General Curriculum Chapter 3 Disorder of vascular flow ZHOU REN 周 韧 Prof., M.D., Ph.D. Institute of Pathology & Forensic Medicine Department of Pathology & Patho-physiology Zhenjiang University Judicial Evidence & Evaluation Center Zhejiang University School of Medicine Course of Basic Medical Sciences Chapter 3 Structure and Function of Vascellum Course of Basic Medical Sciences Chapter 3 Disorder of vascular flow may be divided into general and local categories. The local disorders contain: ①Derangement of local blood volume: hyperemia and ischemia, ②Derangement of blood properties and content: thrombosis, embolism and infarction. ③Derangements of vascular permeability and anatomic integrity: edema, hemorrhage. Course of Basic Medical Sciences Chapter 3 Hyperemia Def. Hyperemia refers to a local increased volume of blood caused by dilatation of the small vessels. Course of Basic Medical Sciences Chapter 3 1. Arterial hyperemia (active hyperemia) It results from an augmented arterial inflow, such as occurs in the muscles during exercise, at sites of inflammation, and in the pleasing neurovascular dilatation termed blushing. Course of Basic Medical Sciences Chapter 3 Active hyperemia causes increase of the volume of local tissue, of the metabolism and function of the organ. It is beneficial to the organism. Active hyperemia of body surface shows red in color and increase in local temperature. Course of Basic Medical Sciences Chapter 3 2. Venous hyperemia (passive hyperemia, congestion) It results from diminished venous flow such as follows cardiac failure or obstructive venous disease. Course of Basic Medical Sciences Chapter 3 Etiology (1)Compression on vein (2)Intravenous obstruction (3)Cardiac failure Course of Basic Medical Sciences Chapter 3 Morphology Congested organ increases in size and weight, solidifies in consistence, and shows dark color and capsular stiffness. Course of Basic Medical Sciences Chronic congestion of lung Chapter 3 Course of Basic Medical Sciences Chronic congestion of liver Chapter 3 Course of Basic Medical Sciences Chronic congestion of liver Chapter 3 Course of Basic Medical Sciences Chapter 3 Hemorrhage Def. Hemorrhage refers to extravasation of blood caused by rupture of blood vessel. Course of Basic Medical Sciences Hematoma: Accumulation of large amount of blood within the tissue of the body. Chapter 3 Course of Basic Medical Sciences Hemothorax, hemopericardium, hemoperitoneum, hemarthrosis: blood accumulation in body cavities as thoracic cavity, pericardial cavity, Peritoneal cavity and arthritic cavity respectively. Chapter 3 Course of Basic Medical Sciences Chapter 3 Petechiae(淤点): Minute hemorrhage into skin, mucous membrane or serosal surface. Purpura (紫癜): Slight larger hemorrhage. Ecchymosis (淤斑): A large subcutaneous hematoma. Course of Basic Medical Sciences Chapter 3 Thrombosis Def. Thrombosis refers to the process of formation of an adherent clotted mass of blood within the cardiovascular system in a living body. Course of Basic Medical Sciences Chapter 3 1. Factors and mechanism of thrombosis (1)Endothelial injury On the one hand, endothelial cells possess antiplatelet, anticoagulant, and fibrinolytic properties; on the other hand they exert procogulant functions. Course of Basic Medical Sciences Chapter 3 Intact endothelium insulates the blood platelets and coagulation proteins from the highly thrombogenic subendothelial components, principally collagen. Course of Basic Medical Sciences Chapter 3 Damage to vascular endothelium is the dominant influence thrombogenesis, and the only one which, by and of itself, may lead to thrombus formation. It may occur in the following situations: ulcerated atherosclerotic plaques; vascular traumatic or inflammatory injury; endocardium in the site of myocardial infarction or myocarditis. Course of Basic Medical Sciences Chapter 3 (2)Alteration of blood flow (stasis and turbulence) In normal laminar blood flow, all of the formed elements are separated from the endothelial surface by a clear plasmatic zone. Course of Basic Medical Sciences Chapter 3 ①disrupt laminar flow and permit platelets to come into contact with the endothelium; ②prevent dilution of activated clotting factors to subcritical concentrations; ③retard the inflow of clotting factor inhibitors; Course of Basic Medical Sciences Chapter 3 ④permit the build-up of platelets aggregates and nascent fibrin either in the sluggish stream or in the pockets of stasis; ⑤promote endothelial cell hypoxia and injury, predisposing to platelet and fibrin deposition as well as reducing release of TPA; ⑥the turbulence is a mechanism for endothelial injury. Course of Basic Medical Sciences Chapter 3 (3)Hypercoagulability Hypercoagulability can be defined as an alteration of the blood or , specifically, the clotting mechanism that in some way predisposes to thrombosis. Hypercoagulability can be seen in many clinical settings such as severe trauma, burns, disseminated cancer, long term use of oral contraceptives. Course of Basic Medical Sciences Morphogenesis of thrombi Chapter 3 Course of Basic Medical Sciences Chapter 3 ①Endotbelial injury→platelets adhesion and aggregation. Platelets activation→release reaction (ADP, TxA2, 5-HT)→platelet aggregation. Course of Basic Medical Sciences ②Intrinsic and extrinsic coagulation sequence: prothrombin→thrombin ↓ fibrinogen ———→fibrin Chapter 3 Course of Basic Medical Sciences White thrombus (head of thrombus): dry, friable gray mass z Transection: darker gray lines of platelets (Zahn’s line) H. Platelet trabeculae formation z Chapter 3 Course of Basic Medical Sciences z mixed thrombus (body) White thrombus intermingled with red thrombus Chapter 3 Course of Basic Medical Sciences Chapter 3 Dark red in color, laminations are not well developed and composed of RBC and fibrin z red thrombus (tail) : Course of Basic Medical Sciences 3. Types of thrombi (1)Arterial thrombi Chapter 3 Course of Basic Medical Sciences ①Mural thrombi Chapter 3 Course of Basic Medical Sciences ②Ball thrombi Chapter 3 Course of Basic Medical Sciences ③Occlusive thrombus Chapter 3 Course of Basic Medical Sciences Chapter 3 Course of Basic Medical Sciences (2)Venous thrombus Chapter 3 Course of Basic Medical Sciences (3)Vegetations Chapter 3 Course of Basic Medical Sciences Chapter 3 The potential outcomes of thrombus: (1)Softening, liquefaction and absorption (2)Detachment of thrombus followed by thromboembolism Course of Basic Medical Sciences Chapter 3 Course of Basic Medical Sciences (3) Organization and recanalization Chapter 3 Course of Basic Medical Sciences (3) Organization and recanalization Chapter 3 Course of Basic Medical Sciences (4)Calcification Chapter 3 Course of Basic Medical Sciences Chapter 3 Course of Basic Medical Sciences Chapter 3 Course of Basic Medical Sciences Chapter 3 Microcirculatory Thrombosis(DIC) Def. Widespread thrombosis in the microcirculation is referred to disseminated intravascular coagulation(DIC). Course of Basic Medical Sciences Chapter 3 Etiology and mechanism DIC is not a primary disease, rather, it is a complication of some underlying diseases (trauma, severe infection, shock, carcinoma etc.) which activate the processes involved in blood clotting. Course of Basic Medical Sciences The simplest mechanism involves the release of tissue factor into the circulation, for example, from the placenta in obstetric complication. Carcinomas may also release other thromboplastic substances such as proteolytic enzymes etc. Chapter 3 Course of Basic Medical Sciences Chapter 3 Morphology The microthrombi are composed of platelets and fibrin and are found principally in the arterioles and capillaries of the kidney, adrenals, brain and heart. Course of Basic Medical Sciences Chapter 3 The bleeding tendency is probably attributable to the rapid consumption of platelets and clotting factors; hence DIC is sometimes also referred to defibrillation syndrome or consumption coagulopathy. Course of Basic Medical Sciences Chapter 3 Embolism Def. Embolism refers to occlusion of some part of the cardiovascular system by any foreign mass carried there in the blood stream. The transported mass is called as embolus. Course of Basic Medical Sciences Chapter 3 1. Routes of embolus transportation (1)Arterial emboli induce embolism in brain, kiney, spleen and lower limbs. (2)Venous emboli usually lodge in the lung. Course of Basic Medical Sciences Chapter 3 (3)Paradoxical embolism: In case of congenital septum defect of the heart, venous emboli may enter from the right into the left heart chambers. (4)Retrograde embolism: Emboli occasionally may travel against the direction of blood flow. Course of Basic Medical Sciences Chapter 3 2. Types of emboli (1)Thromboembolism ①Pulmonary embolism most commonly originates from thrombus of lower limb. The prognosis depends on the size of the occluded vessel and the status of the patient’s cardiovascular system. Course of Basic Medical Sciences Chapter 3 Large embolus: fatal. Mechanical obstruction + severe strain on the right side of the heart (acute cor pulmonale) + reflexive vascular and bronchial spasm. Course of Basic Medical Sciences Chapter 3 Small emboli obstruct small branches of pulmonary artery: The thrombi can be resolved and so of little significance. If bronchial circulation is insufficiency (chronic passive congestion of lung), small emboli may produce either pulmonary hemorrhage or infarction Course of Basic Medical Sciences Chapter 3 ②Arterial embolism Origin: Emboli usually arise from mural thrombi in the left ventricle or atrium, from vegetations on the left side valves, and occasionally from thrombi on the aorta. Course of Basic Medical Sciences Chapter 3 Morphology: They produce occlusion of blood stream most frequently in the spleen, the kidneys, the brain, and lower extremities, often with resultant infarcts in the organs and gangrene in the limbs. Course of Basic Medical Sciences Chapter 3 (2)Fat embolism Etiology: Fracture of the shafts of long bones, soft tissue trauma, burns. Morphology: Sequences: The prognosis of fat embolism depends on the quantity and site of embolism. Course of Basic Medical Sciences ①Pulmonary fat embolism: 9~20g fat→75% pulmonary arteries are occluded→pulmonary edema, hemorrhage, atelectasis→asphyxia, right sided heart failure. Chapter 3 Course of Basic Medical Sciences Chapter 3 ②Lung-brain-kidney-skin embolism syndrome Course of Basic Medical Sciences Chapter 3 (3)Gas embolism ①Air embolism Etiology: As a complication of trauma (chest), cardio-thoracic surgery, various diagnostic or therapeutic procedures, or rupture of veins during delivery. Course of Basic Medical Sciences Sequences: Small volume: absorbed >100ml: acute distress. >300ml: fatal due to pulmonary embolism. Chapter 3 Course of Basic Medical Sciences Chapter 3 ②Decompression sickness (cassion disease) Etiology and mechanism: Decompressed rapidly from high atmospheric pressure to a normal level of pressure (in deep sea divers, in underwater construction workers) or from normal atmospheric pressure to a low pressure (in aviators)→Gas comes out of solution in the blood, tissue fluid, and fat, in the form of minute bubbles which are composed of O2, CO2 and nitrogen. The nitrogen is of low solubility and persists as minute bubbles. Course of Basic Medical Sciences Chapter 3 (4)Amniotic fluid embolism Etiology and mechanism: After rupture of membranes, some of the amniotic fluid may be forced by vigorous uterine contractions between the membranes and the uterine wall and then up to the placentar margin to enter the uterine sinusoids. Amnionic fluid embolism 羊水栓塞 Course of Basic Medical Sciences It is now suspected that vasoactive substances within the amniotic fluid such as prostaglandins may be the cause of pulmonary vasoconstriction. Chapter 3 Course of Basic Medical Sciences Chapter 3 Morphology: The classic findings in the pulmonary arteries and capillaries at autopsy are epithelial squames from fetal skin, lanugo hairs, fat from vernix caseosa, and mucin, presumed to be from the fetal GIT. Course of Basic Medical Sciences Chapter 3 Infarction Def. Ischemic necrosis of tissue or organ caused by occlusion of either its arterial supply or its venous drainage is referred to infarct, the process of infarct formation is called as infarction. Course of Basic Medical Sciences Chapter 3 1. Causes and factors that condition the development of an infarct (1)Nature of vascular supply ①Effective anastomosis ②Double blood supply (liver, lung etc) Course of Basic Medical Sciences Chapter 3 (2)Rate of development of occlusion (3)Vulnerability of the organ or tissue to hypoxia (nerve cells, myocardial muscle>fibroblasts) Course of Basic Medical Sciences Chapter 3 (4)Oxygen carrying capacity of blood: The anemia or cyanotic patient tolerates arterial insufficiency less well than does the normal person. Course of Basic Medical Sciences Chapter 3 2. Types (1) White infarct : It result of arterial occlusion, commonly seen in compact, solid organs with less collateral circulation, such as the kidneys, spleen and heart. Course of Basic Medical Sciences Chapter 3 (2) Red infarct: Red infarct of intestine: Limited venous outflow due to vascular obstruction + by pass channels can’t develop. Course of Basic Medical Sciences Chapter 3 3. Morphology G. All infarcts, red and white, tend to be wedge shape, the occluded vessel at the apex and the periphery of the organ forming the base. Course of Basic Medical Sciences Chapter 3 Shortly after the vascular obstruction, the area involved becomes red and congested as a result of dilatation of the vessels and flowing of blood into the part from adjacent vessels. Hemorrhage occurs as a result of ischemic damage to vessel wall. Course of Basic Medical Sciences Chapter 3 Compact organs have relative little hemorrhage, the necrotic area is gradually decolorized (rbc are lysed and removed from the area), and appears pale or yellow-white (white infarct). Course of Basic Medical Sciences Chapter 3 Organs of soft, loose tissue with double supply, infarcts tend to remain hemorrhagic (Red infarct) Course of Basic Medical Sciences Pulmonary hemorrhagic infarct Chapter 3 Course of Basic Medical Sciences H. Necrotic tissue surrounding with hyperemic and hemorrhagic zone. Chapter 3 Course of Basic Medical Sciences * Septic infarct: When an infarct is produced by a septic embolus, the infarct is converted to an abscess. Chapter 3 Course of Basic Medical Sciences Chapter 3 4. Fate of infarct (1)Small infarct: softened, absorbed (2)Large infarct: organization and scar formation (3)Septic infarct: abscess formation (4)Infarction of brain, myocardium or lung: sometimes may cause sudden death. KEY WORDS and QUESTIONS-THINKING FOR THE CHAPTER ? ? z Congestion z Thrombosis z Embolism z Infarction ?