Brainscape's Knowledge GenomeTM

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


See full index

MD3001 Cardiology > Ischaemic Heart Disease > Flashcards

Ischaemic Heart Disease Flashcards

1
Q

What are the causes of atherosclerotic coronary disease?

A
  • chronic coronary insufficiency (angina)
  • unstable coronary disease (MI/sudden ischaemic coronary death)
  • heart failure
  • arrythmia (acute ischaemia/scar related)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the subendocardial region?

A

the water-shed area of perfusion and the first region to become ischaemic

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

What cusp of the aortic valve becomes the right coronary artery?

A

right

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

What cusp of the aortic valve becomes the left coronary artery?

A

posterior

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

What are the risk factors for atherosclerotic coronary artery disease?

A
  • age
  • hypertension
  • hypercholesterolaemia
  • smoking
  • diabetes
  • obesity
  • physical inactivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the different pathologies of atherosclerotic coronary artery disease

A
  • fatty streak
  • fibro-fatty plaque
  • plaque disruption (rupture/erosion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the formation of the fatty streak

A
  • endothelial cells that line coronary arteries upregulate
  • attaches to monocytes by VCAM-1 adhesion molecules
  • transmigrates and becomes macrophage
  • ingests lipid in subendothelial space to become foam cell and form fatty streak
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the formation of fibro-fatty plaque

A
  • macrophage through interaction with T cells secretes cytokines
  • attracts smooth muscle cells from the tunica media to the subendothelial intimal space
  • they then secrete fibrin and collagen to make an ECM that is very tough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is angina represented on an ECG?

A

depressed ST

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

What is supply angina?

A

the mismatch of supply and demand of coronary blood flow

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

What is demand angina?

A

the mismatch of supply and demand of myocardial oxygen consumption

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

What are the 2 regulatory systems that control coronary circulation?

A
  • autoregulation (myogenic control)

- metabolic regulation

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

Describe autoregulation of coronary blood flow in relation to exercise

A
  • coronary blood flow can increase to accommodate an increase in O2 consumption during exercise
  • a rise in HR accounts for 1/3 of increase in blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the determinants of myocardial oxygen consumption?

A
  • variable per unit mass of tissue:
  • tension development (LV pressure/volume)
  • contractility
  • HR
  • basal activity per unit mass (fixed)
  • mass of tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is angina sometimes unpredictable in determining when it can come on?

A

variability in coronary blood flow due to factors (time of day/induced by the cold etc)

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

How can you anatomically assess for the identification of coronary heart disease?

A
  • CT coronary angiography

- invasive angiography

17
Q

What tests can you carry out to identify inducible ischaemia?

A
  • exercise stress test
  • dobutamine stress echo
  • myocardial perfusion imagine with exercise/pharmacological stress
  • cardiac MRI
18
Q

How can angina be treated?

A
  • therapeutically to reduce myocardial oxygen consumption

- improve coronary flow reserve through percutaneous coronary intervention/CABG/vasodilator drugs

19
Q

What vessels are used for CABG?

A
  • saphenous vein

- left internal mammary artery

20
Q

What are the main causes of MI?

A
  • plaque rupture

- plaque erosion

21
Q

Explain how complete occlusion of a vessel can occur

A
  • rupture/erosion of plaque
  • tissue blood doesn’t normal see is exposed and results in blood clotting
  • arteries adhere platelets which then contract and change shape
  • exposed to prothrombinase complex leading to more clotting
  • thrombus occludes vessel and propagates downstream which seals vessel
  • complete epicardial coronary occlusion
22
Q

Describe the pathology of an unstable plaque

A
  • macrophage changes
  • instead of directing healing factors to make a strong cap secretes MMPs that digest the matrix
  • weak and vulnerable
  • platelets adhere
23
Q

What are the factors that can modify the presentation of an acute MI?

A
  • time of the day
  • inflammatory activity
  • infection
  • elevation in BP
  • catecholamines
24
Q

What are the different ways of classifying MI?

A
  • by site of infarction (transmural/subendocardial)
  • by ECG (STEMI/NSTEMI)
  • by cause (type 1-5)
25
Q

What does STEMI imply?

A

transmural MI

26
Q

Type 1 MI

A

spontaneous MI related to ischaemia due to primary coronary event such as plaque erosion/rupture, fissuring or dissection

27
Q

Type 2 MI

A

MI secondary to ischaemia due to increased O2 demand or decreased supply

28
Q

Type 3 MI

A

Sudden unexpected cardiac death with symptoms suggestive of myocardial ischaemia

29
Q

Type 4 MI

A

MI associated with percutaneous coronary intervention/stent thrombosis

30
Q

Type 5 MI

A

MI associated with cardiac surgery

31
Q

How does age affect STEMI/NSTEMI?

A

NSTEMIs are more common with elderly population

32
Q

How do you diagnose MI?

A
  • clinical history shows ECG changes defining whether STEMI/NSTEMI
  • raised cardiomyocyte markers in blood such as troponin T/I
33
Q

How is STEMI managed?

A
  • anti-platelet agents:
  • aspirin
  • clopidogrel/anti-platelet agent
  • immediate revascularisation by primary PCI
34
Q

What are the adjunctive treatment options for STEMI?

A
  • statin drugs
  • ACE inhibitors
  • B-blockers
35
Q

What are the complications of STEMI?

A

Immediate:

  • ventricular arrhythmia/death
  • acute left heart failure

Early:

  • myocardial rupture
  • mitral valve insufficiency
  • ventricular septal defect
  • mural thrombus and embolisation

Late:

  • LV dilatation and heart failure
  • arrhythmia
  • reccurent MI
36
Q

What does NSTEMI imply?

A

sub-endocardial ischaemia

37
Q

What causes NSTEMI?

A
  • threatened STEMI
  • small branch occlusion
  • occlusion of well collateralised vessel
38
Q

How can you treat NSTEMI?

A
  • anti-platelet therapy
  • ant–ischaemics
  • statins
  • ACE inhibitors
  • coronary angiography and revascularisation

MD3001 Cardiology (56 decks)

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