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Robbins pathology > X - The Blood Vessels > Flashcards

X - The Blood Vessels Flashcards

1
Q

In these arteries, elastic fibers alternate in layers with smooth muscle cells. Examples are the common carotid artery, iliac arteries and pulmonary arteries.

A

Large or elastic arteries

Robbins Basic Pathology, 8th Ed p. 340

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2
Q

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.

A

Medium-sized or muscular arteries

Robbins Basic Pathology, 8th Ed p. 340

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3
Q

These are the principal control points for regulation of physiologic resistance to blood flow.

A

Arterioles

Robbins Basic Pathology, 8th Ed p. 340

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4
Q

These vessels are approximately the diameter of an RBC, have an endothelial cell lining but no media.

A

Capillaries

)Robbins Basic Pathology, 8th Ed p. 341

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5
Q

Diameter of an RBC.

A

7-8 um

Robbins Basic Pathology, 8th Ed p. 341

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6
Q

These are thin-walled, endothelium lined channels that drain excess interstitial tissue fluid, returning it to blood via the thoracic duct.

A

Lymphatics

)Robbins Basic Pathology, 8th Ed p. 341

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7
Q

These are small spherical dilatations, typically in the circle of Willis.

A

Developmental/berry aneurysms

Robbins Basic Pathology, 8th Ed p. 341

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8
Q

These are abnormal, typically small, direct connections between arteries and veins that bypass the intervening capillaries.

A

Arteriovenous fistulas

Robbins Basic Pathology, 8th Ed p. 341

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9
Q

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.

A

Fibromuscular dysplasia

Robbins Basic Pathology, 8th Ed p. 341

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10
Q

Literally means hardening of the arteries, term reflecting arterial wall thickening and loss of elasticity, affecting small arteries and arterioles.

A

Arteriolosclerosis

Robbins Basic Pathology, 8th Ed p. 343

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11
Q

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.

A

Mockenberg medial calcific sclerosis

Robbins Basic Pathology, 8th Ed p. 343

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12
Q

Characterized by intimal lesions called atheromas that protrude into vascular lumina.

A

Atherosclerosis

Robbins Basic Pathology, 8th Ed p. 343

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13
Q

Three principal components of an atheromatous plaque.

A
  1. Cells (SM cells, macrophages, T cells)
  2. Extracellular matrix (collagen, elastic fibers, proteoglycans)
  3. Intracellular and extracellular lipidFibrous cap, central lipid core, neovascularization

Robbins Basic Pathology, 8th Ed p. 344

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14
Q

Non-modifiable risk factors for atherosclerosis. (4)

A

Increasing age
Male gender
Family history
Genetic abnormalities

Robbins Basic Pathology, 8th Ed p. 344

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15
Q

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.

A

Fatty streaks

Robbins Basic Pathology, 8th Ed p. 349

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16
Q

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

A

Abdominal aorta > coronaries > popliteal arteries > internal carotid arteries > circle of Willis
Robbins Basic Pathology, 8th Ed p. 350

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17
Q

Fate of an atheromatous plaque due to rupture of the overlying fibrous cap or the thin-walled vessels in the areas of neovascularization.

A

Hemorrhage

Robbins Basic Pathology, 8th Ed p. 351

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18
Q

Fate of an atheromatous plaque causing discharge of debris into the bloodstream, producing microemboli composed of plaque contents.

A

Atheroembolism

Robbins Basic Pathology, 8th Ed p. 351

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19
Q

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.

A

Aneurysm formation

Robbins Basic Pathology, 8th Ed p. 351

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20
Q

Most common cause of hypertension.

A

Idiopathic (essential hypertension)

Robbins Basic Pathology, 8th Ed p. 355

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21
Q

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.

A

Hyaline arteriolosclerosis

Robbins Basic Pathology, 8th Ed p. 356

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22
Q

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.

A

Hyperplastic arteriolosclerosis

Robbins Basic Pathology, 8th Ed p. 356

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23
Q

It is a localized abnormal dilation of a blood vessel or heart.

A

Aneurysm

Robbins Basic Pathology, 8th Ed p. 357

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24
Q

Aneurysm which involves all three layers of the arterial wall, or the attenuated wall of the heart.

A

True aneurysm

Robbins Basic Pathology, 8th Ed p. 357

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25
Q

A breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space.

A

False aneurysm

Robbins Basic Pathology, 8th Ed p. 357

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26
Q

Arises when blood enters the wall of an artery, as a hematoma dissecting between its layers. Often, but not always aneurysmal in origin.

A

Arterial dissection

Robbins Basic Pathology, 8th Ed p. 357

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27
Q

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.

A

Saccular aneurysms

Robbins Basic Pathology, 8th Ed p. 357

28
Q

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.

A

Fusiform aneurysms

Robbins Basic Pathology, 8th Ed p. 357

29
Q

Two most important causes of aortic aneurysms.

