Question 48

Week 206 - Myocardial Infarction: What is the role of COX-2 receptors?

Answer 48

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.

Question 49

Week 206 - Myocardial Infarction: What is the mechanism behind the anti-platelet activity of aspirin?

Answer 49

Aspirin causes the permanent acetylation of COX in platelets, preventing the synthesis of thomboxane and prostacyclin.

Question 50

Week 206 - Myocardial Infarction: What is the mechanism behind the anti-platelet activity of clopidogrel?

Answer 50

Inhibits the ADP receptor on platelets, which inhibits ADP-dependant platelet activation.

Question 51

Week 206 - Myocardial Infarction: The loss of the CYP2C19 allele is associated with increased risk of atherothrombotic complications following treatment with which medication?

Answer 51

Clopidogrel

Question 52

Week 206 - Myocardial Infarction: Which therapy is required for patients who have had a bare metal stent? How long should the regime last?

Answer 52

Anti-platelet therapy (Aspirin and Clopidogrel) | 1 month in stable angina.

Question 53

Week 206 - Myocardial Infarction: Dual anti-platelet therapy (Clopidogrel and Aspirin) is indicated in which three groups?

Answer 53

* 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.

Question 54

Week 206 - Myocardial Infarction: What is prasugrel indicated for? What is its mechanism of action?

Answer 54

* 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.

Question 55

Week 206 - Myocardial Infarction: NICE recommends the use of prasugrel in which three circumstances?

Answer 55

* Immediate primary PCI * Diabetics * ACS caused by stent thrombosis while taking clopidogrel.

Question 56

Week 206 - Myocardial Infarction: What is the function of Ticagrelor? What is its mechanism? Why is it better than Clopidogrel and Prasugrel?

Answer 56

* 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.

Question 57

Week 206 - Myocardial Infarction: What is the role of glycoprotein IIB-IIIa antogonists in anti-platelet therapy? Give examples.

Answer 57

* 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.

Question 58

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

Answer 58

* 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.