CVS Week 7 TLO

Question 1

Topic 1: Introduction to Myocardial Ischaemia
TLO 7.1.1: Definition of Myocardial Ischaemia

Answer 1

Myocardial ischaemia is a condition where blood flow to the myocardium is reduced, preventing the heart muscle from receiving enough oxygen to meet its metabolic demands. (Robbins & Cotran, Ch. 12)

Question 2

TLO 7.1.2: Determinants of Myocardial Oxygen Demand

Answer 2

• Heart rate
• Myocardial contractility
• Wall tension (Laplace’s law: proportional to pressure and radius, inversely to wall thickness)
• Metabolic activity of the myocardium (Rang & Dale, Ch. 20)

Question 3

TLO 7.1.3: Causes of Myocardial Ischaemia

Answer 3

• Atherosclerosis (most common)
• Coronary artery spasm (e.g., Prinzmetal’s angina)
• Thrombosis or embolism
• Coronary artery dissection
• Increased demand or decreased supply (e.g., anemia, hypotension)
  (Robbins & Cotran, Ch. 12)

Question 4

TLO 7.1.4: Types of Angina

Answer 4

• Prinzmetal’s (Variant) Angina: Caused by coronary artery spasm; occurs at rest; transient ST elevation during pain.
• Chronic Stable Angina: Predictable, triggered by exertion; relieved by rest/nitrates.
• Unstable Angina: Occurs at rest or with minimal exertion; new onset or worsening pattern; precursor to MI.
  (Cecil Essentials, Ch. 8)

Question 5

TLO 7.1.5: ECG Changes in Angina

Answer 5

• Stable Angina: ST depression, T wave inversion during episodes
• Prinzmetal’s Angina: Transient ST elevation during pain
• Unstable Angina: May be normal or show non-specific ST-T changes
  (Robbins & Cotran, Ch. 12)

Question 6

TLO 7.1.6: Management of Angina

Answer 6

• Lifestyle: smoking cessation, weight loss, exercise
• Pharmacologic: nitrates, beta-blockers, calcium channel blockers, antiplatelets
• Revascularization: PCI or CABG in selected patients
  (Rang & Dale, Ch. 20; Cecil Essentials, Ch. 8)

Question 7

Topic 2: Atherosclerosis
TLO 7.2.1: Risk Factors

Answer 7

• Modifiable: smoking, hypertension, hyperlipidemia, diabetes, obesity
• Non-modifiable: age, sex, family history
  (Robbins & Cotran, Ch. 11)

Question 8

Topic 2: Atherosclerosis
TLO 7.2.2: Pathogenesis

Answer 8

• Endothelial injury → Lipid accumulation → Monocyte recruitment → Foam cell formation → Fibrous cap → Plaque development
  (Robbins & Cotran, Ch. 11)

Question 9

TLO 7.2.3: Microscopic Features of Plaques

Answer 9

• Lipid core
• Fibrous cap (smooth muscle cells, collagen)
• Inflammatory cells
• Neovascularization
  (Robbins & Cotran, Ch. 11)

Question 10

TLO 7.2.4: Plaque Rupture vs. Erosion in MI

Answer 10

• Rupture: More common; exposes thrombogenic core, causing occlusive thrombosis
• Erosion: Occurs with less fibrous disruption; also leads to thrombosis
  (Goldman-Cecil, Ch. 41)

Question 11

TLO 7.2.5: Anti-atherosclerotic Therapy

Answer 11

• Lifestyle: diet, exercise, smoking cessation
• Drugs: statins, antihypertensives, antidiabetics
  (Robbins & Cotran, Ch. 11)

Question 12

Topic 3: Lipids in Heart Disease
TLO 7.3.1 & 7.3.2:

Answer 12

• Lipids: Triacylglycerols (energy), phospholipids (membranes), cholesterol (precursor to hormones)
• Lipoproteins: Chylomicrons, VLDL, LDL, HDL
  (Cecil, Ch. 71)

Question 13

TLO 7.3.3: Structure and Function of Lipoproteins (LDL)

Answer 13

• LDL transports cholesterol to peripheral tissues; high levels are atherogenic
  (Rang & Dale, Ch. 22)

Question 14

TLO 7.3.5: LDL and Atherosclerosis

Answer 14

• Oxidized LDL triggers endothelial damage, foam cell formation, and inflammation
  (Robbins & Cotran, Ch. 11)

Question 14

TLO 7.3.4: Apolipoproteins

Answer 14

• Structural components of lipoproteins; ligands for receptors (e.g., ApoB-100 for LDL)
  (Cecil, Ch. 71)

