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PATH30001 - Mechanisms of Disease > Lecture 2 - AMI & Atherosclerosis > Flashcards

Lecture 2 - AMI & Atherosclerosis Flashcards

1
Q

Why is AMI significant?

A

It is the leading cause of death in industrialised countries

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2
Q

What are the two main pathways that lead to sudden coronary death?

A
  1. Myocardial ischema

2. Plaque in coronary arteries

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3
Q

What is atherosclerosis?

A

• Fibrofatty plaques in intima of arteries
due to
• Chronic inflammatory healing response

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4
Q

What is the major underlying cause of AMI?

A

Atherosclerosis (95%)

Lifestyle dependent

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5
Q

How does age and gender affect chance of AMI?

A
  • Chance increases with age

* Men are affected for than women

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6
Q

Describe the time scale during an MI

A 
As time elapses,
very soon:
 • lactate increases
 • ATP decreases
over a matter of hours:
 • decrease in 'salvageable myocardium'
 • increase in dead myocardium
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7
Q

How long does it take for loss of contractility during an MI?

A

< 2 mins

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8
Q

Describe the pathogenesis of atherosclerosis

A
  1. Endothelial injury
  2. Accumulation of lipoproteins
  3. Monocyte adhesion to the endothelium
  4. Platelet adhesion
  5. Factor release from activated immune cells
  6. Smooth muscle cell proliferation and ECM production
  7. Lipid accumulation
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9
Q

Which lipoproteins accumulate in atherosclerosis?

A

Mainly LDL

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10
Q

What does the location of the MI depend on?

A

The coronary artery that is occluded

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11
Q

Compare transmural and non-transmural infarcts

A

Transmural: entire thickness of a portion of the wall is affected

Non-transmural: part of wall is affected

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12
Q

What changes can occur to the plaques in atherosclerosis?

A
  • rupture
  • erosion
  • ulceration
  • haemorrhage
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13
Q

Why do changes to the plaque occur?

A

The plaque is unstable and weak

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14
Q

What is an aneurysm?

A

Ballooning of a portion of an artery

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15
Q

What are the clinical complications of atherosclerosis?

A
  • Aneurysm and rupture
  • Occlusion by thrombus
  • Critical stenosis
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16
Q

In what case does critical stenosis occur?

A

Continual growth of plaque so that the artery is almost completely blocked

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17
Q

What are some risk factors for atherosclerosis?

A
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Immune reactions
  • Toxins
  • Viruses
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18
Q

What is the normal role of monocytes?

A
  • Replenish macrophages and dendritic cells
  • When an immune response is activated, they are recruited in large numbers and differentiate into macrophages for an effective immune response
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19
Q

What is a foam cell?

When are where are they seen?

A
  • A fat laden macrophage

* Seen in atherosclerosis in the intima of vascular wall

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20
Q

What is the role of smooth muscle cells in atherosclerosis?

A
  • Recruited into the intima

* Proliferate

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21
Q

Which part of the myocardium is at risk in a given coronary artery occlusion?

A

The myocardium that derives its blood supply from the portion of coronary artery distal to the blockage

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22
Q

Which part of the wall layer undergoes necrosis first in a coronary artery occlusion?

A
  • The sub-endocardial zone (interal layers)

* The necrosis then extends outward

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23
Q

What does the size of the zone of necrosis depend on?

A
  • Duration of occlusion

* Presence of collateral circulation

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24
Q

What is subacute period of MI?

