edema1 - Dr. Manal Gabril, MD, FRCPC, Msc Assistant...

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Unformatted text preview: Dr. Manal Gabril, MD, FRCPC, Msc Assistant professor Pathology, LHSC, University Campus Introduction 60% of the person’s body weight is water: Distribution of body fluid 40% intracellular Extracellular 5% plasma 15% interstitial 40% 15% 5% 40% 40% Introduction Survival of cells and tissue is depend on Oxygen provided in the blood supply Normal fluid balance Normal fluid balance depends on Starling’s law Systemic factors Intact circulation Overall fluid balance Salt retention Physiologic ranges of Intravascular pressure Osmolarity Homeostasis Process of maintaining a constant internal environment despite changing external conditions Several factors must be regulated including: Temperature Heart rate Respiratory rate Blood pressure Water balance Blood sugar levels Detoxification Altered vascular homeostasis results in: Change in net movement of water across the vascular wall. Artery Vein Capillary Lymphatic Each day about 50% of the total blood proteins leak out of the capillaries into the tissue fluid and return to the blood via the lymphatic vessels. Under normal circumstances only a small amount of fluid leaks from vessels to form interstitial fluid which is removed by lymphatic vessels. Move fluid outward Draw fluid inward Interstitial Fluid osmotic pressure Interstitial fluid oncotic pressure (tissue tension) Starling’s law : movement of fluid between vascular and interstitial spaces (at level of capillaries) is controlled by 4 forces Hydrostatic pressure (HP) Plasma oncotic pressure (OP) Tissue/Interstitial pressure (tissue tension) Interstitial/tissue fluid osmotic pressure Mainly by the opposing effect between HP and OP Hydrostatic pressure Definition: HP: force exerted by a fluid against the capillary wall. (pushing force) Capillary hydrostatic pressure (filtration pressure) forces fluid out of the blood capillaries The fluid contains oxygen and nutrients that move into the surrounding tissue where they are less concentrated Similarly, the tissue contains carbon dioxide and waste products that move into the capillaries where they are less concentrated This process of substances moving from areas of higher concentration to areas of lower concentration is diffusion Hydrostatic pressure: Capillary pressures vary: 32 mmHg at arteriolar end and 12 mmHg at venous end. Mean 25 mmHg. Interstitial Fluid osmotic pressure Interstitial fluid oncotic pressure (tissue tension) Oncotic pressure/plasma osmotic pressure OP is the pressure created by the presence of large molecules that can ’t diffuse and are prevented from moving through the capillary membrane These large molecules are plasma proteins such as albumin They encourage osmosis and they draw water toward them Because capillary blood has a high content of plasma proteins, the capillary has a high oncotic pressure of 26 mmHg Osmotic pressure depends on water and other solutes and a membrane that is permeable to water and not to other large molecules The oncotic pressure doesn't vary from one end of the capillary bed to OP These colloids exert an osmotic pressure of about 26 mmHg The colloid osmotic pressure due to the plasma colloids = oncotic pressure How do we know which direction fluid is moving? Whether there is a net gain or net loss of fluid? The net filtration pressure (NFP) must be calculated. It is the difference between the two pressures, the hydrostatic and the oncotic pressure. Fluid will leave the capillary if hydrostatic > oncotic pressure Fluid will enter the capillary if hydrostatic < oncotic pressure Hydrostatic Pressure = 32 mmHg Oncotic Pressure = 26 mmHg Hydrostatic Pressure = 12 mmHg Oncotic Pressure = 26 mmHg Under normal circumstances At arterial end: Hydrostatic Pressure = 32 mmHg Oncotic Pressure = 26 mmHg water moves out of the capillary with a NFP of +6 mmHg Hydrostatic pressure dominates at the arterial end and net fluid flows out of the circulation. At venous end: Hydrostatic Pressure = 12 mmHg Oncotic Pressure = 26 mmHg water moves into the capillary with a NFP of -14 mmHg Oncotic pressure dominates at the venous