Question 15

TLO 7.3.7: HDL as Defense

Answer 15

• Reverse cholesterol transport
• Anti-inflammatory and antioxidant roles
  (Cecil, Ch. 71)

Question 16

TLO 7.3.6: Lipid-lowering Agents

Answer 16

• Statins: Inhibit HMG-CoA reductase
• Ezetimibe: Inhibits intestinal cholesterol absorption
• PCSK9 inhibitors: Promote LDL receptor recycling
  (Rang & Dale, Ch. 22)

Question 17

TLO 7.3.8: Triglycerides and Therapy

Answer 17

• High TGs associated with pancreatitis and CV risk
• Lowering agents: fibrates, omega-3 fatty acids, niacin
  (Braunwald, Ch. 27)

Question 18

Topic 4: Ischaemic Heart Disease (IHD)
TLO 7.4.1: Epidemiology of MI

Answer 18

• Leading cause of death worldwide
• Incidence increases with age, smoking, and metabolic syndrome
  (Goldman-Cecil, Ch. 40)

Question 19

Topic 4: Ischaemic Heart Disease (IHD)
TLO 7.4.2: Risk Factors

Answer 19

• Same as atherosclerosis: smoking, HTN, hyperlipidemia, DM
  (Goldman-Cecil, Ch. 40)

Question 20

Topic 4: Ischaemic Heart Disease (IHD)
TLO 7.4.3: Pathophysiology

Answer 20

• Plaque rupture → thrombosis → coronary occlusion → myocardial necrosis
  (Goldman-Cecil, Ch. 40)

Question 21

Topic 4: Ischaemic Heart Disease (IHD)
TLO 7.4.4: Clinical Manifestations

Question 22

ECG in NSTEMI vs STEMI

Answer 22

• NSTEMI: ST depression, T wave inversion
• STEMI: ST elevation, new LBBB, later Q waves
  (Goldman-Cecil, Ch. 40)

Question 23

Topic 5: Diagnosis of IHD
TLO 7.5.1: ECG Findings

Answer 23

• See above for STEMI/NSTEMI patterns
• Serial ECGs are crucial
  (Robbins & Cotran, Ch. 12)

Question 24

TLO 7.5.2: Cardiac Biomarkers

Answer 24

* Troponin I/T: Highly sensitive and specific, elevated within 3–12 hrs, peaks at 24–48 hrs * CK-MB: Less specific, used to detect reinfarction (Goldman-Cecil, Ch. 57)

Question 25

Topic 5: Diagnosis of IHD TLO 7.5.3: Imaging Studies

Answer 25

* Echocardiogram, cardiac MRI, coronary angiography, CT angiography (Goldman-Cecil, Ch. 57)

Question 26

TLO 7.5.4: Morphology of MI

Answer 26

* Coagulative necrosis, neutrophil infiltration, granulation tissue, fibrosis (Robbins & Cotran, Ch. 12)

Question 27

Topic 5: Diagnosis of IHD TLO 7.5.5: Investigations

Answer 27

* ECG, troponin, echo, angiography * Consider comorbidities and timing (Goldman-Cecil, Ch. 57)

Question 28

Topic 6: Management of MI TLO 7.6.1: Medical Management

Answer 28

* MONA: Morphine, Oxygen, Nitrates, Aspirin * Beta-blockers, anticoagulants, statins (Braunwald, Ch. 38)

Question 29

Topic 6: Management of MI TLO 7.6.2: Drug Mechanisms

Answer 29

* Aspirin/Clopidogrel: Inhibit platelet aggregation * Nitrates: Vasodilation, reduce preload * Beta-blockers: Decrease oxygen demand * Morphine: Pain relief, reduces sympathetic tone * Anticoagulants (heparin): Prevent thrombus propagation (Rang & Dale, Ch. 20)

Question 29

TLO 7.6.3: Interventions

Answer 29

* PCI (preferred for STEMI) * CABG in selected high-risk patients * Thrombolysis if PCI not available (Braunwald, Ch. 38)

Question 30

Topic 7: Complications and Lifestyle Modifications TLO 7.7.1: Complications of MI

Answer 30

* Arrhythmias (most common cause of early death) * Heart failure, shock * Myocardial rupture, tamponade * Mural thrombus → embolism * Ventricular aneurysm * Dressler’s syndrome (autoimmune pericarditis) (Robbins & Cotran, Ch. 12)

Question 31

Topic 7: Complications and Lifestyle Modifications TLO 7.7.2: Lifestyle Changes

Answer 31

* Smoking cessation, regular exercise, diet (low-fat, Mediterranean) * Weight loss, BP/glucose control * Adherence to medications (statins, antiplatelets) (Goldman-Cecil, Ch. 40, 57)