Chapter 18: Blood
I. Functions and Properties
Involved in respiration, nutrition, waste elimination, thermoregulation, immune
defense, water and pH balance, and communication. 4-6L/ adult.
Consists of plasma and formed elements (cells and platelets).
Hematocrit separates RBCs from plasma, with buffy coat between. Normally,
RBCs ~ 45%.
Properties include: viscosity – 4.5 – 5.5X that of water; osmolarity
regulates fluid and electrolyte balance based on osmosis. Colloid osmotic
pressure especially crucial – created by proteins. When pathologically low, e.g.
kwashiorkor (starvation), BP drops.
II. Plasma
With proteins removed = serum.
(A) Proteins – for clotting, defense and transport.
-1- albumins: smallest and most abundant.
-2- globulins: alpha, beta and gamma.
-3- fibrinogen: precursor of fibrin, for clotting.
Most from liver; gamma globulins (antibodies) from plasma cells.
(B) Nonprotein Nitrogenous Substances
Amino acids and nitrogenous wastes, e.g. urea.
(C) Nutrients: glucose, amino acids, fats, lipids, vitamins, minerals….
(D) Gases: O2, CO2, N2
(E) Electrolytes: Na+ most important.
III. Blood Cell Formation = Hematopoiesis
First from yolk sac, its stem cells migrate to marrow, spleen, liver, thymus. After
infancy, myeloid hematopoiesis in red marrow (all formed elements) and
lymphoid hematopoiesis in lymphoid tissues and elsewhere (only
lymphocytes).
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(A) RBC Production = erythropoiesis. 2.5 million cells/ second!
Stimulated by hormone erythropoietin (EPO). Reticulocytes enter
bloodstream, lose ER to mature into RBCs. RBC count maintained
homeostatically. Stimulated by hypoxemia (low blood O2). Requires iron, which
is selectively absorbed and transported. Also required: Vitamin B12, folic acid,
Vitamin C and copper.
(B) WBC Production = leukopoiesis.
B progenitors; T progenitors; granulocyte-macrophage colony-forming
units (for granulocytes & monocytes). These cells have receptors for CSFs
(colony stimulating factors.
(C) Platelet Production = thrombopoiesis. Stimulated by hormone
thrombopoietin. Megakarycytes produced by DNA replication without cell
divisions. Break into platelets.
IV. Erythrocytes = Red Blood Cells (RBCs)
(A) Form and Function Anucleate biconcave discs. Shape enhances
surface area to volume ratio. Transport O2 and some CO2. Plasma membranes
with glycoproteins and glycolipids which determine blood type.
No organelles, depend upon anaerobic fermentation. Cytoplasm is 1/3
hemoglobin (Hb) which carries gases, enzyme carbonic anhydrase (which
creates carbonic acid from water and CO2).
(B) Hemoglobin 280 million molecules/ RBC! Each with four globin
chains, two alpha & two beta, each has a heme (Fe) group to bind O2. CO2
binds to globin. Adult and fetal Hb (binds O2 more tightly).
(C) Quantities clinically important.
-1- hematocrit: 42-52% in men; 37-48% in women.
-2- hemoglobin: 13-18 g/dL in men, 12-16 in women.
-3- RBC count: 4.6-6.2 million/ microliter in men, 4.2-5.4 in women.
Gender differences due to androgens, menstrual losses, relationship to body fat.
(D) Death and Disposal RBC lifespan no more than 120 days.
Membranes become fragile, many die in spleen (narrow channels). Hemolysis
releases Hb. Globin provides amino acids, Fe recycled from heme, remainder
creates bile pigments biliverdin, then bilirubin. Urobilinogen from bilirubin in
small intestine (responsible for fecal brown). Urochrome from Hb for yellow
urine. High blood bilirubin causes jaundice.
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(E) RBC Disorders
-1- polycythemia = elevated hematocrit. Increases blood viscicity and BP.
Primary (polycythemia vera) due to cancer; secondary due to dehydration,
hypoxemia (common in long-term smokers).
-2- anemias (low hematocrit +/or Hb) result from three causes:
a. inadequate hematopoiesis or Hb formation. Iron or vitamin
deficiency, lack of intrinsic factor (pernicious anemia), old age, destruction of
myeloid tissue (hypoplastic and aplastic anemias).
b. hemorrhagic
c. hemolytic: toxins, drugs, genetically malformed HB (thalassemia,
Sickle Cell disease).
V. Blood Types
Based on antigens = agglutinogens on RBC surfaces. Recognized by
antibodies = agglutinins, created in response to foreign agglutinogens.
(A) ABO Group A and B gene alleles add sugars to glycolipids on
membranes. Transfusion reaction: agglutination between agglutinins and foreign
RBCs. Can be fatal.
(B) Rh Group C, D, E exist but D most important clinically. Antibodies not
present until sensitization in Rh- blood. HDN (hemolytic disease of the newborn)
= erythroblastosis fetalis results from Rh antibodies passing placenta.
Sensitization prevented with Rhogam injections.
(C) Other groups – many. Rarely cause incompatibilities, used for
paternity testing.
VI. Leukocytes = White Blood Cells
Classified, for convenience, based on appearance when stained.
(A) Types
-1- Granulocytes have obvious granules in cytoplasm:
a. neutrophils- mostly phagocytic.
b. eosinophils- fight parasitic worms.
c. basophils: secrete histamine (inflammation) & heparin (blood thinner)
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-2- Agranulocytes:
a. lymphocytes: for immunity
b. monocytes: become macrophages
(B) Abnormal Counts Normal = 5,000-10,000 WBCs/ microliter
-1- leukopenia = deficiency. Heavy metal poisoning, radiation sickness, some
viral infections.
-2- leukocytosis (excessive). Infection, allergy, dehydration. Differential count
used for more useful diagnosis.
-3- leukemias cause extreme leukocytosis.
a. myeloid (granulocytes) vs. lymphoid.
b. acute vs. chronic.
VII. Hemostasis
(A) Platelets: secrete procoagulents, vasoconstrictors, form plugs,
dissolve old clots, phagocytize bacteria, attract WBCs, secrete growth factors to
maintain vessel linings.
(B) Vascular Spasm
(C) Platelet Plug Formation Attraction to exposed collagen, release
chemicals to establish positive feedback loop.
(D) Coagulation Last resort, potentially dangerous, carefully regulated.
Ends with fibrin mesh. Extrinsic mechanism initiated by damaged blood
vessels, much faster. Intrinsic mechanism begins in blood. Leads to reaction
cascade, requires Ca++, various factors (enzymes).
Ultimately, prothrombin becomes thrombin, fibrinogen becomes fibrin.
Involves another positive feedback loop.
Platelets retract the clot, damaged blood vessel repaired. Dissolution =
fibrinolysis, done with plasmin (another + feedback).
Coagulation prevented by platelet repulsion, dilution, anticoagulants
(antithrombin, heparin).
(E) Disorders
-1- hemophiliac: sex linked recessive, lack of clotting factors. Painful
hematomas.
-2- thrombosis: thrombus becomes embolus when traveling, embolism when
lodged.
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