Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Cardiology Teaching Series Session 3 - IschaemiaThe Case Mr P is a 56-year-old man, who is brought into hospital by ambulance. He describes being out on a walk when he noticed a crushing chest pain, as well as pain in his left arm. He remarks feeling quite sweaty at the time as well. Mr P smokes daily, and sees his GP regularly to manage his high blood pressure. What is the likely diagnosis here?Starting from the basics + Tunica adventitia – tough structural layer composed of connective tissue + Tunica media – maintains tone and composed of smooth muscle and elastic fibres + Tunica intima – Endothelial layer, acts as a protective barrier https://training.seer.cancer.gov/anatomy/cardiovascular/blood/classification.htmlPathophysiology of atherosclerosis DOI:10.1042/BSR20212355Back to The Case Mr P is a 56-year-old man, who is brought into hospital by ambulance. He describes being out on a walk when he noticed a crushing chest pain, as well as pain in his left arm. He remarks feeling quite sweaty at the time as well. Mr P smokes daily, and sees his GP regularly to manage his high blood pressure and type 2 diabetes mellitus. What risk factors does Mr P have for heart disease?Risk factors for endothelial activation + Diabetes - Advanced glycation end products + Oxidative stress – smoking + Obesity - inflammatory cytokines + Hypertension + Hypercholesterolaemia + Etc.So why the sudden heart attack? + Unstable plaque → rupture + Exposure of the thrombogenic lipid core + Platelet activation → release thromboxane A2 (TXA2) and ADP + ADP binds to P2Y12 receptors → cross-linking → platelet plug + Conversion of fibrinogen → fibrin,forming a mesh over the plug + This occludes the artery → hypoxia to cardiomyocytes (ischaemia) → death (infarction) + What results might you see in a blood test?Back to The Case Mr P’s ECG is shown below:Localising MIsPharmacology + Unstable plaque → rupture + Exposure of the thrombogenic lipid core ASPIRIN + Platelet activation → release thromboxane A2 (TXA2) and ADP + ADP binds to P2Y12 receptors → cross-linking → platelet plug CLOPIDOGREL + Conversion of fibrinogen → fibrin,forming a mesh over the plug ALTEPLASE + This occludes the artery → hypoxia to cardiomyocytes (ischaemia) → death (infarction)Intervention + Early reperfusion is key: Thrombolysis – Alteplase Percutaneous Coronary Intervention + Secondary prevention: Statin – HMG-CoA reductase inhibitor Aspirin and Clopidogrel ACEi Beta blockerSBA 1 + Which of the following lab findings is most specific for MI? A) Raised CK-MB B) Raised troponin C) Raised myoglobin D) Raised D-Dimer E) Raised ESRSBA 1 + Which of the following lab findings is most specific for MI? A) Raised CK-MB B) Raised troponin C) Raised myoglobin D) Raised D-Dimer E) Raised ESRSBA 2 + Which of the following normally plays the most important role in regulating coronary vasodilation? A) Sympathetic activation B) Endothelin-1 release C) Myogenic reflex D) Nitric oxide release E) Inhibition of the Na-K ATPase pumpSBA 2 + Which of the following normally plays the most important role in regulating coronary vasodilation? A) Sympathetic activation B) Endothelin-1 release C) Myogenic reflex D) Nitric oxide release E) Inhibition of the Na-K ATPase pumpSBA 3 + Why are patients started on ACE inhibitors following a myocardial infarction? A) Increases blood pressure and coronary perfusion B) Reduces platelet aggregation and clot formation C) Prevents adverse ventricular remodelling D) Blocks sympathetic overactivity E) Reduces LDLlevels in the bloodSBA 3 + Why are patients started on ACE inhibitors following a myocardial infarction? A) Increases blood pressure and coronary perfusion B) Reduces platelet aggregation and clot formation C) Prevents adverse ventricular remodelling D) Blocks sympathetic overactivity E) Reduces LDLlevels in the bloodSBA 4 + Why does ST elevation occur in myocardial infarction? A) Increased ventricular depolarisation B) Failure of repolarisation due to ischaemic injury C) Increased sympathetic activity D) Decreased calcium influx into myocytes E) Increased cardiac outputSBA 4 + Why does ST elevation occur in myocardial infarction? A) Increased ventricular depolarisation B) Failure of repolarisation due to ischaemic injury C) Increased sympathetic activity D) Decreased calcium influx into myocytes E) Increased cardiac output