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Vascular abnormalities cause clinical disease by: 1. Progressively narrowing the lumina of vessel and producing ischemia of the tissue perfused by that vessel. 2. Provoking intravascular thrombosis, causing acute obstruction or embolism or both!
Vascular abnormalities cause clinical disease by: 1. Progressively narrowing the lumina of vessel and producing ischemia of the tissue perfused by that vessel. 2. Provoking intravascular thrombosis, causing acute obstruction or embolism or both!
Vascular abnormalities cause clinical disease by: 1. Progressively narrowing the lumina of vessel and producing ischemia of the tissue perfused by that vessel. 2. Provoking intravascular thrombosis, causing acute obstruction or embolism or both!
In general vascular abnormalities cause clinical disease
by: 1. Progressively narrowing the lumina of vessel & producing ischemia of the tissue perfused by that vessel. 2. Provoking intravascular thrombosis, causing acute obstruction or embolism or both!. ". #eakening the walls of vessels there by leading to dilatation or rupture. I.Congenital anomaly: 1.$erry aneurisma. 2.%rteriovenous fistula. II.Atherosclerosis & other forms of arteriosclerosis. A.Atherosclerosis: &haracteri'ed by intimal thickening & lipid deposition. (he basic lesion, the atheroma, or fibrofatty pla)ue consists of a raised focal pla)ue within the intima, having a core of lipid mainly cholesterol & cholesterol ester! and a covering fibrous cap. *eath from cardiovascular disease in +.,. rose from 1- . of all deaths in 1/"0 to 1-. in 1/23. 4isk factors for atherosclerosis : Major: 5iperlipidemia hypercholesterolemia, hypertriglycerimia!. Minor: 6besity, physical inactivity, male gender, increasing age, family history, stress, oral contraceptives, high carbohidrat intake. %therosclerotic pla)ue have three principal components: 1. &ell, including smooth muscle cell, macrophages and other leucocytes. 2. &onnective tissue e7tracellular matri7, including collagen, elastic fibers & proteoglycans. ". Intracellular & e7tracellular lipid deposits. (he complicated lesion of atherosclerosis: 1. &alcification. 2. 8ocal rupture or gross ulceration. ". (hrombosis. -. 5emorrhage. B.MOC!EBE"#$S Arteriosclerosis. 9edial calcific sclerosis!. &haracteri'ed by ring like calcifications within the media of medium si'ed to small muscular arteri. (he calcification is not associated with any inflammatory reaction, and the intima and adventitia are largely un affected. (he calcific deposit do not narrow the lumen. C.A"%E"IOLOSCLE"OSIS. 9arked by proliferation or hyaline thickening of the walls of small arteries & arteriol. III.I&LAMMA%O"' DISEASE( %)E VASC*LI%IDES. +.#iants cell ,tem-oral. arteritis. (he most common of the vasculitides, is a focal granulomatous inflammation of arteries of medium si'e and small si'e that affects principally the cranial vessel, especially the temporal arteries in older individuals rare before age 1:!, but also the vertebrae and ophthalmic arteries!. (he histologic change: 1. ;ranulomatous lesion with giant cell. 2. <on specific white cell infiltration lymphocyte & eosinophils!. ". Intimal fibrosis, /.%A!A'AS*$S Arterities. &linical syndrome characteri'ed principally by ocular disturbances and marked weakening of the pulses in the upper e7tremities pulses disease! related to fibrous thickening of the aortic arch with narrowing of virtual obliteration of the great vessels arising in the arch. (he cause and pathogenesis are unknown. 0.1OL'A"%E"I%IS ODOSA #"O*1 ,1A.. P%< is manifested by necroti'ing inflammation of small or medium si'ed muscular arteries. (ypically involving renal and visceral vessel & sparing the pulmonary circulation. <either glomerulonephritis nor vasculitis of arteriols, capillaries or venules is present. (he most common manifestation are fever of unknown cause & weight loss, hypertention, usually developing rapidly, abdominal pain & melena. *ifuse muscular aches & pains & peripheral neuritis. 