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Phase 2A - Cardiovascular > Conditions - Ischaemic Heart Disease > Flashcards

Conditions - Ischaemic Heart Disease Flashcards

1
Q

What are the different types of ischaemic heart disease?

A

Angina pectoris and myocardial infarction

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2
Q

What is angina pectoris?

A

Central chest tightness/pain caused by myocardial ischaemia

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3
Q

What is the clinical presentation of angina pectoris?

A

Symptoms: Dyspnoea, nausea, sweatiness and syncope

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4
Q

What are the different types of angina pectoris?

A

Stable
Unstable
Decubitus
Prinzmetal

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5
Q

What is stable angina pectoris?

A

It is induced by effort and relieved by rest

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6
Q

What is unstable angina pectoris?

A

Increasing severity and frequency. Minimal exertion and there is a high risk of MI

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7
Q

What is decubitus angina pectoris ?

A

Pain when lying flat

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8
Q

What is prinzmetal angina pectoris?

A

During rest

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9
Q

What is the pathophysiology of stable, unstable and decubitus angina?

A

Atheroma obstructing or narrowing coronary artery

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10
Q

What is the pathophysiology of prinzmetal angina?

A

Coronary artery spasm

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11
Q

What is the aetiology of angina?

A

Atheroma

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12
Q

What are the diagnostic tests done for angina pectoris?

A

ECG

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13
Q

What does an ECG of angina pectoris show?

A

Usually normal
Some ST depression
Flat or inverted T waves

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14
Q

What is the treatment of angina pectoris?

A 
Modify risk factors
Aspirin 
Beta blockers 
Nitrates 
Long -acting calcium channel blockers 
K+ channel activators
Statins
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15
Q

What is the action of aspirin in the treatment of angina pectoris?

A

irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation

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16
Q

What is the action of beta blockers in the treatment of angina pectoris

A

blocking the effect of adrenaline on the heart. This has two major beneficial effects in patients with angina: Slowing of the heart rate, in particular during periods of exercise or stress. Reducing the force of heart muscle contraction

17
Q

What is the action of nitrates in the treatment of angina pectoris?

A

Nitrates work as venodilators and arterial dilators, and by these actions in patients with angina pectoris can reduce myocardial oxygen demands while maintaining or increasing coronary artery flow

18
Q

What is the action of calcium channel blockers in the treatment of angina?

A

The entry of calcium is critical for the conduction of the electrical signal that passes from muscle cell to muscle cell of the heart, and signals the cells to contract.
It also is necessary in order for the muscle cells to contract and thereby pump blood.
In the arteries, the entry of calcium into muscle cells constricts the arteries.
Thus, by blocking the entry of calcium, calcium channel blockers reduce electrical conduction within the heart, decrease the force of contraction (work) of the muscle cells, and dilate arteries.

19
Q

What is the action of K+ channel activators in the treatment of angina?

A

Open or prolong the open state duration of potassium channels. Hence they promote potassium efflux, hyperpolarize the cell membrane, thus preventing intracellular penetration of calcium through the voltage-dependent calcium channels

20
Q

What is a myocardial infarction?

A

Death of heart tissue due to an ischaemic event

21
Q

What are the types of MI?

A

STEMI and NSTEMI

22
Q

What is the clinical presentation of MI? Give 3 symptoms and signs

A

Symptoms: Nausea, crushing chest pain, vomiting, dyspnoea, sweating, fatigue, palpitations
Signs: fever, hyper/hypotension, 3th/4th heart sound and signs of congestive heart failure

23
Q

What is the pathophysiology of MI?

A

Blockage of the coronary artery by a thrombus. This leads to ischaemia in the cardiac tissue

24
Q

What is the aetiology of MI?

A

Atheroma

25
Q

What is the epidemiology of MI?

A

600/100,000 men

200/100,000 women

26
Q

What are the diagnostic tests for MI?

A

ECG, FBC and cardiac enzymes

27
Q

What does an ECG show for MI?

A

For a STEMI, ST elevation
Peaked T waves then T wave inversion
New Q waves
New conduction defects

28
Q

What does a FBC show for MI?

A

It rules out anaemia

29
Q

What do cardiac enzymes show for MI?

A

Elevated levels of troponin T and I are markers for cardiac damage

30
Q

What is the treatment for MI?

A

Thromolytic (aspirin)
PCI - percutaneous coronary intervention
CABG - coronary artery bypass graft
Clopidogrel for 30 days

31
Q

What are the complications of MI?

A

Ischaemia - angina, recurrent infarct
Mechanical - Left heart failure, ventricular septal rupture, free wall rupture, pericardial bleeding, cardiac tamponade, false aneurysm, acute mitral regurgitation
Arrhythmias - ventricular tachycardia, ventricular fibrillations, total AV block, bradycardia
Thrombotic/Embolus - thrombus can form in ventricle wall, DVT, PE
Pericarditis - dressler’s syndrome
Depression

32
Q

What is the sequelae of MI?

A

Shock
Heart failure
Pericarditis

33
Q

What is ACS?

A

Acute coronary syndrome

34
Q

Types of ACS?

A

ST elevation

Non-ST elevation

Phase 2A - Cardiovascular (8 decks)

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