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Revision Cards > Week 206 - Myocardial Infarction > Flashcards

Week 206 - Myocardial Infarction Flashcards

1
Q

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

A

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

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2
Q

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

A

• Pathological Q Waves, T-waves invert.

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3
Q

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

A

• ST depression in leads facing the ischaemia.

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4
Q

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

A

• ST elevation in leads facing the affected area.

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5
Q

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

A

• 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.

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6
Q

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

A

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.

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7
Q

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

A

II, III, aVF.

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8
Q

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

A

I, aVL (Left side)

V5,V6 (Right side)

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9
Q

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

A

V3, V4

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10
Q

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

A

V1, V2

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11
Q

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

A
  • Intake or excretion from the intestine.

* Uptake and secretion from cells.

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12
Q

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

A
  • 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.
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13
Q

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

A

Chylomicrons.

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14
Q

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

A
  • ‘Good Cholesterol’

* Transport cholesterol back to the liver for excretion.

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15
Q

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

A

Frederickson.

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16
Q

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

A

Triglyceride

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17
Q

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

A

Cholesterol

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18
Q

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

A
  • 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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19
Q

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

A

Tendon xanthomata.

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

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20
Q

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

A

• 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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21
Q

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

A

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

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22
Q

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

A

Statins (high dose)

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23
Q

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

A
  • 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.
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24
Q

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

A

Intima

25
Q

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

A
  • Connective tissue cap

* Core - Extracellular lipid with surrounding macrophages.

26
Q

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

A
  • 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
Q

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

A

• 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
Q

Week 206 - Myocardial Infarction: What are foam cells?

A

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

29
Q

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?

A
  • ‘Synthetic phenotype’

* Produces growth factors, proteases, collagen and elastin.

30
Q

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

A
  • Large lipid cores.
  • Unstable cap, in which structure is disorganised.
  • High densities of macrophages.
  • Low densities of smooth muscle cells.
31
Q

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

A

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

32
Q

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

A
  • Pale, Sweaty, Anxious
  • Excess sympathetic tone / Excess parasympathetic tone.
  • Impaired LV function - hypotension, crackles, 3rd heart sound, murmurs.
33
Q

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

A

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

34
Q

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

A
  • ST-depression

* Variable T wave abnormalities

35
Q

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

A
  • PE, septicaemia, Renal failure.

* Myocarditis, trauma, hypertensive crisis.

36
Q

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

A

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

37
Q

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

A

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

38
Q

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

A

• 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
Q

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

A
  • 4a - MI associated with PCI.
  • 4b - MI associated with verified stent thrombosis.
  • 5 - MI associated with CABG.
40
Q

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

A
  • Detection of rise/fall of cardiac markers above 99th centile.
  • Symptoms of ischaemia.
  • ECG changes of new ischaemia.
  • Imaging evidence.
41
Q

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

A
  • Anti-platelet (e.g. Aspirin, Clopidogrel)
  • Anticoagulant (e.g. Heparin)
  • Anti-ischaemic therapy (Beta-blockers, GTN)
42
Q

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

A
  • Anti-platelet (E.g. Aspiring, Clopidogrel)
  • Anticoagulant (Heparin)
  • Anti-ischaemic therapy (Beta-blockers, GTN)
  • Fibrinolytic therapy
  • Immediate PCI
43
Q

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

A
  • Primary PCI

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

44
Q

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

A

Fibrinogen receptor, glycoprotein IIbIIIa receptor.

45
Q

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

A
  • Also known as the fibrinogen receptor, it is the convergence point of the platelet activation pathway.
  • Causes fibrinogen/fibrin binding.
46
Q

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

A

ADP and Thromboxane.

47
Q

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

A

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
Q

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

A

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
Q

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

A

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

50
Q

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

A

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

51
Q

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

A

Clopidogrel

52
Q

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

A

Anti-platelet therapy (Aspirin and Clopidogrel)

1 month in stable angina.

53
Q

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

A
  • 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
Q

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

A
  • 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
Q

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

A
  • Immediate primary PCI
  • Diabetics
  • ACS caused by stent thrombosis while taking clopidogrel.
56
Q

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

A
  • 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
Q

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

A
  • 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
Q

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

A
  • 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.

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