Comprehensive Study Notes – Blood (Chapter 17)

Overall Functions of Blood

• Transport

  • Delivers \text{O}_2 and nutrients to tissues

  • Removes metabolic wastes (e.g., \text{CO}_2, urea)

  • Carries hormones to targets

• Regulation

  • Maintains body temperature (heat distribution & absorption)

  • Preserves constant blood pH via buffers

  • Sustains adequate fluid volume in the circulation

• Protection

  • Hemostasis (prevents blood loss)

  • Immune defense against infection

Basic Composition of Blood

• Two major fractions

  • Plasma (≈ 55\% of whole blood)

  • \approx 90\% water

  • Solutes (≈ 10\%): nutrients, gases, electrolytes, hormones, proteins

  • Major plasma proteins (mostly liver-derived)

    • Albumin: chief contributor to colloid osmotic pressure & carrier for molecules

    • Globulins

    • Fibrinogen

  • Formed elements (≈ 45\%)

  • Erythrocytes

  • Leukocytes

  • Platelets

• Hematocrit = % of blood volume occupied by RBCs

  • Normal adult blood volume ≈ 5\text{ L} (≈ 8\% of body mass)

Erythrocytes (Red Blood Cells)

• Structure

  • Small, biconcave, anucleate

  • Flexible due to spectrin cytoskeleton ⇒ pass through narrow capillaries

  • Packed with hemoglobin (Hb)

• Function

  • Major role: transport of \text{O}_2 (as oxyhemoglobin in lungs; becomes deoxyhemoglobin in tissues)

  • Secondary role: \text{CO}_2 transport

• Lifespan & Turnover

  • ≈ 120 days

  • Aged/damaged RBCs removed by splenic & hepatic macrophages

  • Fate of Hb

  • Iron → stored as ferritin/hemosiderin, recycled

  • Heme → bilirubin → bile

  • Globin → amino acid pool

• Erythropoiesis (RBC production) sequence

  1. Hematopoietic stem cell →

  2. Proerythroblast (committed) →

  3. Basophilic → Polychromatic → Orthochromatic erythroblast

  4. Reticulocyte (still contains ribosomal remnants) → released to blood →

  5. Mature erythrocyte

• Regulation

  • Stimulated by erythropoietin (EPO, mainly renal) and testosterone

  • Requires iron, vitamin \text{B}_{12}, folic acid

• Disorders

  • Anemias (↓ O₂-carrying capacity)

  • Polycythemia (↑ RBC mass, e.g., polycythemia vera)

Leukocytes (White Blood Cells)

• General

  • Nucleated; crucial for immunity

  • Life span generally shorter than RBCs

• Two broad classes

  • Granulocytes (neutrophils, eosinophils, basophils)

  • Neutrophils: active phagocytes

  • Eosinophils: attack parasitic worms; up in allergies

  • Basophils: histamine release ⇒ vasodilation & leukocyte attraction

  • Agranulocytes (lymphocytes, monocytes)

  • Lymphocytes: B & T cells (adaptive immunity)

  • Monocytes → macrophages in tissues

• Leukopoiesis

  • Originates from hematopoietic stem cell

  • Early split: lymphoid stem cell (→ T & B lymphocytes) vs. myeloid stem cell (→ all other formed elements)

  • Granulocyte line: myeloblast → promyelocyte → myelocyte → band cell → mature granulocyte

  • Marrow stores ≈ 10× more granulocytes than circulate; production ratio granulocytes : RBCs ≈ 3:1 because granulocytes live only 0.25 – 9 days

• Leukocyte Disorders

  • Leukemias

  • Infectious mononucleosis

  • Myeloproliferative disorders (e.g., polycythemia vera, leukoerythroblastic anemia, marrow fibrosis)

Platelets

• Fragmented bits of megakaryocytes

• Circulate \approx 10\text{ days}

• Central role in hemostasis: form platelet plug & provide phospholipid surface for clotting cascade

Hemostasis (Stopping Bleeding)

1. Vascular spasm (smooth-muscle constriction)

2. Platelet plug formation (platelet aggregation at injury site)

3. Coagulation (intrinsic & extrinsic pathways converge to activate thrombin → fibrin mesh)

   • Intrinsic pathway: all factors within blood, slower

   • Extrinsic pathway: tissue factor (factor III) from damaged tissue allows pathway to bypass several intrinsic steps

ABO Blood Group System

• Determined by presence/absence of agglutinogens (antigens) A & B on RBC surface

  • Group A: antigen A; plasma antibody anti-B

  • Group B: antigen B; plasma antibody anti-A

  • Group AB: antigens A & B; no anti-A or anti-B antibodies ⇒ “universal recipient” (theoretically)

