BloodHuman AnatomyChapter 10

I. BloodA. General Characteristics

1. body’s only fluid tissuea. connective tissue made of formed elements (45%)

suspended in a liquid matrix (55%)

1) formed elements = red blood cells, white blood cells & platelets

2) matrix = plasma2. main job = transport anything being carried w/in body

a. incl. nutrients, gases, hormones, wastes, heatb. also clots to prevent blood loss & aids immunity

3. Sticky, opaque & metallic tastinga. thicker & more viscous than water

4. Bright scarlet when carrying oxygena. dull maroon when oxygen-poor

5. Slightly alkaline (7.35-7.45 pH)

6. Slightly higher temp than avg. body temp (38o C / 100.4o F)

7. About 8% of body massa. women = about 4-5 L, men = about 5-6 L

B. Plasma1. straw-colored fluid 2. about 55% of total blood volume3. about 90% water plus many dissolved materials

a. incl. nutrients, electrolytes, gases, hormones, wastes, cell products & plasma proteins

4. can be transfused w/out being type-matcheda. helps restore blood protein levels

1) ex. liver surgery, severe blood loss, serious burns

5. three major plasma proteinsa. primarily made in liver

1) except antibodies & protein-based hormonesb. Albumin – important blood buffer, aids osmotic

balance of bloodc. Fibrinogen – aids blood clottingd. Globulins – antibodies to protect from pathogens

and lipid transport molecules

C. Red blood cells (RBC’s) ~ a.k.a. erythrocytes1. function = carry O2 to body cells2. greatest proportion of the formed elements

a. about 40% of total blood volume1) about 1000x more than white cells

3. small, flexible, biconcave discsa. anucleate cells w/ few organelles when matureb. makes room to carry protein hemoglobin

1) iron-containing respiratory pigment a) turns bright red in presence of O2

4. Formed by erythropoiesis in red bone marrowa. 5 – 7 days to mature & enter blood streamb. avg. lifespan = 120 days

5. RBC problemsa. Anemia = decrease in O2-carrying ability of blood

1) may be due to low # of RBCs or abnormal/deficient hemoglobin

2) often a symptom of other health issues3) forms incl. hemorrhagic, hemolytic, pernicious,

aplastic, and iron-deficiency (see p. 342)

b. Sickle cell anemia1) genetic mutation causing misshaped hemoglobin

a) causes cells to become crescent-shaped when unloading O2 or if O2 levels are lower than normal

b) easily rupture, dam up small blood vessels & cause O2-deficiencies in body tissues

c. Polycythemia1) excessive # or abnormal increase in RBCs

a) may be due to living at high altitudes or a side effect of bone marrow cancer

2) increases viscosity of blood, slowing circulation

D. White blood cells (WBC’s) ~ a.k.a. leukocytes1. function = immunity against pathogens & disease2. less than 1% of total blood volume

a. w/ platelets, form “buffy coat” between plasma & RBCs when whole blood is separated

3. 5 types of cells w/ typical organelles & nucleus4. capable of diapedesis

a. can leave blood vessels to work directly where needed for inflammatory or immune response

5. Use positive chemotaxis to locate areas of tissue damage & infectiona. respond to chemicals diffused from cellsb. move through tissues by ameboid motionc. destroy microorganisms & dispose of dead cells

6. Formed by hematopoiesis in red bone marrowa. avg. lifespan varies by cell type from a few hours to

several months or years

White blood cell

life spans& functions

7. WBC count varies a. leukocytosis = WBC count > 11,000 cells/mm3

1) normal response to viral & bacterial infectionsb. leukopenia = abnormally low WBC count

1) common response to corticosteroids, chemotherapyc. leukemia = cancer of bone marrow, creating huge #s of

immature, nonfunctioning WBCs

8. WBC types (see p. 344)

a. Granulocytes – cells w/ lobed nuclei & granules in cytoplasm1) Neutrophils – phagocytes during infections2) Eosinophils – respond to parasitic worms; have a

role in allergy attacks3) Basophils – release histamine at inflammation sites;

release anticoagulant heparin

b. Agranulocytes – cells w/ normal nuclei, lacking visible granules in cytoplasm

1) Lymphocytes – 2 forms found in lymphatic tissue to aid immune responsea) B lymphocytes produce antibodiesb) T lymphocytes directly attack tumors, virus &

grafted tissues2) Monocytes – largest WBCs; become macrophages to

engulf chronic infectious agentsa) ex: tuberculosis

E. Platelets ~ a.k.a. thrombocytes1. function = hemostasis

a. stoppage of bleedingb. begin the clotting cascade to form blood clots

2. irregularly shaped cell fragmentsa. created when multinucleate megakaryocytes pinch

off thousands of pieces

3. avg. lifespan = 8-9 daysa. destroyed in spleen & liver

4. less than 1% of total blood volumea. w/ WBCs, form “buffy coat”

