Secrete chemicals of inflammation (histamine, heparin, serotonin)
Stimulate inflammatory response
Eosinophil Function:
Leave capillaries, enter tissue fluid
Release histaminase and other enzymes that combat effects of inflammatory mediators in allergic reactions
Combat parasitic worms
High count suggests allergic reaction or parasitic infection
Monocyte Function:
Slower to arrive at infection site but arrive in larger numbers, destroy more microbes
Enlarge and differentiate into macrophages
Clean up cellular debris and microbes following infection
Lymphocyte Functions:
B cells destroy bacteria and inactivate bacterial toxins
B cells produce antibodies when stimulated by foreign antigens
T cells secrete perforin (enzyme that perforates cell membranes) and are effective against various pathogens
Helper T cells stimulate T- and B-cells, activate macrophages, necessary for immunity
Regulatory T cells help prevent hypersensitivity reactions, regulate the immune system
Natural killer cells attack microbes and some tumor cells
Differential WBC Count:
Indicates inflammation or infection
Differential count (count of each type of WBC as % of total WBCs) indicates type of pathology (infection, poisoning, leukemia, chemotherapy, parasites, or allergy reaction)
Platelet (Thrombocyte) Anatomy:
Disc-shaped cellular fragments 2-4 µm in diameter
Normal count = 150,000-400,000 cells/mm3 of blood
Complete Blood Count (CBC):
Screens for anemia and infection
Includes total RBC, WBC, platelet counts, differential WBC, hematocrit, hemoglobin
Hemostasis:
Stoppage of bleeding when blood vessels are damaged
Three mechanisms: vascular spasm, platelet plug formation, coagulation (clotting)
Vascular Spasm:
Immediate contraction of damaged vessel wall
Reduces blood loss for several minutes to several hours
Allows time for other hemostatic mechanisms to proceed
Platelet Plug Formation:
Platelet adhesion, release reaction, aggregation
Coagulation (Clotting):
Cascade of reactions resulting in the formation of fibrin threads
Role of Vitamin K:
Produced by bacteria in the large intestine
Required for normal clotting
Not involved in clot formation but required for synthesis of several clotting factors
After clot has formed:
Platelets pull on fibrin threads (retraction) drawing edges of damaged vessel closer together
Serum can still escape, but cells cannot
Eventually new endothelium grows, and scar tissue produced by fibroblasts
Breakdown of small, intravascular clots and clots at a site of completed repair by tissue plasminogen activator (t-PA)
Hemostatic Control Mechanisms:
Fibrin, prostacyclin, anticoagulants
Low dose aspirin inhibits vasoconstriction and platelet aggregation