Hemodynamic & Haemostasis Disturbances.pptx

pathology

1. Heat Redness Swelling Pain Loss Of Func. The 5 Cardinal Signs of

2. Vascular Flow Disorders By: Dr.salem f gerbadi

3. Oedema ( OR edema) Hyperaemia & congestion Overview of normal haemostasis Haemorrhage Thrombosis Embolism Infarction Shock We are Going to Discuss the Following

4. In a 70 kg weight adult male there are: 40 liters of total body water 70% Distributed in: 25 liters of intracellular fluid 15 liters of extracellular fluid divided into: 12 liters of interstitial fluid 3 liters of intravascular fluid ( plasma ) Fluid Compartments

5. Intravascular and extravascular fluid compartments are separated by permeable membranes. Distribution of fluid between these two compartments depend on water movement. Na is the main cation of the extracellular fluid.(interstitial &intravascular) Note

6. Oncotic pressure (or colloid osmotic pressure ) is the pressure exerted by plasma proteins across Blood vessel wall . Hydrostatic pressure is the force that drives fluid through the vessels walls into the interstitial space Pressure gradients

7. Fluid Homeostasis

8. Oedema refers to fluid accumulation in the interstitial space . Causes: Increased hydrostatic pressure Decreased plasma oncotic pressure Lymphatic obstruction Sodium and water retention inflammation Edema

9. Localized : Due to local obstruction example: Venous Thrombosis in lower extremities (local edema). Generalized : Congestive Heart Failure (generalized edema). The serum protein(Albumin) is MOST responsible for the maintenance of colloid osmotic pressure.” I . Increased Hydrostatic Pressure II. Reduced Plasma Oncotic Pressure

10. Increased albumin Loss: Nephrotic Syndrome & intestinal loss. Reduced albumin synthesis: liver disease Protein malnutrition ( Kwashiorkor)and malabsorption II. Reduced Plasma Oncotic Pressure

11. Examples: Infection (e.g. Filariasis in Elephantiasis ) Tumor permeation. E.g. breast p eau d orange (i.e. orange like) Postirradiation Postsurgical Primary lymphatic channel tumor ( lymphangiosarcoma ) Lymphatic Obstruction

12. EDEMA - Summary INCREASED HYDROSTATIC PRESSURE Congestive Heart Failure Ascites Venous Obstruction DECREASED ONCOTIC PRESSURE Nephrotic Syndrome Cirrhosis Protein Malnutrition INCREASED PERMEABILITY Inflammation LYMPHATIC OBSTRUCTION Inflammatory Neoplastic

13. Edema Fluid Exudate Transudate Inflammatory High hydrostatic pr. Cause High 2.5-3.5g\dl Low > 1g\dl Protein content >1.020) <1.012) Specific gravity Rich Absent Inflammatory cells <7.3 >7.3 pH

14. Nephrogenic (kidney) oedema Cardiac oedema (heart) Pulmonary oedema (lung) Cerebral oedema Examples of oedema

15. 15 Oedema

16. HEMORRHAGE

17. Definitions Hyperaemia is the active increase in blood flow Congestion is the passive engorgement of a tissue with blood due to obstruction to venous outflow. 17

18. Is extravasation of blood from vessels into the extravascular space. Hemorrhage can be external or can be confined within a tissue; any accumulation is referred to as a hematoma Petechiae PurPura Ecchymoses HEMORRHAGE

19. Haemostasis .

20. Is the maintenance of the blood in its fluid state inside the vascular tree and solidification of blood (clot) in case of injury to prevent excessive blood loss. Normal haemostasis is an interplay between three components: Endothelial cells Platelets Coagulation system Definition of Haemostasis

21. Hemostatic disorders Thrombosis

22. Is the formation of a solid or a semi-solid mass from the constituents of blood within the vascular system during life. Not from blood embolism Outside vascular system clotting or haemostasis After death clotting Hemostatic disorders Thrombosis

23. Three primary influences predispose to thrombus formation, the so-called Virchow triad : endothelial injury stasis or turbulence of blood flow blood hypercoagulability In other words it results from interaction platelets, damaged endothelial cells and the coagulation cascade. .

24. Virchow’s Triad

25. Either: Physical injury exposure of sub-endothelial collagen Release of tissue factor Loss of anticoagulant effect of normal endothelium OR dysfunction tipping of pro-/anti-thrombotic balance Altered Endothelium

26. Either: Stasis activation of coagulation cascade OR turbulence endothelial dysfunction blood cells get contact with endothelium Altered blood flow

27. Either: (for sake of simplification) Increased coagulation factor activity , OR Decreased natural anticoagulants activity Increased Coagulability

28. Pale thrombus: forms in rapidly flowing blood (e.g. arterial). Grayish and firm Red thrombus: forms in slowly flowing blood (e.g. venous). Dark and gelatinous Mixed thrombus Types of thrombi

29. Venous (most common) oedema Arterial (more serious) necrosis Cardiac (e.g. in narrow mitral valve, thrombus may form in the atrium) Capillary (e.g. during acute inflammation) Site of thrombi

30. Fate

31. Embolism

32. Embolism Is the transference of abnormal material by the blood stream and its impaction in a vessel distant to the site of injury. Embolus is the impacted material Embolism

33. Thromboembolism Fat embolism Amniotic fluid embolism Air embolism Septic emboli Types of Emboli

34. Infarction

35. Ischaemia is deficient supply of blood. Infarction is tissue death due to reduction or loss of blood supply. Such tissue is termed an infarct Infarction can be due to venous or arterial occlusion. Infarction

36. Myocardial infarction Splenic infarction Cerebral infarction Intestinal infarction Examples

37. Anatomy of vascular supply Tissue metabolic rate and type of metabolism Rate of development of occlusion Oxygen content of the blood Factor That Affect Tissue Response to Ischaemia

38. Refresh basic sciences Active attendance learn to read textbooks Use your mind !! Remember :