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AMI pathology and treatment

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AMI

Question 1 of 16

1

Match the artery to the supply of myocardium and leads of ECG
....R) Atrium, SA & AV nodes, Inferior wall of R) ventricle....Lead 1,2 & AVF
...Inferior wall of R) Ventricle, Apex of Heart....Leads 1, 2 & AVF
R) Posterior Interventricular....R) & L) ventricles, Posterior intermuscular septum....Leads (depression)
....L) ventricle anterior wall, Anteroseptal, Anteroapical....V1-4,
....Left Atrium, Left Ventricle, Anterolateral Wall...V5-V6, Lead 1, avL

Drag and drop to complete the text.

    R) Coronary Artery
    R) Anterior Artery
    R) Marginal
    L) Marginal
    L) Circumflex
    L) Interventricular
    L) Anterior Descending
    Great Cardiac Vein
    V1, V2
    V4-V6

Explanation

Question 2 of 16

1

Macrophages which are transformed into foam cells, secrete cytokines which propagate atherosclerosis?

Select one of the following:

  • True
  • False

Explanation

Question 3 of 16

1

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ST segment: The ST segment represents the time interval at the end of ( ventricular depolarisation, Ventricular contraction ) to the time of ( ventricular repolarisation, ventricular contraction ). At this time there is no difference in electrical potential, therefore there is no deflection, and this segment should be isoelectric.
Changes in the ST segment are caused by disturbances in repolarisation and may be reflected in elevation or depression of ST segment.
The ST segment is measured from the ( end, start ) of the QRS complex to the ( beginning, end ) of the T wave.

Explanation

Question 4 of 16

1

Which of these are characteristics of PR interval?

Select one or more of the following:

  • Measured from end of P wave to beginning of QRS?

  • Measured from start of P wave to beginning of QRS?

  • Represent time required for impulse to depolarise atria, traverse AV node and enter ventricular system.

  • Normally 0.08-0.12

  • Normally 0.12-0.20

Explanation

Question 5 of 16

1

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QRS complex: Normal duration/ interval ( 0.08- 0.10, 0.12-0.20 ) secs. The QRS complex reflects ( ventricular, atrial ) depolarisation (NOT ventricular contraction, which is associated with ST). Not every QRS complex contains a Q wave, R wave and S wave; it depends on the position of the lead and underlying myocardium.

Explanation

Question 6 of 16

1

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Angina is caused by decreased blood supply within the coronary arteries causing . It normally occurs during periods of strenuous activity where the heart cannot meet the O2 requirements of the myocardial tissue.
Stable angina- physical exertion, to rest and medication
Unstable angina- does not respond to rest or medication
Variant angina- Caused by spasm

Explanation

Question 7 of 16

1

Treatment of angina is normally through?

Select one or more of the following:

  • GTN- causes vasodilation of the coronary vessels via increased cGMP

  • Aspirin- irreversibly inhibits COX enzymes which reduces prostaglandins and thromboxane

  • Stenting

  • beta-blockers

Explanation

Question 8 of 16

1

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The pathology of coronary artery atherosclerosis involves ( chronic, acute ) endothelial injury, endothelial dysfunction, smooth muscle migration from ( tunica media, tunica externa ) to tunica intima, engulfment by ( macrophages, debris, lipids ), formation of foam cells, proliferation of SMC's and collagen.

Explanation

Question 9 of 16

1

Which layers will typically be first to undergo infarction?

Select one of the following:

  • pericardial

  • myocardial

  • subendocardial

Explanation

Question 10 of 16

1

List the most common pathological conditions affecting the pericardium?

Select one or more of the following:

  • Cardiac Tamponade- fluid within the pericardial sac

  • Pericarditis- inflammation of the pericardium relieved by sitting up and worsened by supine

  • Pericardial effusion which can be haemoserous, fibrinoserous, suppuratives.

  • Pericardial Cancer

Explanation

Question 11 of 16

1

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GTN is A ( prodrug, vasopressor ) which first must be denitrated to produce its active form ( nitrous oxide, nitrous oxide synthase ). Nitrous oxide released increases ( guanylyl cyclase, adenylyl cyclase ) activity this results in increased cyclic GMP dependent protein kinase that activates MLC ( phosphatase, kinase ). MLC ( dephosphorylation, phoshorylation )-- VSMC relaxation.

Explanation

Question 12 of 16

1

B- blockers competitively antagonise B-adrenergic receptors in cardiac nodal tissue and myocytes. They block NA & A from binding. B-adrenergic receptors are couped to a G-Protein, which activates adenylyl cyclase to form cAMP from ATP. Increased cAMP activates a cAMP dependent protein kinase A that phosphorylates L-type calcium channels, which causes increased calcium entry into the cell. Contraindications to b-blockers are?

Select one or more of the following:

  • Unstable angina

  • asthma

  • stroke

  • severe PVD

Explanation

Question 13 of 16

1

Aspirin irreversibly inhibits COX enzyme. Which line of cyclo-oxygenase will regenerate first?

Select one of the following:

  • Prostaglandins

  • Thromboxane

Explanation

Question 14 of 16

1

Which factors does heparin inhibit in order to prevent the coagulation cascade form forming fibrin.

Select one or more of the following:

  • Factor 2

  • Factor 3

  • Factor 7

  • Factor 10

Explanation

Question 15 of 16

1

Warfarin inhibits activation of vitamin K via inhibition of vitamin k epoxide.

Select one of the following:

  • True
  • False

Explanation

Question 16 of 16

1

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Dual therapy of and aspirin is used because the endothelial cells will eventually replenish the levels of prostaglandin and thromboxane, but can inactive platelets for a lengthy period of time until they are replenished by haemopoeisis.

Explanation