Blood Physiology and Mechanism of Blood Clotting Medical Presentation

Blood Physiology PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Download Free Blood Physiology medical powerpoint (ppt) presentation for your medical ppt presentation

Tags : Blood

Published on : Jun 17, 2018 | Views : 6774 | Downloads : 65

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Blood Physiology and Mechanism of Blood Clotting Presented by :- Dr. Neha Singh 2nd yr P.G.
Slide 2-

Contents Introduction. Blood functions. Haematopoiesis. Blood cells and their functions. Haemostasis. Blood Groups. Haemolytic Diseases of the newborn.
Slide 3-

Objective Describe the formed elements of blood, their physiology and functions. Describe Hemoglobin. Describe events in Haemostasis. Classify blood groups.
Slide 4-

Introduction Blood makes up about 7-8% of body weight.
Slide 5-

Blood Functions Transportation. Regulation. Protection.
Slide 6-

Bone Marrow Stem cells ------ Non-lymphoid stem cells Lymphoid stem cells. Non-lymphoid stem cells --- circulating erythrocytes, granulocytes, monocytes and platelets. Lymphoid stem cells --- undergo differentiation.
Slide 7-

ppt slide no 7 content not found
Slide 8-

HAEMATOPOIESIS In the human embryo, the yolk sac is the main site of haematopoiesis in the first few weeks of gestation. By about 3rd month, however, the liver and spleen are the main sites of blood cell formation and continue to do so until about 2 weeks after birth. Haematopoiesis commences in the bone marrow by 4th and 5th month and becomes fully active by 7th and 8th month so that at birth practically all the bones contain active marrow.
Slide 9-

In childhood, red marrow is progressively replaced by fat (yellow marrow), so that in adults normal haematopoiesis is restricted to the central skeleton (vertebrae, pelvis, sternum, ribs, clavicles, skull, upper humeri and proximal femora). However, red marrow can expand in response to increased demands for blood cells. The spleen and liver can also resume their foetal haematopoietic role in certain pathologic conditions and is called extramedullary haematopoiesis.
Slide 10-

ppt slide no 10 content not found
Slide 11-

Blood Cells and their Function Circulating blood normally contains 3 main types of mature cells—the Red cells (erythrocytes), the White cells (leucocytes) and the Platelets (thrombocytes). These blood cells perform their respective physiologic functions.
Slide 12-

The lifespan of these cells in circulating blood is variable. The rates of production of these blood cells are normally regulated in healthy individuals in such a way so as to match the rate at which they are lost from circulation. Their concentration is normally maintained within well-defined limits unless the balance is disturbed due to some pathologic processes.
Slide 13-

Red Cells Red cell precursors formed in the bone marrow from the erythroid (CFU–E) progenitor cells are called erythroblasts or normoblasts.
Slide 14-

Erythroblasts divide and acquire hemoglobin which turns the cytoplasm pink; the nucleus condenses and is extruded from the cell. The first non-nucleated red cell is a reticulocyte which still contains ribosomal material in the cytoplasm, giving these large cells a faint blue tinge (‘polychromasia’).
Slide 15-

Mature red cells circulate for about 120 days. They are 8 μm biconcave discs lacking a nucleus but filled with Hb, which delivers oxygen to the tissues from the lungs. In order to pass through the smallest capillaries the red cell membrane is adapted to be deformable, with a lipid bilayer to which a ‘skeleton’ of filamentous proteins is attached via special linkage proteins. Inherited abnormalities of any of these proteins result in loss of membrane as cells pass through the spleen, and formation of abnormally shaped red cells called spherocytes or elliptocytes.
Slide 16-

The red blood cells have other functions besides transport of hemoglobin. For instance, they contain a large quantity of carbonic anhydrase, an enzyme that catalyzes the reversible reaction between carbon dioxide (CO2) and water to form carbonic acid (H2CO3), increasing the rate of this reaction several thousand fold.
Slide 17-

NORMAL VALUES AND RED CELL INDICES
Slide 18-

Regulation of RBC Production—Role of Erythropoietin
Slide 19-

Hemoglobin
Slide 20-

Normal hemoglobin values at different ages At birth : 25 gm% After 3rd month : 20gm% After 1 year : 17gm% In adult males : 14-16gm% In adult females : 12-15gm%
Slide 21-

