病理学英文课件：血液循环障碍

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1、血 液 循 环 障 碍血 液 循 环 障 碍 Frequently seen in a wide variety of diseases (eg. stroke) Involving all kinds of tissue Either systemic or local Various forms充血和缺血充血和缺血Hyperemia and Ischemia 水肿和出血水肿和出血Edema and Hemorrhage血栓形成、栓塞及梗死血栓形成、栓塞及梗死Thrombosis, Embolism and Infarction 局部血量的异常局部血量的异常血液在血管内外分布异常血液在血管内

2、外分布异常血液性状和血管内容物的异常血液性状和血管内容物的异常 Local increased volume of blood in a particular tissue or areaA-1 Hyperemia 充充 血血 An active process due to augmented tissue inflow because of arteriolar dilation Tissue is redder than surrounding areas because of engorgement with oxygenated blood Examples: Skeletal mu

3、scle during exercise Sites of inflammation After decompression hyperemia blood redistributionAcute appendicitis急性阑尾炎急性阑尾炎Inflammatory hyperemiaInflammatory hyperemiaClinical consequences: positive effect negative effectA-2 Congestion 淤血淤血/ /静脉性充血静脉性充血 passive process resulting from reduced outflow o

4、f blood Systemic congestion: l heart failuresLocal congestion: l external pressure, l internal occlusion (thrombosis), l collateral circulation is failed to set up Morphology Dusky reddish-blue color / cyanosis(紫绀紫绀) because of accumulation of deoxygenated hemoglobin pulmonary congestion 肺淤血肺淤血Acute

5、 pulmonary congestion 急性肺淤血急性肺淤血 Morphology Dilation of venule and capillaryLiver congestion肝淤血肝淤血 Morphology Secondary changes including p Edema p Hemorrhage and Hemosiderin-laden cellp Ischemic tissue injury : Atrophy, degeneration p Congestive fibrosis and sclerosisAcute pulmonary congestion with

6、 edema Acute pulmonary congestion with edema and hemorrhage Chronic pulmonary congestionHemosiderin-laden cell (含铁血黄素细胞含铁血黄素细胞)/Heart failure cells (心衰细胞心衰细胞)Chronic pulmonary congestion-Heart failure cellChronic pulmonary congestion-Heart failure cellprussian blue stainingChronic pulmonary congesti

7、onLiver congestionAtrophyCentrilobular necrosis Fatty changeNutmeg liverCardiac cirrhosisRight heart failureLiver congestion with atrophy Liver congestion with hemorrhage and centrilobular necrosisNutmeg liver槟榔肝槟榔肝 Chronic hepatic congestionCardiac cirrhosisSpleen congestionSpleen congestion with f

8、ibrosis Dysfunction Fibrosis and cirrhosisClinical consequenceEdema 水肿水肿Hemorrhage 出血出血B-1 Edema 水肿水肿 an abnormal increase fluid in interstitial fluid is called edema(水肿水肿). Fluid collections in the body cavities is called hydrops(积水积水). BloodIntracellular waterInterstitium water/ third space water6

9、0% of lean body weight is waterPathophysiologic catogaries of edemauIncreased Hydrostatic Pressure (Impaired venous return)流体静压流体静压 A.Congestive heart failure? B.Liver cirrhosis ? C. Venous obstruction owing to I. Thrombosis II. Compression (eg. tumor) III. Stasis (eg. Lower extremity) Pathophysiolo

10、gic categries of edemauReduced Plasma Colloid Osmotic Pressure 血浆胶体渗透压减少血浆胶体渗透压减少 A. Nephrotic syndrome (glomerular protein leakage) 肾病综合征肾病综合征 B. Liver cirrhosis (loss of plasma protein synthesis) 肝硬变肝硬变 C. Malnutrition 营养不良营养不良 D. Protein-losing gastroenteropathyPathophysiologic categries of edema

11、u Sodium / Water Retention A. Kidney disease B. Renal hypoperfusion(congestive heart failure): Decreased renal perfusion lead to activation of renin-angiotensin-aldosterone axis, retention of sodium / water causes increased hydrostatic pressure and diminished vascular colloid osmotic pressure.Pathop

12、hysiologic categries of edemau Lymphatic Obstruction (lymphedema 淋巴水肿淋巴水肿) A. Inflammation (eg. Filariasis-Elephantiasis) B. Neoplasia C. Surgery/Irradiation Pathophysiologic categries of edemau InflammationProtein-poor transudate(漏出液漏出液)Protein-rich and cellularexsudate(渗出液渗出液)Subcutaneous pitting

