6. blood

Page 1: Blood Cell Types

• Leukocyte: White blood cells, crucial for immune defense.

• Erythrocyte: Red blood cells, responsible for oxygen transport.

• Platelet: Cell fragments essential for blood clotting.

Page 2: Functions of Blood and Interstitial Fluid

• Blood Composition: Composed of plasma and various blood cells.

• Transport: Nutrients and wastes are transported by blood; interstitial fluid bathes the cells.

• Diffusion: Nutrients and oxygen diffuse from blood to interstitial fluid and into cells, while wastes move in reverse.

• Hematology: The study of blood and its disorders.

Page 3: Functions of Blood

• Transportation: Carries O2, CO2, metabolic wastes, nutrients, heat, and hormones.

• Regulation:

  • pH maintenance through buffers.

  • Body temperature regulation via coolant properties of water and vasodilation.

  • Water content of cells regulated by interaction of dissolved ions and proteins.

• Protection: Shielding the body from disease and minimizing blood loss.

Page 4: Properties of Blood

• Volume: Adults have 4-6 L of blood.

• Components: Plasma (clear extracellular fluid) and formed elements (blood cells and platelets).

• Viscosity: Blood is thicker than water, flows slowly.

• Temperature: Approximately 100.4°F.

• pH: Normal is 7.4 (range: 7.35-7.45).

• Body Weight: Comprises 8% of total body weight.

• Blood volume: Average male has 5-6 L; female has 4-5 L. Hormonal feedback maintains blood volume and osmotic pressure.

• Fluid Balance: High molarity causes fluid absorption and high blood pressure; low molarity causes edema, potentially due to plasma protein deficiency.

Page 5: Techniques of Blood Sampling

• Venipuncture: Sampling from a vein using a needle and syringe, typically the median cubital vein because it has less pressure and is closer to the surface.

• ABG: Arterial Blood Gas sampling, involves measuring blood gas content.

• Finger or Heel Stick: Used primarily for diabetics or infants to monitor blood sugar.

Page 6: Components of Blood

• Hematocrit Levels:

  • Plasma: 55%

  • Cells: 45% (predominantly RBCs, followed by WBCs and platelets).

  • RBCs: 99% of cells, < 1% WBCs and platelets.

Page 7: Plasma and Plasma Proteins

• Composition: Plasma is composed mainly of water (>90%), proteins (7%), enzymes, and other substances.

• Serum: Remaining fluid post-clotting.

• Major Plasma Proteins:

  • Albumins: Most abundant, maintain viscosity and osmolarity, influencing blood pressure and fluid balance.

  • Globulins: Including antibodies for immune defense.

  • Fibrinogen: Precursor to fibrin for blood clot formation.

• Synthesis: Most plasma proteins produced by the liver, except gamma globulins from B lymphocytes.

Page 8: Nonprotein Components of Plasma

• Nitrogenous Compounds: Includes amino acids, urea, uric acid, and creatinine removed by kidneys.

• Nutrients: Such as glucose, vitamins, and minerals.

• Gases: Some O2 and CO2 are transported in plasma.

• Electrolytes: Sodium predominates among plasma cations, crucial for blood osmolarity.

Page 9: Formed Elements of Blood

• Types of Blood Cells:

  • Erythrocytes: Red blood cells.

  • Leukocytes: White blood cells (WBCs), classified as granular (neutrophils, eosinophils, basophils) or agranular (lymphocytes, monocytes).

  • Platelets: Fragments essential for clotting.

Page 10: Hematocrit

• Hematocrit Levels:

  • Female Normal Range: 38 - 46% (average 42%).

  • Male Normal Range: 40 - 54% (average 46%).

• Conditions:

  • Anemia: Not enough RBCs or hemoglobin.

  • Polycythemia: Too many RBCs (hematocrit over 65%), which can arise from dehydration or blood doping.

Page 11: Blood Doping

• Definition: Injection of stored RBCs before athletic events to enhance oxygen delivery to tissues.

• Risks: Increases blood viscosity, requiring the heart to work harder.

• Regulation: Banned by the Olympic Committee.

Page 12: Blood Cell Production (Hematopoiesis)

• Replacement: Blood cells require continual production due to limited lifespan.

• Hematopoietic Tissues: Stem cells in yolk sac, liver, spleen, thymus, and bone marrow.

• Post-Birth: Liver stops producing blood cells; spleen and thymus continue producing WBCs.