2.!A3ASA!I S'D"OME. 9ucocutaneous lymph node syndrome!. Is an arteritis involving large, medium si'e & small arteries of the coronary arteries! that is associated with the mucocutaneus lymph node syndrome usually in young children & infant 3:. yonger then four years old!. (he acute illness is manifested by fever, con=unctival & oral erythema & erosion, edema of the hands & feet, erytheme of the palm & soles, a skin rash often with des)uamation & enlargement of cervical lymph node it is usually self limited. 4.Microsco-ic -olyangitis. 9icroscopic polyarteritis , hypersentivity!. (his type of necroti'ing vasculitis generally affects smaller vessel than P%< arteriols, capillaries, & venules!. In a single patients, all lesions tend to be of the same age. Its typically involves the skin, mucous, membrans, lungs, brain, heart, gastrointestinal tract, kidney and muscle. 5.3egener$s gran6lomatosis. (his form of necroti'ing vasculitis is characteri'ed by: 1. %cut necroti'ingngranulomas of the upper & lower respiratory tract nose, sinuses & lung!. 2. 8ocal necroti'ing vasculitis . %ffecting small to medium si'ed vessel. ". 4enal disease in the form of focal or diffuse necroti'ing glomerulitis. 7.%hrom8oangitis o8literans: Is a distinctive disease characteri'ed by segmental thrombosing, acut & chronic inflammation of intermediate & small arteries & sometimes vein of the e7tremities. (he condition had accured almost e7clusively in men who were heavy cigarret smoker. IV.Ane6risma & Dissection. A.An ane6risma is a locali'ed abnormal dilatation of any vessel. 6ccur in any artery or vein of the body, most commonly the aorta. %therosclerosis, the most fre)uent etiology of aneurysm causes arterial wall thinning through medial destruction secondary to pla)ue that originates in the intima. >):?%bdominal aortic aneurysm. ?,yphilitic luetic! aneurysm. B.AO"%IC DISSEC%IO: Is an catastrophic illness characteri'ed by dissection of blood along the luminar planes of the aortic media, with formation of blood filled channel within the aortic wall & that often rupture, causing massive hemorrhage. In contrast to atherosclerotic and syphilitic aneurysm, aortic dissection is not usually associated with marked dilatation of the aorta. ,ome dissection are related to the inherited connective tissue disorder marfan syndrome, an autosomal dominant disease of connective tissue fibrillin, characteri'ed by skeletal, cardiovascular & ocular manifestation. (he serious cardiovascular complication is dilatation of the aortic rootannuloaortic ectasia! and mitral valve prolapsed. V.VEI & L'M1)A%ICS. A.Varicose 9eins. %re abnormali dilated, turtous veins produced by prolonged, increased intraluminal pressure. (he superficial veins of the legs are the preponderant site of involvement. Portal hypertention cirrhosis of the liver! leads to varices in the esophageal & hemorhoidal veins!. B.Lym-hangitis. C.Lym-e:ema: (he most common causes: 1. ,pread of malignant tumor. 2. 4adical surgical procedure. ". Post irradiation fibrosis. -. 8ilariasis. 1. Post inflammatory thrombosis & scarring of lymph channel!. VI.%*MO". +.)emangioma: &apillary hemangioma: %re composed of blood vessels that resemble capillaries, narrow, thin walled & lined by relatively thin endothelium. +sually occurring in the skin, subcutaneous tissue & mucous membrane of the oral cavities & lips, they may occur in internal vicera, such as liver, spleen & kidney. &avernous hemangioma: *istinguished by the formation of large cavernous vascular channels. 6ften occurring in childhood, they have predilection for the skin of the head & neck & mucosal surface of the body, also found in many viscera, particulary the liver, spleen, pancreas, & occasionally the brain. /.#"A*LOMA 1'O#EIC*M ;ranulation tissue type hemangioma!. 6f uncertain neoplastic nature & currently considered a plypoid form of capillary hemangioma, these masses appear as e7ophytic red nodule on the skin & gingival or oral mucosa & are often ulserated. 