中国医科大学病理学英文课件4

null二. The Process and morphology二. The Process and morphology(一) The process of thrombosis: Platelets adhere to extracellular matrix at sites of endothelial injury and become activated. Secrete granule products ( ADP, TXA2 ) Platelets aggregating The intrinsic and extrinsic pathway activate Fibrinogen FibrinnullnullThe process of vein thrombosis(二) Types and morphology(二) Types and morphology1. Pale thrombus : (1) The common sites: arterial lumen: coronary A cardiac valves and chambers Initial site of vein thrombus (2) Gross pale nodule or vegetation rough surface,friable firmly adherent to arterial wall(3) LM: Platelet(main)＋Fibrin (a little) Erythrocyte , degenereting leukocyte (3) LM: Platelet(main)＋Fibrin (a little) Erythrocyte , degenereting leukocyte Pale thrombus in cardiac valvePale thrombus in cardiac valve2. Mixed thrombi2. Mixed thrombi(1) Sites body part of vein thrombus Aneurysm mural thrombi (2) Gross : gray-white alternating with brown dry, adherent to vascular wallnull(3) LM: platelet , fibrin , erythrocytes3. Red thrombus (Venous thrombi)3. Red thrombus (Venous thrombi)(1) Sites vein of the lower extremities Prostate, ovary, uterus tail of the vein thrombus (2) Gross dark red wet →dry friable (3) LM Fibrin + RBC a little WBCVenous thrombusVenous thrombus4. Fibrous thrombus (Hyaline thrombus \ micro thrombus) 4. Fibrous thrombus (Hyaline thrombus \ micro thrombus) occur in capillary (microcirculation) can be seen under LM only compose of acidophilic fibrin most common cause: DIC Fibrin thrombiFibrin thrombi三. Sequelae of thrombi三. Sequelae of thrombi1. Dissolution and absorption 1) Small →dissolved completely →removed by fibrinolytic system 2) Large → dissolved partly, detachment →embolism 2. Organization and recanalization 1) Organization: thrombus is replaced by granulation tissuenull2) Recanalization: In process of thrombus organization, thrombus contraction or partly dissolve and forms fissure, newly formed EC cover the surface of fissure and incorporate to reestablish vascular flow. 3. Calcification: phlebolith ( arteriolith)Organization and recanalizationOrganization and recanalizationnullOrganization and recanalization四. Affections on the body四. Affections on the body(一) Obstructing BV 1. A →obstructed partly →ischemia hypoxia →parenchymal cell atrophy 2. A → obstructed completely, without effective circulation →infarction cerebral A →brain infarction coronary A →myocardium infarctionnull3. Venous thrombosis (phlebothrombosis) without effective branch circulation →congestion, edema, hemorrhage (二) Embolism 1. Thrombi →soften, split →detachment →embolism 2. Deep venous thrombi, heart chamber, valve thrombi(三) Valvular deformation(三) Valvular deformationRheumatic or infectious endocarditis →thrombi organized repeatedly →valve thicken (四) Extensive hemorrhage 1. DIC →microthrombosis 2. Causes:Trauma, burn →release procoagulation F →clotting process →coagulation F depletionSection 4 . EmbolismSection 4 . Embolism Embolism :In circulation, undissolvable abnormal substances are carried by blood to a site distant from its point of origin and block the lumen.nullEmbolus:The abnormal substance which block the lumen called embolus, may be