Hemodynamic Disturbance PDF

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Nineveh University

Asma Mohammadsheet Alhialy

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Hemodynamic disturbance pathology physiology medicine

Summary

This presentation covers hemodynamic disturbance, including definitions and mechanisms of hyperemia, congestion, and edema. It also discusses hemostasis, thrombosis, embolism, and ischemia. The content is suitable for an undergraduate-level medical course.

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Hemodynamic disturbance Lec. Dr. Asma Mohammadsheet Alhialy M.B.Ch.B MSc.(Histopath) CABHS(surgical path.) Pathology Department/Ninevah University/Collage of Medicine Objective ► The student will know and learn the following: 1. Definition of hyperemia and conges...

Hemodynamic disturbance Lec. Dr. Asma Mohammadsheet Alhialy M.B.Ch.B MSc.(Histopath) CABHS(surgical path.) Pathology Department/Ninevah University/Collage of Medicine Objective ► The student will know and learn the following: 1. Definition of hyperemia and congestion and types of congestion 2. Definition of edema, Pathogenesis of edema, Edematous fluid types, Types of edema, Clinical significance of edema and Pathological features of edema 3. Definition of hemostasis 4. Definition of hemorrhage 5. Definition of thrombosis, Morphology of thrombus, Pathogenesis of thrombosis and Fate of thrombus 6. Definition of embolism and its types 7. Definition of ischemia 8. Definition of infarction 9. Definition of shock 10. Types and stages of shock Hemodynamics ► Hemodynamics is the study of dynamics of blood flow. It explains the physical laws that govern the flow of blood in the blood vessels. Hyperemia and Congestion Hyperemia and Congestion both refer to an increase in blood volume within a tissue. But they have different mechanisms Hyperemia Congestion ► is an active process resulting from arteriolar ► is a passive process resulting from impaired dilation and increased blood inflow as occurs in outflow of venous blood from a tissue exercising skeletal muscle(physiological) and in ► it can occur systematically as in cardiac failure, or areas of inflammation(pathological). locally as a consequence of an isolated venous ► Tissue appears redder than normal because of obstruction. engorgement with oxygenated blood. ► congested tissues have an abnormal blue-red color(cyanosis) resulting from accumulation of deoxygenated hemoglobin in the affected area. At high magnification, the alveoli in this lung are filled with a smooth to slightly pink material characteristic for pulmonary edema. Note also that the capillaries in the alveolar walls are congested with many red blood cells. Congestion and edema of the lungs is common in patients with heart failure and in areas of inflammation of the lung. Congestion of the liver: usually follow right-sided heart failure--Grossly: liver moderately enlarged, firm and tender. cutsurface shows mottled appearance of dark areas( centrilobular zone congestion) and pale peripheral areas ( periportal areas ) giving appearance of (nutmeg liver). Microscopically, red cells accumulate in the sinusoids around the central veins surrounded by the peripheral hepatocytes which are better Nutmeg oxygenated because of their ‫ﺟوزه اﻟطﯾب‬ proximity to hepatic arterioles so they are less hypoxic & may only developed fatty changes giving it an appearance called“ nut meg liver". oedema About 60% of lean body weight is water, of which 2/3 is intracellular and 1/3 is extracellular( mainly interstitial). 5% of total body water is plasma. ► There are 2 opposing factors that govern the movement of fluid between vascular and interstitial spaces. Normally at the arterial end the hydrostatic pressure is greater than oncotic pressure so fluid is forced out the capillaries of the microcirculation. While at the venous side, the reverse happen and the fluid attracted back into the vessels. Only small residual amount stay in the tissue which will be drained by lymphatics. Oedema means abnormal and excessive accumulation of “free fluid” in the interstitial tissue spaces and/or body cavities. Free fluid in the interstitial spaces is commonly called oedema , this fluid lies free in the interstitial spaces between the cells. The main ingredient of the fluid is water. Extravascular fluid can also collect in the body cavities such as pleural cavity -------> hydrothorax. peritoneal cavity--------> hydroperitoneum (Ascites). pericardial cavity---------> hydropericardium. Anasarca is severe generalized oedema marked by profound swelling of the subcutaneous tissues and accumulation of fluid in body cavities. https://youtu.be/aRelHSTQiJw?si=ksdjlgKapaS3okPQ Pathogenesis of oedema 1- Increased capillary hydrostatic pressure: congestive heart failure constrictive pericarditis ascites of liver diseases e.g. hepatic cirrhosis venous obstruction e. g. DVT 2- Decreased plasma oncotic pressure a/ decreased synthesis(e.g., liver disease, protein malnutrition). b/increased loss(e.g., nephrotic syndrome , protein-loosing enteropathy). 