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CR/MET PBLs > PBL 3: MIchael O'Conlan > Flashcards

PBL 3: MIchael O'Conlan Flashcards

1
Q

What is angina?

A

A clinical syndrome caused by transient myocardial ischaemia

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2
Q

What are the 3 features of angina?

A
  • chest, jaw, shoulder, back and arm pain
  • exertion
  • relieved by rest and nitrate sprays
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3
Q

What are the main causes of angina?

A

Ischemia due to either reduction in supply or less commonly a uncompensated increase in oxygen supply

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4
Q

What are the causes for a reduction in supply of oxygen?

A
  • coronary artery disease is the common

- severe anaemia

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5
Q

What causes coronary artery disease?

A
  • most commonly atherosclerosis
  • arterial spasms
  • vasculitis
  • radiation
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6
Q

Why might oxygen demand increase?

A
  • left ventricular hypertrophy
  • right ventricular hypertrophy
  • tachycardias
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7
Q

What may be the cause of left ventricular hypertrophy?

A

Aortic stenosis or regurgitation

Hypertension

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8
Q

What may be the cause of right ventricular hypertrophy?

A

Pulmonary hypertension

Pulmonary stenosis

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9
Q

What is the most important diagnosis method?

A

HISTORY

  • where is the pain? = central chest
  • what provokes it? = exertion
  • what is its character? - constricting tightness
  • where does it radiate to? - left arm, right arm, jaw, face, shoulders, neck
  • what alleviates it? - rest/GTN spray
  • how long does it last? - a few minutes post exercise
  • what exacerbates it? - cold weather
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10
Q

What are the different types of angina?

A

Stable and unstable

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11
Q

What is the difference between stable and unstable angina?

A

Unstable - unpredictable attack and may not have a trigger, may continue after rest medical emergency, acute coronary syndrome, partial rupture of a plaque

Stable - predictable, brought on by a trigger (stress or exercise), stops when you rest, due to atherosclerotic plaques restricting vessel lumen

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12
Q

What type of angina does Michael have?

A

Stable as occurs after exercise

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13
Q

How can atherosclerosis cause angina?

A

Narrows the coronary arteries due to the lipid plaque build up
This means less oxygen is supplied to the heart via these coronary arteries resulting in myocardial ischaemia
At rest blood flow is still enough however during exercise demand increases (exercise induced myocardial ischemia)
Pain therefore usually stops 3-10 minutes after begin rest
May get transient breathlessness

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14
Q

What are the risk factors of angina?

A

Smoking, diabetes, obesity, high cholesterol, hypertension

First degree family history of MI, sedentary lifestyle

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15
Q

How is angina diagnosed?

A

Anatomical tests look for coronary artery disease = angiography (CT or invasive)
Functional tests look for ischemia evidence = stress echo/MRI scan, perfusion scans, ECG

First line is CT coronary angiography

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16
Q

What would you see on ECG?

A

When exercise - ST depression, if depression starts prior to exercise this is a poorer prognosis
Pathological Q waves and left bundle branch block indicative of coronary artery disease

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17
Q

What features would not suggest a stable angina?

A
  • continuous/prolonged chest pain
  • chest pain unrelated to activity
  • pain brought on by breathing
  • pain associated with dizziness, palpitations, tingling, swallowing difficulty
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18
Q

How are symptoms managed?

A
  • GTN (glyceryl trinitrate spray) taken sublingually (first line)
  • Beta blocker or CCB - vasoconstriction of coronary arteries and negative ionotropic effects to slow down heart activity (first line)
  • second line = long acting nitrate, ivabradine, nicorandil, ranolazine
  • if these do not work = PCI, CABG
19
Q

What are PCI and CABG?

A

PCI - percutaneous coronary intervention = non-surgically open up narrowed vessels with a stent

CABG - coronary angiography bypass graft = replace damaged vessel with saphenous vein/artery

20
Q

How is angina prevented?

A

Aspirin - antiplatelet and anti-inflammatory drug decreases the chance of clot formation in atheromatous coronary arteries
Statins - inhibit hMG-coA-reductase to prevent cholesterol synthesis in the blood contributing to atherosclerosis
ACE inhibitors - hypertension/diabetes mellitus
P2Y12 receptor antagonist - after PCI or if intolerant to aspirin, receptor involved in platelet aggregation

21
Q

What is acute coronary syndrome?

