Blood Physiology PH (2024) PDF

White Blood Cells  Types of leucocytes Granulocytes Agranulocytes Neutrophils Eosinophils Lymphocytes Monocytes Basophils B T...

White Blood Cells  Types of leucocytes Granulocytes Agranulocytes Neutrophils Eosinophils Lymphocytes Monocytes Basophils B T Normal Total white cell count: 4500-11000 cells/mm3 (Average 7000/mm3)  Granulocytes Neutrophils Eosinophil's White Blood Cells Basophils (Classification) Agranulocytes Monocytes Lymphocytes  Differential white cell count (% distribution of types of leucocytes) Neutrophils 60 - 70 % Eosinophils 1-4% Basophils 0.25 - 0.5 % Lymphocytes 25 - 33 % Monocytes 2-6%  Functions of white blood cells Phagocytic cells. First defenders Neutrophils against bacterial invasion. Count increases in acute bacterial infections Kill parasites and defend in allergic Eosinophils conditions. Count increases in allergy & parasitic infestations Act like mast cells. Synthesize and Basophils store histamine and heparin. May play role in allergic conditions B lymphocytes produce antibodies (humoral immunity) Lymphocytes T lymphocytes directly destroy the target cells (cellular immunity) Monocytes Highly phagocytic. Settle down in the tissues and become macrophages  Leucocytosis refers to excess of Leucocytes Like in Terms infections etc. related to white blood Leucopenia refers to a cells decrease in number of (leucocytes) leucocytes Leukemia is cancer of the blood and bone marrow  Neutrophilia: acute bacterial infection Basophilia: Allergy Conditions with increased white blood Eosinophilia: Parasitic infections cells and allergic reactions (Leucocytosis) Lymphocytosis: Chronic bacterial infection and acute viral infection Monocytes and macrophages: chronic bacterial infection.  It is the ability to resist organisms and toxins capable of damaging the body tissues. Immunity It is of two types: Innate Immunity Acquired immunity  It is “built in” ability to resist damaging organisms and toxins. Innate It is non specific and is present all the time – e.g skin, Immunity – Acid in stomach – tissue neutrophils and macrophages  Acquired Immunity It is “acquired” (developed) after the invasion (attack) by the organism. It is specific for the specific invading organism. Two types: Humoral: Mediated by antibodies produced by Plasma cells derived from B lymphocytes. Cellular: Mediated by T lymphocytes. THANK YOU  HEMOSTASIS (STOPPING THE BLEEDING)  This is a bleeding vessel How hemostasis (stoppage of bleeding) occurs? Steps involved in hemostasis Vascular Blood spasm clotting Formation of platelet plug  Hemostasis means stopping of bleeding (arrest of bleeding from a broken blood vessel) 3 main steps of hemostasis: Vascular spasm ( local vasoconstriction ) Formation of platelet plug Blood coagulation ( clotting ) Hemostasis  Vascular spasm Inherent response of Sympathetic induced vessel to injury vasoconstriction Opposite endothelial surfaces are pressed. They stick to each other & seal off the vessel This process slows blood flow and minimizes blood loss   Immediately after a blood vessel is cut or ruptured, the walls of the vessels contract; this instantaneously reduces the flow of blood from the vessel rupture.  Lasts for less than 1 minute  Contraction of the vessel walls result from:  nervous reflexes Step-1  factors released by platelets Vascular spasm  release of the vasoconstrictor serotonin. (Local Vasoconstriction)  Vascular spasm alone cannot arrest blood loss.  Formed from About Life span Fragments of 350,000/mm3 10 days Megakaryocytes in bone marrow Play essential Platelets Do not have role in nuclei hemostasis (Thrombocytes) Have Have high Removed organelles concentration from circulation that synthesize of actin and by tissue secretory myosin macrophages products  PLATELETS : Not true cells?? Platelets are fragments of Megakaryocytes 150,000- 350,000/mm3 Normal life span 7-10 days. About 1/3 are trapped in the spleen.  Platelet  Platelets attach ( adhere ) to exposed collagen aggregation fibers in sub-endothelial structure of damaged  vessels.  Platelets begin to swell and change shape Formation of  Platelets becomes sticky and attract additional the Platelet platelets, causes them to adhere to the originally activated platelets clump platelet plug. Plug This process is called aggregation of platelets.  Platelet plugs are temporary solution especially if the defect in the vessel is large.  Step-3 Blood clotting A triggered chain reaction involving clotting factors in the plasma results in blood coagulation Formation of a clot on top of the platelet plug supports it and seals off the break in the vessel Coagulation is the body’s most powerful hemostatic mechanism  Step-3: Blood Coagulation ( Clotting ) Transformation of blood from liquid into a solid gel. Clotting depends on a family of plasma proteins known as clotting factors. The clot on top of the platelet plug strengthens and supports the plug. The clotting factors are present in the blood in an inactive form, therefore blood is fluid.  Exposed collagen at the site of vessel injury simultaneously initiates platelet aggregation and clotting cascade The two hemostatic mechanisms positively reinforce each other as they seal the damaged vessel Summary of the clot formation using intrinsic & extrinsic pathways  FIBRIN FORMATION The ultimate step in clot formation Fibrinogen Thrombin Catalyst to convert Fibrinogen to FIBRIN Fibrin (clot) Fibrinogen is a large soluble plasma protein produced by liver and normally present in blood Fibrin is an insoluble thread like molecule  Vessel damage Exposed + collagen + Platelet Activation aggregation of factor XII + + Activation of next factor + Activation of thrombin + Formation Seal of Fibrin damaged vessel (clot) Normal clotting time 3 - 6 minutes (Capillary Tube Method) Normal bleeding time 5 - 10 minutes  Hemophilia Characterized by excessive bleeding due to deficiency of Thrombocytopenic factor VIII purpura Characterized by diffuse capillary hemorrhages visible as purple spots or blotches under skin due to deficiency of platelets Thrombocytopenia Condition where the number of circulating platelets is deficient Thrombocytopenic purpura Patients show small purple blotches on the skin due to spontaneous, widespread hemorrhage https://www.youtube.com/watch?v=x8TLTTyyPfI THANK YOU