Atherosclerosis, MI, Heart Failure Flashcards

1
Q

What is atherosclerosis?

A

Chronic inflammation in the intima of large arteries characterised by intimal thickening and lipid accumulation

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2
Q

Describe the 7 steps of atherosclerosis

A
  1. Endothelial injury
  2. LDL enters intima and is trapped in sub-intimal space
  3. LDL converted into modified & oxidised LDL, causing inflammation
  4. Macrophages take up modified &oxidised LDL, becoming foam cells
  5. Apoptosis of foam cells causes inflammation & cholesterol core of plaque
  6. Inc adhesion molecules on endothelium recruit more macrophages & T cells into plaque
  7. Vascular smooth muscle cells form fibrous cap
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3
Q

State the 3 principal components of atherosclerotic plaques

A

Cells (smooth muscle cells, macrophages, other leucocytes), extracellular membrane (including collagen), intracellular and extracellular lipid

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4
Q

What are foam cells?

A

Macrophages containing modified and oxidised LDL

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5
Q

Is atherosclerosis more prominent in the thoracic or abdominal aorta?

A

Abdominal

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6
Q

Which cells form the fibrous cap?

A

Vascular smooth muscle cells

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7
Q

Where is atherosclerosis most prominent?

A

Sites of slow/ turbulent flow, e.g. ostia of major branches

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8
Q

State at least 3 modifiable risk factors for atherosclerosis

A

Type 2 diabetes mellitus, hypertension, hypercholesterolaemia, smoking

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9
Q

State 3 non-modifiable risk factors for atherosclerosis

A

Male gender, increasing age, family history

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10
Q

Describe the pathogenesis of myocardial infarction

A

A dynamic interaction between coronary atherosclerosis, plaque rupture, superimposed platelet activation, thrombosis, and vasospasm leads to coronary artery occlusion. Occlusion causes ischaemia which progresses to myocardial necrosis

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11
Q

How long does myocardial ischaemia have to be before myocytes die and injury becomes irreversible?

A

20-40 minutes

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12
Q

State at least three mechanical complications of myocardial infarction

A

Contractile dysfunction, congestive cardiac failure, left ventricular infarct and mitral regurgitation, ventricular rupture and haemopericardium, septal rupture, ventricular aneurysm

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13
Q

What does septal rupture lead to?

A

Left to right cardiac shunt

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14
Q

What does a ventricular aneurysm lead to?

A

Persistent ST elevation

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15
Q

What % of patients develop an arrhythmia after a myocardial infarction?

A

90%

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16
Q

When is ventricular fibrillation likely to develop post-MI?

A

Within 24h

17
Q

When is a ventricular aneurysm likely to develop post-MI?

A

After at least 4 weeks

18
Q

What is Dressler’s syndrome?

A

Pericarditis with chest pain, fevers, and effusion weeks to months after a myocardial infarction

19
Q

What causes fibrinous pericarditis?

A

Myocardial infarction extending to the epicardium

20
Q

What is the main risk of left ventricular dysfunction or ventricular aneurysm?

A

Mural thrombus, which can cause stroke

21
Q

What are the histological findings 0-6 hours after a myocardial infarction?

A

Normal histology

22
Q

What are the histological findings 6-24 hours after a myocardial infarction?

A

Loss of nuclei, homogenous cytoplasm, necrotic cell death

23
Q

What are the histological findings 1-4 days after a myocardial infarction?

A

Infiltration of polymorphs then macrophages

24
Q

What are the histological findings 5-10 days after a myocardial infarction?

A

Evidence of removal of debris by macrophages

25
Q

What are the histological findings 1-2 weeks after a myocardial infarction?

A

Granulation tissue, new blood vessels, myofibroblasts, collagen synthesis

26
Q

What are the histological findings weeks to months after a myocardial infarction?

A

Decellularising scar tissue

27
Q

State at least four common causes of heart failure

A

Ischaemic heart disease, valve disease, myocarditis, hypertension, dilated cardiomyopathy, arrhythmias

28
Q

State the four main complications of heart failure

A

Systemic emboli, arrhythmias, DVT and PE, sudden death

29
Q

How does heart failure cause fluid overload?

A

Cardiac damage leads to decreased cardiac output. This activates the renin-angiotensin system, leading to salt and water retention to maintain perfusion. This causes fluid overload

30
Q

Describe the pathophysiology of heart failure

A

Cardiac damage leads to decreased stroke volume. This is detected by baroreceptors which activate the sympathetic nervous system, increasing heart rate and total peripheral resistance to maintain perfusion. This increases afterload, which leads to left ventricular hypertrophy and increased end diastolic volume. The heart becomes dilated with poor contractility

31
Q

What are the symptoms of left ventricular failure?

A

Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, wheeze, fatigue

32
Q

What are the two main causes of right ventricular failure?

A

Left ventricular failure, chronic severe pulmonary hypertension

33
Q

What are the symptoms of right ventricular failure?

A

Peripheral oedema, ascites, facial engorgement

34
Q

What investigations are required to diagnose heart failure?

A

Brain natriuretic peptide (BNP), chest x-ray, ECG, echocardiogram