RED CELL DESTRUCTION Red cells at the end of their lifespan of approximately 120 days are phagocytosed by the reticulo-endothelial system. Amino acids from globin chains are recycled and iron is removed from haem for reuse in hemoglobin synthesis. The remnant haem structure is degraded to bilirubin and conjugated with glucuronic acid before being excreted in bile. In the small bowel, bilirubin is converted to stercobilin; most of this is excreted, but a small amount is reabsorbed and excreted by the kidney as urobilinogen.
Slide 22-

ppt slide no 22 content not found
Slide 23-

ppt slide no 23 content not found
Slide 24-

Leukocytes (White Blood Cells) The leukocytes, also called white blood cells, are the mobile units of the body’s protective system. After formation, they are transported in the blood to different parts of the body where they are needed. 5 types of white blood cells are normally present in the blood. The lymphocytes function is mainly in connection with the immune system.
Slide 25-

Neutrophils Neutrophils, the most common WBC in the blood of adults, are 10–14 μm in diameter with a multilobular nucleus containing 2–5 segments and granules in their cytoplasm. Their main function is to recognise, ingest and destroy foreign particles and microorganisms. A large storage pool of mature neutrophils exists in the bone marrow. Factors such as exercise or catecholamines increase the number of cells flowing in the blood.
Slide 26-

Neutrophils spend 6–10 hours in the circulation before being removed, principally by the spleen. Alternatively, they pass into the tissues and either are consumed in the inflammatory process or undergo apoptotic cell death and phagocytosis by macrophages.
Slide 27-

Eosinophils Eosinophils represent 1–6% of the circulating white cells. They are a similar size to neutrophils but have a bilobed nucleus and prominent orange granules. Eosinophils are phagocytic and their granules contain a peroxidase capable of generating reactive oxygen species and proteins involved in the intracellular killing of protozoa and helminths. They are also involved in allergic reactions.
Slide 28-

Basophils These cells are less common than eosinophils, representing less than 1% of circulating white cells. They contain dense black granules which obscure the nucleus. Mast cells resemble basophils but are only found in the tissues. These cells are involved in hypersensitivity reactions.
Slide 29-

Monocytes Monocytes are the largest of the white cells, with a diameter of 12–20 μm and an irregular nucleus in abundant pale blue cytoplasm containing occasional cytoplasmic vacuoles. These cells circulate for a few hours and then migrate into the tissue where they become macrophages and Kupffer cells. The former phagocytose debris, apoptotic cells and microorganisms.
Slide 30-

Lymphocytes Lymphocytes are derived from pluripotent haematopoietic stem cells in the bone marrow. There are two main types: T cells and B cells. The majority of lymphocytes (approximately 80%) in the circulation are T cells. Lymphocytes are heterogeneous, the smallest cells being the size of red cells and the largest being the size of neutrophils.
Slide 31-

Small lymphocytes are circular with scanty cytoplasm but the larger cells are more irregular with abundant blue cytoplasm. Lymphocyte subpopulations can be defined with specific functions and their lifespan can vary from a few days to many years.
Slide 32-

PLASMA The fluid portion of the blood, the plasma, is a remarkable solution containing an immense number of ions, inorganic molecules, and organic molecules that are in transit to various parts of the body or aid in the transport of other substances. Plasma = Whole Blood – formed elements (Plasma is the liquid portion of the blood). The plasma proteins consist of albumin, globulin, and fibrinogen fractions.
Slide 33-

Plasma Protein and their Functions
Slide 34-

Physiologic Variation : Pregnancy :  in albumin,  in globulin,  in fibrinogen. Pathologic Variation : Increase plasma proteins – Dehydration. Hemorrhage -  in plasma proteins. Burns - Loss of plasma proteins.  albumin - Malnutrition, liver and kidney diseases.  globulin - Tuberculosis, carcinoma, leukemia and infection.
Slide 35-

Platelets Platelets are formed in the bone marrow from megakaryocytes. Megakaryocytic stem cells (CFU–Meg) divide to form megakaryoblasts, which undergo a process called ‘endomitotic reduplication’. This creates mature megakaryocytes, large cells with several nuclei and cytoplasm containing platelet granules.
Slide 36-

