Blood and Hemostasis

Essentials of Human Anatomy and Physiology: Blood

10.1 Anemia in Advanced Kidney Disease

  • Cause of Anemia in Kidney Disease:

    • Many individuals with advanced kidney disease experience anemia.

    • This can be attributed to an imbalance affecting the O₂-carrying ability of blood, manifesting as low blood O₂ levels due to:

    • Decreased Red Blood Cell (RBC) count.

    • Decreased amount of hemoglobin.

    • Decreased availability of O₂.

  • Erythropoiesis Mechanism:

    1. Stimulus for Erythropoiesis: Low blood O₂-carrying ability triggers a response.

    2. Erythropoietin Release:

    • Kidneys (and to a lesser extent, the liver) release erythropoietin to stimulate RBC production in red bone marrow.

    1. Enhanced Erythropoiesis: Results in an increased RBC count, enhancing the blood's O₂-carrying capacity.

10.1.1 Formation of White Blood Cells and Platelets

  • Stimulation of Blood Cell Formation:

    • The process is also hormone-driven, with specific factors involved:

      • Colony Stimulating Factors (CSFs): Stimulate production of leukocytes (white blood cells).

      • Interleukins: Enhance the capability of mature leukocytes for body protection.

  • Trigger Mechanism: These hormones respond to specific chemical signals from the environment (inflammatory chemicals, certain bacteria/toxins).

  • Thrombopoietin:

    • A hormone produced by the liver that accelerates the production of platelets from megakaryocytes, although specifics of regulation are largely unknown.

  • Bone Marrow Biopsy Procedure:

    • If bone marrow abnormalities or diseases (e.g., leukemia) are suspected, a needle is used to extract a small marrow sample from flat bones (iliac crest or sternum) for microscopic examination.

Questions to Consider:

  1. What is the name of the stem cell that gives rise to all formed elements?

  2. What property of RBCs limits their life span to about 120 days?

  3. How does the production of platelets differ from that of other formed elements?

10.2 Hemostasis

10.2.1 Learning Objectives

  • Describe the blood-clotting process.

  • Identify factors that may inhibit or enhance blood-clotting.

10.2.2 Mechanism of Hemostasis

  • Definition: Hemostasis means stopping bleeding; activated by blood vessel injury.

  • Normal Functioning vs. Injury: Under normal conditions, blood flows smoothly; injury leads to hemostasis.

Phases of Hemostasis:

  1. Vascular Spasms:

    • Immediate response to blood vessel injury (vasoconstriction).

    • Blood vessel spasms narrow the vessel and decrease blood loss until clotting occurs.

    • Factors that induce spasms:

    • Direct injury to smooth muscle cells.

    • Stimulation of local pain receptors.

    • Release of serotonin by platelets.

  2. Platelet Plug Formation:

    • Intact endothelium prevents platelet sticking.

    • Upon injury, collagen fibers are exposed; platelets become sticky and adhere to the damaged site.

    • Platelets release chemicals that:

    • Enhance vascular spasms.

    • Attract additional platelets.

    • Formation of a platelet plug occurs as more platelets accumulate.

  3. Coagulation (Blood Clotting):

    • Injured tissues release tissue factor (TF).

    • TF interacts with platelet factor 3 (PF3) and calcium ions (Ca^{2+}) to form an enzyme activator.

    • Produces thrombin, which converts soluble fibrinogen into insoluble fibrin threads, creating a mesh that stabilizes the plug by trapping RBCs.

  • Retracting Clot: Within an hour, the clot retracts, squeezing serum and pulling the vessel edges together.

  • Normal Clotting Time: Blood typically clots within 3 to 6 minutes.

  • Preventing Widespread Clotting: Trigger factors rapidly inactivated to avert excessive clotting.

  • Healing Process: Endothelium regenerates and the clot is finally removed or broken down.

10.2.3 Disorders of Hemostasis
Undesirable Clotting

  • Sometimes clots (thrombi) form in unbroken vessels, especially in legs.

  • Thrombus: A persistent clot that obstructs blood flow, potentially leading to tissue death and hypoxia.

  • Embolus: If a thrombus breaks free, it becomes an embolus and can cause strokes or other complications when lodging in narrower vessels.

  • Risk Factors for Thrombus Formation:

    • Roughened endothelium due to physical impact or fatty deposits.

