PBL 5 - Angina + Myocardial Infarction Flashcards

1
Q

Explain exactly what is meant by ‘acute myocardial infarction’ (AMI) (1 mark)

A

A coronary artery becomes blocked by a thrombus (1/2 mark), causing death (necrosis) (1/2 mark) from ischaemia to some part of the myocardium.

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2
Q

Describe three typical characteristics of the chest pain experienced by someone experiencing an AMI (3 marks)

A

Intense and unremitting for 30-60 minutes

2) Retrosternal and often radiates up to the neck, shoulder, and jaw and down to the ulnar aspect of the left arm
3) Usually described as a pressure sensation that also may be characterized as squeezing, aching, burning, or even sharp
4) In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas

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3
Q

In the context of myocardial infarction, what do the terms STEMI and nonSTEMI stand for?

A

STEMI means ST elevation myocardial infarction (1/2 mark) , nonSTEMI is no ST elevation myocardial infarction (1/2 mark)

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4
Q
  1. What is the significance of a new Q wave in the ECG of a person suffering from a myocardial infarction ? (1 mark)
A

A new Q wave indicates there is a zone of myocardium that has undergone irreversible damage.

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5
Q
  1. Which two classes of enzymes would be measured in the blood on a patient with a suspected AMI? (2 marks) Explain the difference in the time course of the changes in these two enzymes (2 marks)
A

MB subtype of the enzyme creatine kinase: (1 mark: ½ mark for creatine kinase) CK-MB levels increase within 3-12 hours of the onset of chest pain (1/2 mark) , and return to baseline after 48-72 hours (1/2 mark)

Cardiac troponins T (1/2 mark) and I (1/2 mark) The cardiac troponins are released within 4–6 hours of an attack of MI (1/2 mark) and remain elevated for up to 2 weeks (1/2 mark)

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6
Q

What is the main difference between stable and unstable angina

A

In stable angina symptoms only appear during exercise or exertion. (1 mark).

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7
Q

What does a raised C-reactive protein level indicate? (

A

It is a blood marker for inflammation OR it is a marker for increased heart disease risk

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8
Q

Explain the difference between dyspnea and orthopnea (

A

Dyspnea is painful or difficult breathing. (1/2 mark). Orthopnea is difficulty breathing when lying down. (1/2 mark)

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9
Q

Explain why Mr O’Conlan has pains in his left upper arm. (

A

Pain fibres from the heart converge in the spinal cord with pain fibres from the arm and neck (1 mark). Because we have no sensory map of the inside of our body when either set are active the person will feel pain in the arm or neck (1 mark)

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10
Q

Apart from calcium channel blockers and aspirin, List the three other drug types most commonly used to treat angina and explain briefly how each one works (3 marks)

A

Nitrates (1/2 mark) ; eg glyceryl trinitrate (nitroglycerin, GTN)
These drugs release nitric oxide causing coronary vasodilatation (1/2 mark) (and opening of collateral vessels)
Beta-blockers; eg atenolol, metoprolol, propranolol. (1/2 mark)
These drugs have negative inotropic and chronotropic effects due to competitive blockade of cardiac beta-receptors. (1/2 mark)
ACE inhibitors eg captopril (1/2 mark)
Vasodilators that relax coronary vascular smooth muscle by blocking conversion of angiotension 1 to angiotensin 2. (1/2 mark)

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11
Q

List four major reversible risk factors for angina

A

Smoking, Hypertension, Hyperlipidaemia, Obesity, Physical inactivity

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12
Q

Define the terms tachypnea and dyspnea (2)

A

Tachypnoea – Abnormally rapid breathing >16 breaths per minute
Dyspnoea – Difficult or laboured breathing

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13
Q

What causes angina (1)

A

insufficient blood supply to the myocardium leading to ischaemia
Usually atherosclerosis with a narrowed lumen (as you exercise the demand increases to flow isn’t sufficient)

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14
Q

What are risk factors for angina – reversible and irreversible? (4)

A

Reversible - Diabetes, obesity, poor diet, hypertension

Irreversible - Age, male, ethnicity, family history

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15
Q

What changes on the ECG can be seen during the exercise stress test? (2)

A

ST depression
T wave inversion
Pathological Q waves

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16
Q

What is the action of Aspirin, calcium antagonists and statins + why is he given these? (3)

A

Aspirin - COX 1 + 2 inhibitors, anti platelet (blocks thromboxane) decreases probability of vlot forming
Calcium channel antagonist - Amlodipene, diltiazem, verapamil, Causes systemic and coronary vasodilation with negative ionotropic effects for diltiazem and verapamil. Inhibits ca mediated muscle contraction
Statins - Competitive inhibitor of HMG CoA reductase - inhibits formation of excess cholesterol in the blood –> reduces the growth of the atheroma

17
Q

What 2 other drug treatments could he be given and what is the mechanism of these? (2)

A

BB - atenolol, propanolol, negatively ionotropic and chronotropic
Nitrates - Glyceryl trinitrate given sublingually, causes coronary vasodilation by an action on the vascular smooth muscle

18
Q

How do you diagnose a AMI? (2)

A
ECG
	ST elevation – In 2 or more adjacent ECG leads 
	T wave inversion
	Pathological Q waves- dead zone of myocardium --> irreversible 
Cardiac enzymes
-C reactive protein
-Troponin
-Creatine kinase
- AST
- Lactate dehydrogenase 
- Myoglobin
19
Q

How do you treat STEMI? (2)

A
Oxygen
Aspirin
Pain relief 
Percutaneous coronary intervention 
Thrombolytics
20
Q

What is reperfusion therapy? (2)

A

Thrombolytics
and surgery (PCI)
combined to treat STEMI

21
Q

How do you treat NSTEMI? (2)

A

Aspirin
Clipidogrel
Factor Xa inhibitor

22
Q

Why would you give streptokinase? (1)

A

To break down fibrin directly

TPA

23
Q

What complications can occur after an AMI? (3)

A

Afib
2nd MI
Heart failure
Mitral regurgitation

24
Q

How can a MI patient be managed? (2)

A

Aspirin for a year

25
Q

What medications must a MI patient have on discharge? (2)

A

Aspirin
Beta-blocker
In most cases an angiotensin converting enzyme inhibitor
In those with an elevated cholesterol a statin
They should understand the reasons underlying the prescription of these drugs and the
need for long-term treatment

26
Q

What is coronary rehabilitation? (2)

A

Health education

Supervised aerobic exercise

27
Q

How can angina lead to an AMI? (2)

A

If blood clot grows and blocks the artery

28
Q

Angina symptoms

A

Crushing pain
Sweating
Fainting
Breathlessness

29
Q

What is the pathophysiology of MI

A

o Triggering event causes disrupting of unstable atherosclerotic plaque in c.a –> rupture –>clotting cascade –> occlusion of the artery
o Impaired blood flow to heart – ischaemic cascade, heart cells die and do not grow back, collagen scar forms in their place
o Calcium can deposit in the CA and can be detected with CT scans

30
Q

Why can you have diaphoresis in an MI

A

extreme sweating, light headedness

due to surge of catecholamines from Sns in response to pain

31
Q

What is acute Coronary Syndrome

A

Unstable angina
NSTEMI
STEMI

32
Q

Pathological Q wave

A

a dead zone of myocardium that has undergone irreversible damage and
death.