CVS Week 7

Question 1

🔹 Topic 1: Introduction to Myocardial Ischaemia
Q1: What is myocardial ischaemia?

Answer 1

A1: A condition where the heart muscle receives insufficient oxygen due to reduced coronary blood flow.

Question 2

Q2: What are the determinants of myocardial oxygen demand?

Answer 2

A2: Heart rate, contractility, wall tension, and myocardial metabolic activity.

Question 3

Q4: What characterizes Prinzmetal’s angina?

Answer 3

A4: Occurs at rest due to coronary artery spasm with transient ST elevation.

Question 4

Q3: What are the main causes of myocardial ischaemia?

Answer 4

A3: Atherosclerosis, coronary artery spasm, thrombosis, embolism, anemia, and hypotension.

Question 5

Q6: What ECG changes are seen in angina?

Answer 5

A6: ST depression, T wave inversion (stable/unstable); transient ST elevation (Prinzmetal’s).

Question 6

Q5: How is stable angina different from unstable angina?

Answer 6

A5: Stable angina is predictable and exertional; unstable angina is unpredictable and occurs at rest or with minimal exertion.

Question 7

Q7: How is angina managed?

Answer 7

A7: Lifestyle changes, nitrates, beta-blockers, calcium channel blockers, antiplatelets, and possible PCI/CABG.

Question 8

Q9: Describe the pathogenesis of atherosclerosis.

Answer 8

A9: Endothelial injury → lipid accumulation → inflammation → foam cells → fibrous plaque.

Question 8

🔹 Topic 2: Atherosclerosis
Q8: List modifiable and non-modifiable risk factors for atherosclerosis.

Answer 8

A8: Modifiable: smoking, hypertension, hyperlipidemia, diabetes. Non-modifiable: age, sex, genetics.

Question 9

Q12: What therapies help prevent atherosclerosis?

Answer 9

A12: Lifestyle modification and statins, antihypertensives, antidiabetics.

Question 9

Q10: What are the microscopic features of an atherosclerotic plaque?

Answer 9

A10: Lipid core, fibrous cap, inflammato cells, neovascularization.

Question 10

Q11: How does plaque rupture differ from erosion in causing MI?

Answer 10

A11: Rupture exposes core, causing thrombosis; erosion exposes endothelium, also triggering clotting.

Question 11

🔹 Topic 3: Lipids and Heart Disease
Q13: What are major lipid types?

Answer 11

A13: Triacylglycerols, phospholipids, cholesterol (esters).

Question 12

Q14: What are the main lipoproteins?

Answer 12

A14: Chylomicrons, VLDL, LDL, HDL.

Question 13

Q17: How is LDL linked to atherosclerosis?

Answer 13

A17: Oxidized LDL promotes endothelial injury, inflammation, and plaque formation.

Question 13

Q16: What are apolipoproteins?

Answer 13

A16: Protein components of lipoproteins that help in lipid transport and receptor binding.

Question 14

Q15: What is the function of LDL?

Answer 14

A15: Transports cholesterol to tissues; contributes to atherosclerosis.

Question 15

Q18: Name three types of lipid-lowering agents and their mechanisms.

Answer 15

A18: Statins (HMG-CoA reductase inhibitors), ezetimibe (cholesterol absorption inhibitor), PCSK9 inhibitors (increase LDL receptor recycling).

Question 15

🔹 Topic 4: Ischaemic Heart Disease (IHD)
Q21: What is the global significance of MI?

Answer 15

A21: It is one of the leading causes of death worldwide.

Question 15

Q20: How do high triglycerides affect heart disease?

Answer 15

A20: Associated with increased cardiovascular risk; treated with fibrates, niacin, omega-3s.

Question 16

Q19: What role does HDL play in heart protection?

Answer 16

A19: Removes cholesterol from tissues and ha anti-inflammatory effects.

Question 17

Q22: List the risk factors for MI.

Answer 17

A22: Smoking, diabetes, hypertension, hyperlipidemia, obesity.

Question 18

Q23:* What is the pathophysiology of MI?

Answer 18

A23: Plaque rupture → thrombosis → occlusion → myocardial necrosis.

Question 19

Q27: What cardiac biomarkers are used in MI?

Answer 19

A27: Troponin I/T (most specific), CK-MB (for reinfarction).

Question 19

Q24: What are typical symptoms of MI?

Answer 19

A24: Chest pain, dyspnea, diaphoresis, nausea, fatigue.

Question 19

Q28: What imaging modalities are used in MI?

Answer 19

A28: Echocardiogram, coronary angiography, cardiac MRI, CT.

Question 20

Q25: What are the ECG features of NSTEMI and STEMI?

Answer 20

A25: NSTEMI: ST depression/T inversion. STEMI: ST elevation, new LBBB, Q waves.

Question 20

Q26: How is MI diagnosed on ECG?

Answer 20

A26: ST elevation (STEMI), ST depression/T wave inversion (NSTEMI), serial changes.

Question 21

Q29: Describe the histology of a myocardial infarct.

Answer 21

A29: Coagulative necrosis, neutrophil infiltration, granulation tissue, fibrosis.

Question 22

Q30: What are key investigations in IHD?

Answer 22

A30: ECG, troponins, echocardiography, angiography.

Question 23

Q33: What is the mechanism of nitrates?

Answer 23

A33: Vasodilation, reduces preload and myocardial oxygen demand.

Question 23

Q32: What is the mechanism of aspirin in MI?

Answer 23

A32: Inhibits thromboxane A2 to reduce platelet aggregation.

Question 24

🔹 Topic 6: Management of MI Q31: What is the initial medical management of MI?

Answer 24

A31: MONA: Morphine, Oxygen, Nitrates, Aspirin + beta-blockers, anticoagulants, statins.

Question 25

🔹 Topic 7: Complications and Lifestyle Q36: List complications of MI.

Answer 25

A36: Arrhythmias, heart failure, myocardial rupture, mural thrombus, aneurysm, Dressler’s syndrome

Question 25

Q34: How do beta-blockers help in MI?

Answer 25

A34: Reduce heart rate and contractility, lowering oxygen demand.

Question 26

Q35: What are interventional treatments for MI?

Answer 26

A35: PCI (primary treatment for STEMI), thrombolysis, CABG.

Question 27

Q37: What lifestyle changes are recommended post-MI?

Answer 27

A37: Smoking cessation, regular exercise, heart-healthy diet, weight loss, adherence to medications.