Chapter 10: Complete lecture Flashcards
What was discussed in the lecture? (you obvi don’t have to learn this, it’s to illustrate what’s discussed)
• 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
Does the media increase during atherosclerosis with inflammation?
No, it decreases
Does the intima increase during atherosclerosis with inflammation?
Yes
The intima increases because of lipid. How is this lipid also called?
Ceroid
There are cells that try to fagocytose the lipid/ceroid in the intima. What are these cells?
Antibody detecting Macrophages
How does a normal aorta appear (during surgery e.g.)?
You see smooth white substance, the elastin aorta
How does an aorta with minor/medium atherosclerosis look?
You see lesions, and in a worsened state necrosis
How does an aorta with sever atherosclerosis appear?
There are plaques thrombi, might be a dilation with aneurysm, and in the worst state a rupture of the vessel wall
What might be the result of splicing of the wall?
Hemorrhage/thrombosis
What may a dissection be caused by?
- a perforation of an atherosclerotic plaque
- bleeding within the vessel wall, a so-called hematoma (this can be independent of atherosclerosis)
How does mucoid media degeneration affect the vessel wall?
There is loss of elastic fibers (less elastic aorta) and there is mucoid depositions (glycosaminoglycans) causing a weakening of the media
If mucoid media degeneration is found in patients above 45y/o, what is the (probable) cause?
Age
If mucoid media degeneration is found in patients below 45y/o, what is the (probable) cause?
Genetic
What complication can occur because of mucoid media degeneration
Aneurysm development and dissection
Aneurysm and dissection can have a genetic cause: disease of … (2 answers)
fibrilin (stabilizes elastin) or collagen
What type of malformation (in regard to disease of aneurysm/dissection) is found in Marfan Disease?
Thin and fragmented elastin
What type of malformation (in regard to disease of aneurysm/dissection) is found in Ehlers-Danlos?
malformation collagen with a strong variation in collagen fiber diameter
What is degeneration? (in regard to heart valves)
thickening of the valve with fibrosis and inflammation
What is atherosclerosis?
degeneration plus ceroid/calcification
Which heart valves are often degenerated/have atherosclerosis?
aortic valve (in between left ventricle and aorta) and mitral valve (in between left ventricle and left atrium)
True/false: infectious endocarditis is mainly caused by a bacterial infection
True
What cellular responses are seen in infectious endocarditis?
Thrombosis and necrosis of the valve
How can you see the difference between thrombosis and necrosis on a valve? (slide 10)
Thrombosis is red, necrosis is white (very roughly speaking oc)
True/false: there is lipid in the media
False, in the intima
How is lipid phagocytosed?
By macrophages (partly succesful)
What parts of the vessel wall are affected by chronic inflammation? And how?
Intima (increase) /media (decrease) /adventitia (fibrosis)
What is an aneurysm?
Dilation of blood vessel
What is a dissection?
Splicing of blood vessel
Which layer(s) of a blood vessel increase(s) during atherosclerosis: a) Intima b) Media c) Intima and media d) No layer
a) Intima
What is a major complication of atherosclerosis in coronary arteries?
Acute myocardial infarction (AMI)
Please look at the figure to see how e.g. the right corona artery causes failure of the posterior MI
(i don’t think you should know which artery causes which failure, but understand the concept)
What is a stable atherosclerotic plaque?
thick fibrous cap without inflammation in the cap
What is an unstable atherosclerotic plaque?
thin fibrous cap or thick fibrous cap with inflammation in the cap
What may the causes of Acute Myocardial Infarction (AMI) be?
Thrombus, bleeding/hemorrhage, plaque bleeding, dissection
How will a stable plaque with a thick cap become an unstable plaque
Inflammation
Acute Myocardial Infarction (AMI) can also occur in the intramyocardial coronary artery. What are the causes?
- 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)
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?
Signs of cell damage
Another way to show AMI is by nitrobluetetrazolium (NBT), that stains lacatedehydrogenase (LDH). What color is this staining?
Purple
So, if a heart is depicted purple, is this good?
Yes, it means there is no loss of LDH
Explain where neutrophilic granulocytes are present during AMI (with timeline please)
- 6-12h: granulocytes are present in the vessels 2. 12h-3d: granulocytes are in between cardiomyocytes 3. 3-5d: degenerating granulocytes
What happens because of the degeneration of the neutrophilic granulocytes?
Necrosis of cardiomyocytes
1-2w after Acute Myocardial Infarction (AMI), granulation tissue will be formed. Which cells are then seen in the tissue?
Lymphocytes, macrophages and fibroblasts
What are complications of AMI?
Rupture of the papillary muscle -> dysfunction of the heart valve Aneurysm of the heart -> thinning of the ventricle wall
Rupture of the heart in transmural infaction is…..
infarction of the full thickness of the ventircle wall
How is Acute Myocardial Infarction (AMI) treated?
• Drug therapy: Thrombolysis • Minimally invasive: Stent • Surgical: Bypass operation
The teacher told about his research of myocardial infarction. Explain the main concepts
*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
For overview purposes, what are the causes/complications of Myocardial infarction?
*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
The lecturer also told about his research on a venous bypass graft. Explain
*Arterial pressure causes distension of the vein graft when placed on the heart *An elastic external stent can prevent this distension
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
c) Apoptotic and necrotic cardiomyocytes