  • Group O: no A or B antigens; plasma contains both anti-A & anti-B ⇒ “universal donor” (theoretically)

• Unique feature: plasma contains natural (pre-formed) agglutinins beginning \approx 2 months after birth, reaching adult levels by 8–10 years

• U.S. Population frequencies

  • AB: White 4\% | Black 4\% | Asian 7\% | Hispanic 2\%

  • B: 11\% | 19\% | 25\% | 10\%

  • A: 40\% | 26\% | 28\% | 31\%

  • O: 45\% | 51\% | 40\% | 57\% (up to 79\% in Native Americans)

• Caveat: other minor antigens (MNS, Duffy, Kell, Lewis, private antigens) can still trigger reactions

Rh Blood Group System

• ≥ 52 known Rh antigens; five common: C, D, E, c, e

• Rh + individuals (≈ 85\% of Americans): have antigen D

• Rh – individuals: lack antigen D

• Unlike ABO system, anti-Rh antibodies are not pre-formed; they develop after exposure to Rh + RBCs (e.g., transfusion, fetomaternal hemorrhage)

• Second exposure → hemolytic reaction

Hemolytic Disease of the Newborn (Erythroblastosis Fetalis)

• Occurs when Rh– mother carries Rh + fetus

• First pregnancy usually safe; sensitization happens mainly at delivery

• Subsequent Rh + pregnancy ⇒ maternal anti-Rh IgG crosses placenta → fetal RBC lysis

  • Fetal anemia, hypoxia, possible brain damage or death

• Prevention/Therapy

  • RhoGAM (anti-Rh serum) administered during pregnancy & immediately postpartum (also after miscarriage/abortion)

  • Agglutinates fetal Rh antigen in maternal blood, blocking immune sensitization

  • In severe cases: intrauterine or post-delivery exchange transfusions with Rh– blood; transfused cells replaced within \approx 6 weeks

Blood Typing & Cross-Matching

• Essential to determine donor & recipient ABO/Rh before transfusion

• Simple slide test: add anti-A and anti-B sera to diluted blood → observe agglutination pattern (Fig 17.17 concept)

• Cross-match:

  1. Test recipient serum vs. donor RBCs

  2. Test donor serum vs. recipient RBCs

• Ensures compatibility beyond basic ABO/Rh

Transfusion Reactions

• Trigger: infusion of mismatched blood

• Mechanism

  • Recipient antibodies agglutinate donor RBCs (donor antibodies usually too diluted to damage host)

  • Agglutination → vessel blockage

  • RBC lysis → free Hb → renal tubule damage, possible acute renal failure

• Clinical manifestations

  • Fever, chills, hypotension, tachycardia, nausea, vomiting, general toxicity

• Major dangers

  1. Inability of destroyed RBCs to carry \text{O}_2

  2. Blocked microcirculation

  3. Kidney shutdown from Hb overload

• Treatment

  • Rapid infusion of IV fluids & diuretics ⇒ ↑ urine output, “wash out” hemoglobin, prevent tubular necrosis

Autologous Transfusions

• Patient pre-donates own blood (stored for elective surgery)

• Eliminates risk of transfusion reaction & transmission of infections (e.g., HIV)

Specialized Procedures & Terms

• Plasmapheresis

  • Blood removed → plasma separated → formed elements returned

  • Uses: remove antibodies/immune complexes in autoimmune diseases (multiple sclerosis, myasthenia gravis); collect plasma for burn therapy or components for treatment

• Hemochromatosis

  • Genetic iron-overload disorder ⇒ intestine absorbs excess iron

  • Iron deposition (joints, liver, pancreas) forms toxic compounds

• Septicemia

  • “Blood poisoning” = excessive bacteria/toxins in blood

• Myeloproliferative Disorders

  • Group of marrow pathologies with uncontrolled cell division (e.g., polycythemia vera, leukemia, leukoerythroblastic anemia with fibrosis)

Key Ethical & Practical Points

• “Universal donor/recipient” labels are oversimplifications; minor antigens can still provoke reactions

• Rising awareness of transfusion-related infections drives alternative strategies (autologous donation, stringent testing)

• RhoGAM prophylaxis exemplifies preventive medicine, averting a life-threatening neonatal disease

Connections & Real-World Relevance

• Blood typing underpins safe transfusion practices in trauma and surgery

• Plasmapheresis demonstrates therapeutic manipulation of blood components

• Knowledge of hematopoiesis guides treatment of leukemias and aids interpretation of complete blood counts (CBCs)

• Hemostasis & platelet biology inform anticoagulant and antiplatelet drug development