Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1Principles of Biomedicine - MD1 > 57 - Ischaemic Heart Disease > Flashcards

57 - Ischaemic Heart Disease Flashcards

1
Q

Examples of acute ischaemic heart disease

A

Unstable angina, myocardial infarct, sudden cardiac death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Examples of chronic ischaemic heart disease

A

Stable angina, chronic myocardial ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Factors limiting coronary blood flow 1) 2) 3) 4)

A

1) Perfusion pressure 2) Coronary vascular resistance 3) External pressure 4) Intrinsic regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What could lead to decreased perfusion pressure in coronary arteries?

A

Systemic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What could lead to increased coronary vascular resistance?

A

Coronary artery atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What could lead to external compression of the coronary arteries?

A

Muscular wall of the ventricle contracts and compresses coronary arteries. Vessels of the subendocardium particularly get squeezed between contracting muscles and pressure inside the ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Example of intrinsic regulation of coronary vessels 1) 2)

A

1) Endothelium releases prostacyclin, NO, endothelin 2) Adenosine, lactate, hydrogen are local metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Typical blood flow in solid organs

A

Have a hilum. Blood flows from hilum to capsule or periphery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Typical blood flow in hollow organs

A

Fatty external layer contains vessels. Blood flows from outside to inside.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where do infarcts often occur?

A

At end of blood supply (EG: Causing wedge-shaped necrosis in solid organs, causing infarcts near lumen in hollow organs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Part of heart most vulnerable to infarction

A

Subendocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do infarcts spread in the heart?

A

Begin in the inside, spread outwards (non-transmural -> transmural infarcts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Coronary arteries 1) 2) 3) 4) 5)

A

1) Left main 2) Left anterior descending 3) Left circumflex 4) Right coronary 5) Posterior descending

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How to tell where is up and down on a cardiac slice 1) 2) 3)

A

1) Posterior side is more flat 2) Posterior side is less fatty 3) Posterior descending coronary artery is at septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

*Blood supply of the heart

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Blood vessel supplying anterior wall and 2/3 of the septum in the heart

A

Left anterior descending coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Blood vessel supplying lateral wall of heart

A

Left circumflex coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Blood vessel supplying posterior wall of the heart

A

Posterior descending coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where does the posterior descending coronary artery arise from?

A

In right-dominant heart (majority of people), from right coronary artery. In left-dominant people, from left circumflex coronary artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is a heart attack?

A

Myocardial infarction. Imbalance between O2 supply and demand of myocardium, resulting in ischaemia and cell death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Most common cause of myocardial infarct

A

Acute plaque event. Rupture or haemorrhage of atherosclerotic plaque, with formation of occlusive thrombus of coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

30 minutes after myocardial infarct 1) 2) 3) 4)

A

1) No macroscopic, microscopic changes 2) Intracellular changes (EG: mitochondrial swelling) visible on electron microscope 3) Functional loss of contractility 4) Might see ECG changes (ST depression, T wave inversion) 5) Angina - REVERSIBLE INJURY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How long after ischaemia sets in does irreversible injury occur?

A

~30 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Indicators of irreversible cardiac damage 1) 2)

A

1) Leaking of cardiac proteins (creatine kinase, troponin) 2) Leaking of current (ST segment elevation, ST segment depression, myocardial irritability)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How long after an infarct are troponin blood levels detectable?

A

~3-4 hours post-infarction

26
Q

Complications 30 minutes-12 hours post-infarction 1) 2)

A

1) Arrhythmia (damaged myocytes are unstable) 2) Cardiac failure (damaged myocytes can’t contract properly)

27
Q

NSTEMI 1) 2) 3)

A

1) Non-ST elevated myocardial infarction. 2) Leads to a non-transmural infarct. 3) From a transient or partial obstruction of coronary arteries, leading to a regional subendothelial infarct.

28
Q

STEMI 1) 2) 3)

A

1) ST elevated myocardial infarction 2) Leads to a transmural infarct. 3) From a permanent, full-thickness occlusion of coronary artery

29
Q

Histology of heart 30 minutes-12 hours post-infarction 1) 2) 3)

A

1) Wavy myocytes
2) Cell death, with faded nuclei, interstitial red blood cells
3) Early necrosis is present (faintly eosinophilic)

30
Q

Are there any gross morphological changes 30 minutes - 12 hours post-infarct?

A

No

31
Q

What happens 12-24 hours post-infarct?

A

Necrosis and early acute inflammation

32
Q

Histology of cardiac muscle 12-24 hours post-infarct 1) 2)

A

1) Neutrophils present
2) Contraction band necrosis

33
Q

Gross appearance of heart 12-24 hours post-infarct

A

Mottled, haemorrhagic myocardium

34
Q

Gross appearance of heart 1-3 days post-infarct

A

Soft yellowing of wall (necrosis is grossly-apparent)

35
Q

Histological appearance of myocardium 1-3 days post-infarct

A

Heavy neutrophil infiltration Loss of structure.

