Blood Vessel Pathology Presentation PDF
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Ambo University
Dr. Addisu B
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Summary
This document is a presentation on blood vessel pathology, covering topics such as arteriosclerosis, atherosclerosis, and aneurysms. It details the pathogenesis, morphology, and clinical consequences of these conditions, including risk factors and diagnostic features. The presentation explains the different types of vascular diseases and the various processes that contribute to their development, and explains both stable and vulnerable plaques.
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BLOOD VESSEL PATHOLOGY Dr. Addisu B 1 ARTERIOSCLEROSIS Arteriosclerosis literally means “hardening of the arteries” It is a generic term reflecting arterial wall thickening and loss of elasticity...
BLOOD VESSEL PATHOLOGY Dr. Addisu B 1 ARTERIOSCLEROSIS Arteriosclerosis literally means “hardening of the arteries” It is a generic term reflecting arterial wall thickening and loss of elasticity 2 Types of arteriosclerosis Atherosclerosis: A specific type of arteriosclerosis. Arteriolosclerosis: Hardening of small arteries and arterioles. Monckeberg’s sclerosis: Calcification of the arterial media without obstruction. 3 Arteriosclerosis vs. Atherosclerosis Feature Arteriosclerosis Atherosclerosis General term for hardening of A specific type involving plaque Scope arteries buildup Aging, hypertension, or other High cholesterol, smoking, Cause chronic conditions diabetes, and inflammation Affects medium to large arteries Artery Type Can affect any artery specifically Key Impact Hardens and thickens arteries Narrows arteries due to plaque Complications Reduced blood flow Heart attack, stroke, gangrene, etc. 4 ATHEROSCLEROSIS 5 ATHEROSCLEROSIS… Atherosclerosis is characterized by intimal lesions called atheromas (or atheromatous or atherosclerotic plaques) Atheromatous plaques are raised lesions composed of soft friable (grumous) lipid cores (mainly cholesterol and cholesterol esters, with necrotic debris) covered by fibrous caps It underlies the pathogenesis of coronary, cerebral, and peripheral vascular disease 6 ATHEROSCLEROSIS 7 Atheromatous plaque 8 Atherosclerosis is virtually ubiquitous among most developed nations, with prevalence increasing at an alarming pace in developing countries 9 Age Sex Genetics Risk Hypertension Hypercholesterolemia factors Diabetes Smoking Physical activity Obesity 10 Risk factors Others: inflammation: Assessing systemic inflammatory status has become important in overall risk stratification, e.g. CRP Lipoprotein a Stressful lifestyle Metabolic syndrome 11 Atherosclerosis Special form of chronic inflammation Which involves the intima And leads to narrowing of arteries 12 Pathogenesis The currently held view of pathogenesis is embodied in the response- to-injury hypothesis. This model views atherosclerosis as a chronic inflammatory response of the arterial wall to endothelial injury Lesion progression involves interaction of modified lipoproteins, monocytederived macrophages, T lymphocytes, and the cellular constituents of the arterial wall 13 Pathogenesis = chronic inflammation = response - to - injury 14 Pathogenesis… Endothelial Injury EC injury is the cornerstone of the response to injury hypothesis Inflammation Inflammation contributes to the initiation, progression, and complications of atherosclerotic lesions 15 Prolonged exposure to potentially toxic agents [exogenous, endogenous] toxins from cigarette hyperlipidemia smoking Damage the endothelium = injury 16 injury damage of endothelium becames permeable for lipoproteins influx of LDL into intima 17 18 19 20 21 22 MORPHOLOGY The development of atherosclerosis tends to follow a series of morphologic changes described below Fatty Streaks. Atherosclerotic plaques 23 1). Fatty Streaks A fatty streak is an early lesion in the arterial wall consisting mainly of lipid- laden macrophages (foam cells) and some extracellular lipids. Are only minimally raised and do not cause any significant flow disturbance Fatty streaks begin as minute yellow, flat macules that coalesce into elongated lesions, 1cm or more in length. 