中国医科大学病理学英文课件5说课材料.ppt

中国医科大学病理学英文课件5 Still waters run deep.流静水深流静水深,人静心深人静心深 Where there is life,there is hope。有生命必有希望。有生命必有希望ll heart heart l l A VA Vl l N-N-humorhumortytypespeslllocallocal：coronary AScoronary ASllsystemicsystemic：heart faheart failureilurellrelationshiprelationshipll(一一一一)change of blood:)change of blood:1.volume:1.volume:increasehyperemiaincreasehyperemia decreaseischemia decreaseischemia ll2.2.naturenature:ll high coagultionhigh coagultionthrombosisthrombosisll foreign bodythrombusforeign bodythrombusll embolismembolisminfinfarctionarctionll(二二二二)vessel:)vessel:ll 1.high perm 1.high permeabilityeabilityll 2.rupture2.ruptureA.V.(congestion)edema hemorrhage 一一.Arterial hyperemia1.Definition:Increased volume of arterial inflow in an organ or tissue(hyperemia)2.Common types:(1)Physiologic:exercise skeletal muscle(2)Pathologic:at the foci of inflammation(3)Hyperemia after reducing pressure3.Sequelae:(1)Restore:if causes abated(2)Hemorrhage:hypertension,AS二、二、CongestionResulting from an isolate venous obstructionaccumulation of blood in veinlet and capillary(一一)Etiology1.Veins being pressed:Tumor press local vein2.Venous obstruction:thrombosis3.Heart failure:left pulmonary congestion right hepatic congestion(二二)Lesions and results1.Hydrostatic pressure congestive edema,hemorrhage 2.Chronic hypoxia atrophy or degeneration fibrosis,sclerosis(三三)Congestion of important organs1.Pulmonary congestion(acute,chronic):(1)Cause:left heart failure(2)Morphology:Gross:volume weight dark red cut surface consolidated L M:Aalveolar septa capillary engorged with blood become thickened fibrosis Alveolar spaces edema fluid heart failure cells hemorrhageBrown induration:long period congestion,texture become solid and show brown appearance.Chronic pulmonary congestionChronic pulmonary congestion慢性肺淤血慢性肺淤血慢性肺淤血慢性肺淤血Heart failure cells:Hemosiderin-laden M2.Hepatic congestion:(1)Cause:right heart failure(2)Morphology:Acute hepatic congestion:1)Gross:enlarged,dark red2)LM the central vein and sinusoids are engorged with blood central hepatocyte:necrosis peripheral hepatocyte:fatty change Chronic hepatic congestion:1)Gross:nutmeg liver cut surface shows zones of yellow alternating with zones of red,like nutmeg.The central V,sinusoids:distended with bloodCentral hepatocyte:atrophy or necrosis Peripheral hepatocyte:fatty changeCongestive bands among central v2)LM:Chronic hepatic congestion Congestive cirrhosis of liverSection 3.Thrombosis Definition:within living heart or blood vessel blood coagulated(clotting)or some components clump form solid mass(thrombus)一一.Conditions and mechanism of thrombosisThree primary influences predispose to thrombus formation:(1)Endothelial injury(2)Alteration in normal blood flow stasis or turbulence of blood flow(3)Blood hypercoagulability(一一)Endothelial injuryNormal condition:Intact EC inhibit platelet adherence blood clotting.Injury or activated EC augments local blood clotting.1.Functions of Endothelium(1).Antithrombotic properties Screen function of intact endothelium Antiplatelet adhering Anticoagulants Fibrinolytic内内皮皮细细胞胞抑抑制制血血栓栓形形成成作作用用示示意意图图 Activate exogenous coagulation process Promoting adhesion of platelet Inhibiting fibrinolysis2.Functions of Platelets:Adhesion and shape change Secretion(release reaction)Aggregation(2).Prothrombotic properties3.The common disease(1)Endocardial injury:myocardial infarction,valvulitis(2)Vascular injury:traumatic,As ulcerated plaques inflammatory injury(vasculitis),(3)Hypoxia,shock,bacterial endotoxin DIC microthrombus(二二)Alteration in normal blood flow 1.Refer to Stasis or turbulence(1)Disrupt laminar flow and bring platelets into contact with EC.(2)Prevent dilution by fresh flowing blood of activated clotting factors(3)Promote EC activation,predisposing to local thrombosis,leukocyte adhesion.2.Vein is the favored sites:1)Venous valves slow,turbulence2)Fugacious stasis3)Thinner wall pressed easily4)Adherence increased (blood from capillary Vein)(三三)Hypercoagulability1.Inherited causes of hypercoagulability:(1)The most common cause:Mutations in the factor V gene prothrombin gene (2)Inherited lack of the anticoagulants:anti-thrombin protein C,protein S2.Acquired causes of hypercoagulability:1)Widely metastasis of malignant tumor 2)Severe trauma Large area burn Operation of3)Hyperlipemia,AS,smoking,obesityLoss of blood二二.The Process and morphology(一一)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 FibrinThe process of vein thrombosis(二二)Types and morphology1.Artery thrombi(Pale thrombus):(1)The common sites:arterial lumen:coronary A cardiac valves and chambers Injured site of BV(2)Gross pale nodule or vegetation rough surface,friable firmly adherent to arterial wall(3)LM:Platelet(main)Fibrin(a little)Erythrocyte,degenereting leukocyte Pale thrombus in cardiac valve2.Mixed thrombi(1)Sites heart chamber aneurysm,AS(2)Gross:gray-white alternating with brown dry,adherent to vascular wall mural thrombus(3)LM:platelet,fibrin,erythrocytes3.Venous thrombi(Red thrombus)(1)Sites vein of the lower extremities Prostate,ovary,uterus(2)Gross dark red wet dry friable(3)LM Fibrin+RBC a little WBCVenous thrombus4.Fibrin thrombi(Hyaline thrombus)occur in capillary(microcirculation)can be seen under LM only compose of acidophilic fibrin most common cause:DIC Fibrin thrombi