00:00 / 00:00
Bundle branch block
Pulseless electrical activity
Atrioventricular nodal reentrant tachycardia (AVNRT)
Premature atrial contraction
Long QT syndrome and Torsade de pointes
Premature ventricular contraction
Rheumatic heart disease
Atrial septal defect
Coarctation of the aorta
Patent ductus arteriosus
Ventricular septal defect
Hypoplastic left heart syndrome
Tetralogy of Fallot
Total anomalous pulmonary venous return
Transposition of the great vessels
Pericarditis and pericardial effusion
Aortic valve disease
Mitral valve disease
Pulmonary valve disease
Tricuspid valve disease
Coronary steal syndrome
Polycystic kidney disease
Renal artery stenosis
Peripheral artery disease
Subclavian steal syndrome
Superior mesenteric artery syndrome
Human herpesvirus 8 (Kaposi sarcoma)
Chronic venous insufficiency
Deep vein thrombosis
Acyanotic congenital heart defects: Pathology review
Aortic dissections and aneurysms: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Cardiac and vascular tumors: Pathology review
Cardiomyopathies: Pathology review
Coronary artery disease: Pathology review
Cyanotic congenital heart defects: Pathology review
Dyslipidemias: Pathology review
Endocarditis: Pathology review
Heart blocks: Pathology review
Heart failure: Pathology review
Hypertension: Pathology review
Pericardial disease: Pathology review
Peripheral artery disease: Pathology review
Shock: Pathology review
Supraventricular arrhythmias: Pathology review
Valvular heart disease: Pathology review
Vasculitis: Pathology review
Ventricular arrhythmias: Pathology review
0 / 46 complete
0 / 4 complete
Dr Joe reverses his own atherosclerosis
atherosclerosis in p. 305, 733
atherosclerosis p. 305
abdominal aortic aneurysms and p. 305
aortic aneurysms p. 733
diabetes mellitus and p. 350
familial dyslipidemias p. 92
homocystinuria as cause p. 83
sites of p. 733
stable angina with p. 308
transplant rejection p. 117
atherosclerosis in p. 305
atherosclerosis in p. 733
atherosclerosis and p. 305
in atherosclerosis p. 305
So these three words look the same: Arteriosclerosis, Atherosclerosis, and Arteriolosclerosis.
Arteriosclerosis is a general umbrella term describing diseases where the wall of the artery becomes thicker, harder, and less elastic than normal.
You can figure that out right from the name: “arterio” which is Greek for artery, and sclerosis which is Greek for “hardening”.
Now the word arteriolosclerosis is any sort of hardening of small arteries in arterioles.
This is also pretty easy to remember since the “olo” in the middle of the word indicates small arterioles.
And then finally, atherosclerosis is the hardening of any artery (even though it’s usually medium- to large-sized arteries) which is caused by the buildup of plaque.
These plaques are called atheromatous plaques and happen in the innermost wall of the blood vessel called the tunica intima or endothelium. Okay now that we’ve differentiated been all three of those words, let’s first take a look at atherosclerosis.
So the blood vessel endothelium is made up of a single layer of cells and does two jobs: First,it protects the rest of the blood vessel wall from the blood, like a coat of varnish on your wood furniture and then, secondly, it secretes proteins on its surface to prevent the blood from clotting, because blood just inherently likes to clot whenever it gets the chance.
Now, Your endothelium can become damaged in lots of different ways. Low density lipoproteins, chemicals from smoking cigarettes, and high blood pressure all wreak havoc on the endothelium because these irritants break down the endothelium.
The damaged endothelium allow low-density lipoproteins to enter the endothelial wall.
The white blood cells called monocyte follow the low-density lipoproteins and break them down through oxidation.
Okay, so you might think macrophages eating the embedded low-density lipoproteins is a good thing, but if there is a lot of low-density lipoprotein, then the macrophage will eat so much cholesterol that it can die. It basically eats itself to death.
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