24 25 2. Atherosclerotic plaques Is a more advanced lesion in the atherosclerotic process, involving a buildup of lipids, fibrous tissue, calcium, and other substances. The key features of these lesions are intimal thickening and lipid accumulation Have three principal components: Cells, including SMCs, macrophages, and T cells ECM, including collagen, elastic fibers, and proteoglycans Intracellular and extracellular lipid 26 27 Pathologic changes of atherosclerosis Atherosclerotic plaques are susceptible to several clinically important changes 28 Pathologic changes of atherosclerosis Acute Plaque Change Rupture, ulceration, or erosion of the luminal surface of atheromatous plaques exposes the bloodstream to highly thrombogenic substances and induces thrombus formation. Such thrombi can partially or completely occlude the lumen and lead to downstream ischemia 29 cont.…. 30 Hemorrhage into a plaque. Rupture of the overlying fibrous cap or of the thin-walled vessels in the areas of neovascularization can cause intra-plaque hemorrhage The resulting hematoma may cause rapid plaque expansion or plaque rupture 31 Hemorrhage into a plaque 32 Atheroembolism Ruptured plaque can discharge debris into the blood, producing microemboli composed of plaque contents. Aneurysm formation Atherosclerosis-induced pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, causes structural weakening that can lead to aneurysmal dilation and rupture. 33 34 Clinical consequences of atherosclerosis Myocardial infarction (heart attack), Cerebral infarction (stroke), Aortic aneurysm, and Peripheral vascular disease (gangrene of extremities) 35 Clinical consequences of atherosclerosis 36 Clinical consequences of atherosclerosis Other consquences - Sudden cardiac death, - chronic ischemic heart disease & - ischemic encephalopathy due to acutely or chronically diminished arterial perfusion. 37 38 STABLE VS VULNARABLE PLAQUE Stable plaques have densely collagenized and thickened fibrous caps with minimal inflammation and negligible underlying atheromatous cores Whereas vulnerable plaques have thin fibrous caps, large lipid cores, and increased inflammation. Plaques at high risk for rupture are referred to as vulnerable plaques 39 40 Plaque inflammation increases collagen degradation and destabilizing the mechanical reduces collagen synthesis integrity of the cap 41 ANEURYSMS Aneurysms are congenital or acquired dilations of blood vessels or the heart True aneurysms involve all three layers of the artery (intima, media, and adventitia) or the attenuated wall of the heart; these include atherosclerotic and congenital vascular aneurysms, as well as ventricular aneurysms resulting from transmural myocardial infarctions 42 Cont.... A false aneurysm (pseudo aneurysm) results when a wall defect leads to the formation of an extravascular hematoma that communicates with the intravascular space (“pulsating hematoma”). Examples are ventricular ruptures contained by pericardial adhesions and leaks at the junction of a vascular graft with a natural artery. 43 True vs. false aneurysm 44 Cont.... Aneurysms can be classified by shape Saccular aneurysms are discrete outpouchings ranging from 5 to 20 cm in diameter, often with a contained thrombus. Fusiform aneurysms are circumferential dilations up to 20 cm in diameter; these most commonly involve the aortic arch, the abdominal aorta, or the iliac arteries. 45 Pathogenesis Aneurysms occur when alterations in SMCs or ECM compromise the structural integrity of the arterial media Inadequate or abnormal connective tissue synthesis E.g Marfan syndrome (genetic disorder that affects the body's connective tissue) 46 Cont.... Excessive connective tissue degradation : degrading arterial ECM in the arterial wall Loss of SMCs or change in the SMC synthetic phenotype 47 Cont.... The two most important predisposing conditions for aortic aneurysms are :- atherosclerosis hypertension 48 Cont.... Other causes that weaken vessel walls and lead to aneurysms include Trauma, Congenital defects (e.g., berry aneurysms), Vasculitis Infections (mycotic aneurysms), or syphilis. 49 Abdominal Aortic Aneurysm (AAA) Aneurysms occurring as a consequence of atherosclerosis form most commonly in the abdominal aorta and common iliac arteries, May also involve the aortic arch and descending thoracic aorta Abdominal aortic aneurysms (AAAs) occur more frequently in men and in smokers and rarely develop before 50 years of age Abdominal aortic aneurysms typically occur between the renal arteries and the aortic bifurcation; 50 AAA… 51 AAA… 52 AAA… Atherosclerotic aneurysms occur most frequently in the abdominal aorta (abdominal aortic aneurysm) But the common iliac arteries, the arch, and descending parts of the thoracic aorta can also be involved 53 AAA… The clinical consequences of AAA include: - Rupture into the peritoneal cavity or