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Summary Pathology second exam
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summary of the pathology course for. the second exam. The summary is complete and is made using the lectures and the book :)
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Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster 9780323353175 Chapter 1-24 | Complete Guide A+
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TEST BANK FOR Robbins Basic Pathology (Robbins Pathology) 10th Edition by Vinay Kumar & Abul K. Abbas , ISBN: 9780323353175 |Chapters 1-24| Guide A+
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Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster 9780323353175 Chapter 1-24 | Complete Guide A+
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Types of tumorsType of tumor Cell type
Carcinoma Epithelial cells
Sarcoma Soft and connective tissue
Melanoma melanocytes
Lymphoma Cancer of lymphocytes
Leukemia Blood cells
adenoma Benign tumor of epithelial cells
Chapter 10/11 cardiovascular pathology
Veins and arteries
Atherosclerosis
Atherosclerosis is deposition of ceroid/lipids in the intima, which induces inflammation.
Macrophages are present in the intima layer, while lymphocytes are present in the intima,
media, and adventitia. Phagocytosis of lipids by macrophages is partly successful which
causes plaques to form. Plaques can cause many complications such as
- Thrombosis
- ruptures of vessel wall
- dilation of the vessel wall due to an aneurysm
- dissection: splicing of the vessel wall (e.g., splicing between media and adventitia)
Aneurysm and dissection can have a genetic cause: disease of fibrillin (stabilizes elastin or
collagen:
- marfan disease: thin and fragmented elastin
- Ehlers-danlos: malformation collagen with a strong variation in collagen fiber
diameter
1
,mucoid media degeneration
a vascular disorder where mucinous is deposited in the intima and media layers, which
weakens the media. Elastic fibers are lost, which means that the aorta becomes less elastic.
Mucoid media degeneration of the vessel wall can play a role in aneurysm development and
dissection. In patients above 45 years it is age dependent, while in younger people it can
also have genetic cause. Elastic fibers are lost, which means that the aorta becomes less
elastic.
2
,Atherosclerosis in the coronary arteries: acute myocardial infarction
(AMI)
Occlusion of a specific coronary artery means oxygen can’t go to the
heart properly. Ischemia leads to death of cardiomyocytes
(=infarction). The level of ischemia is depicted by the level of stenosis
in the artery.
Stable vs unstable plaque:
- Stable: thick fibrous cap without inflammation in the cap
- Unstable: thin fibrous cap with inflammation in the cap
à patients with a stable plaque, have a risk at an unstable cap!
Causes AMI:
Arteries outside the myocardium:
- Thrombus
- Microscopic thrombus
- Plaque bleeding (increase intima): plaque bleeding is related to malformation of
newly formed vessels within the plaque
- Dissection of the coronary artery
Arteries inside the myocardium:
- Small vessel disease: thickness in basal membrane, which causes decrease in oxygen
diffusion
- Myocardial bridging: increase in intima, as a cause artery won’t dilate during the
diastole, so they can’t fill with blood.
What happens to cardiomyocytes after AMI?
- Changes in the mitochondria of the myocytes. Calcium deposits in mitochondria, so
not enough ATP is formed (2-3 hours after AMI)
- Nitrobluetetrazolium (NBT) stains lactatedehydrogenase (LDH) purple, after an
infarction there is a detectable loss of NBT (2-3 hours after AMI)
- Acute and chronic inflammation:
o Neutrophilic granulocytes leave blood vessels (6-12 hours after AMI)
o Neutrophilic granulocytes are in between the cardiomyocytes (12 hours- 3
days after AMI)
o Neutrophilic granulocytes are degenerated; however, they have secreted
many enzymes and ROS which jeopardize the cardiomyocytes (3-5 days after
AMI)
3
, Complications of AMI:
- Rupture of the papillary muscle of the heart valve: disfunction of the heart valve
- Arrythmia: partly related with fibrosis
- Pericarditis: 2-3 days post AMI: inflammation and/or thrombosis
- Aneurysm of the heart: thinning of the ventricle wall of the heart
- Rupture of the heart: infarction of the full thickness of the ventricle wall
Intervention of AMI:
- Drug therapy: thrombolysis
- Minimally invasive: stent, this is a long term protection of the vessel wall, after a
balloon decreases the plaque area
- Surgical: bypass operation
Summary
Myocardial infarction: causes and complications
- 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
Research venous bypass graft
- Arterial pressure causes distension of the vein graft when placed on the heart
- An elastic external stent can prevent this distension
Heart valves
Atherosclerosis or degeneration of heart valves
- Degeneration: thickening of the valve with fibrosis and inflammation
- Atherosclerosis: degeneration plus calcification
à occurs mainly at the valves at the left side of the heart, due to the high pressure
Infectious endocarditis
Mainly caused by a bacterial infection
- Thrombosis of the valve: can cause a brain infarction
- Necrosis of the valve causes disfunction of the valves
à Can occur at all ages
4
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