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Blood Vessels

Blood Vessels. The Structure and Function of Blood Vessels. Basic Constituents of walls of blood vessels Endothelial cells Smooth muscle cells Extracellular matrix Three concentric layers Intima Media Adventitia Three types of arteries Large, elastic Medium-sized , muscular

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Blood Vessels

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  1. Blood Vessels

  2. The Structure and Function of Blood Vessels • Basic Constituents of walls of blood vessels • Endothelial cells • Smooth muscle cells • Extracellular matrix • Three concentric layers • Intima • Media • Adventitia • Three types of arteries • Large, elastic • Medium-sized , muscular • Small arteries • Arterioles- principle points of physiologic resistance to blood flow • Capillaries – thin wall, slow flow= ideal for exchange between blood and tissues • Venules – vascular leakage and leukocyte exudation occur preferentially • Veins –predisposed to irregular dilation, compression, easy penetration • Lymphatics –important pathway for disease dissemination

  3. Vessel Development, Growth, and Remodeling • Vasculogenesis – de novo formation of blood vessels during embryogenesis • Angiogenesis – neovascularization in mature organism • Arteriogenesis – remodeling of existing arteries

  4. Congenital Anomalies • Developmental (berry) aneurysms • Arteriovenous fistulas • Fibromuscular dysplasia

  5. Vascular Wall Cells and Their Response to Injury • Endothelial Cells • Weibel-Palade bodies – von Willebrand’s factor • Endothelial cell properties and functions - Table 11-1 • Endothelial ativationvs dysfunction – Figure 11-2 • Vascular smooth muscle cells • Proliferate when stimulated • Synthesize ECM • Elaborate growth factors and cytokines • Vasoconstriction or dilation • Intimal thickening – a stereotypic response to vascular injury • Vascular injury – with endothelial loss or even just dysfunction – stimulates smooth muscle cell growth and associated matrix synthesis that thickens the intima • Neointimal smooth muscle cells divide but do not contract • Healing response results in permanent intimal thickening

  6. Hypertensive Vascular Disease • Types and causes of hypertension – Table 11-2 • 95% is essential hypertension • Complex, multifactorial disorder • Interactions of mutations and polymorphisms at several loci that influence blood pressure, with a variety of environmental factors • Regulation of Blood Pressure – Figure 11-4 • Function of cardiac output and peripheral vascular resistance • Malignant hypertension - >200/120 mmHg • Retinal hemorrhages and exudates, +/- papilledema • Renal failure

  7. Hypertensive Vascular Disease • Vascular pathology in hypertension • Benign – hyaline arterioslerosis • Malignant – hyperplastic asteriolosclerosis • “onion-skinning” • Necrotizing arteriolitis

  8. Arteriosclerosis • Arteriosclerosis • Monckeberg medial sclerosis • Atherosclerosis

  9. Atherosclerosis • Epidemiology • Pathogenesis of Atherosclerosis • Endothelial Injury • Smooth Muscle Proliferation – PDGF, FGF, TGF-alpha -> ECM production • Overview • Consequences of Atherosclerotic Disease

  10. Epidemiology • Major risk factors • Nonmodifiable • Increasing age • Male gender • Family history • Genetic abnormalities • Modifiable • Hyperlipidemia • Hypertension • Cigarette smoking • Diabetes mellitus • Additional risk factors • Inflammation – CRP • Hyperhomocystinemia • Metabolic syndrome • Lipoprotein (a) • Factors affecting hemostasis • Other factors – Type A, etc

  11. Pathogenesis • Response-to-injury hypothesis • Atherosclerosis is a chronic inflammatory and healing response of the arterial wall to endothelial injury. Lesion progression occurs through the interaction of modified lipoproteins, monocyte-derived macrophages, and T-lymphocytes with the normal cellular constituents of the arterial wall. • Endothelial injury -> Accumulation of lipoproteins -> monocyte adhesion to the endothelium -> platelet adhesion -> factor release -> smooth muscle recruitment, proliferation, and ECM production -> lipid accumulation

  12. Endothelial Injury • Endothelial dysfunction • Hemodynamic disturbances • Nonturbulent laminar flow leads to athero-protection • Lipids • Cholesterol and cholesterol esters • Oxygen free radical production • Oxidized LDL - cytotoxic • Inflammation – Dysfunctional endothelial cells express adhesion molecules for leukocytes • Infection – Herpesvirus, CMV, C. pneumoniae detected in plaques

