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Unit 2.docx

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Department
Pathology
Course Code
PATH 3610
Professor
Andrew Vince

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Description
Unit 2 Normal fluid exchange Normal fluid exchange Osmosis- solvent passing from less. concentration to greater ‘Oncotic pressure’- pressure generated by osmosis ‘Hydrostatic pressure’- pressure of water , influenced by heart activity, elasticity + recoil of blood vessels, the quantity of blood w.i a vessel, etc. Normally hydrostatic & oncotic pressures are near 0, so contribute little to fluid exchange. Normal capillary, at arteriolar end of capillary bed, vascular hydrostatic pressure (pushing fluid out of vessels) is higher than vascular oncotic pressure (drawing fluid into vessels). Net effect drives fluid into tissues (to deliver nutrients and O2to tissues). At venular end, v. hydrostatic pressure lower than v. oncotic pressure, driving fluid back into blood vessels, carrying away metabolic waste byproducts of tissue. Usually balanced so gains and losses of fluid equal. Fluid moves out of capillaries at the pores, which permit only small molecules through. This fluid is then called ultrafiltrate. Most of this returns to capillary via the “pull” of the oncotic pressure of the plasma proteins in the capillary. The rest drains via the lymphatic system (which eventually drains into bloodstream). Edema  accumulation of excess fluid in the interstitium (tissue space)  mostly seen in skin and associated subcutaneous tissues  localized edema (ex. spider bite) : result of localized disturbance of the fluid exchange mechanism in the tissue  generalized edema (ex. congestive heart failure): excess fluid seen in many tissues When fluid accumulates in body cavities (ex. pleural space, pericardial sac) the term effusion is used (eg. pleural effusion); sometimes see hydropericardium because refers to water. Anasarca indicates massive edema of whole body. Localized edema example  EX. TUMOR: if venous drainage of capillary bed is obstructed, hydrostatic force at the venular end will increase so HP>OP. Fluid will leave capillaries normally at arteriolar end of capillary bed (HP>OP) but can not return to capillaries as easily bc. HP still exceeds OP. So the fluid remains in tissue spaces as edema.  Lymphatic drainage could be obstructed by mass (may cause edema over time), although usually cause is venous obstruction. Acucmulation of small protein molecules over time leads to increased tissue colloid oncotic pressure which will favour fluid remaining in the tissue spaces. The “pull” of plasma colloid osmotic pressure is not sufficient to move adequate amounts of fluid back into capillaries so edema will develop. If this edema persists tissue may undergo fibrosis causing affected area to become firm and thick  SO. Two important causes of localized edema are: 1. venous obstruction 2. lymphatic obstruction  Two other causes are 1. acute inflammation (ex. spider bite) and 2. acute allergic reactions (ex. hives), both of which increase capillary permeability allowing fluid and plasma proteins to move out of capillaries and into tissues Generalized edema **edema most noticed in dependent parts of body (ex. lower legs, ankles) bc. gravity  increased venous pressure (in heart failure) causing systemic and pulmonary edema; st 1 major cause of generalized edema  In congestive heart failure, heart is failing in role as a forward pump o right ventricular failure: venous blood backs up in systemic circulatory system (“body-wide” venous obstruction) causing a generalized increase in venous hydrostatic pressure. Causes fluid to build in interstitium, leading to generalized edema o left ventricular failure: blood builds up in pulmonary circulation causing an increase in pulmonary v. hydrostatic pressure (so fluid remains in lungs as edema). Differs from right bc. normally pulmonary functions with HP
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