Vascular Pathology PDF

Vascular Pathology ❑Classification of arteries according to their size & structure into: 1. Large (elastic arteries): Example: AORTA & ITS BANCHES. 2. Medium size arteries (muscular arteries): like coronary, renal arteries. 3. Small arteries (less than 2mm in diameter) & Arterioles (20 to 100 mic...

Vascular Pathology ❑Classification of arteries according to their size & structure into: 1. Large (elastic arteries): Example: AORTA & ITS BANCHES. 2. Medium size arteries (muscular arteries): like coronary, renal arteries. 3. Small arteries (less than 2mm in diameter) & Arterioles (20 to 100 microns).  Vascular diseases I. Vascular anomalies: main two anomalies are; a. Berry aneurysm (discussed later). b. Arteriovenous Fistula. Arteriovenous fistula II. Arteriosclerosis: & means thickening & loss of elasticity of arterial walls it occurs in three forms: 1. Atherosclerosis, the most frequent & important form (later discuss). 2. Monckeberg medial calcific sclerosis; Characterized by calcific deposits in the walls of muscular arteries in persons older than 50 years, Radiological visible & often palpable calcifications without occlusion of their lumens. 3. Arteriolosclerosis: (Disease of small arteries & arterioles); seen in old ages and in patient with hypertension & diabetes mellitus. Monckeberg calcific medial sclerosis Hyaline arteriolosclerosis Hyperplasic arteriolosclerosis  Atherosclerosis (ATH) characterized by; Intimal lesion called Atheromas, or atheromatous (fibro- fatty) plaques, that protrude into & obstruct vascular lumen. ATH contributes for more than 50% of all deaths as a result of ischemic heart diseases or cerebrovascular accidents. ❑ Pathogenesis of ATH: E The most acceptable theory of pathogenesis of ATH is called Response to injury hypothesis as result of chronic endothelial injury by the following causes;  Risk Factors of ATH: ❑ Major risk factors: include; 1 , 55 · i A. Unmodifiable major risk factors 1. Age: ATH is not usually clinically evident until middle age or later. 2. Male gender (Sex): Male more prone to ATH than the female (due to protective hormonal effect of estrogen in females). 3. Familial predisposition: Familial predisposition to ATH & IHD is most likely Polygenic, may be related to other risk factors (e.g. hypertension, diabetes mellitus). 4. Genetic abnormalities, like abnormality in lipoprotein metabolism, such as familial hypercholesterolemia. B. Modifiable Major risk factors (Potentially controllable). 1. Hyperlipidemia 2. Hypertension: Is a major risk factor for ATH in all ages. 3. Cigarettes smoking 4. Diabetes Mellitus ❑ Lesser, Uncertain, Non-quantitated risk factors: i. Obesity. ii. Physical inactivity. iii. Stressful life style (type-A personality). iv. High carbohydrate intake. v. Postmenopausal estrogen deficiency. vi. Unsaturated fat intake. vii. Chlamydia pneumoniae infection. Clinical Significance of ATH: In small arteries; Atheromas can occlude lumina of arteries by superadded thrombosis; resulting in ischemia of supplies parts of body. In large & medium sized arteries; Plaques of ATH are destructive, resulting in weakening the affected vessel wall causing aneurysm.  & - ⑯ Morphology of ATH: The ATH passes in 3 stages: ( % 352 1) Fatty streaks: characterized by intimal thickening & accumulation of Lipid-filled foam cells and are not significantly raised and thus do not cause any disturbance in blood flow. Lipilm cel 2) Atheromatous Plaques: These are raised focal lesions within the intima, also called (Fibro-fatty or Fibro-lipid Plaques). varied in size from 0.3 to 1.5cm in diameter, sometimes they are coalesces to form large masses that protruded into lumen. · The atheromatous plaques consist of two parts: I. Cap (fibrous cap): Is composed of SMCs and relatively dense collagen. II. Core (lipid core): Deep to the fibrous cap is a necrotic core, containing lipid (primarily cholesterol and cholesterol esters), debris from dead cells, foam cells (lipid-laden macrophages and SMCs). so Immen is] complet - obstructio Stage 2: Atheromatous plaques (Mic) 3) Advanced atheromatous lesions: As the disease become advanced, these lesions become diffusely involving the arterial wall leading to a condition called advanced atheromatous lesion Varying degrees of ATH in the Aorta  -- Pathological changes (complications) in ATH lesions: -6) S/ : + +- 58 1. Focal rupture, ulceration, erosion, and superadded thrombosis. 