  13. Overview • Fatty streaks • Earliest lesions • Lipid-filled foamy macrophages • Atherosclerotic plaque • Components • Superficial fibrous cap – Smooth muscle cells and collagen • “Shoulder” – beneath and to the side – macrophages, T cells, smooth muscle cells • Necrotic core – lipid, debris from dead cells, foam cells, fibrin, variable organized thrombus, plasma proteins • Periphery – neovascularization • Calcification • Clinically important changes • Rupture, ulceration, erosion -> thrombosis • Hemorrhage into a plaque • Atheroembolism • Aneurysm

  14. Consequences of Atherosclerotic Disease • Major consequences • Myocardial infarction • Cerebral infarction • Aortic aneurysms • Peripheral vascular disease

  15. Consequences of Atherosclerotic Disease • Principal outcomes depend on: • Size of the involved vessels – smaller vessels can become occluded compromising the distal blood supply • Relative stability of the plaque itself – ruptured plaques can cause embolism causing distal vessel obstruction or acute thrombosis • Degree of degeneration of the arterial wall – aneurysm formation with rupture and/or thrombosis

  16. Consequences of Atheroscerotic Disease • Atherosclerotic stenosis • Early stages – outward remodeling of the media tends to preserve lumen diameter • Critical stenosis – usually around 70% - symptoms start • Chronically diminished blood supply • Mesenteric occlusion and bowel ischemia • Chronic IHD • Ischemic encephalopathy • Intermittent claudication

  17. Consequences of Atherosclerotic Disease • Acute plaque changes • Rupture/fissuring – exposing highly thrombogenic plaque constituents • Erosion/ulceration – exposing the thrombogenicsubendothelial basement membrane to blood • Hemorrhage into the atheroma – expanding its volume • Precipitating lesion in patients who develop MI and other acute coronary syndromes is not necessarily a severely stenotic and hemodynamically significant lesion before its acute change • Events that trigger acute changes • Intrinsic – plaque structure and composition • Extrinsic – blood pressure and platelet reactivity • Vulnerable plaque vs stable plaque

  18. Consequences of Atherosclerotic Disease • Thrombosis – potent activator of multiple growth-related signals in smooth muscle cells leading to growth of atherosclerotic lesions • Vasoconstriction – compromises lumen size and increases local mechanical forces • Stimulated by circulating adrenergic agonists, locally released platelet contents, impaired secretion of endothelial relaxing factors( NO)

  19. Aneurysms and Dissection • Abdominal Aortic Aneurysm • Thoracic Aortic Aneurysm • Aortic Dissection

  20. Aneurysms and Dissection • Aneurysm = localized abnormal dilation of a blood vessel or the heart • Types • True aneurysm – involves an intact attenuated arterial wall of thinned ventricular wall of the heart • False (pseudo-) aneurysm – defect in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space • Dissection – blood enters the arterial wall itself as a hematoma dissecting between the layers • Saccular – spherical outpouchings • Fusiform – diffuse, circumferential dilation of a long vascular segment

  21. Anuerysms and Dissection • Pathogenesis • Structure or function of the connective tissue within the vascular wall is compromised • The intrinsic quality of the vascular wall connective tissue is poor • E.g. Marfan syndrome – defect in synthesis of fibrillin • E.g. Loeys-Dietz syndorme – abnormalities in elastin and collagen I and II • E.g. Ehlers-Danlos syndrome – Defective type III collagen • Scurvy – altered collagen cross-linking

  22. Aneurysms and Dissection • Pathogenesis • The balance of collagen degradation and synthesis is altered by local inflammatory infiltrates and the destructive proteolytic enzymes they produce - MMP • The vascular wall is weakened through the loss of smooth muscle cells or the inappropriate synthesis of noncollagenous or nonelastic ECM • Two most important disorders that predispose to aortic aneurysms are atherosclerosis and hypertension • Other - trauma, vasculitis, congenital defects, infections (mycotic)

  23. Anuerysms and Dissection • Abdominal aortic aneurysm • Increased age • Males • Smokers • Clinical consequences • Rupture into the peritoneal cavity or retroperitoneal tissues with massive potentially fatal hemorrhage- rate of rupture related to size • Obstruction of a branch vessel resulting in ischemic injury of downstream tissues • Embolism from atheroma or mural thrombus • Impingement on an adjacent structure • Presentation as an abdominal mass

  24. Aneurysms and Dissection • Thoracic aortic aneurysms • Hypertension • Marfan, etc • Syphilis • Clinical presentation • Encroachment on mediastinal structures • Respiratory difficulties • Difficulty in swallowing • Persistent cough • Pain caused by erosion of the bone • Cardiac disease – aortic valve or coronary ostia involvement • Rupture

