X - The Blood Vessels Flashcards
In these arteries, elastic fibers alternate in layers with smooth muscle cells. Examples are the common carotid artery, iliac arteries and pulmonary arteries.
Large or elastic arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
In these arteries, tunica media is composed primarily of smooth muscle cells, with elastin limited to the internal and external elastic lamina. Examples are the coronaries and renal arteries.
Medium-sized or muscular arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
These are the principal control points for regulation of physiologic resistance to blood flow.
Arterioles(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
These vessels are approximately the diameter of an RBC, have an endothelial cell lining but no media.
Capillaries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Diameter of an RBC.
7-8 um(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are thin-walled, endothelium lined channels that drain excess interstitial tissue fluid, returning it to blood via the thoracic duct.
Lymphatics(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are small spherical dilatations, typically in the circle of Willis.
Developmental/berry aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are abnormal, typically small, direct connections between arteries and veins that bypass the intervening capillaries.
Arteriovenous fistulas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Focal, irregular thickening of the walls of medium and large muscular arteries. Segments of the vessel wall are focally thickened by combination of irregular medial and intimal hyperplasia and fibrosis, causing luminal stenosis.
Fibromuscular dysplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Literally means hardening of the arteries, term reflecting arterial wall thickening and loss of elasticity, affecting small arteries and arterioles.
Arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Characterized by calcific deposits in muscular arteries, typical in persons older than 50 yrs old. The radiographically visible, palpable calcifications do not encroach on the vessel lumen, and are not clinically significant.
Mockenberg medial calcific sclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Characterized by intimal lesions called atheromas that protrude into vascular lumina.
Atherosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Three principal components of an atheromatous plaque.
- Cells (SM cells, macrophages, T cells)2. Extracellular matrix (collagen, elastic fibers, proteoglycans)3. Intracellular and extracellular lipidFibrous cap, central lipid core, neovascularization(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 344
Non-modifiable risk factors for atherosclerosis. (4)
Increasing ageMale genderFamily historyGenetic abnormalities(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 344
Composed of lipid-filled foam cells but are not significantly raised and thus do not cause any disturbance in blood flow. Can appear as early as 1 year, and present in virtually all children older than 10 years old.
Fatty streaks(TOPNOTCH)
Composed of lipid-filled foam cells but are not significantly raised and thus do not cause any disturbance in blood flow. Can appear as early as 1 year, and present in virtually all children older than 10 years old.
Fatty streaks(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 349
Arrange in descending order, based on which blood vessel is most extensively involved in development of atherosclerosis.Popliteal arteries, internal carotid arteries, circle of Willis, coronaries, abdominal aorta
Abdominal aorta > coronaries > popliteal arteries > internal carotid arteries > circle of Willis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 350
Fate of an atheromatous plaque wherein the luminal surface exposes the bloodstream to highly thrombogenic substances and induces thrombus formation.
Rupture, ulceration or erosion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atheromatous plaque due to rupture of the overlying fibrous cap or the thin-walled vessels in the areas of neovascularization.
Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atheromatous plaque causing discharge of debris into the bloodstream, producing microemboli composed of plaque contents.
Atheroembolism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atherosclerotic plaque due to increased pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, leading to weakness of the vessel wall.
Aneurysm formation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Most common cause of hypertension.
Idiopathic (essential hypertension)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 355
This vascular lesion consists of a homogenous pink hyaline thickening of the walls of arterioles with loss of underlying structural detail and with narrowing of the lumen. A major morphologic characteristic in benign nephrosclerosis.
Hyaline arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 356
Characteristic of malignant hypertension, associated with “onion-skin” concentric, laminated, thickening of the walls of arterioles with luminal narrowing. These laminations consist of smooth muscle cells and thickened duplicated basement membrane.
Hyperplastic arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 356
It is a localized abnormal dilation of a blood vessel or heart.
Aneurysm(TOPNOTCH)
It is a localized abnormal dilation of a blood vessel or heart.
Aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysm which involves all three layers of the arterial wall, or the attenuated wall of the heart.
True aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
A breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space.
False aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Arises when blood enters the wall of an artery, as a hematoma dissecting between its layers. Often, but not always aneurysmal in origin.
Arterial dissection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysms which are spherical outpouchings, involving only a portion of the vessel wall, varying in size from 5-20cm in diameter and often contain thrombi.
Saccular aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysms which involve diffuse, circumferential dilation of a long vascular segment, varies in diameter and length, and can involve extensive portions of the aortic arch, abdominal aorta,and iliacs.
Fusiform aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Two most important causes of aortic aneurysms.
AtherosclerosisCystic medial degeneration of the arterial media(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Infection of a major artery that causes weakness to its wall.
Mycotic aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
This disease can more commonly affects men >50 years old. Lesion usually positioned below the renal arteries and above the aortic bifurcation. Can be saccular or fusiform.
Abdominal aortic aneurysm (AAA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
Abdominal aortic aneurysm characterized by dense periaortic fibrosis containing abundant lymphoplasmacytic infiltrate with manybmacrophages and often giant cells.
Inflammatory AAA(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 358
Atherosclerotic lesions infected by lodging of circulating microorganisms in the wall, particularly in the setting of bacteremia from a Salmonella gastroenteritis. Suppuration further destroys the media, potentiating rapid dilation and rupture.
Mycotic abdominal aortic aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
Small blood vessels and vasa vasorum show luminal narrowing and obliteration (obliterative endarteritis), scarring of the vessel wall and a dense surrounding rim of lymphocytes and plasma cells that may extend into the media. Characteristic of the tertiary stage of syphilis.
Syphilitic aortitis(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 359
Most common point of origin of an aortic dissection.
Ascending aorta, 10 cms from the aortic valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 360
Most frequent pre-existing histologically detectable lesion in aortic dissection, characterized by elastic tissue fragmentation and separation of the elastic and smooth muscle cell elements of the media by cystic spaces filled with amorphous proteoglycan-rich extracellular matrix.
Cystic medial degeneration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Classification of aortic dissection involving either them ascending aorta only or both the ascending and descending aorta.
Type A dissections (proximal) Type I DeBakey - ascending aorta only Type II DeBakey - ascending and descending aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Classification of aortic dissections involving the descending aorta only, usually distal to the subclavian artery.
Type B dissection / type III DeBakey(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Granulomatous inflammation frequently involving the temporal artery, occuring in patients >50 years old, associated with polymyalgia rheumatica.
Giant cell (Temporal) arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 363
Granulomatous inflammation usually occuring in patients younger than 50 years old. Classically involves the aortic arch, with intimal hyperplasia and irregular thickening of the vessel wall. Origin of great vessels are obliterated causing weakness of peripheral pulses.
Takayasu arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
Used to distinguish between giant cell arteritis and takayasu arteritis of the aorta.
Age of patient40 Giant cell arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364