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Summary chapter 10/11 (HC 10) of the book basic pathology
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a comprehensive summary after the lecture on chapter 10/11. Everything that has been covered in the lecture is in this explanation summary.
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COMPLETE TEST BANK _ ROBBINS BASIC PATHOLOGY| ROBBINS PATHOLOGY| 10TH EDITION, BY VINAY KUMAR, ABUL K. ABBAS & JON C. ASTER ALL CHAPTERS 1-24| LATEST VERSION WITH DETAILED EXPLANATION| GRADE A+
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Test Bank Complete_ Robbins Basic Pathology| Robbins Pathology| 10th Edition, By Vinay Kumar, Abul K. Abbas & Jon C. Aster All Chapters 1-24| Latest Version With Detailed Explanation| Grade A+
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Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster | all 25 chapters covered | complete guide | graded a+
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Chapter 10: Atherosclerosis/Chapter 11: the heartAtherosclerosis:
A normal artery is composed of intima, media (smooth muscle, elastin) and adventitia (fat
and blood vessels). In arteriosclerosis, increased intima because of inflammation, decrease
media and fibrosis in adventitia.
Aorta can be dilated due to arteriosclerosis= aneurysm. Due to inflammation less strength
media (loss of elastin).
Aorta can also dissect because of atherosclerosis. The splicing can become a haemorrhage
due to perforation plaque or bleeding in vessel wall.
Mucoid media degeneration = loss of elastin. Under the age of 45 may be genetic cause.
Aneurysm and dissection can have genetic cause: Marfan disease (thin fragmented elastin)
or Ehlers-Danlos (malformation collagen)
Myocardial infarction: 4 causes:
Atherosclerosis coronary artery, LAD is most common to get AMI.
1. The level of stenosis also determines the change of AMI.
2. A stable plaque without inflammation on top of the stenosis has lower change of
getting AMI. If it gets inflamed more change of getting an AMI.
3. If the plaque gets new malformed blood vessels, also higher risk the plaque bleeding
and increased intima.
4. Dissection of the coronary artery.
5. Intramyocardial coronary artery, hypertension. Cannot dilate in diastole.
6. Small vessel disease > decreased O2 diffusion.
Infarction: The mitochondria deposit calcium > less ATP production. No LDH > diseased
cardiomyocytes. More PMN = more neutrophilic granulocytes. First in the vessels and later
between the cardiomyocytes.
Acute phase proteins: ischemia causes sPLA2-IIA can bind to CRP, activate complement.
PX-18 causes inhibitor sPLA2-IIA and no membrane flip. So no Annexin-V can bind.
Complications: rupture of papillary muscle, less function heart valve. Arrhythmia by fibrosis
(Due to multiple AMI). Pericarditis Is inflammation heart sac. Aneurysm of the heart =
thinning of the ventricle wall of the heart. Total wall of left ventricle is necrotic, rupture wall
Intervention: drug therapy by thrombolysis. There can be a stent or a bypass operation by a
vein graft > add fibrin to prevent dilation to prevent rupture.
Valve disease:
Mitral valve and aortic valve (pressure higher there). Degeneration = thickening of the valve
with fibrosis with inflammation. Atherosclerosis = degeneration + calcification. CRP/sPLA2-
IIA are more present in atherosclerosis.
Infectious endocarditis: bacterial infection causes thrombosis (brain infarction) and necrosis
(no function properly) of the valve.
Myocarditis:
Inflammation of the heart. Can be infectious or non-infectious. Can happen at all age.
Viral infection causes lymphocytic myocarditis can cause; arrhythmia, vasospasm, heart
failure (huge increase interleukins) When extensive cell death = fulminant myocarditis.
Neutrophilic granulocytes; bacteria (no TBC) of fungi.
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