IHD patho final

Question 1

What is ischaemic heart disease (IHD)?

Answer 1

Reduced coronary arterial blood flow due to narrowing of the coronary artery lumen resulting in insufficient oxygen delivery to the myocardium.

Question 2

Define angina.

Answer 2

Chest pain caused by myocardial ischaemia without myocardial necrosis.

Question 3

Define myocardial infarction (MI).

Answer 3

Irreversible death of heart muscle due to prolonged lack of blood supply.

Question 4

What is Acute Coronary Syndrome (ACS)?

Answer 4

A group of conditions caused by sudden reduction or blockage of coronary blood flow.

Question 5

What conditions make up ACS?

Answer 5

Unstable angina, NSTEMI, STEMI.

Question 6

Severity progression in coronary disease?

Answer 6

Stable angina → Unstable angina → NSTEMI → STEMI.

Question 7

Why does myocardial ischaemia cause chest pain?

Answer 7

Low oxygen → anaerobic metabolism → lactate accumulation → acidosis → stimulation of cardiac sensory nerves.

Question 8

List the steps in the development of atherosclerosis.

Answer 8

• Endothelial injury; LDL entry into intima;
• LDL oxidation;
• Monocyte adhesion and migration; Macrophage formation;
• Foam cell formation; Fatty streak formation; Smooth muscle cell migration and proliferation;
• Extracellular matrix deposition (collagen, calcium);
• Fibrous cap formation;
• Plaque growth with necrotic lipid core; Plaque rupture;
• Platelet activation and thrombosis.

Question 9

Causes of endothelial damage?

Answer 9

• Smoking- toxin
• hypertension - shear stress
• Diabetes - hyperglycaemia
• high LDL cholesterol.

Question 10

What happens after endothelial injury?

Answer 10

Increased permeability to LDL and increased leukocyte adhesion.

Question 11

What adhesion molecules are expressed by damaged endothelium?

Answer 11

VCAM-1 and ICAM-1.

Question 12

Function of VCAM-1 and ICAM-1?

Answer 12

Allow leukocytes (especially monocytes) to stick to the vessel wall and migrate inside.

Question 13

What receptors detect damage and activate inflammation?

Answer 13

Toll-like receptors (TLRs).

Question 14

What is TNF-α and its role?

Answer 14

A pro-inflammatory cytokine that activates endothelial cells and recruits immune cells.

Question 15

What is MCP-1?

Answer 15

Monocyte chemoattractant protein-1.

Question 16

Function of MCP-1?

Answer 16

Attracts monocytes from blood into the arterial intima.

Question 17

What is IL-1?

Answer 17

A pro-inflammatory cytokine that amplifies vascular inflammation and promotes smooth muscle activation.

Question 18

What happens to monocytes after entering the intima?

Answer 18

They differentiate into macrophages.

Question 19

Role of macrophages in atherosclerosis?

Answer 19

Phagocytose oxidised LDL and release inflammatory mediators.

Question 20

What happens to LDL in the vessel wall?

Answer 20

It becomes oxidised LDL (oxLDL).

Question 21

Why is oxidised LDL dangerous?

Answer 21

It is toxic, pro-inflammatory, and strongly taken up by macrophages.

Question 22

What are foam cells?

Answer 22

Lipid-laden macrophages filled with oxidised LDL.

Question 23

What is a fatty streak?

Answer 23

Early atherosclerotic lesion composed of foam cells within the intima.

Question 24

Which cells release PDGF?

Answer 24

Macrophages and platelets.

Question 25

Function of PDGF?

Answer 25

Stimulates smooth muscle cell migration and proliferation into the intima.

Question 26

What does TGF-β do?

Answer 26

Promotes collagen production and fibrous cap formation.

Question 27

Role of IL-1 in plaque growth?

Answer 27

Enhances smooth muscle proliferation and inflammation.

Question 28

What do smooth muscle cells produce in plaques?

Answer 28

Collagen, extracellular matrix, and calcium.

Question 29

What is an atheromatous plaque composed of?

Answer 29

Fibrous cap, lipid necrotic core, and inflammatory cells.

Question 30

Why do plaques rupture?

Answer 30

Thin fibrous cap weakened by inflammatory macrophages and enzymes.

Question 31

What pro-coagulant substance is released by foam cells?

Answer 31

Tissue factor.

Question 32

Function of tissue factor?

Answer 32

Activates coagulation cascade leading to thrombin and fibrin clot formation.

Question 33

What happens when plaque ruptures?

Answer 33

Platelets adhere to exposed collagen.

Question 34

What do activated platelets release?

Answer 34

ADP (recruits platelets); Thromboxane A2 (vasoconstriction and aggregation); Serotonin (vasoconstriction).

Question 35

Role of thromboxane A2 in ACS?

Answer 35

Promotes platelet aggregation and coronary vasoconstriction.

Question 36

Final result of plaque rupture?

Answer 36

Thrombus formation causing coronary artery occlusion and ACS.

Question 37

Definition of stable angina?

Answer 37

Predictable exertional chest pain relieved by rest.

Question 38

Pathophysiology of stable angina?

Answer 38

Fixed narrowing of coronary artery.

Question 39

Troponin in stable angina?

Answer 39

Normal.

Question 40

ECG in stable angina?

Answer 40

Usually normal.

Question 41

Cause of unstable angina?

Answer 41

Plaque rupture with partial occlusion.

Question 42

Symptoms of unstable angina?

Answer 42

Pain at rest lasting more than 20 minutes.

Question 43

ECG in unstable angina?

Answer 43

ST depression or T-wave inversion.

Question 44

Troponin in unstable angina?

Answer 44

Normal.

Question 45

Define NSTEMI.

Answer 45

Subendocardial myocardial necrosis from partial occlusion.

Question 46

ECG in NSTEMI?

Answer 46

ST depression.

Question 47

Troponin in NSTEMI?

Answer 47

Elevated.

Question 48

Define STEMI.

Answer 48

Complete coronary artery occlusion causing transmural infarction.

Question 49

ECG in STEMI?

Answer 49

ST elevation.

Question 50

ST elevation V1–V4 indicates what?

Answer 50

Left anterior descending artery occlusion.

Question 51

Major complications of STEMI?

Answer 51

Heart failure, arrhythmias, cardiogenic shock, death.

Question 52

What is troponin T?

Answer 52

Structural protein in cardiac muscle cells.

Question 53

Why does troponin rise after MI?

Answer 53

Released after myocardial cell membrane rupture.

Question 54

Troponin time course?

Answer 54

Rises 3–6 hours, peaks 24–48 hours, remains elevated 7–10 days.

Question 55

What does ECG assess?

Answer 55

Electrical activity of the heart.

Question 56

Stress test finding of ischaemia?

Answer 56

ST depression greater than 1 mm during exercise.

Question 57

What does echocardiography show in MI?

Answer 57

Regional wall motion abnormality.

Question 58

What does coronary angiography show?

Answer 58

Exact site of arterial blockage.

Question 59

Three treatment goals in IHD?

Answer 59

Decrease oxygen demand, increase oxygen supply, prevent clot formation.

Question 60

Why statins?

Answer 60

Lower LDL and reduce inflammation.

Question 61

Why beta-blockers?

Answer 61

Reduce heart rate and myocardial oxygen demand.

Question 62

Why antiplatelets?

Answer 62

Prevent platelet aggregation and thrombosis.

Question 63

Why ACE inhibitors?

Answer 63

Protect endothelium and prevent cardiac remodeling.