13、edem(凹陷性水肿凹陷性水肿)Brain edemaAcute pulmonary congestion with edema Extravasation of blood into the extravascular space due to injury B-2 Hemorrhage 出血出血 Petechiae （出血点出血点）: Minute（1- 2mm）hemorrhage into skin, mucosa, serosa Commonly associated with increased intravascular pressure, low platelet counts

14、 （3mm hemorrhage Commonly associated with increased intravascular pressure, low platelet counts, vasculitis, fragility, trauma Ecchymoses （瘀斑）（瘀斑）: 1cm hemorrhage Subcutaneous bleeding Red cell degraded and phagocytosis Hematoma (血肿血肿）: Bleeding enclosed by tissue Bleeding into body cavities: hemoth

15、orax 胸腔积血胸腔积血 Hemopericardium 心包腔积血心包腔积血 Hemoperitoneum 腹腔积血腹腔积血 hemarthrosis 关节腔积血关节腔积血Subarachnoid hemorrhageBrain bleedingHemosiderinDepending on the volume and rate of bleedingClinical consequences Local effect (eg. Brain) Shock (shock is characterized by systemic hypotension due either to reduc

16、ed cardiac output or to reduced effective circulating blood volume. The consequences are impaired tissue perfusion and cellular hypoxia. At the outset the cellular injury is reversible; prolonged shock leads to irreversible tissue injury that often proves fatal. Anemia(iron deficiency anemia)Thrombo

17、sis 血栓形成血栓形成Thrombus 血栓血栓Thrombosis refers to the formation of a insoluble clot within a vascular lumen or cardiac cavity of living organism.An aggregate of coagulated blood containing platelets, fibrin, and entrapped cellular elements.l A well regulated processl Maintains blood in a fluid, clot fre

18、e state in normal vessels l Induces the rapid formation of a localized hemostatic plug at the site of vascular injury Normal HemostasisRolls of endotheliumAntithrombotic properties:u Antiplatelet properties A.Physical barrier B.producing PGI2, NO and ADPase, platelet adhesion or aggregationu Anticoa

19、gulant properties A.Heparin-like molecules (肝素肝素 样分子样分子) B.Thrombomodulin (凝血酶调节蛋白凝血酶调节蛋白) (binding to thrombin anticoagulant)u Fibrinolytic properties: Synthesis of t-PA(组织纤溶酶原激活物组织纤溶酶原激活物)Prothrombotic propertities:u Platelet effectsProducing vWF(cofactor for platelet binding to EMC)u Procoagulant

20、 effects:cytokine (IL-1, TNF) and endotoxin stimulation releasing tissue factor from endothelium extrinsic clotting cascadeu Antifibrinolytic effects:secreting PAIs(纤溶酶原活化物抑制因子纤溶酶原活化物抑制因子)Role of platelets in hemostasis1.Platelet adhesion: Reaction between platelet surface receptors, vWF, and collag

21、en2.Platelet secretion: Release of granule secretory products that promote platelet-plug formation3.Platelet aggregation: ADP and thromboxane promote primary hemostasis. Platelet contraction and fibrin formation lead to secondary hemostatic plug.Fibrinolytic pathwayp Endothelial cells play key rolls

22、 in the homeostasis Intact non-activated endothelial cells inhibit platelet adhesion and blood clotting. Endothelial injury or activation results a procoagulant phenotype that enhances thrombus formation.Vasculitis and thrombosisEndothelial injuryl Particularly important in thrombus formation in the

23、 heart and arterial circulation (e.g., myocardial infarction or valvulitis, severely atherosclerotic arteries, traumatic or inflammatory vascular injury)p Alteration in normal flow(Stasis and turbulence) Activating endothelium Disrupt laminar flowlTurbulence contributes to arterial and cardiac throm

24、bosis 涡流涡流lStasis is a major factor in the development of venous thrombi 血流缓慢血流缓慢 淤滞淤滞Venous Thrombus Thrombus of Iliac arteryMural thrombus 附壁血栓附壁血栓From othersMural thrombusHemangioma 血管瘤血管瘤p Hypercoagularity(高凝状态高凝状态) Platelets and clotting factors Fibrinolytic cascade 纤维蛋白溶解系统的活性纤维蛋白溶解系统的活性 Prima