0.#LOM*S %*MO".,#lomangioma.. % benign but e)uisitely painful tumor that arise from the modified smooth muscle cell of the glomus body. % neuromyoarterial receptor that is sensitive to variation in temperature & regulates arterial flow. 2.VASC*LA" EC%ASIA ,%elangiectasia.. *esignates a group of abnormally prominent capillaries, venules & arteriol that created a small focal red lesion, usually in the skin or mucous membrane. 4.)EMA#IOEDO%)ELIOMA intermediate malignancy!. % true neoplasma of vascular origin composed predominantly of masses of endothelial cell growing in and about vascular lumina. 5.A#IOSA"COMA ,)EMA#IOSA"COMA.. Is a malignant neoplasma of vascular origin, characteri'ed by masses of endothelial cell displaying the celluler atypia & anaplasia characteristic of malignancy. 7.)EMA#IO1E"IC'%OMA ,malignant. (he origin of these tumors to pericyte most of these neoplasms are small. (hey consist of numerous capillary channel surrounded by & enclosed within nest & masses of spindle shaped cells. (hat these cell are outside the basement membrane of the endothelium. ;.!A1OSI$S SA"COMA. &onsist spindle shaped stromal cell containing irregular, angulated, slit like spaces filled with red cells & lined by recogni'able endothelium, interwined with normal vascular channels. B.L'M1)A#IOMA: +.SIM1LE ,ca-illary lym-hangioma.. (hese masses composed of small lymphatic channels tend to occur subcutaneously in the head & neck region & in the a7illa. /.CAVE"O*S L'M1)A#IOMA ,cystic hygroma.. &omposed of cavernous lymphatic spaces and therefore are analogous to cavernous hemangioma. 0.L'M1)A#IOSA"COMA. (he tumor is composed of channels lined by anaplastic endothelial cells. %)E )EA"% &auses of cardiovascular dysfunction: 1. @oss of blood. 2. Iregular heart beat. ". 6bstructed flow. -. 4egurgitant flow. 1. Pump failure. ?&ontractile dysfunction systole failure!. ?Inade)uate filling diastolic failure!. I.CO#ES%IVE )EA"% &AIL*"E ,C)&.. #hen sufficiently severe or advanced, may ultimately impair cardiac function and render the heart unable to maintain an output sufficient for the metabolic re)uirements of the tissues & organs of the body, producing congestive heart disease. %s stated &58, occurs either because of a decreased myocardial capacity to contract or because of an inability to fill the cardiac chambers with blood. CA"DIAC )'1E"%"O1)'. (he compensatory response of the myocardium to increased work. 9yocardial hyperfunction induces increased myocite si'e cellular hypertrophy! that increase in the overall mass and si'e of the hearts. &aused the cardiac hypertrophy: 1. 5ypertension. Pressure overload. 2. Aalvular disease. Pressure andBor volume overload. ". 9yocardial infarction. 4egional dysfunction with volume overload. II.ISC)EMIC )EA"% DISEASE ,I)D.. Is the generic designation for a group of closely related syndrome resulting from ischemia. *epending on the rate of development and ultimate severity of the arterial narrowing and the myocardial response, four ischemiac syndrome may result. +.Angina -ectoris. Is a symptom comple7 of I5* characteri'ed by paro7ysmal attacks of substernal or precordial chest discomfort variously described as constricting, s)uee'ing, choking or knife like! caused by transient 11 secons to 11 minutes!. (here are three pattern of angina pectoris ?,table or typical angina. ?Prin'mental. ?+nstable or crescendo angina. /.Myocar:ial Infarction. 9yocardial ischemia that falls short of inducing the cellular necrosis that difines infarction. (here are two types of myocardial infarction each having differing morphology & clinical significance. %ransm6ral infarct: In which the ischemic necrosis involve the full thickness of the ventricular wall. (his pattern of infarction is usually associated with coronary atherosclerosis, pla)ue rupture & superimposed thrombosi S68en:ocar:ial infarct: &onstitutes an area of ischemic necrosis limited to the inner one?third or at most one?half of the ventricular wall. (he clinical diagnosis of acut myocardial infarction is mainly based on : ?,ymptoms. ?