• Red Bone Marrow: Main site for producing RBCs, WBCs, and platelets from pluripotent stem cells (hemocytoblasts).

• Signaling: Stimulation by erythropoietin for RBCs, thrombopoietin for platelets, and CSFs for WBCs.

Page 13: Hematopoiesis Continued

• Differentiation: Stem cells (hemocytoblasts) develop through committed cells to precursor cells leading to formed elements in blood circulation.

Page 14: Stages of Blood Cell Formation

• Stem Cell Differentiation: Pluripotent stem cells (0.1% of red marrow cells) differentiate into myeloid or lymphoid stem cells leading to specific blood cell types.

• Myeloid Line Development: Includes progenitor and blast cells which progressively differentiate into mature cell types; specialized progenitor cells for red blood cells.

Page 15: Hematopoietic Growth Factors

• Roles: Regulate differentiation and proliferation of blood cells.

• Key Factors:

  • Erythropoietin (EPO): Increases RBC production.

  • Thrombopoietin (TPO): Stimulates platelet formation.

  • Cytokines: Local hormones produced by leukocytes that promote WBC proliferation.

Page 16: Medical Uses of Growth Factors

• Recombinant Products: Used in treating decreased RBC production, especially in kidney disease or during chemotherapy for stimulating WBC formation.

Page 17: Erythrocytes (RBCs)

• Production Rate: 2 million RBCs enter circulation per second.

• Structure: Disc-shaped, thick rim, enhances gas transport.

• Functions:

  • Major function is gas transport (O2 delivery and CO2 removal).

  • Cytoplasm mainly consists of hemoglobin (33%).

  • Enzyme carbonic anhydrase aids pH balance and gas exchange.

Page 18: Erythrocyte Production

• Erythropoiesis: Produces red blood cells from stem cells, involving several developmental stages.

• Key Stages: Includes proerythroblast, erythroblast, normoblast, and reticulocyte, which develops after nucleus discarding.

Page 19: Normal Reticulocyte Count

• Count Range: Should be between 0.5-1.5% of circulating RBCs.

• Diagnostic Implications:

  • Low count may indicate bone marrow issues or nutritional deficiencies.

  • High count may suggest recent blood loss.

Page 20: Erythrocyte Homeostasis

• Feedback Mechanism: A drop in RBC count causes hypoxemia, stimulating EPO production and subsequent stimulation of bone marrow.

• Common Stimuli: Low atmospheric O2, intense exercise, or significant blood loss.

Page 21: RBC Life Cycle

• Lifespan: Approximately 120 days; worn-out cells are removed by macrophages in the spleen and liver.

• Recycling: Breakdown products are recycled to manufacture new blood cells.

Page 22: Nutritional Needs for Erythropoiesis

• Iron: Crucial for hemoglobin synthesis, with recommended daily intake higher than loss rates due to absorption.

• Other Vitamins: B12 and folic acid for cell division; C and copper for enzyme function in RBC synthesis.

Page 23: Recycling of Hemoglobin Components

• Breakdown: In macrophages, globin is recycled to amino acids, and heme is divided into iron and biliverdin.

Page 24: Fate of Components of Heme

• Iron Transportation: Attached to transferrin, stored as ferritin or hemosiderin.

• Bilirubin: Secreted into bile, eventually converted by bacteria in the intestine, processed for excretion.

Page 25: Hemoglobin Structure

• Composition: Four protein chains with heme groups that bind oxygen; fetal hemoglobin has different chain components.

Page 26: Transport of Gases

• O2 and CO2 Transport: Hemoglobin carries oxygen to tissues, regulates CO2 removal, and aids in nitric oxide transportation for blood pressure regulation.

Page 27: Erythrocytes and Hemoglobin

• Indicators: RBC count and hemoglobin concentration determine oxygen-carrying capacity.

  • Hematocrit: 42-52% for men, 37-48% for women; hemoglobin levels: men 13-18 g/dL, women 12-16 g/dL.

Page 28: Erythrocyte Disorders

• Polycythemia: Excess RBCs due to various causes, dangerous for circulatory health.

• Anemia: Defined by insufficient RBCs or hemoglobin affecting oxygen delivery.

Page 29: Anemia - Deficiency of RBCs or Hb

• Causes of Anemia: Vary from dietary deficiencies to genetic disorders affecting RBC production.

• Symptoms: Reduced oxygen capacity leads to fatigue, cold intolerance, and lethargy.