2. Hemorrhage into the plaques; (mainly in coronary arteries), may result in formation of Hematoma. 3. Atheroembolism; Plaque rupture can discharge debris into the bloodstream, producing microemboli composed of plaque contents. 4. Aneurysmal dilatation: Atherosclerosis-induced aortic aneurysm.. Occlusive atheromas in the coronary arteries Complications of ATH: Cholesterol emboli &  ANEURYSMS An aneurysm is a localized abnormal dilatation of a blood vessel or heart, two types. & i. True aneurysm (involve all three layers of the wall, intima, media, and adventia)). ii. False aneurysm (wall is composed of hematoma or fibrous tissues). MCPS Causes of aneurysm: alp Ssls - 1. ATH. 2. Cystic medial degeneration of arterial media. 3. Trauma. 4. Congenital defect (Berry aneurysm) 5. Infections (Mycotic aneurysm).or Syphilis. Complications of ATH (formation of Aneurysm)  % /nyers if 125450 Aneurysm Aortic Dissection (Dissecting Hematoma) or dissecting aneurysm: Dissection of blood between & along the laminar planes within the media, with the formation of blood filled channel within the wall of aorta. ❑ Etiology of aortic dissection: 1. Mostly unknown. 2. Hypertension. Surgical 3. Marfan syndrome. d 4. Complication of arterial cannulation or catheterization. (Iatrogenic aortic dissection). 5. Sometimes for unknown causes dissection occurs during or after pregnancy. Aortic dissection / Gross Aortic dissection /microscopically Hypertensive Vascular Diseases (Hypertension) ▪ Sustained diastolic pressure in excess of 90 mmHg or a sustained systolic pressure in excess of 140 mmHg is considered as hypertension. Systolic blood pressure is more important than diastolic blood pressure in determining cardiovascular risk. ❑ Types of systemic Hypertension: a. Idiopathic (essential hypertension) forming 95% of all cases of hypertension. ( 95% are benign & 5% are malignant accelerated hypertension), which are blood pressure over200/120mmHg, with renal failure, and retinal hemorrhages and exudates, with or without papilledema). b. Secondary hypertension forming 5% of cases of hypertension; (95% of cases are malignant & 5% are benign hypertension). Causes of secondary hypertension: Renal causes, Endocrine causes, Cardiovascular causes, & Neurologic causes. Papilledema Retinal hemorrhage Malignant hypertension  Inflammatory diseases of blood vessels (Vasculitides) 1. Infectious Vasculitis; Bacterial (e.g., Neisseria), Spirochetal (syphilis), Fungal (aspergillosis), & viral. 2. Immune-mediated Vasculitis (non infectious Vasculitis); the main immunologic mechanisms that initiate noninfectious vasculitis are; (1) immune complex deposition, (2) antineutrophil cytoplasmic antibodies (ANCAs), and (3) anti-endothelial cell antibodies. 3. Vasculitides associated with other disorders: Rheumatoid arthritis, SLE, inflammatory bowel diseases …etc. Giant Cell (Temporal) Arteritis 11/ &S most common form of the Vasculitides, it is a chronic, typically granulomatous inflammation of large to small-sized arteries. Site: principally affects the arteries in the head-especially the temporal arteries-but also the vertebral and ophthalmic arteries, as well as the aorta (giant-cell aortitis). Ophthalmic artery involvement can lead to sudden and permanent blindness. Age: older individuals, rare before the age of 50. Symptoms of giant cell arteritis are either; - Facial pain or headache, more intense along the course of the superficial temporal artery, - OR only vague, fever, fatigue, weight loss-without localizing signs Very high erythrocytes sedimentation rate (ESR). Giant cell arteritis/ Gross Giant cell arteritis/ Mic Polyarteritis Nodosa E Polyarteritis nodosa (PAN) is a systemic vasculitis of small or medium-sized muscular arteries (but not arterioles, & capillaries, or venules), typically involving renal and visceral vessels but sparing the pulmonary circulation.. 