>lectrocardiographic >&;!. ?>levation of specific serum en'yme creatine phosphokinase &PC! & @actate dehidrogenase @*5!. 0.C)"OIC ISC)EMIC )EA"% DISEASE. Is used here for the hearts in patients often but not e7clusively elderly, insidiously develop &58, some times fatal, as a conse)uences of ischemic myocardial damage. Its must instances there has been a history of angina & usually prior episodes of myocardial infarction, often as remote as 1 to 1: year before the onset of the &58. 2.S*DDE CA"DIAC DEA%) 9ost commonly sudden cardia death ,&*! is defined as une7pected death from cardiac causes early usually within 1 hour!. %fter or without the onset of symtoms. III.)'1E"%ESIVE )EA"% DISEASE. Is the response of the heart to the increased demands induced by systemic or pulmonary hypertension. A.Systemic ,left(si:e:. hy-ertensi9e heart :isease. (he minimal criteria for diagnosis: 1. @eft ventricular hypertrophy usually concentric! in the absence of other cardiovascular pathology that might have induced it. 2. % history of hypertension. B.16lmonary ,right(si:e:. hy-ertensi9e heart :isease. ,CO" 1*LMOALE.. &ontitutes the rights ventricular enlargement, secondary to pulmonary hypertention caused by disorder that affect the lung or pulmonary vasculature. *isorders predisposing to cor pulmonale: 1. *iseases of the lung. 2. *iseases of pulmonary vessels. ". *isorders affecting chest movement -. *isorder inducing pulmonary arteriolar constriction IV.CO#EI%AL )EA"% DISEASE. %.@eft to?right shunts? late cyanosis. +.Atrial se-tal :efect ,ASD.. %n abnormal opening in the atrial septum that allows free communication of blood between the right & left atria. (he three ma=or types of %,*: ?,ecundum type %,*. ?Primum anomaly ?sinus venosus. /.Ventric6lar se-tal :efect ,VSD.. %n abnormal opening in the ventricular septum that allows free communication between right & left ventricles. 0.1atent :6ct6s arterios6s ,1DA.. 4esuts when ductus arteriosus, a normal aortopulmonary vascular channel during intra uterine life remain open after birth. 2.Atrio9entric6lar se-tal :efect. 4esult from abnormal development of the embryologic atrioventricular canal, which the superior & inferior endocardial cushion fail to fuse ade)uately, resulting in complete closure of the %A septum & inade)uate formation of the septal tricuspid & anterior mitral leaflefts. B."ight to left sh6nts( early cyanosis. +.%etralogy of fallot: (he four features , the most common form of cyanotic congenital heart disease are: a. A,*. b. 6bstruction to the right ventricular outflow tract subpulmonary stenosis!. c. %n aorta that overrides the A,*. d. 4ight ventricular hypertrophy. /.%rans-osision of great anomaly. (ransposision implies ventriculoarterial discordance such that the aorta arise from the right ventricle and the pulmonary artery emanates from the left ventricle. 0.%r6nc6s arterios6s. (he persistent truncus arteriosus anomaly arises from a developmental failure of separation of the embryologic truncus arteriosus into aorta & pulmonary artery. 2.%ric6s-i: atresia: &omplete occlusion of the tricuspid valve orifice is know as tricuspid atresia. It results embryologically from une)ual division of the %A canal, thus the mitral valve is large than normal. C.O8str6cti9e congenital anomaly. 1.&oarctatio aorta narrowing, constriction!. 6f the aorta ranks, high in fre)uency among the common structural anomalies. 2.Pulmonary stenosis or atresia with intact ventricular septum. ".%ortic stenosis & atresia. V.VALV*LA" )EA"% DISEASE 1.*egenerative calcific aortic valve stenosis. #ith either tricuspid or bicuspid valve is heaped up calcifified masses within the aortic cusps that ultimately protrude through the outflow surface into the sinuses of valsava. 2.&ongenitally bicuspid aortic valve. ".9itral annular calcification. In elderly individuals, especially women, degenerative calcific deposit can develop in the ring annulus! of the mitral valve!. -.9itral valve prolapse. 