Heart Flashcards

1
Q

Define Acute plaque change.

A

It is the unpredictable and sudden conversion of a stable atherosclerotic plaque into an unstable and potentially fatal atherothrombotic lesion through rupture/ superficial erosion/ ulceration/ fissuring/ deep haemorrhage.

  • It is usually associated with inflammation.
  • Leads to formation of a superimposed thrombus.
  • Partially /completely occludes they coronary artery
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2
Q

What is an Ischemic Heart Disease? What are its causes? Give examples.

A

IHD is a group of disordered which occur due to myocardial ischemia, which is due to imbalance between myocardial supply and cardiac demand for oxygenated blood.

Causes are:

  1. Decreased supply of blood:
    - Atheromatous narrowing of one or more epicardia coronary arteries (CAD)
    - Risk depends on: Extent and severity of occlusion, type of atheromatous plaque (vulnerable or stable), degree of stenosis (70% is critical), rate of development (slowly developing plaque allows time for collaterals to grow)
  2. Increased demand : Cardiac hypertrophy, tachycardia

Examples of IHD: There are 4 types.
MI, Angina pectoris, Chronic IHD , Sudden Cardiac Death

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3
Q

What is a stable and a vulnerable plaque.

A

Stable plaque

  1. Dense collagenous fibrous cap
  2. Minimal inflammation
  3. Less foam cells and less necrotic core
  4. Not likely to rupture

Vulnerable plaque:

  1. Thin fibrous cap
  2. Lot of inflammation and foam cells, with extra cellular lipids
  3. Necrotic core is large
  4. Likely to rupture
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4
Q

Define angina pectoris. Types.

A

It is a type of IHD characterised by:

  • Recurrent and paroxysmal attacks of
  • Substernal or precordial chest pain
  • Caused by transient (15s to 15 min) ischemia
  • which is not sufficient to cause myocardial necrosis

Types: 3 types
1) Stable angina - substernal chest pain induced by exercise

2) Variant/Prinzmetal Angina - spasm of coronary artery having atherosclerosis, not related to physical activity, heart rate,
or blood pressure. Occurs during rest or sleep.

3) Unstable Angina (it is a type of Acute coronary syndrome)- rupture of an atherosclerotic plaque complicated by thrombosis/ embolization/vasospasm. May be a precursor of MI.

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5
Q

Define MI. What is the etiology/cause?

A

Coagulative necrosis of cardiac muscle due to prolonged severe ischemia.

Etiology:

  1. Coronary Arterial Occlusion: (90% cases) Due to Acute Plaque change
  2. Other causes (10% cases) : Vasospasm/Emboli in left atrium causing fibrillation/Amyloidosis etc.
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6
Q

Pathogenesis of M.I.

A
  1. Acute Plaque Change: Sudden conversion of stable plaque into a fatal atherothrombotic lesion. May be due to:
    - Rupture/Fissure: Thrombogenic plaque contents released–> thrombus formation and occlusion
    - Erosion: Thrombogenic subendothelial collagen exposed– thrombosis and occlusion
    - Hemorrhage into plaque: It grows in size and occludes lumen
  2. Platelet activation, adhesion and aggregation- formation of microthrombi- partial or complete occlusion
  3. Vasospasm: Due to TxA2 and other mediators released by platelets
  4. Coagulation: by tissue factor and other mediators - formation of a growing thrombus
  5. Complete occlusion: Usually within minutes
  6. Myocardial necrosis: Ischemic, coagulative necrosis of the area supplied by the occluded artery (Area at risk)
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7
Q

What are the myocardial response in MI with timing.

A
  1. Onset of ATP deception : within sec
  2. Loss of contractility: <2mins
  3. ATP reduced to 50% of normal: 10 mins
  4. ATP 10% of normal : 40 mins
  5. Irreversible injury: 20-40 mins
  6. Micro vascular injury: >1 hour
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8
Q

What is the TTC stain for gross examination of MI?

A

If MI is less than 12 hours old, TTC stain can be used.

TTC= Triphenyl Tetrazolium chloride

Tissue section immersed in TTC:

  • Normal Myocardium appears red (LDH intact)
  • Infarcted area appears white (LDH has leaked out and is lost)
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