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
Coronary steal syndrome
Coarctation of the aorta
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 / 80 complete
0 / 10 complete
autoantibody p. 113
as granulomatous disease p. NaN
labs/findings p. 721
Sometimes the body confuses the innermost layer of the blood vessel, which is the endothelial layer, with a foreign pathogen and directly attacks it.
To be a little bit more specific, the white blood cells of the immune system mix up the normal antigens on the endothelial cells with the antigens of foreign invaders like bacteria simply because they look similar—and this is called molecular mimicry.
This autoimmune confusion is thought to be the cause several types of medium-vessel and large-vessel vasculitides.
Other times the immune system attacks healthy cells that are near the vascular endothelium, and the endothelial cells are only getting indirectly damaged.
Once the endothelium is damaged either directly or indirectly, almost all vasculitis diseases progress in a similar way.
The damaged endothelium exposes the underlying collagen and tissue factor, and these exposed materials increase the chance of blood coagulation.
The blood vessel walls themselves get weaker as they’re more damaged, making aneurysms more likely.
And finally as the vessel wall heals, it becomes harder and stiffer because fibrin is deposited into the vessel walls as part of the healing process.
And actually, that’s vasculitis in a nutshell.
Vasculitis is a condition in which there is inflammation of the blood vessels, typically caused by immune-mediated damage to the endothelial cells. The inflammation can affect blood vessels of different sizes, ranging from small capillaries to larger arteries and veins. There are many different types of vasculitis, which can affect various parts of the body, including the skin, joints, and internal organs.
Symptoms may include fever, fatigue, weight loss, joint pain, skin rashes, and organ dysfunction, depending on the type and location of the vasculitis. Treatment for vasculitis may involve medications to suppress the immune system and reduce inflammation, such as corticosteroids.
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