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Atherosclerosis & The heart

51 important questions on Atherosclerosis & The heart

What are the layers of an artery?

From inside → outside:
- Tunica intima
- Tunica media (smooth muscle cells, elastin)
- Tunica adventitia (fat, blood vessels)

What are the three major changes in someone with atherosclerosis?

- Intima: increase in thickness because of inflammation (of the fat that is stored inside)
- Media: decrease in thickness, because of the smooth muscle cells that migrate from the media to the intima
- Adventitia: inflammation & fibrosis

What induces the chronic inflammation of the intima?

The macrophages that are recruited, that want to phagocytose the lipid molecules, but that is often not possible, and then they are trapped.

What are some possible implications of atherosclerosis on the blood vessel?

- decreased elasticity (because of thrombosis & loss of elastin in media)
- later stage: dilatation, aneurysm (because of decrease of the media)
- splicing of the blood vessel wall (can also be caused by a hematoma of the bood vessels in the blood vessel wall)

What protein stabilizes elastin?

Fibrillin.

What genetic disease causes the elastin to be thinner?

Marfan disease (because of decrease in fibrillin).

What kind of disease is Ehlers-Danlos?

A genetic disease in which the diameter of collagen fibers is variable (instead of constant).

When is an aneurysm or dissection of the aorta likely to be caused by genetic defects?

- When multiple people in the family have an aneurysm/dissection
- When the patients is less than ~45 years old
- When the patient doesn't have hypertension

What is the difference between degeneration and atherosclerosis of the heart valve?

Degeneration = thickening of the heart valve with fibrosis and inflammation
Atherosclerosis = degeneration + ceroid (lipid)/calcification

What causes acute inflammation in an atherosclerotic valve?

- In atherosclerosis of the valve, also acute fase proteins (C-reactive Protein, complement) are activated,
- which attract neutrophils and granulocytes to the valve,
- causing an acute inflammation.

What is the disease pattern of infectious endocarditis?

- The infection causes necrosis of the cells in the heart valve,
- and the necrosis causes thrombosis,
- which can cause problems in the brain or the lung when it detaches from the valve.

What causes acute myocardial infarction?

- A major factor is stenosis (narrowing, can be really severe).
It's caused by atherosclerosis, so an increase in the intima.
- Problems with the intramyocardial coronary arteries.

For the risk of getting an acute myocardial infarction, what feature of the stenosis is important?

The stability of the plaque:
- Stable plaque: plaque has lipids, but also fibrosis above it (picture) → less risk of AMI
- Unstable plaque: plaque has a thin fibrous cap (picture) OR is a thick plaque, but has inflammation

What are complications of plaques?

- Instable plaques: the formation of a thrombus,
- bleeding inside the plaque, because of malformations of the (newly formed) blood vessels (within the plaque) → causes even more severe stenosis
- dissection of the coronary artery

What are problems with the intramyocardial coronary arteries?

- Small vessel disease
- Myocardial bridging

What is small vessel disease?

A disease in which the basal membrane of small vessels is way thicker than it should be (→ decrease in oxygen diffusion), the cause is unknown.

What is myocardial bridging?

- The coronary artery, that should be in the fat layer on the epicardial side, is now in the myocardium.
- Due to fibrosis, the artery does not dilate during the diastole

If a patient has an AMI, what are the first signs you could spot?

An increase of calcium in the mitochondria (= sign of ischemia).

3> hours after the onset of the AMI, how can you then spot the AMI?

By staining with NBT → the dead cells lack lactate dehydrogenase (LDH), so they are white/yellow & living cells are stained purple

In an AMI, what are the first cells to arrive after the inflammation has started?

Neutrophils, recruited by complement in the tissue.

What are the two types of damage to the cardiomyocytes caused by an AMI?

- Reversible
- Irreversible

What is the difference between reversibly and irreversibly damaged cardiomyocytes?

Following the ischemia, there is 'flip-flop' of the plasma membrane (negative phospholipids to the outside), which
- can attract C-reactive protein & complement → inflammation → necrosis
- sometimes does not attract inflammatory mediators → survival

What can inhibit the inflammation to occur?

PX-18, which inhibits the flip-flop, and the recruitment of inflammatory mediators.

In what state of the cell does flip-flop occur?

In a state of dying, so both in necrosis and apoptosis.

Why are there only very few cells that die of apoptosis during an AMI?

- the AMI causes lack of oxygen (ischemia),
- and for apoptosis, oxygen is needed.
→ so apoptotic cells turn into secondary necrotic cells

Except for rythmic problems, what are (5) possible complications of an AMI?