A

Days old

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25
What is the role of apoptosis in MI?
Occurs rapidly post-ischemia
26
What happens in MI if there is no reperfusion?
Necrosis, which is complete after 6-12 hours
27
Compare 'salvage', 'partial salvage' and 'complete infarct'
This depends on how much time passes before reperfusion Salvage: no necrosis, slight dysfunction Partial salvage: necrosis with haemorrhage & contraction bands Complete infarct: necrosis
28
What happens to the infarct site over the next few days?
* monocyte infiltration * phagocytosis of necrotic cells * repair; scar tissue formation
29
What are the necrotic cells replaced with after an MI?
Collagenous scar tissue
30
What are the possible medical interventions to prevent MI?
* Balloon angioplasty * Thrombolysis * Coronary artery bypass graft
31
What are the markers of myocardial infarction?
* Creatinine phosphokinase * Troponin These are released by the now leaky membrane of the myocytes
32
Which tests are done to detect MI?
* Troponin assay (most specific) | * CK-MB assay
33
Why does reperfusion injury occur?
* The new blood flowing in is ischemic, as are the cells in the blood. * These cells are producing free radicals * Free radicals cause mitochondrial damage * Necrosis
34
How can reperfusion injury be avoided?
With pharmaceuticals: • Xanthine oxidase inhibitors • Blood without polymorphs • Activation of RISK pathway through ischemic post conditioning
35
What is 'preconditioning'?
Repeated, short-lived ischemia | • Provides protection from later ischemia
36
What is mPTP?
Mitochondrial permeability transition pore • Protein pore in the inner membrane of the mitochondria, which forms under pathological conditions • Increase in permeability of the mitochondrial membrane
37
What does the mPTP lead to?
Cell death (apoptosis or necrosis) 1. mPTP 2. Cytochrome c lost from mitochondria into cytosol 3. Activation of caspases 4. Activation of endonucleases & degradation of cytoskeleton 5. Apoptosis
38
What are some complications of AMI?
* Arrythmias * Contractile dysfunction * Rupture * Pericarditis
39
What is VI?
Vascular insufficiency
40
What is Acute myocardial infarction due to?
Macroscopic cell death of myocardium due to Vascular Insufficiency
41
Why does hypertrophy often occur in myocardial infarction?
Heart not pumping as well, so muscle hypertrophies to compensate
42
What is the composition of the plaque?
Cholesterol | Fibrous material
43
What is the initial event in AMI? | When does this occur?
Sudden change in the plaque | This can take decades to get to this point
44
What causes vasopasm?
Mediators released from platelets
45
Is necrosis of heart muscle after AMI fatal?
No | It depends on how much of the heart muscle is affected
46
How quickly does ATP depletion occur in AMI?
Starts after a few seconds | Most ATP is gone after about 40 mines
47
Once there is even a very small injury to endothelium, what starts to occur?
Accumulation of lipoproteins
48
Described changes to the smooth muscle layer in arteries during atherosclerosis
Smooth muscle thickens
49
What determines whether an infarct is transmural or non-transmural?
Transmural caused by complete blockage of coronary artery Non-transmural caused by partial blockage
50
What is global hypotension?
When there is narrowing of all coronary arteries This leads to circumferential sunendocardial infarct
51
What do small occlusions of coronary arteries lead to?
Microinfarcts
52
Compare the smooth muscle layer in arteries of infants and in aging adults
Infants: think muscle layer | Aging adult: thickened, reduced diameter of artery
53
What is happening when a plaque ruptures?
Plaque is normally covered by fibrotic tissue | Rupture leads to plaque spilling out through the fibrotic tissue, bringing about an acute inflammatory response
54
What is a thrombus?
Aggregation of platelets | i.e. a clot
55
Why are smooth muscle cells recruited in atherosclerosis?
Abnormal growth factor release recruits them
56
What do macrophages attempt to do in atherosclerosis?
They phagocytose fat in an aim to resolve the problem | This adds to the problem
57
Why does the inner part of the heart muscle become necrotic first?
Further away from the blood supply
58
How do apoptosis inhibitors affect the size of the infarct?
They reduce the size of the infarct
59
How quickly does reperfusion need to occur so that there is no necrosis?
20 mins
60
What is happening 3-4 days after an AMI?
Massive neutrophil infiltration
61
What is happening 7-10 days after an AMI?
Necrotic cells
62
What is happening 21 days after an AMI?
Collagen deposition
63
What is the structure of the tissue 60 days after an AMI?
Scar tissue
64
What clinical signs indicate AMI?
• Abnormal ECG • Biomarkers in blood: - Troponin - CK
65
Up to half of the region of necrosis can be due to:
Reperfusion injury
66
What does xanthine oxidase do?
Leads to production of ROS in neutrophils
67
What is done before reperfusion?
Ischemic postconditioning
68
What is the effect of ischemic postconditioning?
Inhibit / close the mPTP (mitochondrial permeability transport pore) Ie blocking the mechanism of apoptosis
69
Why are mPTPs opened after ischemia?
It is part of the apoptosis pathway
70
Under what conditions can complete rupture of the myocardium occur?
``` When there has been a previous heart attack and there is necrotic tissue The second (or third...) AMI then causes rupture of hge weakened tissue ```
71
Describe the pathogenesis of atherosclerosis
(learn diagram) 1. Exposure 2. Epithelial injury 3. Monocyte recruitment and adhesion 4. Monocyte → macrophage 5. LDL crosses from blood stream into intima of blood vessel, then into macrophage Macrophage → foam cell 6. Smooth muscle cell precursor recruitment 7. Hypertrophy, ECM production, necrosis (plaque formation)
72
Why is blood without polymorphs used to avoid reperfusion injury?
The polymorphs are producing ROS, so we want fewer of these reaching the at risk tissue

PATH30001 - Mechanisms of Disease (34 decks)

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