end and net fluid will flow into the bloodstream. At arterial end: Hyrostatic P – oncotic P results in 14 ml of fluid into interstitial space Osmotic reabsorption of 12 ml /min at venous side 2ml/min reabsorbed by lymphatics Vascular hemodynamics abnormalities Blood flow- normal fluid homeostasis edema Hyperemia Hemorrhage Maintenance of blood as a liquid Thrombosis Embolism Infarct Shock Edema Means accumulation of the fluids in the interstitial tissue or swelling of the subcutaneous tissues. • Increase hydrostatic pressure at venous end •Reabsorption is decreased •Lymphatics drain Hydrostatic edema Clinical conditions Congestive Heart failure, Right side failure peripheral edema Left side failure lung edema Deep venous thrombosis Right-sided heart failure (CHF) When the heart's function is compromised, it cannot pump blood as effectively -> venous hydrostatic pressure rises This rise in venous pressure diminishes the region where fluid is reabsorbed into the plasma Results in a net loss of fluid from plasma to interstitial space The resulting edema can be seen in the swollen ankles (and other tissues) that are symptomatic of congestive heart failure Pitting edema Pulmonary edema A venous thrombus has caused increased hydrostatic pressure in the leg, shifting fluid to the extravascular spaces. •Loss of albumin •Decrease oncotic pressure •Excess fluid goes to the interstitial fluid. Clinical conditions Liver disease as cirrhosis (liver failure) Decrease synthesis of albumin Hepatic ascites Renal failure Loss of albumin in urine Malnutrition Lymphatic obstruction: Accumulation of interstitial fluid because of insufficient reabsorption deficient removal of proteins ---- increase the interstitial fluid pressure of the interstitial space. LYMPEDEMA Increase permeability Inflammatory and traumatic edema Local or systemic Vascular bed becomes leaky following injury to the endothelium •Inflammatory and traumatic edema •Vascular bed becomes leaky following injury to the endothelium In conclusion Causes of edema Increased hydrostatic pressure Decreased plasma oncotic pressure Lymphatic obstruction/ increased interstitial oncotic pressure. Increased permability Sodium/water retention Sodium retention Sodium is the major cation that determines the osmolarity of the extracellular fluid volume Increase total body sodium must balanced by more extracellular water to maintain constant osmolarity Sodium retention Kidney diseases Increase intake Increase retention of the water Increase plasma volume: Hypervolemia Increase hydrostatic pressure (Expansion of intravascular fluid volume) Decrease in oncotic pressure edema Edema classified into 2 types: Localized edema Vascular/venous obstruction Lymphatic obstruction (lymphedema) Tumor Inflammation Postsurgical postradiation Burns edema by disrupting the local permeability of local vasculature “Localized” Edemaunilateral secondary to inflammation Non-pitting edema Localized Edema post radiotherapy for breast cancer “lymphatic obstruction ” Generalized edema (Anasarca): affecting the visceral organs and the skin of trunk and lower extremities Increase HP Heart failure Decrease OP Loss of albumin in renal failure (nephrotic syndrome) Decreased synthesis of albumin in liver failure (Ascites) Malnutrition Sodium retention Kidney disease Fluid in body cavities: Hydrothorax Fluid in chest cavity Hydropericardium Fluid in pericardium Hydroperitoneum Fluid in abdominal cavity Ascites Transudate vs exudate Transudate Results from disturbances in starling forces Protein <3 g/dl Specific gravity <1.012 Exudate results from damage to capillary wall Protein >3 g/dl Specific gravity >1.012 In conclusion Mechanism of edema Starling’s forces Local factors Lymphatic obstruction Vascular permeability Systemic factors Cardiovascular function Overall fluid balance Salt retention ? An individual with left heart failure would develop edema of the kidneys. liver. intestines. lungs. legs. ...
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This note was uploaded on 02/08/2012 for the course PATHOLOGY 3245 taught by Professor X during the Spring '11 term at UWO.

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