In the ambulance, a paramedic initiates oxygen therapy and administers morphine to SA (patient) for pain relief, as well as a low dose of aspirin. After SA arrives at the hospital, investigations confirm that he is suffering from an acute myocardial infarction. SA receives an intravenous infusion of the fibrinolytic agent streptokinase, as well as the anti-dysrhythmic amiodarone for ventricular tachycardia. Cardiac enzyme level test indicate that the damage to the myocardium is extensive.
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After prolonged hospital stay, SA is discharged. He goes on to develop chronic heart failure, which is managed with an ACE inhibitor, a diuretic and a peripheral vasodilator.
What is the rationale for the use of fibrinolytic drugs in acute myocardial infarction (AMI)? Are there any constraints regarding the timing of administration of these drugs in AMI?(4 marks)
Compare and contrast the mechanisms of action of the fibrinolytic drugs streptokinase and aspirin.(3 marks)
What adverse reactions should be monitored during and after fibrinolytic drug therapy?(3 marks)
Describe the mechanism of action of the antidysrhythmic agent amiodarone.
To which Vaughan Williams antidysrhythmic drug class does it belong?(4marks)
Compare and contrast the actions of heparin and streptokinase(3 marks)
Outline the pathophysiology of heart failure(4 marks)
Describe the mechanism of action of ACE inhibitors and indicate why they are a drug of choice in heart failure(4 marks)
Pulmonary oedema is caused by alterations in fluid distribution between pulmonary blood vessels and the lung tissue. Using fluid dynamics and changes in fluid pressure, explain the link between heart failure and pulmonary oedema. (3 marks)
Compare and contrast the actions of the loop and thiazide diuretics(4 marks)
At what stages do the diuretics and the peripheral vasodilators interrupt the pathophysiology of heart failure? (3 marks)
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