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Pathology dt2 > Chapter 10: Complete lecture > Flashcards

Chapter 10: Complete lecture Flashcards

1
Q

What was discussed in the lecture? (you obvi don’t have to learn this, it’s to illustrate what’s discussed)

A

• Atherosclerosis: complications aneurysm / dissection • Myocardial infarction: causes and complications • Valve disease: infectious / non-infectious • Myocarditis: infectious / non-infectious • Cardiomyopathy: hypertrophic, dilated, restrictive, arrhythmogenic • Tumours: metastasis, myxoma

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2
Q

Does the media increase during atherosclerosis with inflammation?

A

No, it decreases

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3
Q

Does the intima increase during atherosclerosis with inflammation?

A

Yes

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4
Q

The intima increases because of lipid. How is this lipid also called?

A

Ceroid

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5
Q

There are cells that try to fagocytose the lipid/ceroid in the intima. What are these cells?

A

Antibody detecting Macrophages

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6
Q

How does a normal aorta appear (during surgery e.g.)?

A

You see smooth white substance, the elastin aorta

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7
Q

How does an aorta with minor/medium atherosclerosis look?

A

You see lesions, and in a worsened state necrosis

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8
Q

How does an aorta with sever atherosclerosis appear?

A

There are plaques thrombi, might be a dilation with aneurysm, and in the worst state a rupture of the vessel wall

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9
Q

What might be the result of splicing of the wall?

A

Hemorrhage/thrombosis

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10
Q

What may a dissection be caused by?

A
  • a perforation of an atherosclerotic plaque
  • bleeding within the vessel wall, a so-called hematoma (this can be independent of atherosclerosis)
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11
Q

How does mucoid media degeneration affect the vessel wall?

A

There is loss of elastic fibers (less elastic aorta) and there is mucoid depositions (glycosaminoglycans) causing a weakening of the media

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12
Q

If mucoid media degeneration is found in patients above 45y/o, what is the (probable) cause?

A

Age

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13
Q

If mucoid media degeneration is found in patients below 45y/o, what is the (probable) cause?

A

Genetic

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14
Q

What complication can occur because of mucoid media degeneration

A

Aneurysm development and dissection

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15
Q

Aneurysm and dissection can have a genetic cause: disease of … (2 answers)

A

fibrilin (stabilizes elastin) or collagen

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16
Q

What type of malformation (in regard to disease of aneurysm/dissection) is found in Marfan Disease?

A

Thin and fragmented elastin

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17
Q

What type of malformation (in regard to disease of aneurysm/dissection) is found in Ehlers-Danlos?

A

malformation collagen with a strong variation in collagen fiber diameter

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18
Q

What is degeneration? (in regard to heart valves)

A

thickening of the valve with fibrosis and inflammation

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19
Q

What is atherosclerosis?

A

degeneration plus ceroid/calcification

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20
Q

Which heart valves are often degenerated/have atherosclerosis?

A

aortic valve (in between left ventricle and aorta) and mitral valve (in between left ventricle and left atrium)

21
Q

True/false: infectious endocarditis is mainly caused by a bacterial infection

A

True

22
Q

What cellular responses are seen in infectious endocarditis?

A

Thrombosis and necrosis of the valve

23
Q

How can you see the difference between thrombosis and necrosis on a valve? (slide 10)

A

Thrombosis is red, necrosis is white (very roughly speaking oc)

24
Q

True/false: there is lipid in the media

A

False, in the intima

25
Q

How is lipid phagocytosed?

A

By macrophages (partly succesful)

26
Q

What parts of the vessel wall are affected by chronic inflammation? And how?

A

Intima (increase) /media (decrease) /adventitia (fibrosis)

27
Q

What is an aneurysm?

A

Dilation of blood vessel

28
Q

What is a dissection?

A

Splicing of blood vessel

29
Q

Which layer(s) of a blood vessel increase(s) during atherosclerosis: a) Intima b) Media c) Intima and media d) No layer

A

a) Intima

30
Q

What is a major complication of atherosclerosis in coronary arteries?