Page 30: Sickle-cell Anemia (SCA)

• Genetic Mutation: Altered hemoglobin leads to distorted RBC shapes, causing rupturing and clumping, prevalent in malaria-prone areas due to a heterozygote advantage.

Page 31: Sickle-Cell Diseased Erythrocyte

• Appearance: Distorted sickle shape versus normal RBCs, characteristic of SCA.

Page 32: WBC Anatomy and Types

• Leukocyte Overview: Nucleated cells lacking hemoglobin, classified into two main groups based on granules.

Page 33: Leukocyte Production (Leukopoiesis)

• Cell Development: Committed progenitor cells develop in response to stimuli; WBCs have varying lifespans and are largely maintained outside of blood circulation.

Page 34: Neutrophils (Granulocyte)

• Characteristics: Most abundant WBC type, with segmented nuclei and fine granules, increasing in numbers during infections.

Page 35: Eosinophils (Granulocyte)

• Structure: Bi-lobed nucleus with distinct orange-red staining granules.

• Function: Primarily involved in combating parasitic infections.

Page 36: Basophils (Granulocyte)

• Features: Large granules obscuring nuclei, least common type; involved in inflammatory responses and allergic reactions.

Page 37: Lymphocyte (Agranulocyte)

• Types: Includes B, T, and natural killer cells, with roles in adaptive immunity and increased activity during infections.

Page 38: Monocyte (Agranulocyte)

• Largest WBC Type: Unique kidney-shaped nucleus; develops into macrophages, engaging in tissue repair and pathogen destruction.

Page 39: WBC Physiology

• Count: WBCs are less numerous than RBCs; their fluctuation indicates health status (leukocytosis vs leukopenia).

Page 40: Emigration & Phagocytosis in WBCs

• Process: WBCs migrate to injury sites via a series of adherence and movement steps, engaging in phagocytosis to eliminate debris and pathogens.

Page 41: Neutrophil Function

• Response to Bacteria: Fastest acting WBC, utilizing enzymes and oxidants for bacterial destruction, elevated during infections.

Page 42: Monocyte Function

• Defense Role: Slower to respond but effective in clearing infections through differentiation into macrophages.

Page 43: Basophil Function

• Inflammatory Response: Play roles in allergic reactions, releasing vasodilators to enhance inflammation.

Page 44: Eosinophil Function

• Parasite and Allergy Defense: Leave blood circulation to combat infections, contributing to inflammatory responses.

Page 45: Lymphocyte Functions

• Adaptive Immunity: B cells produce antibodies; T cells target infected or cancerous cells; natural killer cells destroy diverse pathogens.

Page 46: Differential WBC Count

• Importance: Assesses relative proportions of WBC types to diagnose infections, leukemias, and allergies.

Page 47: Abnormalities of Leukocyte Count

• Leukopenia and Leukocytosis: Risks associated with low or high WBC counts, indicating underlying health issues.

Page 48: Normal and Leukemia Blood

• Visualization: Smears showing varying WBC and platelet counts in normal versus leukemic conditions.

Page 49: Bone Marrow Transplant

• Procedure: Transfer of healthy marrow post-destruction of diseased marrow, crucial for conditions like leukemia.

Page 50: Platelet (Thrombocyte) Anatomy

• Description: Small disc-shaped fragments aiding clot formation, with normal counts between 150,000-400,000 per drop of blood.

Page 51: Platelet Production (Thrombopoiesis)

• Process: Derived from megakaryocytes, which replicate their DNA before fragmenting into platelets released into circulation.

Page 52: Megakaryocytes & Platelets

• Structural Relation: Connection between red and white blood cells and their progenitors, the megakaryocytes responsible for platelet formation.

Page 53: Platelets Description and Function

• Roles: Key functions include secreting growth factors, forming temporary plugs, and supporting immune responses.

Page 54: Hemostasis

• Definition: Mechanisms to stop bleeding when blood vessels are injured; involves vascular spasm, platelet plug formation, and coagulation.

Page 55: Vascular Spasm

• Initial Response: Sudden constriction of blood vessels to minimize blood flow and initiate the healing process.

Page 56: Platelet Plug Formation

• Steps: Platelets adhere to damaged sites, releasing chemicals necessary for aggregation and healing.

Page 57: Platelet Plug Formation Continued

• Positive Feedback Loop: Activated platelets amplify their response, ensuring site is sealed effectively.

Page 58: Platelet Adhesion

• Mechanism: Platelets adhere to exposed collagen in damaged vessel walls to begin clot formation.