9y7omatous degeneration of the mitral valve!. In this valvular abnormality, one or both mitral leaflets are enlarged, redundant or DfloppyE & prolapse or balloon back into the left atrium during systole. 1.4heumatic fever & 4heumatic heart disease. Is an acute, often recurrent, inflammatory disease principally of children 1?11 year! that generally follows a pharyngeal but not skin! infection with group % beta hemolytic streptococcus. 48 is the result of an immune response to streptococcal antigen inciting either a cross reaction to tissue antigens or streptococcal induced autoimmune reaction to normal tissue antigens. 48 is characteri'ed by fever, anthralgia & a constellation of findings that includes. %.9a=or manifestations: 1. 9igratory polyarthritis of the large =oints. 2. &arditis, . ". ,ubcutaneus nodules -. >rythema marginatum of the skin. 1. ,yndenhamFs chorea % neurologic disorder with involuntary purpose, rapid movementFs. $.9inor manifestation: 8ever, athralgia , or elevated acute phase reactant. (he diagnosis is established by the Gones criteria. >vidence of a preceding group % streptococcal infection with the presence of two ma=or manifestation or of one ma=or and one minor manifestation. 5.Infecti9e en:ocar:itis. Is characteri'ed by coloni'ation or invasion of the heart valves or the mural endocardium by a microbiologic agent. &omplication: Aalvular insufficiency, myocardial ring abcess, emboli, infarction renal, glomerulonephritis. 7.on 8acterial throm8otic en:ocar:itis. Is a form of vegetative endocarditis most often encountered in debilitated patients, such as those with cancer or sepsis. ;.En:ocar:itis of systemic l6-6s erythematos6s. In ,@> mitral & tricuspidal valvulitis is occasionally encountered & leads to the development of small sterile vegetation. <.Carcinoi: heart :isease. In patient with carcinoid tumor, cardiac involvement, principally of the endocardium & valve of the right heart. VI.M'OCA"DIAL DISEASE. +.Dilate: car:iomyo-athy. Idiophatic *& is characteri'ed by the gradual chamber hypertrophy & dilatation of the heart of unknow cause. /.)y-ertro-hic car:iomyo-athy. Idiopathic hyperthrophic subaortic stenosis, obstructive cardiomyopathy!. Its characteri'ed by a heavy muscular hypercontracting heart. 0."estricti9e car:iomyo-athy. (he ventricles are appro7imately normal si'e or slightly enlarged. (he cavities are not dilated & the myocardium is firm. $iaterial dilatation is commonly observed. 9icroscopically: (here is patchy or difuse interstitial fibrosis which can vary from minimal to e7tensive. $ut the cause is unknown. 2.Myocar:itis: Is best defined as an inflammatory involvement of the heart muscle, characteri'ed by a leucocyte infiltrate & resultant non ischemic necrosis or degeneration of myocytes. VII.1E"ICA"DIAC DISEASE. %.%ccumulation of fluids in the pericardium normally therenis ":?1: ml of thin, clear,strow?collored, translucent fluid in the pericardial space. 5emopericardium, is the accumulation of pure blood in tpericardial sac, distint from hemorrhagic pericarditis, a condition in which there is an inflammatory e7udates containing blood mi7ed with pus. B.1ericar:itis. Inflammation of the pericardium are usually secondary to systemic disorder or to metastases from neoplasms arising in remote site. C."he6matoi: heart :isease. (he most common finding is a fibrinous pericarditis that may progress to fibrous thickening of visceral & parietal pericardium with dense adhesions. 4heumatoid inflammatory granulomatous nodule resembling those that occur subcutaneously may be identifiable deep to the pericardial surface. VII.EO1LAS%IC )EA"% DISEASE. +.My=oma: %re the most common primary tumor of the heart in adults. %bout /:. are located in the atria. /.Li-oma: 9ay occur in the subendocardium, subepicardium or within the myocardium. ".Papillary fibroelastoma. 2."ha8:omyoma. 4.Sarcoma.