(From Path book and lecture, 11-13 Jan 2001, by Brian Buschman)
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This is based on BP Ch. 10
These are three types of arteriosclerosis:
Atherosclerosis is very common in developed countries usually where white people are the majority. Innate risk factors include:
1) Age
2) Sex – females catch up with men after menopause.
3) Familial predisposition often relate to hyperlipidemia.
4) Homocysteinemia
1) Hyperlipidemia
2) Hypertension
3) Smoking
4) Diabetes
Stresses can be either mechanical or chemical. With time they lead to atherogenesis. They may be chemical from things like smoking, viruses or homocysteine or physical from shear stresses and turbulence.
Plaques tend to develop at points of turbulence like at beginnings of vessels and on the posterior wall of the descending and abdominal aorta.
Hyperlipidemia, specifically hypercholesterolemia causes endothelial damage to the intima. Oxidized LDL causes chemotaxis of macrophages, stimulates growth factors (that make ECM) and cytokines and is easily taken in by macrophages.
1) Endothelial injury occurs.
2) Macrophages cross the intima and smooth muscle cels migrate from the media.
3) They engulf oxidized LDL and repair (lay ECM) making fatty streaks of foam cells.
Plaques tend to be found in descending levels of severity:
1) Abdominal aorta
2) Coronary arteries
3) Internal carotid artery
4) Circle of Willis
It is rare to find atheromas in the renal arteries, mesenteric arteries, upper extremities (except at these ostia or opening) and aortic arch.
Composition of the thrombi is:
1) Cells that include macrophages (blood) and smooth muscle cells.
2) C.T. and ECM
3) Lipids
A thrombi can form atop of an atheroma and fuse. In this case it’s called a mural thrombi.
Thrombi end up with one of four complications:
1) Calcification as in Monekeberg medial calcification.
2) Rupture of the luminal surface.
3) Superimposed thrombi like Mural thrombi.
4) Hemorrhage that may balloon the plaque and lead to rupture.
Hypertension may be primary or secondary. Either may be benign, it rises and stays constant, or malignant meaning that it continues to rise and death is usually close.
2o hypertension may be renal, cardiovascular, endocrine or neurologic. One interesting one is increased intracranial pressure caused by head trauma.
Renal artery stenosis reduces glomerular flow and pressure in the afferent arteriole causing renin secretion from the JG cells leading to hypertension.
Vasculites have many causes but one of the most significant is immune complexes. Immune complexes (type III hypersensitivity) cause an Arthus reaction. This is often from antibodies and some particle in the vessel such as DNA/anti-DNA in SLE. It is also common with Hep B and C.
Another cause is anti-neutrophil cytoplasmic antibodies (ANCA). There are two types, P-ANCA which attack myeloperoxidase of the neutrophils and C-ANCA which attacks neutral leukocyte protease. C-ANCA is seen in Wegener’s granulomas while P-ANCA is seen in polyarteritis nodosa and primary glomerular disease.
Polyarteritis is a trans-mural (whole thickness) necrotizing inflammation that affects small to medium sized arteries all over the body except for the lungs (this helps differentiate it from Wegener’s Granulomatosis and Leukocytoclastic Polyangiitis). It produces an aneurysm and/or infarcts. It has a high degree of neutrophil infiltration. You can find PAN in different stages at different points in the body at any given time (unlike Leukocytoclastic Polyangiitis).
If PAN has renal involvement then it will probably first cause hypertension. P-ANCA’s correlate with polyarteritis nodosum. About 30% of patients have Hep-B antigen.
Wegener’s granulomatosis is a triad of:
1) Acute necrotizing granulomas of the upper or lower respiratory tract.
2) Necrotizing vasculitis of small to medium sized arteries of the lungs.
3) Crescentric (crescent-shaped) glomulonephritis.
C-ANCAs are usually seen with Wegener’s Granulomatosis. Morality is high and symptoms appear similarly to polyarteritis nodosa.
Leukocytoclastic polyangiitis is a “pauci-immune” injury of arterioles, capillaries and venules of most any organ.
Clinically patients experience as a result of administration of an agent but show few immune deposits hence the name pauci-immune. Signs include hemoptysis (spitting blood), hematouria, bowel pain/bleeding and often necrotizing glomerulonephritis.
Most show P-ANCA. All legions are the same age (unlike Polyarteritis Nodosa) and it shows involvement of both lungs and other organs (unlike PAN or Wegener’s Granulomatosis).
This is a strange arteriitis that tends to affect the aorta and branches of the carotid arteries in elderly women. Symptoms are related to the type of artery blocked. Often this leads to blindness unilaterally from blocking one of her ophthalmic arteries.
Fibrous thickening of the aorta which leads it to be called the pulse less disease. It usually appears in patients within their first 40 years of life.
Kawasaki’s is a sequeli of coronary artery arteriitis beginning in early childhood. It is self limiting. Initially smaller vessels are involved but later larger arteries come into play. Myocarditis, pericarditis or valvulitis may appear. It will go away on it’s own but during recovery may cause aneurysm or thrombosis.
Thromboangiitis is related to smoking in individuals 25-50. It primarily affects medium sized arteries such as the ulnar and tibial and then spreads to bother adjacent nerves.
Aneurysms are an abnormal dilation of a blood vessel. Atherosclerosis is a major cause while infection is a minor one. Tertiary syphilis tends to have them as syphilis is primarily a vascular problem.
In tertiary syphilis the problem involves destruction of the vaso vasorum leading to the downward spiral. This can lead to encroachment on pathways causing respiratory difficulties, difficulty swallowing, persistent cough, bone pain (bone erosion) and cardiac disease.
Aortic dissection is the opening of a channel for blood to flow within the walls of the aorta. If it ruptures it can cause cardiac tamponade.
Patients tend to be 40-60 years old or younger if they have Marfan. Marfan patients often have tunica media degeneration called cystic medial necrosis. This is often seen in Marfan because Marfan is related to a defective fibrillin gene.
Varicose veins are most common in women due to the venous stasis of pregnancy. The most common sites are the anorectal veins causing hemorrhoids and in esophageal veins due to portal hypertension.
They may thrombose, have painful ulceration or be asymptomatic and just ugly depending on the site and the individual involved.
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