3- Lymphatic obstruction (e.g. inflammation or neoplasia)--> obstruction lymphatic drainage e.g. filariasis--> fibrosis of regional LN-->oedema of lower limbs(elphantiasis). In ca breast, obstruction of superficial lymphatics ---> oedema of overlying skin-( peaud orange). ► 4- increased capillary permeability: capillary endothelial injury by toxins and their products ( e.g. histamin, anoxia, venoms, certain drugs, chemicals).—> increased capillary permeability causing leakage of plasma proteins into interstitial fluid—>more reduction in plasma oncotic pressure —> inflammatory oedema. 5- Sodium and water retention: Derangement in normal regulatory mechanisms of sodium and water balance—> increased capillary hydrostatic pressure which leads to oedema. example: oedema of renal diseases e.g. nephrotic and nephritic syndrome. Clinical classification of oedema ► localized oedema: when limited to an organ or limb e.g. a- inflammatory oedema b-lymphatic oedema due to lymphatic obstruction. c- Oedema due to localized venous congestion. d- pulmonary oedema. ► Generalized Oedema: a-Cardiac oedema seen in right sided heart failure. b-Nutritional oedema: due to hypoproteinemia seen in: - malnutrition -malabsorption -chronic liver diseases( decreased protein synthesis). c- Renal oedema: particularly starts around the eyelids (periorbital)then become generalized. Oedema can be classified according to the nature of accumulated fluid into: Transudate: protein poor fluid results from ► disturbance of Starling forces specific gravity 1.012, protein ► content>3g/dl. Pathological Features of Oedema oedema is most easily recognized grossly. M/S oedema fluid is reflected as a clearing and separation of the extracelluar matrix elements. oedema most commonly seen in subcutaneous tissues, lungs and brain. Subcutaneous oedema: this can be diffused or more prominent in areas with high hydrostatic pressure. dependent oedema is a prominent feature of cardiac failure particularly of the right ventricle. As a result of gravity, it can be in the legs when standing, or involving the sacrum when recumbent. Oedema due to renal dysfunction or nephrotic syndrome starts in loose tissues around the eyes(periorbital) then become generalized. HEMOSTASIS ► DEFINITION - Heme = blood - stasis = to stop ► It is the process of forming clots in the wall of damaged blood vessels & preventing blood loss while maintaining blood in a fluid state with in the vascular system. ► Defects in hemostasis can lead to an increased risk of bleeding (hemorrhage) or clotting (thrombosis). Events in Hemostasis ► Vascular Constriction -Damaged blood vessels constrict ► Formation of platelet Plug - Platelets adhere to damaged endothelium to form platelet plug (primary hemostasis). ► Blood Coagulation - Clots form upon the conversion of fibrinogen to Fibrin, and its addition to the platelet plug (secondary hemostasis). STAGES OF PRIMARY HEMOSTASIS ► Platelet Adhesion ► Platelet Activation ► Platelet Aggregation Secondary hemostasis ► If there is a large hole in the blood vessel, a blood clot is additionally required. ► Cascade of reactions It states that ‘inactive’ enzymes are activated, and the ‘activated’ enzymes in turn activates other inactive enzymes until final step is reached. THE CLOTTING MECHANISM INTRINSIC EXTRINSC Collagen Tissue Thromboplastin XII XI VII IX VIII X V FIBRINOGEN (I) PROTHROMBIN THROMBIN (II) (III) FIBRIN Fibrinolytic phase ► The fibrinolytic system does not allow the fibrin clot to grow and block a vessel, which would cause serious complications. The dissolution of a clot, called fibrinolysis (dissolving of fibrin fibers), is brought about by the formation of the active enzyme plasmin from plasminogen HEMOSTASIS in summery ► DEPENDENT UPON: Vessel Wall Integrity Adequate Numbers of Platelets Proper Functioning Platelets Adequate Levels of Clotting Factors Proper Function of Fibrinolytic Pathway Hemorrhage indicate extravasation of blood from blood vessels. Causes: 1- chronic congestion. 2-Hemorrhagic diathesis. 3- vascular injury( trauma, atherosclerosis, inflammation, neoplastic erosion). patterns include: External bleeding. Internal bleeding---> hematoma formation, hematothorax, hematoperitoneum). petechiae (1-2mm). Purpura (>3mm). Ecchymoses (1-2cm). Clinical significance of any bleeding depends on: volume of blood loss and rate of bleeding rapid loss of up to 20% of blood volume or slow loss of even larger amounts may have little effect on healthy adults however, greater looses can lead to hemorrhagic (hypovolemic shock). The site of hemorrhage is also important, a trivial bleeding in the subcutaneous tissues can lead to death if occur in the brain. Duration of bleeding (acute versus chronic or recurrent). Thank you

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