0 % & 20. Polyateritis nodosa Wegener Granulomatosis It is a necrotizing vasculitis characterized by the triad of 1 a) Acute necrotizing granulomas of the upper respiratory 2 tract (ear, nose, sinuses, throat) or the lower respiratory 3) tract (lung) or both. b) Necrotizing or granulomatous vasculitis affecting small to medium-sized vessels (e.g., capillaries, venules, arterioles, and arteries), most prominent in the lungs and upper airways. c) Renal disease in the form of focal necrotizing, often crescentic, glomerulonephritis. (Mb C) Sil (SY % - , - Wegner grandomatosis Wegener's granulomatosis Thromboangiitis Obliterans (Buerger Disease) characterized by segmental, thrombosing, acute and chronic inflammation of medium-sized and small arteries, principally the tibial and radial arteries and sometimes secondarily extending to veins and nerves of the extremities. Age: before the age of 35 years male in most cases. Sex: heavy cigarettes smokers. Pathogenesis: 1. Direct endothelial cell toxicity by some tobacco products or hypersensitivity to them), which impaired endothelium-dependent vasodilatation. 2. Anti-endothelial cell antibodies have also been found. 3. Increased prevalence in association with certain MHC haplotypes, especially HLA-A9 and HLA-B5 in these patients. 4. Genetic influences: are suggested by an increased prevalence in certain ethnic groups (Israeli, Indian subcontinent, Japanese). Buerger disease Raynaud phenomena Results from an exaggerated vasoconstriction of digital arteries and arterioles. jis 5 ,. 4) These vascular changes induce paroxysmal pallor or cyanosis of the digits of the hands or feet; infrequently, the nose, earlobes, or lips can also be involved. Characteristically, the involved digits show red, white, and blue color changes from most proximal to most distal, correlating with proximal vasodilation, central vasoconstriction, and more distal cyanosis. Raynaud phenomenon may be a primary disease entity (called Raynaud’s disease) or be secondary to a variety of conditions (called Secondary Raynaud phenomenon ), and caused by other entities including; SLE, Scleroderma, Buerger disease, Atherosclerosis. Raynaud’s disease Varicose veins abnormally dilated, tortuous veins produced by prolonged increase in intraluminal pressure and loss of vessel wall support. The superficial veins of the upper and lower leg are typically involved. Some 10% to 20% of adult males and 25% to 33% of adult females develop lower extremity varicose veins; Obesity increases the risk. Higher incidence in women is a reflection of the elevated venous pressure in lower legs caused by pregnancy. A familial tendency toward premature varicosities results from imperfect venous wall development Varicose veins of lower limb  TUMORS of the vascular system Tumors of blood vessels and lymphatics range from benign hemangiomas (capillary hemangioma, cavernous hemangioma, & lymphangioma, and pyogenic granuloma), to intermediate lesions malignint type X that are locally aggressive but infrequently metastatic (Kaposi’s sarcoma and haemangioendothelioma), to relatively very rare, highly malignant angiosarcomas ▪ Primary tumors of large vessels (aorta, pulmonary artery, and vena cava) are extremely rare and are mostly connective tissue sarcomas. ▪ Vascular neoplasms can be derived from; a) Endothelial cells e.g., hemangioma, lymphangioma, angiosarcoma b) Or can arise from cells that support and/or surround blood vessels (e.g., glomus tumor, hemangiopericytoma). Hemangioma /gross Hemangioma / mic Angiosarcoma/ Gross Angiosarcomas / mic THANK YOU