Page 59: Platelet Release Reaction

• Activation: Platelets extend projections, activate more platelets, and release key vasoconstrictors.

Page 60: Platelet Aggregation

• Plug Formation: Activated platelets aggregate to form a stable mass, reinforced by fibrin threads from the clotting cascade.

Page 61: Coagulation Process

• Clot Formation: Blood thickens into a gel, separating into serum and fibrin clot; crucial for hemostasis.

Page 62: Coagulation Cascade

• Mechanism: Clotting factors activate one another sequentially to form fibrin threads essential for clot stability.

Page 63: Overview of the Clotting Cascade

• Common Pathway: Both intrinsic and extrinsic paths lead to the activation of prothrombinase, crucial for effective clotting.

Page 64: Extrinsic Pathway

• Rapid Activation: Tissue injury rapidly initiates clotting through the release of tissue factors into the bloodstream.

Page 65: Intrinsic Pathway

• Delayed Activation: Requires several minutes and involves interactions within the blood itself and damaged vascular endothelium.

Page 66: Final Common Pathway

• Thrombin Action: Thrombin converts fibrinogen to fibrin, facilitating stable clot formation.

Page 67: Enzyme Amplification in Clotting

• Efficiency: Each activated enzyme generates many more enzymes, accelerating the clotting response.

Page 68: Role of Vitamin K in Clotting

• Essential Nutrient: Vitamin K is necessary for synthesizing several key clotting factors, ensuring proper hemostasis.

Page 69: The Fate of Blood Clots

• Clot Retraction: Stabilizes the clot and brings edges of vessels closer to facilitate repair; involves factors released from platelets.

Page 70: Blood Clot Dissolution

• Fibrinolysis: Dissolution of clots involves the activation of plasminogen leading to breakdown of fibrin threads.

Page 71: Hemostatic Control Mechanisms

• Regulation: Fibrinolytic mechanisms ensure that clots remain localized; natural anticoagulants regulate clotting factors.

Page 72: Intravascular Clotting

• Thrombosis: Unbroken vessel clotting poses risks, potentially leading to embolisms and associated complications.

Page 73: Anticoagulants and Thrombolytic Agents

• Medicinal Interventions: Agents to prevent clots or dissolve them, like heparin, warfarin, and other thrombolytics offer vital therapeutic options.

Page 74: Medicinal Leeches

• Use in Medicine: Leeches can be applied therapeutically for clot removal in specific medical scenarios.

Page 75: Hemophilia

• Genetic Disorders: Inability to produce specific clotting factors results in bleeding disorders, potentially severe without medical intervention.

Page 76: Blood Types

• RBC Antigens: Surface antigens dictate blood type; mismatch during transfusions can trigger severe reactions.

Page 77: The ABO Group

• Types: A, B, AB, and O blood types are defined by the presence or absence of A/B antigens and corresponding antibodies in plasma.

Page 78: Landsteiner’s Rule

• Antibody Presence Rule: Individuals will have antibodies against the antigens not present on their own RBCs.

Page 79: Agglutination of Erythrocytes

• Visual Mechanism: Antibodies trigger clumping of RBCs, crucial for identifying mismatches in transfusions.

Page 80: Mismatched Transfusion Reaction

• Consequences: Agglutinated RBCs can block vessels, leading to severe complications like tissue damage and shock.

Page 81: The Rh Group

• Blood Typing: Similar process to ABO but with separate risks associated with Rh factor in pregnancy and transfusions.

Page 82: Hemolytic Disease of Newborn

• Pathological Consequence: Fetal-maternal blood mixing leads to severe anemia in subsequent pregnancies if untreated.

Page 83: Transfusion and Transfusion Reactions

• Risks of Incompatibility: Reactions from mismatched RBC transfusions can be life-threatening and are taken seriously in clinical settings.

Page 84: Universal Donors and Recipients

• Implications: Type O- blood can theoretically be given universally, while type AB+ is the universal recipient but requires cross-matching for safety.

Page 85: Anemia - Not Enough RBCs

• Symptoms: Fatigue, pallor, and cold intolerance result from inadequate oxygen transport; various types affect different mechanisms.

Page 86: Disseminated Intravascular Coagulation (DIC)

• Complex Disorder: DIC causes simultaneous clotting and bleeding, often leading to organ failure due to severe resource depletion.

Page 87: Leukemia

• Types: Acute and chronic leukemias affect blood cell production and can be categorized by the type of cell affected, leading to severe health consequences.