Up to 3000 platelets then fragment off from each megakaryocyte into the circulation in the marrow sinusoids. The formation and maturation of megakaryocytes are stimulated by thrombopoietin produced in the liver. Platelets circulate for 8–10 days before they are destroyed in the reticulo-endothelial system. Some 30% of peripheral platelets are normally pooled in the spleen and do not circulate.
Slide 37-

Under normal conditions platelets are discoid, with a diameter of 2–4 μm.
Slide 38-

Haemostasis Blood must be maintained in a fluid state in order to function as a transport system, but must be able to solidify to form a clot following vascular injury to prevent excessive bleeding, a process known as haemostasis. Successful haemostasis is localised to the area of tissue damage and is followed by removal of the clot and tissue repair. This is achieved by complex interactions between the vascular endothelium, platelets, coagulation factors, natural anticoagulants and fibrinolytic enzymes.
Slide 39-

Dysfunction of any of these components may result in haemorrhage or thrombosis.
Slide 40-

Clotting factors The coagulation system consists of a cascade of soluble inactive zymogen proteins designated by Roman numerals. When proteolytically cleaved and activated, each is capable of activating one or more components of the cascade. Clotting factors are synthesized by the liver, although factor V is also produced by platelets and endothelial cells. Factors II, VII, IX and X require post-translational carboxylation to allow them to participate in coagulation.
Slide 41-

ppt slide no 41 content not found
Slide 42-

Coagulation occurs by two pathways; it is initiated by the extrinsic pathway and amplified by the intrinsic pathway.
Slide 43-

Initiation of Coagulation : Formation of Prothrombin Activator Prothrombin activator is generally considered to be formed in two ways, although, in reality, the two ways interact constantly with each other: by the extrinsic pathway that begins with trauma to the vascular wall and surrounding tissues. by the intrinsic pathway that begins in the blood itself.
Slide 44-

ppt slide no 44 content not found
Slide 45-

The stages of Haemostasis. Stage 1 Pre-injury conditions encourage flow The vascular endothelium produces substances (including nitric oxide, prostacyclin and heparans) to prevent adhesion of platelets and white cells to the vessel wall. Platelets and coagulation factors circulate in a non-activated state.
Slide 46-

Stage 2 Early haemostatic response: platelets adhere; coagulation is activated. At the site of injury the endothelium is breached, exposing subendothelial collagen. Small amounts of tissue factor (TF) are released. Platelets bind to collagen via a specific receptor, glycoprotein Ia (GPIa), causing a change in platelet shape and its adhesion to the area of damage by the binding of other receptors (GPIb and GPIIb/IIIa) to von Willebrand factor and fibrinogen respectively. Coagulation is activated by the tissue factor (extrinsic) pathway, generating small amounts of thrombin.
Slide 47-

Stage 3 Fibrin clot formation: platelets become activated and aggregate; fibrin formation is supported by the platelet membrane; stable fibrin clot forms. The adherent platelets are activated by many pathways, including binding of ADP, collagen, thrombin and adrenaline (epinephrine) to surface receptors. The cyclo-oxygenase pathway converts arachidonic acid from the platelet membrane into thromboxane A2, which causes aggregation of platelets. Activation of the platelets results in release of the platelet granule contents, enhancing coagulation further.
Slide 48-

Thrombin plays a key role in the control of coagulation: the small amount generated via the TF pathway massively amplifies its own production; the ‘intrinsic’ pathway becomes activated and large amounts of thrombin are generated. Thrombin enhances clot formation by cleaving fibrinogen to produce fibrin. Fibrin monomers are cross-linked by factor XIII, which is also activated by thrombin.
Slide 49-

Having had a key role in clot formation and stabilisation, thrombin then starts to regulate clot formation in two main ways: (a) activation of the protein C (PC) pathway (a natural anticoagulant), which reduces further coagulation; (b)activation of thrombin-activatable fibrinolysis inhibitor (TAFI), which inhibits fibrinolysis.
Slide 50-

Stage 4 Limiting clot formation: natural anticoagulants reverse activation of coagulation factors. Once haemostasis has been secured, the propagation of clot is curtailed by anticoagulants. Antithrombin is a serine protease inhibitor synthesised by the liver, which destroys activated factors such as XIa, Xa and thrombin (IIa). Its major activity against thrombin and Xa is enhanced by heparin, explaining its anticoagulant effect.
Slide 51-

