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Year 3 - CR > Chest Pain and Breathlessness > Flashcards

Chest Pain and Breathlessness Flashcards

1
Q

Name the three clinical syndromes of ischaemic heart disease

A
  • Angina (stable and unstable)
  • Myocardial infarction
  • Sudden cardiac death
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2
Q

What can cause ischaemic heart disease

A
  • Atheroma of coronary arteries (95% cause)
  • coronary artery vasculitis (inflammation of the vessel)
  • coronary artery vasospasm
  • anaemia
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3
Q

What is the primetime for males to have there first heart attack

A

55

- Women have ischaemic heart disease later in life

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4
Q

What are the risk factors for ischaemic heart disease

A
  • sex (male)
  • age
  • family history
  • hyperlipidaemia
  • hypertension
  • diabetes mellitus
  • smoking
  • obesity
  • stress
  • lack of exercise
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5
Q

Name differences between stable and unstable angina

A

unstable

  • comes on at rest
  • unpredictable
  • unstable plaque of atheroma that is changing and growing and complicating

stable

  • coronary artery disease causing the atheroma is stable
  • plaque is not changing a lot
  • lasts about 5-15 minutes, with exercise and emotional stress, reduces when relaxing or taking nitrates
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6
Q

What is the main cause of IHD

A
  • Atheroma of coronary arteries (95% cause)
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7
Q

What are the theories as to how atheroma has formed

A
  • Encrustation (Rokitansky) - platelet thrombi over injured endothelium
  • Imbibition (Virchow) - low grade inflammation leads to increase plasma filtration
  • Reaction to injury (Ross and Glomset) - endo injury with increase permeability and macro/smooth muscle accumulation
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8
Q

Describe Rokitansky theory as to how atheroma has formed

A
  • platelets stick to the inside of the platent wall and this is due to the endothelium being injured
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9
Q

Describe Virchow theory as to how an atheroma has formed

A
  • cells - low grade inflammation leads to increased plasma filtration
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10
Q

Describe Ross and Glomset theory as to how an atheroma has formed

A
  • idea that there is a reaction to a vessel wall due to endothelium injury, this increases permeability and macro/smooth muscle accumulation
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11
Q

What part of the artery is the atheroma in

A

Tunica intima

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12
Q

Describe the pathogenesis of atherosclerosis

A
  • At some stage there is a problem
  • contents get stuck to the vascular wall
  • platelets get stuck and form a thrombi
  • endothelium cells either damaged directly or due to the turbulence get dislodged and expose the underlying connective tissue
  • this triggers thrombosis due to the damage of the endothelium
  • this triggers inflammation
  • the plaques becomes more pronounced
  • the smooth muscle cells migrate to the intima and become foam cells
  • macrophages also take up the fat and become foam cells
  • the plaque becomes bigger
  • collagen is laid down
  • get a plaque that is more fibrous and cellular
  • the blood is still trying to get through the lumen
  • get necrosis in the centre eventually
  • then there is an attempt at healing and vaso vasorum grow into the intima and supply it with blood in an attempt to heal the necrosis
  • dyanmic situation has occurred in the coronary artery, the plaque has ulcerated and liberated the necrotic centre and stimulated local thrombosis causing occlusion
  • or the atheroma plaque has caused critical thrombi dynamic changes that cause the occlusions of the vessel
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13
Q

What are the complications of an atheroma

A
  • ulceration
  • fissuring
  • haemorrhage
  • thrombosis
  • aneurysm - dilatation of a vessel (seen in an abdominal aorta due to atheroma)
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14
Q

What are the two main types of acute myocardial infarction

A
  • Transmural (most cause ST elevation(STEMI))

- Subendocardial (most do not cause ST elevation (NSTEMI))

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15
Q

Describe a transmural actue MI

A
  • involves the whole thickness of the ventricular wall - starts from the endocardium right through the myocardium to the epicardium
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16
Q

What is the most likely cause of a transmural acute MI

A
  • underlying lesions is an atheromatous plaque in a coronary artery that has undergone fissuring and occlusive thrombosis
17
Q

Describe a subendocardial infarction

A
  • confined to the inner third or half of the myocardium - this gets in oxygen last
18
Q

What is a subendocardial infarction due to

A
  • results from generalised under-perfusion of the myocardium
  • caused by generalised atheroma of all of the coronary circulation
    or
  • e.g. anaemia on top of something else
  • Lung disease
19
Q

If there is an occlusion of

  • Main left coronary artery
  • Left anterior descending
  • Left circumflex
  • Right coronary artery

What part of the heart does it affect?

