PHYSIOLOGY

RED BONE MARROW

55% IS PLASMA, 45% IS FORMED ELEMENTS

91.5% IS WATER, 7% PROTEINS, 1.5% SOLUTES OTHER THAN PROTEINS

ERYTHROCYTES- REPLENISH 2 MILLION/SEC, BICONCAVE SURFACE CAN AFFECT THE LIFESPAN OF THE RBC, MATURE AFTER 1-2 DAYS OF BEING RELEASED FROM BONE MARROW LEUKOCYTES- LIVE ONLY 1-2 DAYS BUT T AND B CELLS CAN EXIST FOR YEARS

NEUTROPHILS- LARGEST IN #, FIRST RESPONDER TO BACTERIAL INVASION, PHAGOCYTES AND LYSOZYME ACTION EOSINOPHILS-RELEASE ENZYMES THAT COMBAT INFLAMMATION IN ALLERGIC REACTIONS, INVOLVED IN SOME BACTERIAL AND PARASITIC WORMS BASOPHILS-INTENSIFY INFLAMMATORY REACTIONS

LYMPHOCYTES- B CELLS (ANTIBODY), T CELLS (VIRUSES, FUNGI, TRANSPLANTED CELLS, CANCER CELLS), NK CELLS (INFECTIOUS MICROBES AND CERTAIN CANCERS) MACROPHAGES- LARGEST WBC, CAN BE FIXED OR WANDERING MACROPHAGES, MIGRATE TO SITE OF INFECTION AFTER NEUTROPHILS IN LARGE NUMBERS, CLEAN UP DEBRIS POST INFECTION

Erythropoiesis is the process of developing RBC’s. EPO (Erythropoietin) is the hormone produced by the kidney regulates it. Iron, globin, Vitamin B12, Erythropoietin are the “raw ingredients”.

The 8 different types of blood are A+, A-, B+, B-, AB+, AB-, O+, and O-. An antigen is a foreign molecule that has the potential to induce immune responses. It is on the surface of the RBC. An antibody is a protein that is produced when an antigen is introduced in the body. It can bind to the antigen and neutralize its treat presented by the foreign molecule. Each blood typing system is based upon the presence or absence of specific antigens on the surface of RBCs. The ABO system assesses RBCs for the presence of the A or B antigen. The Rh system is based upon the presence of absence of the Rh antigen.

Hemostasis is a sequence of responses that stops bleeding when blood vessels are injured. 1. Vascular Spasm- when a blood vessel is damaged the smooth muscle contracts immediately (Thromboxine A2 maintains contracts) 2. Platelet Plug-positive feedback stops blood loss by plugging injury 3. Blood clotting

Platelet adhesion initiates plug formation. 1. Platelet adhesion- encourages platelets to stick to damaged blood vessel 2. Platelet release action- platelets contact each other and release chemicals (ADP and Seratonin) which activate nearby platelets and encourage vascular spasm to decreased blood flow 3. Platelet aggregation/platelet plug- surrounding platelets gather at site of injury and form an aggregate to help stop blood loss

Extrinsic pathways- outside the blood vessel, rapid, damaged tissue releases tissue factor (TF) that is eventually converted to prothrombinase Intrinsic- takes several minutes, happens inside the blood vessel, endothelial cells become damaged and send signals to release prothrombinase but there are several reactions that occurThe 2 pathways are similar because they both complete hemostasis and form prothrombinase and clot blood

When the fibrin clot tightens over time. Platelets contain a very high concentration of actin and mysosin which are stimulated to contract in aggregated platelets. This pulls the edges of damaged wound together which decreases the risk of further damage and since it is a smaller area to heal, it is speedy in repair of damage

Fibrinolysis is the process by which clots dissolve. Plasminogen is an inactive precursor and once it is activated into plasmin it begins to digest fibrin threads (takes insoluble fibrin into soluble fibrin). It dissolves clots

Antithrombin III- small protein that inactivates thrombin, can break up and clots (Heparin-like)Plasminogen- Tissue Plasminogen Activator (TPA) converts plasminogen to plasmin. This breaks down fibrin. If used within 3 hours or 6 hours direct- Factor XIIa and thrombin also activate plasminogen. Gets into blood stream it can breakdown clot in the heart or brain and restore blood flow

The flow of air in and out of the lungs