    • Slowly flowing or pooled blood (common in immobilized patients).

  • Clinical Anticoagulants: Medications like aspirin, heparin, and warfarin used to mitigate thrombus risks.

Bleeding Disorders

  • Common problems include platelet deficiency (thrombocytopenia) and clotting factor deficits (due to liver impairment or genetics).

  • Thrombocytopenia: Low platelet count causes spontaneous bleeding, evidenced by petechiae (purple spots).

  • Liver-Related Conditions: Impaired liver leads to severe bleeding due to lack of clotting factors. Vitamin K deficiency can be corrected with supplements.

  • Hemophilia: Genetic disorders causing a lack of clotting factors, leading to prolonged and life-threatening bleeding. Treatment includes plasma transfusions and clotting factor injection, though risks include transmission of blood-borne diseases.

Questions to Consider:

  1. What factors enhance thrombus formation in intact vessels?

10.3 Blood Groups and Transfusions

10.3.1 Learning Objectives

  • Describe the ABO and Rh blood groups.

  • Explain transfusion reaction mechanisms.

Blood Loss Compensation

  • When blood is lost, blood vessels constrict, and bone marrow increases blood cell formation.

  • Compensation Limits: Losses of 15-30% can lead to weakness; losses exceeding 30% can result in fatal shock.

Whole Blood Transfusions

  • Utilized for substantial blood loss, severe anemia, or thrombocytopenia.

  • Procedure: Blood is collected with an anticoagulant for preservation.

10.3.2 Human Blood Groups

  • Importance of Compatibility: Transfusion of incompatible blood can lead to fatal reactions.

  • Blood Antigens: RBC membranes express unique antigens that determine blood type.

  • Definition: An antigen is a foreign substance recognized by the immune system, prompting antibody production.

  • Transfusion Reaction Mechanism:

    • Antibodies in the recipient’s plasma can agglutinate the transfused RBCs with foreign antigens, leading to clotting and hemolysis.

ABO Blood Grouping

  • Types:

    • Type A: Presence of A antigens, forms anti-B antibodies.

    • Type B: Presence of B antigens, forms anti-A antibodies.

    • Type AB: Presence of both A and B antigens, forms no antibodies (universal recipient).

    • Type O: Absence of antigens, forms both anti-A and anti-B antibodies (universal donor).

Rh Blood Grouping

  • Identified from Rhesus monkeys; involves Rh antigen D. Most Americans are Rh-positive.

  • Autoantibody Formation: Rh-negative individuals do not initially produce anti-Rh antibodies unless they receive Rh-positive blood.

  • Pregnancy Complications: Rh sensitization can lead to hemolytic disease of the newborn in subsequent pregnancies. Treatment includes RhoGAM to prevent sensitization and subsequent issues with Rh-positive infants.

Blood Typing Procedures

  • Determining blood group involves mixing blood with anti-A and anti-B immune serum, with agglutination signifying positive results. Crossmatching assesses compatibility between donor and recipient blood.

Questions to Consider:

  1. What classes define human blood groups?

  2. What are consequences of mismatched blood transfusion?

  3. What ABO blood type does a typical person possess?

  4. What distinguishes an antigen from an antibody?

10.4 Developmental Aspects of Blood

10.4.1 Learning Objectives

  • Understand the physiological basis of jaundice in newborns.

  • Identify age-related blood disorders.

  • Embryonic Development: Blood system develops early with multiple hematopoietic sites before the fetal liver and red marrow become principal blood cell production sites.

  • Fetal Hemoglobin: Fetal hemoglobin (HbF) binds oxygen more efficiently than adult hemoglobin (HbA).

  • Physiological Jaundice: Occurs when fetal RBCs are destroyed faster than excretion of hemoglobin breakdown products; typically resolves without intervention.

Age-Related Blood Disorders

  • Common blood pathologies include:

    • Genetic disorders (e.g., hemophilia, sickle cell anemia).

    • Nutritional deficiencies (e.g., iron-deficiency anemia).

    • High incidence of leukemias and other blood disorders among the young and elderly.

    • Increased prevalence of pernicious anemia due to deficiency of intrinsic factors affecting Vitamin B12 absorption with advancing age.

Questions to Consider:

  1. How does fetal hemoglobin differ from adult hemoglobin?

  2. What blood disorders are prevalent in the elderly?