5. 3 key qualities for blood clottinga. adhesiveness, aggregation, agglutination

1) stickiness, joining w/ more, clumping together

6. Platelet disorders a. Thrombocytopenia = insufficient # of platelets circulating

1) creates petechiae on skin & frequent bleedinga) small purplish blotches

2) caused by suppressed bone marrow, heredity, kidney issues, alcohol abuse

b. Thrombocytosis = too many platelets1) may be due to abnormal bone marrow or another illness

(cancer, anemia, inflammation, etc.)2) causes spontaneous clots in arms & legs, increasing risk for

heart attack or stroke

Formed elements ~ size comparison

II. Blood Groups and TransfusionsA. General background

1. antigens = identifying proteins on surfaces of cell membranesa. in blood typing, refer to antigens on RBCsb. recognize “self” from foreign “invaders”

1) stimulates immune response against invadersc. a.k.a. “agglutinogens”d. over 30 common human RBC antigens

1) 2 main groups – ABO & Rh

2. antibodies = plasma proteins that respond & bind to foreign antigens a. a.k.a. “agglutinins”b. in blood, causes agglutination

1) RBCs clump together, blocking small blood vesselsc. can lead to transfusion reactions

1) fever, chills, nausea, kidney failure, death

B. ABO blood group1. discovered by Dr. Karl Landsteiner, 19012. type of blood is based on RBC antigens

a. type A = A antigens b. type B = B antigens c. type AB = both present

d. type O = none present3. frequency of each type varies with ethnicity and

geographic region1) ex: most common in US = type O

4. Plasma antibodies form during infancy against the opposite antigen

a. type A = Anti-B antibodiesb. type B = Anti-A antibodiesc. type AB = no antibodies

1) universal recipient – will accept all blood groupsd. type O = Anti-A & Anti-B antibodies

1) universal donor – may donate to all blood groupse. important for blood transfusions

5. Blood type is hereditary a. 3 possible blood type alleles

1) each parent contributes 1 allele to offspring2) offspring’s 2 alleles work together for blood type

b. type A = IAIA or IAi1) type A is dominant over type O

c. type B = IBIB or IBi1) type B is dominant over type O

d. type AB = IAIB

1) type AB is codominant – both alleles are expressede. type O = ii

1) type O is recessive to either A or B; only expressed if both alleles are for type O

Type of genes present = genotype

ex: IAIA or IBi Outward expression of genes = phenotype

ex: type A or type B

Allele = a form a gene for a trait

6. Blood donors / recipientsa. Type A blood – donate to A, AB

1) receive from A, Ob. Type B blood – donate to B, AB

1) receive from B, Oc. Type AB blood – donate only to AB

1) receive A, B, AB or O (universal recipient)

d. Type O blood – donate to A, B, AB or O (universal donor)

1) receive only O

C. Rh blood group1. discovered by Dr. Karl Landsteiner & A.S. Weiner, 19402. several antigens, esp. Rh D

a. Rh+ = D antigen is present1) 85% of humans2) genotypes = DD or Dd (dominant to -)

b. Rh– = D antigen is missing1) 15% of humans2) genotypes = dd (recessive to +)

3. antibodies form differently than ABOa. Rh+ lacks antibodiesb. Rh– only forms antibodies after 1st exposure to Rh+ blood

Named after Rhesus monkeys, who were thought to have the same antigens

4. Important for transfusions, pregnanciesa. Rh+ can receive either Rh+ or Rh–b. Rh– can only receive Rh–c. Rh– moms carrying Rh+ fetuses have problems

1) 1st pregnancy usually fine – antibodies only begin forming

2) 2nd & later Rh+ pregnancies, mom’s antibodies attack baby’s blooda) causes hemolysis (rupture of RBCs) & lead to

erythroblastosis fetalis (& possibly fetal death)b) can be prevented w/ RhoGAM vaccine to prevent

mom from forming antibodies

III. HemostasisA. Stoppage of bleeding

1. triggered by injured blood vessels2. involves platelets, plasma proteins for clotting

B. 3 phases1. Vasoconstriction

a. vascular spasms narrow the blood vessel until clotting can occur

Heme = blood; stasis = standing still

2. Platelet plug formsa. broken endothelium in damaged vessel exposes its

collagenb. collagen causes platelets to stick to damaged areac. platelets release chemicals for more constriction & to

attract more platelets1) creates a white thrombus (a.k.a. platelet plug)

3. Coagulation = series of chemical reactions a. enzyme thrombin is createdb. joins w/ fibrinogen proteins from plasmac. transforms into insoluble fibrin mesh to trap RBCs &

platelets, forming a clotd. clot begins retracting, squeezing out serum

1) serum = plasma minus clotting proteins2) draws injured vessel edges together

4. Typically, clotting takes 3-6 minutes5. As vessel is repaired, clot is broken down & dissolves6. Clotting problems

a. undesired clotting in healthy tissues1) thrombus = stationary in a vessel

a) may prevent blood flow to an area2) embolus = breaks away & enters blood stream

a) usually only a problem if it gets lodged in a narrow vessel, esp. toward heart or brain

b. Hemophilia1) several hereditary disorders preventing blood from

clotting properlya) carried on X chromosome, mostly affects men

2) due to missing or insufficient production of clotting factors

3) can be treated with plasma transfusions or purified clotting factor injections