Chapter 14 Notes — Blood: Composition, Formed Elements, Hemostasis, and Blood Groups
14.1 Characteristics of Blood
Blood is the only type of connective tissue with a liquid matrix (plasma).
Functions: transports vital substances, regulates processes for homeostasis, maintains stability of interstitial fluid, distributes heat.
Blood volume varies with body size, changes in fluid/electrolyte concentration, and adipose tissue levels.
Blood is about $8\%$ of body weight; adult blood volume is about $4$ to $5$ L in a female and $5$ to $6$ L in a male.
Blood contains formed elements (cells and cell fragments): red blood cells (RBCs), white blood cells (WBCs), and platelets.
Formed elements are formed mostly in red bone marrow and are collectively called the formed elements.
Key terms:
RBCs = erythrocytes
WBCs = leukocytes
Platelets = thrombocytes (cell fragments)
Blood also contains plasma, the liquid matrix in which formed elements are suspended.
14.2 Formed Elements (Hematopoiesis and origins)
Hematopoiesis = origin and formation of formed elements (RBCs, WBCs, platelets).
Formation occurs primarily in red bone marrow.
Hematopoietic stem cells (HSCs) are also called hemocytoblasts.
HSCs give rise to two main lineages:
Lymphoid stem cells → lymphocytes.
Myeloid stem cells → all other formed elements (RBCs, other WBCs, platelets).
HSCs give rise to more stem cells and to differentiated cells in response to hematopoietic growth factors.
Figure reference: Blood Cells development involves pathways from hematopoietic stem cells to erythroblasts, myeloblasts, lymphoblasts, megakaryocytes, etc.
14.3 Plasma
Plasma = clear, straw-colored liquid portion of blood; 55% of blood volume; 92% water.
Plasma contains organic and inorganic chemicals, transports nutrients, gases, hormones, vitamins, and helps regulate fluid and electrolyte balance and pH.
Plasma proteins are the most abundant dissolved substances in plasma and are typically not used as an energy source.
Table 14.6 (plasma proteins) overview:
Albumins ≈ $60\%$ of total plasma protein; origin: liver; Function: maintain colloid osmotic pressure.
Globulins ≈ $36\%$; subdivided into:
Alpha globulins (liver): transport lipids and fat-soluble vitamins.
Beta globulins (liver): transport lipids and fat-soluble vitamins.
Gamma globulins (lymphatic tissues): antibodies of immunity.
Fibrinogen ≈ $4\%$; origin: liver; Essential for blood coagulation.
Nonplasma components:
Gases and nutrients: Oxygen, Carbon dioxide; amino acids, simple sugars, nucleotides, lipids (including triglycerides, phospholipids, cholesterol).
Nonprotein nitrogenous substances (NPNs): Urea, uric acid, amino acids, creatine, creatinine; BUN = blood urea nitrogen (indicator of kidney health).
Plasma electrolytes: Na$^+$, K$^+$, Ca$^{2+}$, Mg$^{2+}$, Cl$^-$, HCO$3^-$, PO$4^{3-}$, SO$_4^{2-}$; Na$^+$ and Cl$^-$ are the most abundant.
14.4 Hemostasis
Hemostasis = stoppage of bleeding; three main mechanisms operate to limit blood loss in small vessel injuries:
Vascular (vascular) spasm.
Platelet plug formation.
Blood coagulation (clot formation).
Vascular spasm:
Triggered by cut/break in a small vessel.
Smooth muscle contracts rapidly to slow blood loss; lasts a few minutes and can persist for about $30$ minutes.
Serotonin released from platelets reinforces vasoconstriction.
Platelet plug formation:
Platelets adhere to rough surfaces or exposed collagen, forming a temporary plug.
Coagulation (clot formation):
A cascade of enzymatic reactions converts soluble fibrinogen to insoluble fibrin threads that trap RBCs and platelets.
Initiated by two pathways: Extrinsic and Intrinsic clotting mechanisms; both use calcium ions ($Ca^{2+}$) and end with a common pathway producing a fibrin clot.