A

Atherosclerosis
Cystic medial degeneration of the arterial media
Robbins Basic Pathology, 8th Ed p. 357

30
Q

Infection of a major artery that causes weakness to its wall.

A

Mycotic aneurysm

Robbins Basic Pathology, 8th Ed p. 357

31
Q

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.

A

Abdominal aortic aneurysm (AAA)

Robbins Basic Pathology, 8th Ed p. 358

32
Q

Abdominal aortic aneurysm characterized by dense periaortic fibrosis containing abundant lymphoplasmacytic infiltrate with manybmacrophages and often giant cells.

A

Inflammatory AAA

Robbins Basic Pathology, 8th Ed p. 358

33
Q

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.

A

Mycotic abdominal aortic aneurysm

Robbins Basic Pathology, 8th Ed p. 358

34
Q

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.

A

Syphilitic aortitis

Robbins Basic Pathology, 8th Ed p. 359

35
Q

Most common point of origin of an aortic dissection.

A

Ascending aorta, 10 cms from the aortic valve

Robbins Basic Pathology, 8th Ed p. 360

36
Q

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.

A

Cystic medial degeneration

Robbins Basic Pathology, 8th Ed p. 361

37
Q

Classification of aortic dissection involving either them ascending aorta only or both the ascending and descending aorta.

A

Type A dissections (proximal),
Type I DeBakey - ascending aorta only,
Type II DeBakey - ascending and descending aorta

Robbins Basic Pathology, 8th Ed p. 361

38
Q

Classification of aortic dissections involving the descending aorta only, usually distal to the subclavian artery.

A

Type B dissection / type III DeBakey

Robbins Basic Pathology, 8th Ed p. 361

39
Q

Granulomatous inflammation frequently involving the temporal artery, occuring in patients >50 years old, associated with polymyalgia rheumatica.

A 
Giant cell (Temporal) arteritis
Robbins Basic Pathology, 8th Ed p. 363
40
Q

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.

A

Takayasu arteritis

Robbins Basic Pathology, 8th Ed p. 364

41
Q

Used to distinguish between giant cell arteritis and takayasu arteritis of the aorta.

A

Age of patient40 Giant cell arteritis

Robbins Basic Pathology, 8th Ed p. 364

42
Q

In this disease, affected blood vessels develop nodular intimal thickening, granulomatous inflammation within the inner media centered on the internal elastic membrane, and fragmentation of the internal elastic lamina. Typically involves temporal and ophthalmic arteries.

A

Giant - cell/Temporal arteritis

Robbins Basic Pathology, 8th Ed p. 364

43
Q

A systemic vasculitis causing transmural necrotizing inflammation of small to medium sized vessels, with mixed infiltvrate of neutrophils, eosinophils, and mononuclear cells, frequently accompanied by fibrinoid necrosis.Typically involves renal arteries but spares pulmonary vessels.

A 
Polyarteritis Nodosa (PAN)
Robbins Basic Pathology, 8th Ed p. 365
44
Q

Arteritis associated with mucocutaneous lymph node syndrome, which usually occurs in children. Coronary arteries can be involved with aneurysm formation or thrombosis. Fibrinoid necrosis usually less prominent.

A

Kawasaki disease

Robbins Basic Pathology, 8th Ed p. 366

45
Q

Granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels, including cresencteric glomerulonephritis. Associated with c-ANCA.

A

Wegener granulomatosis

Robbins Basic Pathology, 8th Ed p. 367

46
Q

A necrotizing vasculitis that generally affects capillaries, arterioles and venules, with few or no immune deposits. Necrotizing glomerulonephritis and pulmonary capillaritis are common. Associated with p-ANCA.

A

Microscopic polyangiitis

Robbins Basic Pathology, 8th Ed p. 368

47
Q

Eosinophil-rich and granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels. Associated with asthma and blood eosinophilia. Associated with p-ANCA.

A

Churg-Strauss syndrome

Robbins Basic Pathology, 8th Ed p. 368

48
Q

Characterized by sharply segmental avute and chronic vasculitis of medium sized and small arteries, predominantly of the extremities. There is acute and chronic inflammation accompanied by luminal thrombosis, containing microabscess composed of neutrophils surrounded by granulomatous inflammation. Stromg relationship with cigarette smoking.

A

Thromboangiitis obliterans (Buerger disease)

Robbins Basic Pathology, 8th Ed p. 368

49
Q

Results from an exaggerated vasoconstriction of digital arteries and arterioles, inducing paroxysmal pallor or cyanosis of the digits of the hands and feet.

A

Raynaud phenomenon

Robbins Basic Pathology, 8th Ed p. 369

50
Q

Reflects an exaggeration of central and local vasomotor responses to cold or emotion. Structural changes in the arterial walls are absent except late in course when intimal thickening can appear.