25、ry (Genetic) hypercoagulability 原发性原发性(遗传性遗传性)高凝状态高凝状态 Secondary (Acquired) hypercoagulability 继发性继发性(获得性获得性)高凝状态高凝状态 Primary (Genetic) hypercoagulability Factor V Leiden mutations(2-15%Caucasians, recurrent deep venous thrombosis, mutant factor V resistant to cleavage by protein C) Prothrombin muta

26、tion（G20210A） Antithrombin III deficiency Protein C or S deficiency Secondary (Acquired) hypercoagulability Pronged bed rist or immobilization Myocardial infarction Tissue damage (surgery, fracture, burn) Advanced malignant tumor DIC Hyperlipidemia Hyperestrogenic states Coronary atherosclerosis Ora

27、lontraceptive use Smoking血栓头：血栓头： 血小板和少量纤维素血小板和少量纤维素血栓体：血栓体： 纤维素网络红细胞、纤维素网络红细胞、 血小板血小板血栓尾：血栓尾： 血液凝固后形成血液凝固后形成 Venous Thrombosis Types of thrombus White thrombus / Pale thrombus白血栓白血栓 Mixed thrombus 混合血栓混合血栓 Red thrombus 红血栓红血栓 Fibrinous thrombus/ Hyaline thrombus/Microthrombus纤维素性血栓纤维素性血栓/ /玻璃样血栓玻璃样

28、血栓/ /微血栓微血栓White thrombus 白血栓白血栓 Atrial surfacePapillary musclesChordae tendineaFrom othersFibrinous thrombus/ Hyaline thrombus/Microthrombus纤维素性血栓纤维素性血栓/ /玻璃样血栓玻璃样血栓/ /微血栓微血栓Mixed thrombus 混合血栓混合血栓laminationRed thrombus 红血栓红血栓Postmortem clots (chicken fat)鸡脂样凝血鸡脂样凝血 Fate of thrombusl Propagation: C

29、ontinued growth may obstruct critical vessell Dissolution: Fibrinolysis may dissolve clotl Organization (fibrosis) and Recanalization: re-establish some vascular flowl Calcification: phlebolith(静脉石静脉石) From othersOrganization of thrombusOrganization and RecanalizationVenous thrombus Congestion, edem

30、a, hemorrhage, necrosis Arterial thrombus Ischemia, infarctionEmbolismClinical consequences Embolism (栓塞栓塞): any material carried by blood flow from its point of origin lodging in blood vessels in another place and thereby obstructing the lumen Embolus (栓子栓子): a movable, intravascular mass that is c

31、arried from one site to another by blood flow Forms of emboli: Thromboemboli 血血 栓栓 (98-99%) Fat emboli 脂肪栓子脂肪栓子 Amniotic fluid emboli羊水栓子羊水栓子 Gas emboli 气体栓塞气体栓塞 Tumor emboli肿瘤栓子肿瘤栓子Embolism 栓塞栓塞 Possible pathwayl From left heart cavity or arterial systeml From right heart cavity or venous systeml F

32、rom portal veins 门静脉门静脉l Paradoxical embolism 交叉性栓塞交叉性栓塞l Retrograde embolism 逆行性栓塞逆行性栓塞From others 200,000 deaths per year in US95% Emboli from venous thromboses of lower extremitiesFrom others5%60-80%10-15%3%Pulmonary ThromboembolismClinical consequences: Most pulmonary emboli(60-80%) are clinical

33、 silent because they are small Sudden death occurs when emboli obstruct 60% or more of the pulmonary circulation Embolism of medium-sized arteries usually does not cause pulmonary except in the setting of left sided cardiac failure. Multiple emboli over time may cause pulmonary hypertension and righ

34、t ventricular failureEconomic Cabin Syndrome Systemic thromboembolism 体动脉体动脉血栓血栓栓塞栓塞 80% from the heart（mural thrombi） Travel to a wide variety of siteslower extremities (75%),brain (10%)Intestines, kidneys, spleen Consequences depending on size of emboli, caliber of vessel, collateral circulation,

35、tissue sensitivity to ischemia Etiology Fracture of long bones Soft tissue trauma Burns 10% patients having clinical findings 1-3days after injury, suddent onset of dyspnea ,tachycardia and irritability Pathogenesis involves both mechanical obstruction and biochemical injury Morphology: fat in micro