Vitamin K is required for functioning of certain clotting factors.
The balance between procoagulants and anticoagulants regulates clotting.
Major end point: Conversion of fibrinogen ($F I$) to fibrin ($F I$) by thrombin; fibrin forms the clot network.
Clotting factors (summary from Table 14.9):
I (fibrinogen) — synthesized in the liver — participates in both intrinsic and extrinsic pathways.
II (prothrombin) — synthesized in the liver; requires vitamin K; converted to thrombin.
III (tissue thromboplastin) — released by damaged tissue; extrinsic pathway initiator.
IV (Ca$^{2+}$) — plasma electrolyte; required in both pathways.
V (proaccelerin), VII (serum prothrombin conversion accelerator), VIII (antihemophilic factor), IX, X, XI, XII, XIII — various roles in coagulation; many require vitamin K; pathway specifics summarized in Table 14.8.
Fibrinolysis and clot dissolution:
Plasmin digests fibrin threads, dissolving the clot.
Abnormal clot formation terms:
Thrombus: abnormal clot formed in a vessel.
Embolus: clot moving through circulation.
Thrombosis: clot in a vessel supplying a vital organ.
Infarction: tissue death due to blocked vessel.
Embolism: clot travels and blocks a distant vessel (e.g., pulmonary embolism).
Atherosclerosis can contribute to abnormal clot formation.
Deep Vein Thrombosis (DVT) & prevention (Clinical Application 14.3):
Clot formation due to pooling of stagnant blood, especially in femoral/popiteal veins or deep pelvic veins.
Pulmonary embolism is a major risk if clot travels to lungs.
Risk factors include prolonged immobility; examples include long flights.
Symptoms: deep muscle pain, cramping, redness, swelling; phlebitis may occur.
Prevention: anticoagulants, compression stockings, and physical activity during travel.
Inhibition of coagulation and prevention of clot spread:
Prostacyclin (PGI$_2$) from healthy endothelium prevents platelet adhesion.
Fibrin binds thrombin to limit spread of clotting.
Antithrombin inhibits thrombin; heparin from mast cells and basophils also inhibits clotting.
14.5 Blood Groups and Transfusions
ABO blood group system foundations:
Blood types are determined by surface antigens (A and B) on RBC membranes; antigens are carbohydrates on glycolipids.
Antibodies (in plasma) react against non-self antigens; agglutination occurs when antibodies bind incompatible antigens on donor RBCs.
Safe transfusions require knowledge of donor and recipient blood types and crossmatching for agglutination.
Antigens and antibodies (key definitions):
Antigens: any molecule that can evoke an immune response; in transfusion, RBC antigens trigger antibodies if mismatched.
Antibodies: plasma proteins that react against specific antigens.
Agglutination: clumping of RBCs due to antibody-antigen interaction.
ABO transfusion compatibility (example): Type A blood has antigen A and anti-B antibodies; Type B has antigen B and anti-A antibodies; Type AB has antigens A and B and no anti-A/anti-B antibodies; Type O has neither A nor B antigens but has both anti-A and anti-B antibodies.
ABO blood type frequencies in the United States (example data):
Type O roughly around $40$–$49\%$, Type A around $27$–$40\%$, Type B around $11$–$20\%$, Type AB around $4$–$6\%$ depending on population group. (Refer to Table 14.12 for population-specific values.)
Universal donor and recipient concepts:
Type O = universal donor for RBCs (lacks A and B antigens on RBCs) but anti-A/anti-B antibodies may be present in plasma; transfusion is often slow and controlled.
Type AB = universal recipient for RBCs (lacks anti-A/anti-B antibodies in plasma).
Rh blood group:
Rh factor refers to the presence of the D antigen on RBC membranes.
Rh positive = presence of antigen D; Rh negative = absence of D antigen.
Anti-Rh antibodies form in Rh-negative individuals after exposure to Rh-positive RBCs (sensitization).
Clinical relevance: Rh incompatibility can cause erythroblastosis fetalis (hemolytic disease of the newborn) in subsequent Rh-positive pregnancies if the mother has developed anti-Rh antibodies.