solid, liquid, gas. The most common : dislodged thrombus Rare form droplets of fat bubbles of air tumor fragment amniotic fluid1. Emboli of V system and right heart:1. Emboli of V system and right heart:(1) Most: pulmonary artery and its branch (2) Small emboli with elasticity (fat) alveolar capillary left heart arterial circulation一.The traveling pathways of embolinull2. Aortic system and left heart2. Aortic system and left heart all the organ brain, spleen, kidney and extremities 3. Portal V system: portal V S (mesenteric V) portal V braches in liver 4. Crossed embolism (paradoxical) 4. Crossed embolism (paradoxical) Rarely: Right heart or cava system pass through an interatrial or interventricular defect gain access to the systemic circulation 5. Retrograde embolism v. cava inferior →sudden increased pressure in chest or abdomen (cough) →emboli retrogress to liver, kidney 二、Types and affection二、Types and affection(一) Thromboembolism 99% of all emboli represent some part of thrombus →the most common cause 1. Pulmonary thromboembolism (1)The origin: In more than 95% of emboli deep leg vein thrombi above the level of the knee (popliteal, femoral, and iliac veins)(2) Sequences:(2) Sequences:1) Middle and small emboli: i) Embolize small branches of pulmonary artery dual blood flow into the area from branchial circulation doesn’t cause infarction ii) In the setting of LH failure (pulmonary congestion) hemorrhagic infarction.null2) Large embolus : pulmonary truncus or large branch sudden death 3) Multiple small emboli : small end-arteriolar of pulmonary branches right heart failure →sudden deathPulmonary thromboembolismPulmonary thromboembolismPulmonary thromboembolismPulmonary thromboembolism 2. Systemic thromboembolism: 2. Systemic thromboembolism:(1) Sources of emboli: 80% from LH SBE mural thrombus Others AS ulcerated plaque; aneurysm →thrombus Rare: cava V. →crossed embolism(2) Major sites(2) Major sites Lower extremities(75%), the brain(10%) Intestine, spleen, kidney, upper extremities involved to a lesser extent (3) Results: infarction collateral vascular supply tissue’s vulnerability to ischemia sites of embolism dependent onnull[病例]: 患者 男 20岁建筑工人某日施工 中不慎右脚掌被锈钉扎伤。逐 渐出现伤脚红肿，并蔓延到右 下肢。以后又反复发作多次， 一个月后, 在厕所内排便中突然 大叫一声口吐白沫，抽搐死亡。 null 讨论： 1. 此患死亡原因是什么? 2. 疾病是如何发生、发展的？ 3. 经验教训是什么？(二) Fat embolism(二) Fat embolism1. Fat embolism: There are fat globules in the circulation. 2. Origin of emboli : fracture of long bone adipose tissue injury , burn enters the circulation by rupture of marrow, vascular sinusoids or V3. Sites3. SitesEmboli >20μm→pul embolism Emboli <20μm →cap →pul.V →LH →multiple organs The most common site: ① Brain →edema, hemorrhage →delirium, coma ② Lung →sudden onset of tachypnea, dyspnea, tachycardia4. Sequences: 4. Sequences: Depend on the site number of fat globules A small amount of fat →phagocyted Large amount of fat →pul circulation →acute R H failure →deathnull [病例]: 患者男32岁, 意外被轿车撞伤,左股骨剧痛变形, 由急救车送中国医大急诊室, X-ray摄影检查见左股骨干中段粉碎性骨折,入院后2小时,突然出现呼吸困难,口唇紫绀,经多方抢救无效死亡。 讨论: 此患猝死的原因是什么？ 机理是什么？nullPulmonary fat embolism(三) Gas embolism(三) Gas embolism Definition: Gas enter the circulation rapidly or bubbles dissolved in the blood out of solution . 1. Air embolism (1) Causes: obstetric procedure chest wall injury (operation or trauma) gas enter circulation (2) Sequences: (2) Sequences:Depend on the entering speed and volume 1) In excess of 100cc →V →RH →a large amount bubbles with heart pulsating →circulation dysfunction 2) Bubbles →pul. A embolism →small branch →cap →LH →organs 2. Decompression sickness (caisson disease or diver’s disease): 2. Decompression sickness (caisson disease or diver’s disease): (1) Causes: exposed to changes in atmospheric pressure deep sea diver or underwater worker →ascend too rapidly →nitrogen out of solution (2) Site skeletal M, Intestine, extremities →pain bone →ischemic necrosis; coronary A →circulation disorder c(四) Amniotic fluid embolism(四) Amniotic fluid embolism1. A rare complication during process of parturition, mortality rate in excess of 85% 2. Sites (1) Pul. embolism: LM →pul small A and cap →squamous c, fetal skin, lanugo hair (2) Systemic circulation: small amount of amniotic fluid →pul. cap →LH3. Sequences:3. Sequences:① Pul. embolism →sudden death clinical: sudden onset of dyspnea, cyanosis, shock →death ② Mechanism of sudden death: i) Metabolic products in amniotic fluid →allergic shock ii) Amniotic fluid emboli obstruct pul. A and BV activated substance →BV spasm iii) Amniotic fluid →thrombin function →DIC(五) Others (五) Others 1. Neoplastic c, bone marrow c → cell embolism 2. Cholesterol crystal in AS foci → detachment 3. Parasite → portal V 4. Bacteria, fungi → blood nullEmbolism of Neoplastic cellSection 5. InfarctionSection 5. InfarctionDefinition: Ischemic necrosis caused by occlusion of the arterial supply or the venous stasis. 一. Causes and conditions of infarction (一) Causes 1. Thrombosis: the most common coronary A → myocardial infarct cerebral A → cerebral infarct mesenteric V → intestine infarct2. Arterial embolism2. Arterial embolism Thromboembolism (common) gas, amniotic fluid, fat embolism infarct of spleen, kidney, lung, brain 3. Arterial spasm (vasospasm): coronary A with AS →spasm →infarct 4. Extrinsic compression of a vessel: tumor, intestine twist, twist of ovary cyst(二) Conditions(二) Conditions1. The nature of the vascular supply: (1) Organs with dual blood supply : Lung: pul. A and bronchial artery Liver: hepatic A and portal V circulation Hand , forearm: radial and ulnar arteries (2) Splenic, renal circulations are end arterial → generally cause infarction2. Vulnerability of a tissue to hypoxia:2. Vulnerability of a tissue to hypoxia:① NC: undergo irreversible damage when deprived of their blood supply for only 3-4 min. ② Myocardial: sensitive and die after only 20~30min of ischemia 二. Lesions and types of infarct二. Lesions and types of infarct(一) Morphologic features 1. Shape: depend on the distribution of BV. (1) Spleen, kidney, lung: wedge-shaped, cut surface →triangle apex →occluded vessel base →capsule (organ surface) (2) Myocardial: irregular map-like shape (3) Intestine: segmental shapenull2. Texture: depend on the types of necrosis Heart spleen kidney: coagulative necrosis Brain: liquefactive necrosis 3. Color: 1) Large amount of hemorrhage: hemorrhagic infarct (red infarct) 2) Small amount of hemorrhage : anemic infarct (white infarct)(二) Types(二) Types1. Anemic infarct (white infarct) (1) Sites: in compact solid organs with less collateral circulation such as kidney, spleen, and heart. (2) Gross gray-white, wedge-shape occluded vessel at the apex periphery of organ forming the base margin: narrow rim of hyperemia and hemorrhagenullAnemic infarct of kidneynullnullAnemic infarct of spleennull(3) LM: coagulative necrosis Nuclear changes and Presence of tissue structure outline Margins congestion , hemorrhage inflammatory response Anemic infarct of kidneyAnemic infarct of kidney 2. Hemorrhagic (red) infarct: 2. Hemorrhagic (red) infarct:(1) Conditions: 1) Severe congestion: lung congestion →red infarct ovary cyst →twist →red infarct 2) Loose tissue: lung, small intestine null(2) Common types: 1) Pulmonary hemorrhagic infarct: ① Site: lower lobe of lung →common ② Gross wedge →shape; apex →hilum of lung; base →visceral pleura ③ LM necrosis and outline exist; alveolar space: full of RBC margin: congestion, hemorrhage nullPulmonary hemorrhagic infarctnullPulmonary hemorrhagic infarct2) Intestinal hemorrhagic infarct2) Intestinal hemorrhagic infarct① Causes: mesenteric A.V → thrombosis; intestinal twist; tumor pressed ② Gross: dark-red , segmental 3. Septic infarct: ① Embolus: fragmentation of bacterial vegetation from heart valve ② Morphology infarct change abscess formation 三. Affection and consequences三. Affection and consequences(一) Affection : depend on organs, size, site , with or without infection (1) Myocardial infarct →heart failure →death Brain infarct →death (2) Spleen, kidney, lung →local symptom (二) Consequences 1. Organization 2. Encapsulation and calcification病例四病例四女，30岁，农民 主诉：间歇性心悸，气短1年，伴下肢浮肿、 少尿一个月 现病史：于1年前开始出现劳动后心悸、气 短，休息后好转，1个月前因着凉而发 热、咽痛，心悸、气短加重，同时出现 双下肢浮肿，少尿，右上腹部胀痛，食 欲减退，不能平卧，治疗无效收入院 既往史：10年前常有咽痛、关节疼痛病史null 查体：半坐卧位，慢性病容，四肢末稍及口唇发绀。颈静脉怒张，两肺背部有中、小水泡音。心尖部有舒张期震颤。心界向左右两侧扩大。心率110次/分，血压110/70mmHg，心律不整。心尖部有雷鸣样舒张期杂音，Ⅲ级吹风样收缩期杂音。肝在肋下3厘米，剑突下5厘米，质韧，轻度压痛，肝颈静脉回流征阳性。双下肢凹陷性水肿。null检查：尿常规：尿蛋白(+)、红细胞1-2个/ 高倍视野，透明管型1-2/高倍视野。 X线检查：心脏向左右扩大，双肺纹理 增强 临床诊断: (1)风湿性心脏病 (2)二尖瓣窄漏 (3)全心功能衰竭null思考题： 1. 临床诊断全心功能衰竭依据是什么？ 2. 根据临床特点，你认为此病人有哪 些病变？ 病例四答案病例四答案(1)左心衰(肺淤血) 半坐卧位，心界向左扩大，两肺背部中、小水泡音，心尖部舒张期震颤，雷鸣样舒张期杂音，Ⅲ级吹风样收缩期杂音 (2)右心衰(肝淤血) 肝肋下3cm，剑突下5cm，质韧，颈静脉怒张，心界向右扩大，肝、颈静脉回流征阳性，双下肢凹陷性水肿 (3)病变:慢性肺淤血、慢性肝淤血病 例 五病 例 五男，24岁，工人 现病史：半年前于工地施工中，不慎左脚被钉子刺伤，当时局部感染化脓，下肢红肿，约2周后逐渐恢复，此后左小腿又有数次疼痛和肿胀。2个月前左小腿疼痛肿胀达到膝关节周围，收入院治疗症状有所减轻。4天前左下肢肿胀，疼痛加重，并有发冷发烧。昨日开始咳嗽，咳痰，今晨咳痰带有少量血液，无胸痛。null查体:左下肢浮肿外，其它未见明显异常。 今日下午2点15分左右患者由厕所回病房途中大叫一声倒在地上，医务人员赶到时见患者四肢痉挛、颜面青紫、口吐白沫、瞳孔散大，抢救无效，于2点50分死亡。 临床诊断:急死、死因不清 申请病理解剖:要求查明死亡原因null解剖记录摘要： A1138，身长174厘米，体重60.6公斤 大体检查：左下肢浮肿，以膝关节以下为显著，左脚面有一外伤愈合的小瘢痕。剖开左腿见左股动脉及其分支无明显异常改变。左股静脉：大部分变粗变硬。从腘窝至卵圆孔一段股静脉内完全被凝固的血液成分堵塞，该血液凝固物长约40厘米与血管壁连接不紧密，大部分呈暗红色，表面粗糙，质较脆，有处呈灰白色与血管连接紧密。肺动脉的主干及两大分枝内均被凝血块样的团块堵塞，该团块呈暗红色无光泽，表面粗糙、质脆，与肺动脉壁无粘连。左肺内较小的动脉分枝内也有血凝块样物质堵塞。null左股静脉:主要为红色血栓结构(纤维素网内充满 大量红细胞，少处为混合血栓结构(可见少 量血小板梁)，靠近血管壁处有肉芽组织长 入血栓内。 肺动脉主干及两大分枝内:大部分为红色血栓结 构。左肺小动脉分枝内血凝块样物仍为红色 血栓，靠近血管壁处血栓有肉芽组织长入。显 微 镜 检 查null思考题： 1. 左股静脉内有什么病变？为什么能形成 这种病变？为什么股动脉无此改变？ 2. 肺动脉内为何种病变？根据是什么？ 3. 病变是如何发展的? 4. 死亡原因是什么？病例五答案病例五答案1.血栓形成:左脚钉子刺伤→静脉炎→(血栓形成条件)静脉管内膜损伤→血栓形成。股动脉深在，壁厚不易损伤 2.肺动脉内血栓栓塞:根据为肺动脉主干及大分枝为暗红色凝血块样物，无光泽，表面粗糙，质脆与肺动脉壁无粘连，镜下为红色血栓,机化，无慢性肺淤血null3. 发展过程:静脉损伤→静脉炎→血栓形成→肺主动脉大分枝栓塞→猝死 4. 死亡原因: 肺栓塞猝死. 肺主动脉主干及大分枝栓塞→患者突然呼吸困难、发绀和休克等急性呼吸循环衰竭死亡