36
Q

Peak of troponin levels in the blood

A

Around 2 days post-infarct

37
Q

How long post-infarct can troponin be detected?

A

Up to two weeks

38
Q

What is happening 3-7 days post-infarct?

A

End of acute inflammation and beginning of granulation

39
Q

Histological appearance of myocardium 3-7 days post-infarct 1) 2) 3)

A

1) Macrophages ingesting dead myocytes. 2) Fibroblasts, vessels of granulation tissue appear. 3) Collagen begins being laid down 5-6 days post-infarct

40
Q

Gross appearance of heart 3-7 days post-infarct

A

Central yellowing (necrosis) surrounded by red rim (vascularised granulation tissue)

41
Q

Complications 1-3 days post-infarct 1) 2) 3) 4) 5)

A

1) Arrhythmia (damaged myocytes are unstable) 2) Cardiac failure (damaged myocytes can’t contract) 3) Mural thrombus (damaged wall isn’t moving properly) 4) Rupture (necrotic wall is weak) 5) Pericarditis (preponderance of inflammatory mediators)

42
Q

Three ways in which infarcted heart can rupture 1) 2) 3)

A

1) Rupture of free ventricular wall 2) Rupture of papillary muscle 3) Rupture of IV septum

43
Q

Outcomes of a rupture of free ventricular wall 1) 2)

A

1) Blood can seep into pericardium - Haemopericardium 2) Haemopericardium can compress heart until it stops - Cardiac tamponade

44
Q

Outcomes of a ruptured papillary muscle 1) 2) 3)

A

1) New onset murmur 2) Mitral regurgitation 3) Cardiac failure

45
Q

Effect of a ruptured IV septum 1) 2) 3)

A

1) New onset murmur 2) Ventricular septal defect 3) Cardiac failure

46
Q

What can lead to cardiogenic shock?

A

Rupture of papillary muscle of IV septum. Cardiogenic shock is when the heart can’t generate blood pressure to supply brain

47
Q

Histological appearance of heart 1-8 weeks post-infarct 1) 2)

A

1) Early granulation tissue - High cellularity, vascularity, little collagen 2) Late granulation tissue - Gradual reduction in cells, vessels, increase in collagen

48
Q

Possible complications of heart 1-8 weeks post-infarct 1) 2) 3) 4)

A

1) Lesser chance of arrhythmia or cardiac failure 2) Mural thrombus (damaged wall isn’t moving properly) 3) Aneurysm (the wall is stronger because of collagen, but is flexible to wall stress, and might bulge out) 4) Aneurysm exacerbates risk of mural thrombus.

49
Q

Histological appearance of heart over 8 weeks post-infarct

A

Densely-collagenous scar

50
Q

Complications over 8 weeks post-infarct 1) 2) 3)

A

1) Arrhythmia (damaged myocytes have been cleared, but there are isolated islands of autorhythmic myocytes) 2) Aneurysm, mural thrombus (aneurysm can form, but is unlikely to rupture with strong scar tissue) 3) Cardiac failure (biggest threat. Damaged myocytes can’t be replaced, LV remodelling might occur, decompensation can occur)

51
Q

Non-atherosclerotic possible causes of MI 1) 2) 3)

A

1) Coronary artery dissection 2) Thrombosis due to vasculitis 3) thromboembolism from heart (EXTREMELY RARE. So much so that this isn’t really relevant)

52
Q

Difference between stable and unstable angina

A

Stable angina is reproducible chest pain that is induced by exertion, disappears with cessation of exertion. Unstable angina presents as cardiac chest pain at rest or with minimal exertion

53
Q

What is angina?

A

Transient ischaemia of cardiac muscle. Can lead to infarction (which is irreversible damage)

54
Q

What is stable angina due to?

A

Atherosclerotic narrowing of coronary artery. Symptoms appear with over ~70% stenosis

55
Q

What can bring about unstable angina?

A

Acute plaque event (EG: coronary artery thrombosis)

56
Q

What brings about chronic myocardial ischaemia

A

Chronic narrowing of coronary arteries

57
Q

Outcomes of chronic narrowing of coronary arteries? 1) 2) 3) 4)

A

1) Chronic myocardial ischaemia 2) Small areas of subendothelial ischaemia 3) Patchy myocyte necrosis, replacement by fibrosis 4) Similar risk of cardiac failure and arrhythmia as LV hypertrophy

58
Q

Sudden cardiac death

A

Unexpected cause, death within an hour of symptoms. In a person with no previous diagnosis of a fatal condition. Frequently an arrhythmic event, but can also be a complication of a silent MI within the last few days

59
Q
A
60
Q
A

1Principles of Biomedicine - MD1 (157 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions