Lecture 6 Hemodynamic Disorders I - University of Al-Ameed PDF

University of Al-Ameed College of Medicine Department of pathology and forensic medicine 3rd year / 2024-2025 Lecture 6 Hemodynamic disorders I Professor Dr. Rahem M. R. Hemodynamic disorders include: 1. Hyperemia and congestion 2. Edema 3. Throm...

University of Al-Ameed College of Medicine Department of pathology and forensic medicine 3rd year / 2024-2025 Lecture 6 Hemodynamic disorders I Professor Dr. Rahem M. R. Hemodynamic disorders include: 1. Hyperemia and congestion 2. Edema 3. Thrombosis 4. Hemorrhage 5. Embolism 6. Infarction 7. Shock  HYPEREMIA & CONGESTION Hyperemia – Active process – Resulting from arteriolar dilation and increased blood inflow. – Examples: 1. at sites of inflammation. 2. exercising skeletal muscle. 3. menopausal flush. 4. high grade fever. 5. emotional stress. – Grossly: Hyperemic tissues are redder than normal because of engorgement with oxygenated blood.  Congestion is a passive process Resulting from impaired outflow of venous blood from a tissue. Systemically: as in cardiac failure. Locally: as a consequence of an isolated venous obstruction. Grossly: Congested tissues have an abnormal blue-red color (cyanosis) due to accumulation of deoxygenated hemoglobin in the affected area.  In chronic congestion, inadequate tissue perfusion and persistent hypoxia may lead to: 1. Parenchymal cell death. 2. Secondary tissue fibrosis. 3. Elevated intravascular pressures: edema. rupture capillaries, producing focal hemorrhages. MORPHOLOGY Grossly: Cut surfaces of hyperemic or congested tissues: 1. feel wet 2. ooze blood.  Main examples of congestions: 1. Systemic venous congestion: engorgement of systemic veins, chronic venous congestion as in RVF. 2. Pulmonary venous congestion: when the pressure in the left atrium will increase. 3. Hepatic congestion: the commonest cause is right heart diseases. 4. Local venous congestion: occur at any part of the body when the vein is obstructed. Main examples of congestions: o Systemic venous congestion o Pulmonary venous congestion o Hepatic congestion o Local venous congestion Systemic venous congestion (SVC): Engorgement of systemic veins, chronic venous congestion. Occur in RVF - Pulmonary stenosis - Various lung disease which interfere with pulmonary blood flow. Cor-pulmonale: RVF due to chronic lung disease Pulmonary venous congestion It develop when the pressure in the left atrium will increase. This pressure will increase in: - LVF (coronary artery disease, systemic HT) - Mitral valve stenosis. A. Acute pulmonary congestion: is marked by blood-engorged alveolar capillaries. variable degrees of alveolar septal edema Intra-alveolar hemorrhage. B. Chronic pulmonary congestion: The septa become thickened and fibrotic, the alveolar spaces contain numerous macrophages laden with hemosiderin (“heart failure cells”) derived from phagocytosed red cells. The brown coarsely granular material in macrophages in this alveolus is hemosiderin that has accumulated as a result of the breakdown of RBC's and release of the iron in heme. Hepatic congestion: In acute hepatic congestion: 1. The central vein and sinusoids are distended with blood. 2. Necrosis of centrally located hepatocytes. 3. The peri-portal hepatocytes, better oxygenated {may develop only reversible fatty change}. In chronic passive congestion of the liver: Grossly : The central regions of the hepatic lobules are red-brown and slightly depressed (owing to cell loss) and are accentuated against the surrounding zones of uncongested tan-fatty liver (nutmeg liver). In long-standing, severe hepatic congestion (with heart failure), hepatic fibrosis (cardiac cirrhosis) can develop. "Nutmeg liver” (chronic venous stasis) EDEMA  Approximately 60% of body weight is water 2/3 intracellular. Most of the remaining water is interstitial fluid. 5% in blood plasma. Edema: is an accumulation of interstitial fluid within tissues. Extravascular fluid can also collect in body cavities {as effusions}. Examples: 1. in the pleural cavity (hydrothorax) 2. the pericardial cavity (hydropericardium) 3. the peritoneal cavity (hydroperitoneum, or ascites). Factors influencing fluid movement across capillary walls Fluid movement between the vascular and interstitial spaces is controlled mainly by two opposing forces: 1. Vascular hydrostatic pressure. 2. Colloid osmotic pressure produced by plasma proteins.  Increased hydrostatic pressure or reduced intravascular colloid = Edema (protein-poor transudate) by contrast, Increased vascular permeability in inflammation = Edema (protein-rich exudate) Edema may be caused by: 1. Increased hydrostatic pressure (e.g., heart failure) 2. Increased vascular permeability (e.g., inflammation) 3. Decreased colloid osmotic pressure resulting from reduced plasma albumin a. Decreased synthesis (e.g., liver disease, protein malnutrition) b. Increased loss (e.g., nephrotic syndrome) 4. Lymphatic obstruction (e.g., inflammation or neoplasia) 5. Sodium retention (e.g., renal failure). Excess edema fluid is removed by lymphatic drainage and is returned to the bloodstream by way of the thoracic duct.  Morphology of Edema Edema is easily recognized on gross inspection. Microscopic examination: clearing and separation of the extracellular matrix (ECM) elements. Edema is mostly seen in: Subcutaneous tissues, lungs, and brain. 1. Subcutaneous edema: Pitting edema Periorbital edema. 2. Pulmonary edema: Frothy, sometimes blood-tinged fluid consisting of (a mixture of air, edema fluid, and red cells). 3. Brain edema: Can be localized (e.g., because of abscess or tumor) or generalized. With generalized edema: the sulci are narrowed as the gyri swell and become flattened against the skull Clinical features of edema: 1. Cardiac edema: gravitational distribution, pitting edema 2. Renal edema: Peri-orbital edema 3. Pulmonary edema: Dyspnea 4. Brain edema: Headache, vomiting, convulsion 5. Serous cavities: hydrothorax, ascites 6. Skin: Stretched or shiny Many other features accordingly …. Edema can be generalized or localized I. Generalized edema: A. Cardiac edema B. Renal edema C. Famine edema D. Allergic edema II. Localized edema: A. Venous obstruction B. Lymphatic obstruction C. Inflammatory edema All type of edema are pitting except lymphatic obstruction is non-pitting edema Anasarca: Severe , generalized edema, marked by profound swelling of subcutaneous tissues and accumulation of fluid in body cavities. Thrombosis Definition: Thrombosis is formation of solid or semisolid mass from blood constitutes within the vascular system during the life (while clot formed during the death). Thrombi can develop anywhere in the cardiovascular system. Hemostasis: Formation of a blood clot, which serves to prevent or limit the extent of bleeding at site of vascular injury in collaboration of platelets, clotting factors, and endothelium. Main steps for normal arrest of bleeding at site of injury are: 1. Vasoconstriction 2. Primary hemostasis 3. Secondary hemostasis 4. Clot stabilization and re-sorption Main factors which control the normal hemostasis are: 1. Platelets 2. Coagulation factors and natural coagulation inhibitors 3. Endothelial cells of blood vessel 4. Fibrinolytic system Virchow triad: The primary abnormalities that lead to intravascular thrombosis are: 1. Endothelial injury 2. Stasis or turbulent blood flow 3. Hypercoagulability of the blood I. Endothelial injury: Mechanical injury to ECs with exposure of VWF and tissue factors. Inflammation and other noxious stimuli. Degeneration: atherosclerosis, aneurysm, varicose vein. II. Abnormal blood flow (stasis): Turbulence contributes to arterial and cardiac thrombosis. Stasis is a major factor in the development of venous thrombi. Both turbulence and stasis: 1. Promote endothelial cell activation. 2. Promote platelets and leukocytes to come into contact with the ECs. 3. Slows the washout of activated clotting factors. 4. Impedes the inflow of clotting factor inhibitors. III. Hypercoagulability: Hypercoagulability refers to an abnormally high tendency of the blood to clot. Typically caused by alterations in coagulation factors. MORPHOLOGY: Arterial thrombosis vs venous thrombosis Lines of Zahn Mural thrombosis Vegetations Thrombosis vs clot  Arterial thrombosis vs Venous thrombosis Phlebothrombosis Typically arise at sites of endothelial Typically occur at sites of stasis or injury or turbulence. hypercoagulable state. Extend toward the heart and grow in a Extend in the direction of blood flow. retrograde direction from the point of attachment. Are frequently occlusive and well attach Are almost invariably occlusive and to the wall of BV. loosely attach to the wall of BV. and therefore prone to form embolus. Pale thrombi (Platelets rich) Red thrombi (RBC and Fibrin rich) Usually use antiplatelets in treatment Usually use fibrinolytics in treatment Usually superimposed on a ruptured The veins of the lower extremities are atherosclerotic plaque, vasculitis and most commonly affected. Example DVT trauma. Example MI.  Thrombi can have grossly apparent laminations called lines of Zahn. Lines of Zahn represent pale platelet and fibrin layers alternating with darker red cell–rich layers. Only found in thrombi that form in flowing blood. Distinguish antemortem thrombosis from the bland non-laminated clots that form in the postmortem state.  Thrombi occurring in heart chambers or in the aortic lumen are designated as mural thrombi. Caused by: Abnormal myocardial contraction Endomyocardial injury Ulcerated atherosclerotic plaques and aortic aneurysm Thrombi on heart valves: are called vegetations. Non sterile: Bacterial or fungal bloodborne infections can cause valve damage, leading to the development of large thrombotic masses (infective endocarditis). Sterile vegetations also can develop on noninfected valves in hypercoagulable states—the lesions of so-called “non-bacterial thrombotic endocarditis”.  Thrombus vs Clot Phlebothrombosis Located in intravascular , in circulating Located in IV or EV in stagnant blood after blood during life. death (at Autopsy). Compose mainly from platelets with Compose mainly of fibrin with RBC and fibrin, RBC and WBC. WBC and lack the platelets. Firmly attach to the wall of BV. Usually not attach to BV. Presence of line of Zahn. Lack of line of Zahn. Usually rubbery, gelatinous, moisty and Usually granular, dry friable with shape. lack of shape. Usually White, pale or may be red or Usually intense red or may be yellow. mixed. Fate of thrombus: 1. Propagation: The thrombus enlarges and spread along the blood stream. 2. Embolization: Part or all of the thrombus is detached. 3. Dissolution: By action of fibrinolytic system for newly formed thrombus, while old one is resistance to lysis. 4. Organization and recanalization. Older thrombi become organized by the ingrowth of endothelial cells, smooth muscle cells, and fibroblasts. Capillary channels are re-establishing the continuity of the original lumen. 5. Infection & aneurysm: instead of organizing, the center of a thrombus undergoes enzymatic digestion. If bacterial seeding occurs, the resulting infection may weaken the vessel wall, leading to the formation of a mycotic aneurysm. Good Luck