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ELM2 - pathology > lecture 5/tutorial 6/7 - atherosclerosis & ischaemic heart disease > Flashcards

lecture 5/tutorial 6/7 - atherosclerosis & ischaemic heart disease Flashcards

1
Q

What is the most common pathology that causes ischaemic heart disease?

A

Atherosclerosis of coronary arteries

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2
Q

What are the non-modifiable risk factors for atherosclerosis?

A

genetic condition, family history, increasing age, male sex

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3
Q

What are the modifiable risk factors for atherosclerosis?

A

high cholesterol, hypertension, smoking, diabetes, inflammation

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4
Q

Which arteries are affected by athersclerosis?

A

Elastic arteries & large/medium muscular arteries

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5
Q

Why do veins and small arteries/arterioles not get atherosclerosis?

A

Because the pressure is too low to cause endothelial damage

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6
Q

What is the key driver of the formation of an atherosclerotic plaque?

A

Endothelial injury

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7
Q

What are the steps in the pathogenesis of atherosclerosis?

A
  1. endothelial cell injury causes low grade inflammation
  2. increased vascular permeability, recruitment of inflammatory cells
  3. due to increased permeability, oxidised LDL can accumulate in intima
  4. cytokines released attracting monocytes which migrate, become macrophages and take up lipids to form foam cells.
  5. smooth muscle cells proliferates, ECM deposited,T cells recruited
  6. Fibrous cap forms
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8
Q

What are the structural features of an atherosclerotic plaque?

A

Fibrous cap,
Necrotic centre

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9
Q

What are some of the complications of atherosclerosis?

A

Mechanical obstruction of vessel lumen, aneurysm (e.g. AAA), acute plaque change

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10
Q

What is acute plaque change?

A

When an atherosclerotic plaque has haemorrhage into the plaque from new vessels formed by angiogenesis, resulting in ulceration or rupture of the plaque which causes thrombosis

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11
Q

What are the complications of angiogenesis in the development of an atherosclerotic plaque?

A

Very thin, weak vessels form in the plaque, and if they rupture they can bleed into the plaque causing acute plaque change

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12
Q

What is the morphological difference between a stable and vulnerable atherosclerotic plaque?

A

Stable has a thicker fibrous cap with a smaller lipid core and less angiogenesis

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13
Q

What percentage stenosis of an artery is considered ‘critical’?

A

75% occlusion

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14
Q

What are some of the presentations of iscahemic heart disease?

A

Angina pectoris (stable/unstable), myocardial infarction, sudden cardiac death, heart failure

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15
Q

What is stable angina?

A

Chest pain caused by coronary occlusion due to a stable atherosclerotic plaque. Brought on by increased cardiac O2 demand, such as during exercise.

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16
Q

What is unstable angina?

A

Prolonged chest pain caused by plaque change and thrombus occlusion of coronary vessels. Not relieved by rest.

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17
Q

Why does stable angina come on with exercise and resolve with rest?

A

Caused by narrowed coronary artery which will limit blood supply during periods of high O2 requirements. However, when resting again, blood supply will be sufficient even with the narrowed artery.

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18
Q

What causes the pain experienced with angina pectoris?

A

Transient and reversible myocardial ischaemia

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19
Q

What are acute coronary syndromes?

A

Pathologies involving the acute plate change and ischaemia, including unstable angina and MI

20
Q

What is the physiological sequence of an MI?

A
  1. thrombus forms at plaque in coronary artery
  2. myocardium is ischaemic
  3. local acidosis because lactic acid builds up with anaerobic metabolism
  4. ATP used up causing increased extracellular K+, reducing contractility
  5. damage spreads through the wall, resulting in ventricular failure
  6. MABP drops as cardiac output reduces, reducing coronary perfusion
21
Q

What are the cardiac markers that rise in an MI, and in which order do they rise?

A

memory aid = TCAL (like telephone call)
- T - troponins
- C - creatine kinase
- A - aspartate aminotransferase
- L - lactate dehydrogenase
idk if we have to know last 2

22
Q

What areas of the heart will be ischaemic with a LAD MI?

A

anterior left ventricle, anterior septum

23
Q

What areas of the heart will be affected with an RCA MI?

A

Posterior left ventricle, posterior septum, right ventricle

24
Q

What areas of the heart will be affected with a Left circumflex artery MI?

A

Lateral left ventricle

25
Q

What is the gross morphology of the heart up to 12 hours post MI?

A

minimal or no change, may be pale and swollen

26
Q

What is the gross morphology of the heart 12-24 hours post MI?

A

dark mottling due to red necrotic tissue filled with stagnant blood

27
Q

What is the gross morphology of the heart 1-3 days post MI?

A

Mottling with pale yellow infarct centre due to coagulation necrosis and neutrophil infiltration

28
Q

What is the gross morphology of the heart 10-14 days post MI?

A

Red hyperaemic border (a rim of vascular granulation tissue)

29
Q

What is the gross morphology of the heart 2-8 weeks post MI?

A

Grey-white collagenous scar

30
Q

What is the microscopic morphology of the heart 4-12 hours post MI?

A

early coagulative necrosis, oedema, haemorrhage

31
Q

What is the microscopic morphology of the heart 12-24 hours post MI?

A

infiltration by neutrophils, hypereosinophilia of necrotic myocytes

32
Q

What is the microscopic morphology of the heart 1-3 days post MI?

A

myocytes lose nuclei and striations and are infiltrated by neutrophils

33
Q

What is the microscopic morphology of the heart 3-7 days post MI?

A

infiltration by macrophages to clear necrotic debris

34
Q

What is the microscopic morphology of the heart 10-14 days post MI?

A

granulation tissue formation

35
Q

What is the microscopic morphology of the heart 2-8 weeks post MI?

A

collagenous scar

36
Q

What are the complications of an MI?

A

acute heart failure, cardiogenic shock, arrhythmias. myocardial rupture, pericarditis, mural thrombus and embolism, ventricular aneurysm

37
Q

What is the potentially fatal arrhythmia that sometimes arises after an MI?

A

Ventricular fibrillation

38
Q

What is cardiac tamponade?

A

Compression of the heart due to effusion in the pericardial sac

39
Q

How long after an MI will myocardial rupture potentially occur?

A

5-7 days

40
Q

What are some of the possible myocardial ruptures that can occur post MI?

A

ventricular free wall rupture, septum rupture, papillary muscle rupture

41
Q

What complication is the leading cause of death in acute MI patients?

A

Cardiogenic shock

42
Q

Why does MI increase the risk of stroke?

A

Mural thrombi can form in areas overlying the infarct due to stasis and endothelial damage. These thrombi can then embolise causing stroke, etc.

43
Q

How does chronic ischaemic heart disease cause heart failure?

A

Accumulating ischemic damage results in worsening heart function

44
Q

How does left heart failure cause secondary right heart failure?

A

Increased pressure in the pulmonary circulation causes pressure overload on the right side

45
Q

What is the gross findings of a liver that is chronically congested due to right heart failure?

A

Nutmeg liver

46
Q

What are the 4 key components of primary hospital pharmacological treatments for MI?

A

‘MONA’
- Morphine
- Oxygen
- Nitrates
- Aspirin

47
Q

What are some of the drugs used in treatment of STEMI?

A

Alteplase (thrombolytic), metoprolol (anti-arrhythmic), warfarin (prevent DVT)

ELM2 - pathology (19 decks)

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