Tissue factor pathway inhibitor (TFPI) binds to and inactivates VIIa and Xa. Activation of PC occurs following binding of thrombin to membrane-bound thrombomodulin; activated protein C (aPC) binds to its co-factor protein S (PS), and cleaves Va and VIIIa. PC and PS are vitamin K dependent and are depleted by coumarin anticoagulants such as warfarin.
Slide 52-

Stage 5 Fibrinolysis: plasmin degrades fibrin to allow vessel recanalisation and tissue repair. The insoluble clot needs to be broken down for vessel recanalisation. Plasmin, the main fibrinolytic enzyme, is produced when plasminogen is activated, e.g. by tissue plasminogen activator (t-PA) or urokinase in the clot. Plasmin hydrolyses the fibrin clot, producing fibrin degradation products.
Slide 53-

This process is highly regulated; the plasminogen activators are controlled by an inhibitor called plasminogen activator inhibitor (PAI), the activity of plasmin is inhibited by α2-antiplasmin and α2-macroglobulin, and fibrinolysis is further inhibited by the thrombin-activated TAFI.
Slide 54-

Blood Groups 2 particular types of antigens are much more likely than the others to cause blood transfusion reactions. They are the O-A-B system of antigens and the Rh systems.
Slide 55-

Blood Types with Their Genotypes and Their Constituent Agglutinogens and Agglutinins
Slide 56-

Titer of the Agglutinins at Different Ages Immediately after birth, the quantity of agglutinins in the plasma is almost zero. Two to 8 months after birth, an infant begins to produce agglutinins—anti-A agglutinins when type A agglutinogens are not present in the cells, and anti-B agglutinins when type B agglutinogens are not in the cells. A maximum titer is usually reached at 8 to 10 years of age, and this gradually declines throughout the remaining years of life.
Slide 57-

The Rh Group It is a system composed primarily of the C, D, and E antigens. Unlike the ABO antigens, the system has not been detected in tissues other than red cells. D is by far the most antigenic component, and the term Rh-positive as it is generally used means that the individual has agglutinogen D. The Rh-negative individual has no D antigen and forms the anti-D agglutinin when injected with D-positive cells. The Rh typing serum used in routine blood typing is anti-D serum.
Slide 58-

Haemolytic Disease of the Newborn Another complication due to Rh incompatibility arises when an Rh-negative mother carries an Rh-positive fetus. Small amounts of fetal blood leak into the maternal circulation at the time of delivery, and some mothers develop significant titers of anti-Rh agglutinins during the postpartum period. During the next pregnancy, the mother’s agglutinins cross the placenta to the fetus. In addition, there are some cases of fetal–maternal hemorrhage during pregnancy, and sensitization can occur during pregnancy.
Slide 59-

In any case, when anti-Rh agglutinins cross the placenta to an Rh-positive fetus, they can cause hemolysis and various forms of hemolytic disease of the newborn (erythroblastosis fetalis). If hemolysis in the fetus is severe, the infant may die in utero or may develop anemia, severe jaundice, and edema (hydrops fetalis).
Slide 60-

Because sensitization of Rh-negative mothers by carrying an Rh-positive fetus generally occurs at birth, the first child is usually normal. However, hemolytic disease occurs in about 17% of the Rh-positive fetuses born to Rh-negative mothers who have previously been pregnant one or more times with Rh-positive fetuses. Fortunately, it is usually possible to prevent sensitization from occurring the first time by administering a single dose of anti-Rh antibodies in the form of Rh immune globulin during the postpartum period. Such passive immunization does not harm the mother and has been demonstrated to prevent active antibody formation by the mother
Slide 61-

Kernicterus, a neurologic syndrome in which unconjugated bilirubin is deposited in the basal ganglia, may also develop, especially if birth is complicated by a period of hypoxia. Bilirubin rarely penetrates the brain in adults, but it does in infants with erythroblastosis, possibly in part because the blood–brain barrier is more permeable in infancy. However, the main reasons that the concentration of unconjugated bilirubin is very high in this condition are that production is increased and the bilirubin - conjugating system is not yet mature.
Slide 62-

References Davidson’s Principles and Practice of Medicine : 21st Edition. Guyton & Hall; Textbook of Medical Physiology. Harsh Mohan; Textbook of Pathology : 6th Edition.
Slide 63-

ppt slide no 63 content not found