A
  • Main left coronary artery = massive anterolateral MI
  • Left anterior descending = anteroseptal MI
  • Left circumflex = lateral MI
  • Right coronary artery = Posterior (inferior) MI
20
Q

Describe the macroscopic appearance of the MI

  • 0-12 hours
  • 12-24 hours
  • 24-72 hours
  • 3-10 days
  • weeks - months
A
  • 0-12 hours = no changes
  • 12-24 hours = pale with blotchy discolouration
  • 24-72 hours = soft, pale and yellow
  • 3-10 days = soft, yellow-brown with hyperaemic border
  • weeks - months = white fibrous scar
21
Q

Describe the histology appearance of the MI

  • 0-12 hours
  • 12-24 hours
  • 24-72 hours
  • 3-10 days
  • weeks - months
A
  • 0-12 hours = No changes
  • 12-24 hours = bright eosinophilia of muscle fibres reflecting onset of coagulation necrosis; intracellular oedema
  • 24-72 hours = coagulative necrosis with loss of nuclei and striations, beginning of acute inflammatory response with heavy interstitial neutrophil infiltrate
  • 3-10 days = replacement of infarcted area by granulation tissue
  • weeks - months = collagenous scar tissue
22
Q

How does a pathologist diagnose cardiac death due to MI after death

A

Cut along the coronary artery and find the infract

23
Q

What are the short term complications of MI

A

 left ventricular failure
 cardiac dysrhythmias
 rupture of ventricular wall - blood will just go left to right
 papillary muscle infarction - can cause mitral regurgitation
 mural thrombus - if it embolisms it can convert to stroke
 fibrinous pericarditis
 deep vein thrombosis

24
Q

What are the long term complications of MI

A

 intractable left ventricular failure
 ventricular aneurysm - thin wall where the scar is
 Dressler’s syndrome
 recurrent myocardial infarction

25
Q

What do the effects of a pulmonary embolus depend on

A
  • Size of the occluded vessel
  • number of the emboli
  • adequacy of the bronchial blood supply
26
Q

what does a saddle embolus do

A
  • this is when it blocks both pulmonary arteries

- this can lead to circulatory collapse

27
Q

Where can the PE get stuck

A
  • large embolus coils within one major pulmonary artery

- saddle embolus - blocks both pulmonary arteries

28
Q

duel blood supply….

A

protects lungs from effects of pulmonary artery obstruction

29
Q

How does Dressler’s syndrome present (long term complication of MI)

A

fever, pleuritic pain, pericardial effusion and raised ESR – type of pericarditis thus treated with NSAIDs

30
Q

How does ventricular aneurysm present (long term complication of MI)

A

persistent ST elevation and left ventricular failure

31
Q

How does left ventricular wall rupture present (short term complication of an MI)

A
  • 1-2 weeks afterwards, raised JVP, pulsus paradoxus, diminished heart sounds
    – treated with pericardiocentesis and thoracotomy
32
Q

How does a papillary muscle infarction present (short term complication of an MI)

A

– hypotension and pulmonary oedema may occur, Patients are treated with vasodilator therapy but often require emergency surgical repair

33
Q

How does an VSD present (short term complication of an MI)

A
  • VSD – usually occurs in the 1st week – features include acute heart failure associated with a pan systolic murmur
34
Q

What are the classes of anti-arrhythmic

A
  • Class I - Sodium-channel blockers = E.g. quidine, lidocaine, flecanide
  • Class II - Beta-blockers- Propranolol, Metoprolol
  • Class III - Potassium-channel blockers. – Amiodarone, Sotalol
  • Class IV - Calcium-channel blocker – Verapamil, Dilitiazem

Year 3 - CR (44 decks)

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