A

Acute myocardial infarction (AMI)

31
Q

Please look at the figure to see how e.g. the right corona artery causes failure of the posterior MI

A

(i don’t think you should know which artery causes which failure, but understand the concept)

32
Q

What is a stable atherosclerotic plaque?

A

thick fibrous cap without inflammation in the cap

33
Q

What is an unstable atherosclerotic plaque?

A

thin fibrous cap or thick fibrous cap with inflammation in the cap

34
Q

What may the causes of Acute Myocardial Infarction (AMI) be?

A

Thrombus, bleeding/hemorrhage, plaque bleeding, dissection

35
Q

How will a stable plaque with a thick cap become an unstable plaque

A

Inflammation

36
Q

Acute Myocardial Infarction (AMI) can also occur in the intramyocardial coronary artery. What are the causes?

A
  1. hypertension 2. small vessel disease (thickening of the wall so less oxygen diffusion..) 3. Thickening intima cor art. (see also myocardial bridging cor art) (more info see slide 18&19)
37
Q

An Acute Myocardial Infarction (AMI) is seen on the electron microscopy after 2-3h, and there is calcium related depositions of mitochondria. What does this show?

A

Signs of cell damage

38
Q

Another way to show AMI is by nitrobluetetrazolium (NBT), that stains lacatedehydrogenase (LDH). What color is this staining?

A

Purple

39
Q

So, if a heart is depicted purple, is this good?

A

Yes, it means there is no loss of LDH

40
Q

Explain where neutrophilic granulocytes are present during AMI (with timeline please)

A
  1. 6-12h: granulocytes are present in the vessels 2. 12h-3d: granulocytes are in between cardiomyocytes 3. 3-5d: degenerating granulocytes
41
Q

What happens because of the degeneration of the neutrophilic granulocytes?

A

Necrosis of cardiomyocytes

42
Q

1-2w after Acute Myocardial Infarction (AMI), granulation tissue will be formed. Which cells are then seen in the tissue?

A

Lymphocytes, macrophages and fibroblasts

43
Q

What are complications of AMI?

A

Rupture of the papillary muscle -> dysfunction of the heart valve Aneurysm of the heart -> thinning of the ventricle wall

44
Q

Rupture of the heart in transmural infaction is…..

A

infarction of the full thickness of the ventircle wall

45
Q

How is Acute Myocardial Infarction (AMI) treated?

A

• Drug therapy: Thrombolysis • Minimally invasive: Stent • Surgical: Bypass operation

46
Q

The teacher told about his research of myocardial infarction. Explain the main concepts

A

*Flip-flop of the plasma membrane of cardiomyocytes facilitates post-MI inflammation and thus increases the infarction area in days after AMI *Flip-flop= translocation of negative loaded phospholips to the outer membrane, f.i. PS: this can be detected by Annexin V *Acute phase proteins (sPLA2-IIA, CRP, complement): bind to the flip-flopped membrane *PX-18: prevents flip-flop and inhibits sPLA2-IIA: inhibition post-MI inflammation

47
Q

For overview purposes, what are the causes/complications of Myocardial infarction?

A

*Causes: atherosclerosis coronary artery with unstable plaques/ thrombi; plaque rupture; plaque bleeding; dissection coronary artery; myocardial bridging; vasospasm coronary artery; hypertension related changes vasculature; small vessel disease *Complications: death, arrhythmia, rupture papillary muscle; heart failure; aneurysm heart; rupture heart wall (tamponade); pericarditis

48
Q

The lecturer also told about his research on a venous bypass graft. Explain

A

*Arterial pressure causes distension of the vein graft when placed on the heart *An elastic external stent can prevent this distension

49
Q

Annexin V binds to phosphatidylserine. Which cardiomyocytes bind Annexin V?

a) Apoptotic cardiomyocytes
b) Necrotic cardiomyocytes
c) Apoptotic and necrotic cardiomyocytes
d) Annexin V binds not to cardiomyocytes

A

c) Apoptotic and necrotic cardiomyocytes

Pathology dt2 (39 decks)

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