Practical implications and cross-matching:
Transfusion safety relies on avoiding agglutination by ensuring ABO and Rh compatibility.
Crossmatching tests recipient serum against donor RBCs to detect agglutination before transfusion.
Ethical and clinical considerations include informed consent, infection risk minimization, and the use of universal donor/recipient strategies in emergencies when needed.
Connections to foundational principles and real-world relevance
Hematopoiesis illustrates stem cell differentiation and growth factor signaling, linking developmental biology to clinical hematology.
Oxygen transport by RBCs (hemoglobin) connects cellular biology to respiratory physiology and metabolic demand.
Negative feedback (erythropoiesis control by erythropoietin) exemplifies endocrine-like regulation of blood cell production.
Hemostasis integrates vascular biology, platelet function, and coagulation cascades, highlighting how multiple systems coordinate to prevent blood loss while preserving vessel patency.
Plasma composition and nutrient transport underline homeostasis, nutrition, and the systemic distribution of hormones and metabolites.
Blood typing and transfusion medicine demonstrate practical applications of immunology (antigens/antibodies) in clinical care and patient safety.
Equations, constants, and key numerical references (LaTeX)
Blood volume percentage: of body weight.
Typical adult blood volume (female): ; (male): .
Formed elements proportions in typical centrifuged sample: plasma ; RBCs ; WBCs + platelets < (buff coat).
Hematocrit values (RBCs) in centrifuged sample: female ; male .
RBC life span: .
Platelet count: .
Blood coagulation pathways require Ca$^{2+}$ and vitamin K for certain factors.
RBC production steps in erythropoiesis: hemocytoblast → erythroblast → reticulocyte → erythrocyte; life cycle driven by erythropoietin.
Normal WBC count range: .
ABO antigen/antibody example: Type A RBCs carry antigen A and have anti-B antibodies in plasma; Type B carries antigen B and has anti-A antibodies; Type AB carries both A and B antigens with no anti-A/anti-B antibodies; Type O lacks A and B antigens but has both anti-A and anti-B antibodies.
Ethical, philosophical, and practical implications
Universal precautions emphasize the ethical obligation to protect healthcare workers and patients from bloodborne pathogens (HIV, Hepatitis B/C) and to minimize transmission risk.
Safe transfusion practices (crossmatching, donor screening) reflect a commitment to patient safety and reduce iatrogenic harm.
Treatments for blood disorders (e.g., leukemia, sickle cell disease) involve weighing benefits and risks of aggressive therapies (chemotherapy, bone marrow transplants) against potential mortality and morbidity.
Blood banking and donor programs raise public health considerations about access, equity, and consent.
The potential for transfusion reactions and alloimmunization highlights the importance of personalized medicine and patient-specific considerations in treatment planning.
Summary connections to the broader course concepts
Blood serves as a dynamic transport and regulatory system tightly integrated with endocrine, immune, and integumentary systems.
The study of blood components, their production, and their regulation provides a practical framework for understanding homeostasis, pathophysiology of anemia, coagulation disorders, and transfusion medicine.
Quick reference (selected bullet highlights)
Blood volume percentages and typical volumes: $8\%$ of body weight; female $4$–$5$ L; male $5$–$6$ L.
RBC life span: ; erythropoiesis stimulated by erythropoietin released from the kidneys (and liver) in response to low blood O$_2$.
Plasma proteins: Albumins ; Globulins ; Fibrinogen .
Hemostasis order: Vascular spasm → Platelet plug → Coagulation (fibrin clot) → clot dissolution by plasmin.
Platelet count range: to .
ABO compatibility basics: transfusion safety relies on matching donor RBC antigens with recipient antibodies to avoid agglutination.
Rh incompatibility risks primarily arise in Rh-negative mothers with Rh-positive fetuses; management is crucial in perinatal care.
Common clinical applications include treating DVT to prevent pulmonary embolism; using anticoagulants and compression therapy; and recognizing signs of hemostatic disorders.