36、vasculature of pulmonary and brainFat embolism 脂肪栓塞脂肪栓塞Fat embolism Fat staining 见于分娩或流产、输液、心肺手术、潜水员病。Gas Embolism Air Embolism空气栓塞空气栓塞 Nitrogen Embolism氮气栓塞氮气栓塞 Gas bubbles within the circulation can obstruct blood flow Etiology Intravenous therapeutic procedures Obstetric procedures 分娩、流产分娩、流产 Cli

37、nical effect: 100mL Form frothy masses in vessel and occlude the vesselsAir Embolism 空气栓塞空气栓塞Caisson disease /Decompression sickness潜水员病潜水员病/减压病减压病 Etiology: Sudden decreasing in atmospheric pressure Nitrogen embolism Clinical consequences Lung: edema, hemorrhage, focal atelectasis or emphysema, lea

38、ding to choke Multiple foci of ischemic necrosis of bones, brain, heart Pneumoderma 发生机率1/8万，发生后80% 病人死亡。Amniotic Fluid Embolism 羊水栓塞羊水栓塞 Incidence: 1/50 000 deliveries Mortality rate : 80% Etiology :Infusion of amniotic fluid into the maternal circulation via a tear in the placental membranes and r

39、upture of uterine veins Characterized clinical onset:Sudden severe dyspnea, cyanosis, hypotensive shock, seizures and coma, DIC Morphology:Squamous cells, Lanugo hair, fat, mucin in the pulmonary microcirculationAmniotic fluid embolism Other Forms of Embolisman area of ischemic necrosis caused by oc

40、clusion of either arterial supply or venous drainage in a particular tissuecaused by thrombosis, embolism (99%) extrinsic compression, 受压受压 twisting of the vessels 痉挛痉挛 atheroma 粥瘤粥瘤 Factors that influence development of an infarction：Nature of vascular supply: Alternative blood supply is most impor

41、tant (eg，lung and liver)Rate of development of occlusion: Collateral development limits infarctionTissue vulnerability to hypoxia: Neurons (3 min), Heart (25 min), Connective tissue (hours) Blood oxygen content: Patients with anemia or cyanotic are more susceptible Shape: Wedge-shaped 楔形楔形/ /扇面型扇面型

42、Segmental 节段型节段型 Irregular 不规则不规则 Nature of necrosis: Coagulative necrosis 凝固性凝固性 Liquefactive necrosis 液化性液化性 Types: White infarcts白色梗死白色梗死 ( anemic infarcts贫血性梗死贫血性梗死) Red infarcts红色梗死红色梗死( hemorrhage infarcts出血性梗死出血性梗死) Infarction of spleenWhite infarct (anemic infarct)Infarction of kidneyWhite i

43、nfarct (anemic infarct)Infarction of heartWhite infarct (anemic infarct)Infarction of cerebrumInfarction of small intestineRed infarcts ( hemorrhage infarcts) Pulmonary infarctionRed infarcts ( hemorrhage infarcts) Clinical consequences我国第三次居民死因调查结果我国第三次居民死因调查结果: 城市前五位死亡原因依次是：恶性肿城市前五位死亡原因依次是：恶性肿瘤、瘤、

44、脑血管病、心脏病脑血管病、心脏病、呼吸系统疾病、损伤和中毒；农村依次是：、呼吸系统疾病、损伤和中毒；农村依次是：脑血管病脑血管病、恶性肿瘤、呼吸系统疾病、心脏病、损伤和中毒。、恶性肿瘤、呼吸系统疾病、心脏病、损伤和中毒。 男男,75,75岁岁, ,因股骨颈骨折入院因股骨颈骨折入院。先行外固定制动治疗先行外固定制动治疗, ,同时完同时完善各项检查。于入院后第三天行股骨头置换术善各项检查。于入院后第三天行股骨头置换术, ,手术进行过手术进行过程中患者突然出现心动过速程中患者突然出现心动过速, ,呼吸困难呼吸困难, ,很快进入昏迷状态很快进入昏迷状态, ,经抢救无效死亡。经抢救无效死亡。 既往史既往史: :高血压病高血压病2525年年, ,吸烟多年。吸烟多年。 问题问题: :请分析该患者的可能死亡原因及其发生机制。请分析该患者的可能死亡原因及其发生机制。课后作业：病例分析课后作业：病例分析