  25. Aneurysms and Dissection • Aortic dissection • Blood splays apart the laminar planes of the media to form a blood-filled channel within the aortic wall • Occurs principally in two groups • Pressure-related mechanical injury and/or ischemic injury • Clinical features • Men aged 40-60 with antecedent hypertension • Younger patients with abnormalities affecting the connective tissue • Classification – Figure 11-21 • Type A – more common, proximal (DeBakey I and II) • Type B – distal lesions not involving the ascending part, usually distal to the subclavian (Debakey III) • Excurciating pain beginning in the anterior chest, radiating to the back, and moving downward • The most common cause of death is rupture of the dissection outward into the pericardial, pleural, or peritoneal cavities

  26. Vasculitis • Noninfectious Vasculitis • Giant-Cell (Temporal) Arteritis • Takayasu Arteritis • PolyarteritisNodosa • Kawasaki Disease • Microscopic Polyangiitis • Churg-Strauss Syndrome • Wegener Granulomatosis • ThromboangiitisObliterans(Buerger Disease) • Vasculitis Associated with other Disorders • Infectious Vasculitis

  27. Vasculitis • Vasculitis = vessel wall inflammation • Classification – Table 11-4 • Two most common Immune-mediated Direct-invasion by infectious pathogens • Clinical features • Depend on the vascular bed involved • Constitutional signs and symptoms

  28. Noninfectious Vasculitis • Three main mechanisms • Immune complex deposition • Drug hypersensitivity – serum sickness • Viral infections – polyarteritisnodosa • Pauci-immune • Antineutrophil cytoplasmic antibodies (ANCAs) • Circulating antibodies that react with neutrophil cytoplasmic antigens • Anti-myeloperoxidase (MPO-ANCA) – formerly called perinuclear (p-ANCA) – microscopic polyangiitis and Churg-Strauss • Anti-proteinase-3 (PR3-ANCA) –formerly called cytoplasmic ( c-ANCA) – Wegener granulomatosis • Anti-endothelial cell antibodies – Kawasaki disease

  29. Giant-Cell (Temporal) Arteritis • Most common form of vasculitis among elderly in US and Europe • Granulomatous inflammation of arteries in the head • Fever, weight loss, fatigue, facial pain, headache, tender, superficial temporal artery, ocular symptoms • Segmental nodular intimal thickening, medial granulomatous inflammation, elastic lamina fragmentation, T cell and macrophage infiltration, multinucleated giant cells

  30. Takayasu Arteritis • Granulomatous vasculitis • Ocular disturbances and marked weakening of pulses in the upper extremities (pulseless disease) • Transmural fibrous thickening of the aorta particularly the aortic arch and great vessels, severe luminal narrowing of the great vessels • Under 50 – Takayasu • Over 50 – Giant-cell aortitis • Initial symptoms – non-specific – fatigue, weight loss, fever

  31. PolyarteritisNodosa • Systemic vasculitis of small or medium-sized muscular arteries, typically involving renal and visceral but sparing pulmonary • 30% have chronic hepatitis B with HBsAg-HbsAb complexes in affected vessels • Classic idiopathic –segmental transmural necrotizing inflammation. Weakens the wall, impaired perfusion • Malaise, fever, weight loss, hypertension, abdominal pain and melena, diffuse muscular aches and pains, peripheral neuritis

  32. Kawasaki Disease • Leading cause of acquired heart disease in children • Acute, febrile, usually self-limited illness associated with arteritis affecting large to medium-sized, and even small vessels • Predilection for coronary artery involvement – leading to aneurysms, rupture and acute MI • Also known as mucocutaneous lymph node syndrome • Conjunctival and oral erythema and erosion, edema of hands and feet, erythema of the palms and soles, desquamative rash, cervical lymph node enlargement • IVIG and aspirin

  33. Microscopic Angiitis • Necrotizing vasculitis generally affecting capillaries, arterioles, and venules • Also called hypersensitivity or leukocytoclasticvasculitis • Necrotizing glomerulonephritis and pulmonary capillaritis

  34. Churg-Strauss Syndrome • Allergic granulomatosis and angiitis • Small vessel necrotizing vasculitis associated with asthma, allergic rhinitis, lung infiltrates, peripheral eosinophilia, and extravascular necrotizing granulomas

  35. Wegener Granulomatosis • Acute necrotizing granulomas of the upper respiratory tract • Necrotizing or granulomatous vasculitis of the lungs and upper respiratory tract • Renal disease, often foal necrotizing, often crescentic GN

  36. ThromboangiitisObliterans (Buerger Disease) • Segmental, thrombosing, acute and chronic inflammationof medium-sized and small arteries principally tibial and radial arteries • Almost exclusively associated with smoking • Superficial nodular phlebitis, cold sensitivity of Raynaud type, instep claudication, severe pain even at rest, chronic ulcerations