retroperitoneal tissues with massive, potentially fatal hemorrhage Obstruction of a branch vessel resulting in downstream tissue ischemic injury-for example, iliac (leg), renal (kidney), mesenteric (gastrointestinal [GI] tract), or vertebral (spinal cord) arteries Embolism from atheroma or mural thrombus Impingement on an adjacent structure (e.g., compression of a ureter or erosion of vertebrae) Presentation as an abdominal mass (often palpably pulsating) that simulates a tumor 54 Aortic Dissection Aortic dissection occurs when blood splays apart the laminar planes of the media to form a blood-filled channel within the aortic wall This development can be catastrophic if the dissecting blood ruptures through the adventitia and escapes into adjacent spaces 55 Aortic Dissection … 56 Aortic Dissection… 57 Aortic Dissection … In arterial dissections, pressurized blood gains entry to the arterial wall through a surface defect and then pushes apart the underlying layers 58 Aortic Dissection … Hypertension is the major risk factor for aortic dissection Abrupt , transient increase in blood pressure, as may occur with cocaine abuse, is also known to cause aortic dissection. 59 Aortic Dissection … - Aortic dissection occurs principally in two epidemiologic groups (1) Men aged 40 to 60 years, with antecedent hypertension (more than 90% of cases of dissection) (2) Younger patients with systemic or localized abnormalities of connective tissue affecting the aorta (e.g., Marfan syndrome) 60 Aortic Dissection … - The classic clinical symptoms of aortic dissection are the sudden onset of excruciating pain, usually beginning in the anterior chest, radiating to the back between the scapulae, and moving downward as the dissection progresses; the pain can be confused with that of myocardial infarction 61 Aortic Dissection … - The most common cause of death is rupture of the dissection outward into any of the three body cavities (i.e., pericardial, pleural, or peritoneal). 62 Aortic Dissection … - Thus, common clinical manifestations include cardiac tamponade, aortic insufficiency, and myocardial infarction or extension of the dissection into the great arteries of the neck or into the coronary, renal, mesenteric, or iliac arteries, causing critical vascular obstruction 63 VASCULITIS Vasculitis is a general term for vessel wall inflammation. The two most common pathogenic mechanisms of vasculitis are Immune-mediated inflammation and Direct vascular invasion by infectious pathogens. 64 Varicose Veins Varicose veins are abnormally dilated tortuous veins Produced by chronically increased intraluminal pressures and weakened vessel wall support 65 Varicose Veins… 66 Varicose Veins… Clinical Features Varicose dilation renders the venous valves incompetent and leads to lower-extremity stasis, congestion, edema, pain, and thrombosis. The most disabling sequelae include persistent edema in the extremity and secondary ischemic skin changes, including stasis dermatitis and ulcerations. 67 VASCULAR TUMORS Tumors of blood vessels and lymphatics include benign hemangiomas (extremely common), locally aggressive neoplasms that metastasize infrequently, and rare, highly malignant angiosarcomas Vascular neoplasms arise either from endothelium (e.g., hemangioma, lymphangioma, angiosarcoma) or cells that support or surround blood vessels (e.g., glomus tumor) 68 Benign Tumors and Tumor-Like Conditions 1. Vascular Ectasias Ectasia is a generic term for any local dilation of a structure, Telangiectasia is used to describe a permanent dilation of preexisting small vessels (capillaries, venules, and arterioles, usually in the skin or mucous membranes) that forms a discrete red lesion 69 2. Hemangiomas Hemangiomas are very common tumors composed of blood-filled vessels These lesions constitute 7% of all benign tumors of infancy and childhood; Most are present from birth and initially increase in size, but many eventually regress spontaneously 70 Hemangiomas … 71 Malignant Tumors 1. Kaposi Sarcoma Kaposi sarcoma (KS) is a vascular neoplasm caused by Kaposi sarcoma herpesvirus (KSHV, also known as human herpesvirus-8, or HHV-8) Virtually all KS lesions are infected by KSHV (HHV-8). It is transmitted both through sexual contact and potentially via oral secretions and cutaneous exposures 72 2. Angiosarcomas Angiosarcoma is a rare and aggressive form of cancer that originates in the endothelial cells Are malignant endothelial neoplasms ranging from highly differentiated tumors resembling hemangiomas to wildly anaplastic lesions. 73 Thanks 74