- Rupture of the papillary muscle of the heart valve → necrosis of the muscle → dysfunction of the valve
- Fibrosis → arrythmia
- Pericarditis (inflammation/thrombosis at the outside of the heart)
- Aneurysm of the heart: thinning of the ventricular wall of the heart
- Rupture of the heart: thrombus in the pericardial sac

What are 3 possible interventions for an AMI?

- Drugs: thrombolysis
- Minimally invasive procedure: stent
- Surgical: bypass

A bypass is often done by replacing the artery by a vein. What is a complication of this?

- The arterial pressure is way higher than the pressure the vein is build for,
- and this high pressure causes disruption of the endothelial cells,
- which recruits thrombocytes.
→ can be prevented by fibrin glue

How can lymphocytic myocarditis cause heart failure?

Because in the (viral) infection, interleukins are recruited, which have a negative impact on the contractability of the heart.

The patients that die of lymphocytic myocarditis, what is their direct cause of death?

Not the lymphocytic myocarditis itself, because the number of cardiomyocytes that die is quite low, but because of the complications (heart failure, arrythmia, vasospasm)

What have mice model studies shown about the inflammatory cells in a lymphocytic myocarditis?

That lymphocytes are present in high numbers for up to 14 days (which means that there is an extensive time period for inflammation to happen)

What type of immune cells are found in a viral myocarditis, and what type of cells are found in a bacterial myocarditis?

- Viral: primarily lymphocytes
- Bacterial/fungi: loads of neutrophilic granulocytes (except in tuberculosis)

When you (as a pathologist) see neutrophilic granulocytes in a myocarditis, how do you distinguish between an AMI and a bacterial/fungus infection?

- AMI: neutrophils are diffused throughout the tissue
- Bacterial/fungus infection: neutrophils are gathered in one place

What two options are there for the diagnosis when you find eusinophilic granulocytes in a myocarditis?

- Eusinophilic granulocytes without cardiomyocyte death: by parasites or by drugs
- Eusinophilic granulocytes with cardiomyocyte death: hypereusinophilic syndrome

What could be going on when you find granulomas and/or giant cells in a myocarditis?

- Tuberculosis (giant cells)
- Sarcoidosis (you don't find cardiomyocyte death)
- Giant cell myocarditis: extensive necrosis of cardiomyocytes → poor prognosis

What is an extra complication of non-infectious myocarditis (or: stress-myocarditis)?

- There are also increased numbers of inflammatory cells at the endocardium,
- which gives the risk of thrombus formation and migration to the brain/lungs

What are possible causes of non-infectious myocarditis (or: stress-myocarditis)?

- Tumor of the adrenal glands
- Brain injury
- Lungemboli
- Sepsis (bacteria in the blood)

What is hypertrophic cardiomyopathy?

An enlargement of the heart, as well as asymmetric thickness of the heart walls.

In hypertrophic cardiomyopathy, what are abnormal cell patterns called, and what do they look like?

- 'Whorls',
- which are places where the actin and myosin are not properly aligned

What can hypertrophic cardiomyopathy be caused by?

By a genetic defect in the genes coding for sarcomeres

What is dilated cardiomyopathy?

A decrease in the thickness of the wall, due to a loss of cardiomyocytes.

What can dilated cardiomyopathy be caused by?

- Genetic defect: phenotype of cardiomyopathy is only cause by a specific event, like infarction or myocarditis
- Alcohol
- Chronic viral myocarditis
- Pregnancy
- Idiopathic (no cause known)

What is typical for an alcoholic cardiomyopathy?

Increase in fat tissue in the wall of the heart.

What is restrictive cardiomyopathy?

A storage disease, for example amyloid, in which the myofibrils are replaced by amyloid. This causes a decrease in heart function.
(Amyloid storage disease can also occur in blood vessels, which can cause myocardial infarction.)

What can restrictive cardiomyopathy also be caused by (except for amyloid storage problem)?

- A glycogen storage disease
- Hemosiderosis: an iron storage disease
→ both glycogen and iron can replace the myofibrils in the heart.

What is arrythmogenic cardiomyopathy?

Replacement of myofibrils in the right ventricle by fatty tissue, which can also come together with fibrosis.
It can have a genetic cause, and it can cause arrythmia.

If you find fatty changes in the whole heart, or only the left ventricle, what is most likely the diagnosis?

Dilated cardiomyopathy
(fatty changes in ONLY the right ventricle: arrythmogenic cardiomyopathy.)

Tumors are very uncommon in the heart. What kind of tumors are most prevalent in the heart?

Metastases.

What is the most common tumor of the heart?

A myxoma, which is benign.

What is typical for a myxoma?

Abnormal blood vessels, and macrophages with iron (from the erythrocytes)

What is the most common malignant tumor of the heart?

An angiosarcoma, which has a poor prognosis because it spreads through the heart and it metastasizes easily.

The question on the page originate from the summary of the following study material:

Pathology Part II

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