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BISC 101 (292)
Lecture

Week 10 Circulation & Immunity

37 Pages
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Department
Biological Sciences
Course Code
BISC 101
Professor
Derek Bingham

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Description
BIOL 1103 – Week 10 Circulation III Resistance & Immunity Circulation III Circulation III  Origin and characteristics of formed elements (platelets and blood cells)  Platelets  Leucocytes  Erythrocytes  Mechanisms of haemostasis (reduction and prevention of blood loss) Resistance and Immunity I  General and specific resistance to disease organisms, including:  Non-specific resistance  Roles of leucocytes in resistance and immunity  Antigen- antibody interactions  ABO and Rh blood groups  Significance of blood types in transfusions  Maternal-foetal Rh incompatibilities 4 Objective 1: T ypes of Leukocytes SPECIFY THE TYPES OF LEUC(WHITE BLOOD CE)THEIR ORIGINS AND RELATIVE QUANTITIES IN .ORMAL BLOOD 5 Pluripotent  A developmental term which means that a particular stem cell (all stem cells are capable of differentiation (or specialization) can develop into one of an array of several advanced cell types. Compare Pluripotency with T otipotency Totipotent refers to a stem cell situation in which the stem cell can become ALL possible types of cells. Basophils and Eosinophils Basophils and eosinophils are easily identified on a microcoscope slide because of their distinctly coloured granules. Nevertheless, they are often difficult to find on a microscope slide blood smear because:  They are so small  The granules look like dirt  They break apart when they are spread  There are not many of them  They move too quickly 9 Numerous macrophages with large numbers of ingested zymosan particles visible in their cytoplasm 10 Mechanism of Macrophage Action  The macrophage’s cell membrane will emit extensions called pseudopods, which in turn encapsulate the foreign invader or particle or substance and bring the foreign agent into the macrophage’s cytoplasm. The entire foregoing process is the first part of a process known as phagocytosis.  Macrophages originate from monocytes. Mechanism of Macrophage Action (cont’d)  Once the foreign agent is within the confines of the macrophage’s cytoplasm, special enzymes will “attack” the foreign particle by literally breaking it down into its smallest components (digestion) after which the foreign agent can effectively be deemed as being destroyed and no longer capable of causing harm to the host. Objective 2: Platelets ORIGI, HARACTERISTI,ANDFUNCTION 13 Objective 3 ESCRIBE THE MAJOR FACTORS THAT STIMULATE THE BO.Y TO PRODUCE MORE ERYTHROCYTES AND LEUKOCYTES Erythrocyte Production  Low oxygen supply to tissues stimulates the production of more erythrocytes  Hormone erythropoietin from the kidney stimulates red bone marrow to produce more erythrocytes. Leukocyte Production  Acute infections – increase neutrophils  Chronic infections – increase monocytes  Viral infections – increase lymphocytes  Cancers (e.g. leukemia) – increase in immature leucocytes 14 Objective 4: T ests DESCRIBE THE PRO,THE INFORMATION ,AND THE NORMAL RANGE OF RESULTS FOR T.E FOLLOWING TESTS Haemoglobin (Hb): Differential Count:  Anaemia may be due to low amount  A count of leucocytes to determine of haemoglobin the relative proportions of each type.  Blood is haemolysed and the density  Normal ranges: of the red colour is compared to  Neutrophils - 60-70 % standards.  Lymphocytes – 20-25 %  Normal range is 12-18 gms/100 mls  Monocytes - 1-6 % of blood (equivalent to 12-18 % by  Eosinophils – 1-4 % weight)  Basophils - 0-1 % Hematocrit (Hct):  Anemia may be due to lack of red blood cells  Hematocrit test is what you did in the lab.  Normal pcv (packed cell volume) is 42-54% (men) and 38-46% (women) 15 Objective 5: Hemostasis Define and describe vascular spasm, platelet plug formation, and blood clotting Vascular Spasm  Contraction of smooth muscle in the walls of a cut blood vessel to reduce blood flow and blood loss.  Effective for up to 30 minutes (in some situations - a few hours)  Helps until other longer term mechanisms have an effect Platelet Plug Formation  Platelets stick to damaged vessel walls.  Platelets change. They swell and extend projections and become sticky . They also release various chemicals that cause vascular spasms and make other platelets sticky.  Platelet plug forms Blood Clotting 1. Formation of prothrombinase (in biology , the suffix “ase” almost always indicates that one is dealing with an ENZYME (as opposed to “ose” which indicates a CARBOHYDRA TE)). 2. Conversion of prothrombin to thrombin (“pro” = precursor molecule) 3. Conversion of fibrinogen to fibrin Extrinsic Pathway Intrinsic Pathway Damaged cells outside blood Damage to blood vessel lining vessels Exposed collagen fibres activate Tissue protein leaks into blood platelets Form platelet plug Causes prothrombinase production ++ + Ca Active prothrombinase Prothrombin Thrombin ++ + Ca Thrombin (active) Fibrinogen FIBRIN (threads of the clot) 20 21 Objective 6: Hemostasis Disorders Thrombus  Blood clot in an uninjured vessel Embolus  Blood clot or other material that is flowing freely in a blood vessel.  e.g., air bubbles, globules of fat, blood clot Hemophilia  An inherited deficiency in the ability to form blood clots.  Due to a deficiency in the ability to produce specific clotting factors.  Most common is haemophila A due to deficiency of factor 22 Objective 7: Blood Clotting DESCRIBE HOW THE PROCESS OF BLOOD CLOTTI…G IS REGULATED IN RESPECT TO Prevention of Blood Clotting: Localization of Blood Clotting  Anticoagulants (chemical  Clotting factors are rapidly inhibitors of blood clotting) diluted in fast flowi
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