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Y2 MECHANISMS OF DISEASE > Ischaemic Heart Disease > Flashcards

Ischaemic Heart Disease Flashcards

1
Q

What is the definition of ischaemic heart disease?

A

pathophysiological syndromes due to inadequate blood supply to the myocardium

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2
Q

What are the 2 reasons why there may be inadequate blood supply to the myocardium in IHD?

A
  1. reduced coronary blood flow due to atheroma +/- thrombus

2. myocardial hypertrophy due to systemic hypertension

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3
Q

What are the 5 factors involved in preventing IHD?

A
  1. stop smoking
  2. lose/manage weight
  3. lower blood pressure
  4. encourage exercise
  5. calculate risk and prescribe relevant treatment
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4
Q

What is the main risk score calculation used in IHD?

A

The Framingham risk score calculation

It estimates a patient’s 10 year risk of having a heart attack

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5
Q

What are 2 other commonly used risk calculators?

A
  1. SCORE

2. QRISK3

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6
Q

What is involved in the pathogenesis of IHD?

A
  1. acute and/or chronic ischaemia
  2. loss of autoregulation of coronary blood flow with >75% vessel occlusion
  3. low diastolic flow leading to subendocardial hypoperfusion
  4. myocyte dysfunction/death from ischaemia
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7
Q

When is recovery possible from IHD?

A

If there is rapid reperfusion within 15-20 minutes

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8
Q

At what point does IHD become symptomatic?

A

When there is >75% vessel occlusion

This is critical stenosis and gives angina-like symptoms

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9
Q

What are the 4 IHD syndromes?

A
  1. angina pectoris
  2. acute coronary syndrome
  3. sudden cardiac death
  4. chronic ischaemic heart disease
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10
Q

What typically causes acute ischaemia?

A
  1. atheroma + acute thrombosis/haemorrhange

Lipid rich plaques are most at risk

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11
Q

What does acute ischaemia in the heart lead to?

A

regional transmural myocardial infarction

this is different to a subendocardial MI

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12
Q

If someone has an MI and dies within 24 hours, what morphology would be present?

A

Morphology would be normal

e.g. in a sudden cardiac death

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13
Q

What would the MI morphology look like after 1-2 days?

A

it would be pale and oedematous

there would be neutrophils and myocyte necrosis

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14
Q

What would the MI morphology look like after 3-4 days?

A

it would be yellow with a haemorrhagic edge

there would be macrophages and myocyte necrosis

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15
Q

What would the MI morphology look like after 1-3 weeks?

A

it would be red-grey to grey-white

it becomes pale and thin

granulation tissue forms, followed by fibrosis

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16
Q

What would the MI morphology look like after 3-6 weeks?

A

there would be a dense fibrous scar

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17
Q

What is a ‘STEMI’?

A

ST-elevation myocardial infarction

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18
Q

What causes a STEMI?

A

blockage of one of the major coronary arteries

this is the most serious type of heart attack caused by COMPLETE OCCLUSION of a coronary artery

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19
Q

What is an example of an NSTEMI?

A

subendocardial MI

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20
Q

What is an NSTEMI?

A

non-ST-elevation myocardial infarction

an acute ischaemic event causing myocyte necrosis

21
Q

What is the perfusion of the subendocardial myocardium like under normal conditions?

A

it is relatively poorly perfused under normal conditions

22
Q

What can lead to the subendocardial myocardium infarcting without any acute coronary occlusion?

A
  1. stable atheromatous occlusion of the coronary circulation
  2. an acute hypotensive episode

this can lead to subendocardial MI

23
Q

What is the most common blood marker of cardiac myocyte damage?

A

Troponins T and I

24
Q

Under what circumstances may troponins T and I be raised?

A
  1. post-MI
  2. pulmonary embolism
  3. heart failure
  4. myocarditis
25
Q

When are troponins T and I detectable?

When do they peak?

A

detectable after 2-3 hours

peaks after 12 hours

still detectable for up to 7 days

26
Q

When is creatine kinase MB detectable as a sign of cardiac myocyte damage?

A

detectable after 2-3 hours

peaks at 10-24 hours

detectable for up to 3 days

27
Q

What are 3 other cardiac enzymes that can show damage to the cardiac myocytes?

A
  1. myoglobin
  2. lactate dehydrogenase isoenzyme 1
  3. aspartate transaminase
28
Q

What is the problem with using myoglobin as a marker of cardiac injury?

When does it peak?

A

It peaks after 2 hours

It is also released from damaged skeletal muscle

29
Q

When is lactate dehydrogenase isoenzyme 1 detectable?

When does it peak?

A

Peaks after 3 days

Detectable for up to 14 days

30
Q

Why is aspartate transaminase less useful as a marker of myocardial damage?

A

it is also present in the liver

31
Q

What % of MI patients experience sudden cardiac death?

A

20%

They have 1-2 hour mortality

32
Q

What is the prognosis of MI patients who do not experience sudden cardiac death?

A

10-15% = early hospital mortality

7-10% - further 1 year mortality

3-4% mortality per year in subsequent years

33
Q

What % of MI patients experience complications?

A

80-90%

34
Q

What are the 4 main complications of MI?

A
  1. arrhythmias, ventricular fibrillation & sudden death
  2. left ventricular failure and shock
  3. pericarditis
  4. cardiac mural thrombus and emboli
35
Q

What are the 4 less common complications of MI?

A
  1. DVT and pulmonary embolus
  2. myocardial rupture
  3. ventricular aneurysm
  4. autoimmune pericarditis +/- pleurisy for 2 weeks-months post MI
36
Q

What tends to be involved in myocardial rupture?

A

tamponade, ventricular septal perforation and damage to papillary muscle

37
Q

What are the 3 stages involved in MI diagnosis?

A
  1. taking a history and finding the symptoms
  2. examination - pulse, breathing
  3. investigations - ECG, cardiac enzymes
38
Q

What is the MONA of MI treatment?

A

M - morphine

O - oxygen

N - nitrates

A - aspirin

39
Q

What reperfusion technique is used to treat MI?

A

PCI - percutaneous coronary intervention

this is better than thrombolysis

40
Q

What are the further measures for treating MI?

A

managing the complications of MI and secondary prevention

41
Q

What drugs are given in the secondary prevention of MI?

A
  1. ACEi, anti-platelets and anti-coagulants
  2. anti-arrhythmics and beta-blockers
  3. statins
42
Q

What causes chronic ischaemic heart disease?

A

decompensated myocardium or coronary artery atheroma produces relative myocardial ischaemia

It may be a result of previous MIs or congestive heart failure

43
Q

What does the heart look like in congestive heart failure?

A

it is enlarged, hypertrophied and dilated

44
Q

What is the risk of chronic ischaemic heart disease?

A

risk of sudden cardiac death or MI

45
Q

What causes familial hypercholesterolaemia?

A

mutations in genes involved in cholesterol metabolism

46
Q

What are the most common mutations in familial hypercholesterolaemia?

A
  1. low density lipoprotein receptor gene

2. apolipoprotein B

47
Q

What is the most common symptom of someone who is heterozygous for familial hypercholesterolaemia?

A

development of xanthomas and early progressive atherosclerosis

xanthomas develop in the tendons, periocular and corneal arcus

48
Q

What is the treatment for heterozygous familial hypercholesterolaemia?

A

early primary treatment with statins

49
Q

How does treatment for homozygous hypercholesterolaemia differ to heterozygous?

A

treatment is more complex and less effective

Y2 MECHANISMS OF DISEASE (36 decks)

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