Lecture - Pathology (Ischaemic Heart Disease)

Question 1

Terminology:

For each other these terms, explain what they are in your words (with your understanding)

• Ischaemia
• Hypoxia
• Infarct(-ion)
• Coagulative (coagulation) necrosis
• Liquifactive necrosis

Which one of ischemia or hypoxia is worse? Why?

Answer 1

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Question 2

Ischaemic heart disease (IHD)

What is the clinical presentation? One or more of what?

Answer 2

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Question 3

Normal Heart and Coronary Arteries

1. Describe what a normal artery looks like in terms of:
   - intima
   - IEL
   - Media
   - Adventitia
2. Surface of an aorta from inside
   - what do the valves look like?
3. Epicardial surface of the heart

Answer 3

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Question 4

Ischaemic Heart Disease - Pathogenesis

1. Insufficient _____ ____ relative to what?
2. What are most cases due to?
3. What does the term ‘atherosclerosis’ literally mean?
4. What arteries in the diagram are usually involved? (order them)

Answer 4

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Question 5

Atherosclerosis

1. List some modifiable and some non-modfiable risk factors
   - for some, maybe explain why they lead to athero

It’s Pathogenesis

2. What lies at the heart of athero?
3. What is atherosclerosis considered to be? Like, its definition almost
4. What does ‘endothelial cell injury’ mean? Does it have to be a physical injury?
5. What does it mean by “the endothelial cells have 2 sides to them”? How does this relate to athero?
6. What is the typical response to vascular injury?
7. Okay, in your own words - describe the pathogensis (“response to injury” hypothesis) of atherosclerosis
8. What’s an atheroma?
   - what’re the layers
   - what’s the deal with new BV? (neovascularization)
   - what’s the deal with it bring crunchy -why?
   - why do you need to have an intact endothelium?

It’s Morphology

1. What does it look like in its early phase? I mean, what will you tend to see (even on your own BV)?
   - both gross and microscopic
2. What will mature plaques look like gross and microscopic?

It’s complications

1. Okay, what does it most logically lead to?
   - what’s the critical percentage?
2. Something to do with media…….
3. Something to do with new vessels….
4. There’s another very obvious complication with an athero plaque…..
5. Which of the above complications are “Acute Plaque Changes” that lead to more acute symptoms?
6. Okay, now list the clinical consequcnes of that - just following on from all the above complications (where the athero is = you’ll get that clinical consequence)
7. What are stable vs vulnerable plaques? How does this relate to thrombosus?
8. What do complicated plaques (with thrombis) look like gross and microscopically?

Answer 5

7. Alright so you have the regular response where when there is an edothelial injury and dysfucntion, there is increased vascular permeability, leukocyte and platelet adhesion. But then there is accumulation of lipoproteins in the vessel wall - mainly LDL and its oxidised form…this is a factor that leads to the chronic endothelial cell injury. Cytokines released will attract monocytes and that’ll migrate into the intima, transform into activated marophages that engulf lipids and become foam cells - these are cells that look like foam under the microscope. This will show up as a fatty streak on the vessel wall. For the macrophages, the oxidised form of LDL is mroe palatable. Now that you have the activated EC, SMCs, platelets and macrophages - this will lead to more cytokine and growth factors so SMC recruitment from media or from circulating precursors happens. These SMC will proliferate and produce extracellular matrix deposition. They will also engulf lipids (foam cells) just like macrophages. Then the T cells are recruited. Now an atheroscleortic plaque forms within the intima and this encroaches on the vascular lumen.

Question 6

IHD - Pathogeneis

1. Okay so there is chronic vascular _____ by atherosclerosis
   - what stenosis is considered ‘critical’?
   - How many of the LAD, RCA, LCX are affected for IHD?
2. What are the acute plaque changes? (that lead to more acute symptoms)
3. An element of _______ _______ can also

IHD - Clinical Presentation

1. There are four differnet clinical presentations of ischaemia in the heart - what are they?
2. Which of these presentations is “acute coronary syndrome” and is the result of the acute plaque changes (like the thrombus or haemorrahge into the plaque)

Question 7

IHD - Angina Pectoris

1. What is this?
   - _____ recurrent attacks of _____ or precordial chest pain lasting how long?
2. What is the pain a consequence of? What does it stimulate?
3. What sort of ischaemia can occur in diabetic pateints?
4. What is the pain described like?
5. There are three types of angina - what are they?
   - what’s each associated with?
   - relieved by?

Answer 7

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Question 8

IHD: MI

1. What’s this? Ischaemia severe enough to…..
2. Caused by what?
3. Platelet-derived mediators cause what? Explain this a little more
   - Can you relieve this by vasodilators?
4. SO the thrombus can expand to _____ occlude the vascular lumen
5. What’s the timeline of the events of myocardial ischaemia?
6. What are the cardiac biomarkers for the stuff that leaks out of the necrotic myocytes?
7. Where does ischaemia start (aka what dies first?) and then it becomes transmural so what does that mean about how fast we should intervene?
   - why does the subendocardial necrotic tissue still have a layer of healthy tissue on it?
8. On slide 34 is the MI distribution according to what artery is occluded - go label
   - what happens sometimes in shock?
9. What’s the gross morphology in MI from 12h to 8 weeks?
   - go look at the slides of the MI and their ages - imp bc in exams
   - go do the same with the microscopic
10. MI - complications
    - what are the types of complications you can get with myocardial cells dyring in MI? Be logiccal