A

Myocardial Infarction and unstable angina

22
Q

How does myocardial infarction occur?(pathogenesis)

A

Atherosclerotic plaques form in coronary arteries
If a plaque is unstable the fibrous cap can rupture -> thrombus formation -> occlusion of coronary artery -> no blood or oxygen supply to myocardium which stops contracting and cardiomyocytes die -> troponin released

23
Q

What is the difference between a STEMI an a NSTEMI?

A

STEMI = ST elevation where there is a sudden complete blockage of a coronary artery, transmural involving whole thickness of ventricular wall

NSTEMI = severely narrowed artery but not completely blocked so no ST elevation, subendocardial confined to the inner part of myocardium

24
Q

What risk factors are associated with which type of MI?

A

Aspirin increases risk of NSTEMI

Smoking increases risk of STEMI

25
Q

What is the difference in an ECG from angina and from MI?

A

Angina - ST depression

MI - ST elevation if STEMI or ST not affected/ST depression if NSTEMI

26
Q

What are the signs of an MI?

A

Tachycardia
4th heart sound (late diastolic, before S1)
Low grade fever

27
Q

What are the symptoms of MI?

A

Chest pain - acute crushing central/left sided, lasts more than 20 minutes, radiates to jaw/left arm/epigastric region
Autonomic disturbances (sweating, nausea, vomiting)
Dyspnoea
Syncope

28
Q

What are the risk factors of MI?

A

Unmodifiable = old age, male, family history of ischemic heart disease

Modifiable = smoking, hypertension, diabetes mellitus, hyperlipidaemia, obesity

29
Q

How is an MI diagnosed?

A

ECG
Cardiac enzymes - creatine kinase, LDH, aspartate transaminase
Intracellular proteins - troponin I and T when myocytes necrosis occurs

30
Q

How would an ECG differ between STEMI and NSTEMI?

A

STEMI - ST elevation, tall T waves, left bundle branch block

NSTEMI - ST depression, T wave inversion, or normal

31
Q

Why is an ECG important in an MI?

A

Can localise the MI

Can determine if it is a STEMI or NSTEMI

32
Q

When would troponin I and T be released and when would levels decrease?

A

Released 2-4 hours following MI

Remain elevated for up to 2 weeks

33
Q

When would creatine kinase be released and when would levels decrease?

A

Rises 3-12 hours after MI

Returns to baseline within 48 hours

34
Q

What is the immediate emergency management of an MI?

A

If ACS suspected:
brief history, quick physical exam, ECG

MONA - morphine, oxygen, nitrates, aspirin

35
Q

How would a STEMI be managed?

A
  • antiplatelet aspirin
  • reperfusion (PCI is gold standard, then thrombolysis - streptokinase IV up to 12 hours after or TPA)
  • act quick as more greater degree of necrosis for greater length of time
36
Q

How is thrombolysis carried out?

A

Administrate tissue plasminogen activator to produce active plasmin enzyme to degrade fibrin clots restoring blood flow

37
Q

What are the 5 medications patients take home?

A 
Aspirin
Statins
Beta blockers
ACE inhibitors
Second antiplatelet agent
38
Q

What are some complications of MI?

A

Arrhythmias - tachycardia, ventricular fibrillation
Heart failure
Pericarditis
Thromboembolism

39
Q

What does aspirin do?

A
  • COX inhibition of thromboxanes

- needed for platelet activation and aggregration

40
Q

What is clopidogrel?

A

P2Y12 receptor antagonist

  • blocks this receptor on platelets for ADP which is required for platelet aggregation and fibrin cross linking
  • antiplatelet
41
Q

What are the indications for special referral with angina?

A
  • new onset
  • worsening in patient with previously stable symptoms
  • new/recurrent angina in patient with history of AMI/coronary revascularisation
42
Q

What do you give for an NSTEMI?

A
  • antiplatelet aspirin
  • antiplatelet clopidogrel
    (ANTIPLATELETS)
43
Q

What is variant angina?

A

Also called Prinzmetal’s angina
Comes in waves due to vasospasm rather than exertion
So can happen at night/rest in coronary arteries

44
Q

What is microvascular angina?

A

In small arteries coming off coronary arteries

CR/MET PBLs (15 decks)

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