Atherosclerosis

cont

Morphology
Fatty Streaks y Fatty streaks are composed of lipid-filled foam cells . y They are not significantly raised . y Begin as multiple minute yellow, flat spots that can fuse together into elongated streaks, 1 cm or longer. y NOTE:-Not all fatty streaks are destined to
y

become advanced atherosclerotic lesions

Aorta with fatty streaks (arrows), associated largely with the ostia of (arrows), branch vessels

Microscopical view of fatty streak in the wall of an artery, demonstrating intimal, macrophage-derived foam cells (arrow) intimal, macrophage(arrow)

Morphology
Atherosclerotic Plaque y Grossly :-appear white - yellow; & if thrombosis superimposed over the surface of ulcerated plaques it will give a red-brown in color. y Plaques vary from 0.3 -1.5 cm in diameter but can coalesce to form larger masses. y They are patchy, usually involving only a portion of the arterial wall. "eccentric.
y

Eccentric lesion of atheroma ;notice that the arrow refer to the normal part in the wall

Why focal ?
y

Local flow disturbances, such as turbulence at branch points, leads to certain portions of a vessel wall being more susceptible to plaque formation.

Commonly affected arteries

1-the lower abdominal aorta, y 2-the coronary arteries, y 3-the popliteal arteries, y 4-the internal carotid arteries, y 5- the vessels of the circle of Willis.
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Components of the atherosclerotic plaques

(1) Cells, including SMCs, macrophages, and T cells. y (2) ECM, including collagen, elastic fibers, and proteoglycans. y (3) Intra & extracellular lipid.
y

How these components distributed in the plaque

1-The superficial fibrous cap is composed of SMCs with dense collagen. y 2-Beneath and to the side of the cap (the "shoulder") is a more cellular area containing macrophages, T cells, and SMCs. y 3-Deep to the fibrous cap is a necrotic core, containing lipid ,debris, foam cells &plasma proteins; the cholesterol content is frequently present as an empty "clefts" . y 4-The periphery of the lesions, show neovascularization .
y

Architecture of mature plaque demonstrating fibrous cap (F) and a central (F necrotic (largely lipid) core (C). The lumen (L) has been moderately narrowed. (C (L In this section, collagen has been stained blue (Masson's trichrome stain).

Pathologic changes of the plaques:

1-Rupture, ulceration, or erosion of the luminal surface of atheromatous plaque. y 2-Hemorrhage into a plaque. Rupture of the thinwalled vessels in the areas of neovascularization can cause intra-plaque hemorrhage. y 3-Atheroembolism. Plaque rupture can discharge debris into the bloodstream, producing microemboli composed of plaque contents. y 4-Aneurysm formation. Atherosclerosis-induced pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, causes weakness of the vessel wall and development of aneurysms that may rupture.
y

Atherosclerotic plaque rupture. Plaque rupture (arrow) (arrow) without superimposed thrombus.

photograph of a section of the plaque, stained for elastin (black), plaque, black), demonstrating that the internal and external elastic membranes are destroyed and the media of the artery is thinned under the most advanced plaque (arrow). (arrow).

Acute coronary thrombosis superimposed on an atherosclerotic plaque with focal disruption of the fibrous cap (arrow), triggering fatal myocardial infarction (arrow),

Summary

Diseases of veins

1-Varicose Veins
They are abnormally dilated, tortuous veins produced by prolonged increase in intraluminal pressure and loss of vessel wall support. y Mainly affect The superficial veins of the leg. y About 10% - 20% of adult males and 25% - 33% of adult females develop lower extremity varicose veins.
y

Predisposing factors
Any factor that can raise the venous pressure: y 1-obesity y 2-pregnancy. y 3-Pelvic mass or tumor e.g. large uterine leiomyoma. y 3-A familial tendency due to imperfect venous wall development.
y

Morphology
1-Wall thinning at the points of maximal dilation y 2- Smooth muscle hypertrophy and intimal fibrosis in adjacent segments; y 3- Elastic tissue degeneration and spotty medial calcifications y 4- Focal intraluminal thrombosis (due to stasis).
y

Esophageal varices: causes

2-portal vein obstruction 1-Liver cirrhosis hepatic vein thrombosis

portal vein hypertension

Pathogenesis
Portal hypertension leads to the opening of porto-systemic shunts, increasing blood flow into veins at the gastroesophageal junction (forming esophageal varices), y the rectum (forming hemorrhoids), y and periumbilical veins of the abdominal wall (forming a caput medusa).
y

Esophageal varices notice the blue numerous venous channels at lower part of the organ.

Section of the esophagus show many dilated submucosal veins in patient with liver cirrhosis.

Thrombophlebitis &Phlebothrombosis
Sites:y 1-The deep leg veins account for more than 90% of cases. y 2-The periprostatic venous plexus in males & the pelvic venous plexus in females. y 3- The large veins in the skull and the dural sinuses.
y

Causes
1-Peritoneal infections (e.g., peritonitis,) can lead to portal vein thrombosis. y 2-(DVT) of legs caused by CHF, neoplasia, pregnancy, obesity, the postoperative state, and prolonged bed rest or immobilization. 3-Genetic hypercoagulability syndromes can also be associated with venous thrombosis 4-In patients with adenocarcinomas, hypercoagulability occurs as a paraneoplastic syndrome related to elaboration of procoagulant factors. In this case venous thromboses called migratory thrombophlebitis (Trousseau sign) .
y

Diseases of Lymphatic vessels

1- Lymphangitis:- is the acute y inflammation elicited when bacterial infections spread into and through the lymphatics; the most common agents are group A -hemolytic streptococci.

Lymphedema y Diveded into primary & secondary y Primary lymphedema usually the cause is heridetary resulting from lymphatic agenesis or y hypoplasia. y Secondary lymphedema result from blockage of a previously normal lymphatic.

Causes of secondary lymphedema

1-Malignant tumors obstructing either the y lymphatic channels or the regional lymph nodes. 2-Surgical procedures that remove regional y groups of lymph nodes (e.g., axillary lymph nodes in radical mastectomy) 3-Postirradiation fibrosis. y 4-Filariasis. y 5-Postinflammatory thrombosis and scarring. y