  37. Raynaud Phenomenon • Exaggerated vasoconstriction of the digital arteries and arterioles • Red, white, blue changes – proximal vasodilation, central vasoconstriction, distal cyanosis • Primary - 3-5% general population, usually young woman • Secondary – e.g. SLE, Buerger,scleroderma

  38. Veins and Lymphatics • Varicose Veins • Thrombophlebitis and Phlebothrombosis • Superior and Inferior Vena Caval Syndromes • Lymphangitis and Lymphedema

  39. Varicose Veins Varicose veins = Abnormally dilated, tortuous veins produced by prolonged, increased intraluminal pressure and loss of vessel wall support 10-20% men, 25-33% woman, obesity, pregnancy, familial Stasis, congestion, edema, pain, thrombosis, stasis dermatitis, varicose ulceration Portal hypertension -> esophageal varices, hemorrhoids, caput medusa

  40. Thrombophlebitis and Phlebothrombosis • Deep leg veins are the site of 90% • Others – periprostatic venous plexus, pelvic venous plexus, large skull veins, dural sinuses, portal vein • Prolonged immobilization resulting in decreased blood flow through the veins is the most important predisposing factor • Systemic hypercoagulability • Trousseau sign – migratory thrombophlebitis in cancer • Homan sign may or may not be present • Pulmonary embolism is a serious complication of DVT and in many cases is the first manifestation

  41. Superior and Inferior Vena Caval Syndromes • Superior Vena Cava – neoplasms that compress or invade the SVC leading to marked dilation of the veins of the head, neck, and arms and cyanosis (bronchogenic carcinoma or mediastinal lymphoma) • Inferior Vena Cava – Neoplasms that invade or compress or by thrombus leading to marked lower extremity edema, distension of the superficial collateral veins of the lower abdomen, massive proteinuria (hepatocellular carcinoma or renal cell carcinoma)

  42. Lymphangitis and Lymphedema • Lymphangitis – acute inflammation elicited when bacterial infections spread into the lymphatics, most common Group A beta-hemolytic strep, red painful streaks, enlargement of lymph nodes • Lymphedema • Primary – simple congenital lymphedema or Milroy disease (heredofamilial congenital lymphedema) • Secondary – tumors, surgical procedures involving nodes, irradiation filiarisis, post-inflammatory thrombosis and scarring • Peaud’orange • Chylous ascites, thorax, pericardium caused by rupture of dilated lymphatics

  43. Tumors • Benign Tumors and Tumor-like Conditions • Hemangiomas • Lymphangiomas • Glomus Tumor (Glomangioma) • Vascular Ectasias • Bacillary Angiomatosis • Intermediate-Grade (Borderline) Tumors • Kaposi Sarcoma • Hemangioendothelioma • Malignant Tumors • Angiosarcoma • Hemangiopericytoma

  44. Benign Tumors and Tumor–like Conditions • Hemangioma – very common, increased numbers of normal or abnormal blood vessels filled with blood • Capillary hemangioma – most common variant, skin, subcutaneous tissues, mucous membranes, liver, spleen, kidney • Cavernous hemangioma – Large, dilated channels, less well circumscribed, more frequently involve deep structures, von Hippel-Lindau disease • Pyogenic granuloma – Rapidly growing pedunculated red nodule, bleeds easily, often ulcerated , pregnancy tumor, associated with trauma, proliferating capillaries, inflammation, exuberant granulation -like tissue

  45. Benign Tumors and Tumor-like Conditions • Lymphangiomas • Simple (capiilary) • Caverous (cystic hygromas) – neck and axilla of children, Turner syndrome • Glomus tumor (glomangioma) • Very painful, modified smooth muscle cells of the glomus body • Distal portion of the digitd, especially under the fingernails • Vascular ectasias • Nevus flammeus – “birthmark”, port wine stain – Sturge-Weber syndrome • Spider telangiectasia – high estrogen • Hereditary hemorrhagic telangiectasia ( Osler-Weber-Rendu disease) • Bacillary angiomatosis – • Vascular proliferation resulting from an opportunistic infection

  46. Intermediate-grade (Borderline Tumors) • Kaposi sarcoma • Chronic KS • Lymphadenopathic KS (African or endemic) • Transplant- associated KS • AIDS-associated KS (epidemic) • HHV-8 • Red to purple macules, raised plaques, nodules • Hemangioendothelioma

  47. Pathology of Vascular Interventions • Angioplasty and Endovascular Stents • Vascular Replacement • Act like a vascular injury leading to stenosis, etc

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