A

Primary Raynaud phenomenon (Raynaud disease)

Robbins Basic Pathology, 8th Ed p. 369

51
Q

Reflects vascular insufficiency of the extremities in the context of arterial disease caused by other entities including SLE, Buerger disease, or atherosclerosis.

A

Secondary Raynaud phenomenon

Robbins Basic Pathology, 8th Ed p. 370

52
Q

Abnormally dilated, tortous veins produced by prolonged increase in intraluminal pressure and loss of vessel wall support. Veins show wall thinning at the points of maximal dilation with smooth muscle hypertrophy and intimal fibrosis. Focal thrombosis and venous valve deformities are common.

A

Varicose veins

Robbins Basic Pathology, 8th Ed p. 370

53
Q

Most common blood vessels involved in development of varicose veins.

A

Superficial veins of the upper and lower leg

Robbins Basic Pathology, 8th Ed p. 370

54
Q

Three sites of varices produced in the presence of portal hypertension.

A

GEJ (Esophageal varices)Rectum (Hemorrhoids)Periumbillical veins (Caput medusae)

Robbins Basic Pathology, 8th Ed p. 370

55
Q

Common and serious complication of of deep vein thrombosis (DVT).

A

Pulmonary embolism

Robbins Basic Pathology, 8th Ed p. 371

56
Q

The acute inflammation elicited when bacterial infections spread into and through the lymphatics.

A

Lymphangitis

Robbins Basic Pathology, 8th Ed p. 371

57
Q

These are bright red to blue lesions, that vary from a few millimeters tomseveral centimeters in diameter. Unencapsulated aggregates of closely packed, thin-walled capillaries, usually blood-filled and lined by flattened endothelium. Vessels are separated by scant connective tissue stroma.

A

Capillary hemangiomas

Robbins Basic Pathology, 8th Ed p. 372

58
Q

Appears as red-blue, soft, spongy masses 1-2 cm in diameter, which can affect large subcutaneous areas of the face, extremities, and othe body regions. Mass is sharply defined but not encapsulated, composed of large, cavernous, blood-filled spaces.

A

Cavernous hemangioma

Robbins Basic Pathology, 8th Ed p. 372

59
Q

This form of capillar hemangioma is a rapidly growing peduncular red nodule on the skin, gingival, or oral mucosa, bleeds easily and is often ulcerated.

A

Pyogenic granuloma

Robbins Basic Pathology, 8th Ed p. 373

60
Q

These are round, slightly elevated, red-blue firm nodules, less than 1 cm diameter that can resemble a minute focus of hemorrhage UNDER THE NAIL. Histologically, these are aggregates, nests, and masses of tumor cells intimately associated with branching vascular channels.

A

Glomus tumor (Glomangioma)

Robbins Basic Pathology, 8th Ed p. 373

61
Q

A specialized arteriovenous structure involved in thermoregulation.

A

Glomus body

Robbins Basic Pathology, 8th Ed p. 373

62
Q

This lesion is the ordinary “birthmark” and is the most common form of ectasia. Characteristically a flat lesion on the head or neck, ranging in color from light pink to deep purple.

A

Nevus flammeus

Robbins Basic Pathology, 8th Ed p. 374

63
Q

This non-neoplastic vascular lesion grossly resembles a spider. There is radial, often pulsatile array of dilated subcutaneous arteries or arterioles about a central core, that blanches when pressure is applied to its center.

A

Spider telangiectasia

Robbins Basic Pathology, 8th Ed p. 374

64
Q

An opportunistic infection in immunocompromised persons that manifest as vascular proliferations involving skin, bone, brain and other organs. Characterized grossly by red papules and nodules, or rounded subcutaneous masses. Histologically, there is capillary proliferation with prominent epitheloid EC’s showing nuclear atypia and mitoses. Lesions contain stromal neutrophils, nuclear dust nd purplish granular material.

A

Bacillary angiomatosis

Robbins Basic Pathology, 8th Ed p. 374

65
Q

Common in patients with AIDS, caused by HHV 8, causing skin lesions ranging from patches, plaques to nodules.

A

Kaposi sarcoma

Robbins Basic Pathology, 8th Ed p. 375

66
Q

These are malignant endothelial neoplasms, with varying histology from plump, anaplastic but recognizable endothelial cells producing vascular channels to widely undifferentiated tumors having solid, spindle cell appearance and producing nondefinite blood vessels.

A

Angiosarcoma

Robbins Basic Pathology, 8th Ed p. 376

67
Q

Plaque changes fall into three general categories

A

Rupture/fissuring- exposing highly thrombogenic plaque constituents

Erosion/ulceration- exposing the thrombogenic subendothelial basement membrane to the blood

Hemorrhage into the atheroma expanding it volume

Robbins pathology (23 decks)

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