Download Chapter 18: Blood

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Transport
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Protection
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WBCs, antibodies, and platelets
Regulation
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18-2
O2, CO2, nutrients, wastes, hormones, and heat
fluid regulation and buffering
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You have about 11 pints of
blood (4 to 6 liters)
The plasma portion (fluid
portion) is mostly water
Cells float in the plasma
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Red cells are also called
erythrocytes
White cells are also called
leukocytes
Platelets are pieces of cells
also called thrombocytes
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Viscosity - resistance to flow
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whole blood 5 times as viscous as water
Osmolarity
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total molarity of dissolved particles
 sodium ions, protein, and RBCs
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high osmolarity
 causes fluid absorption into blood, raises BP
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low osmolarity
 causes fluid to remain in tissues, may result in edema
18-4
18-5
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Plasma – liquid portion of blood
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serum remains after plasma clots
3 major categories of plasma proteins
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albumins - most abundant
 contributes to viscosity and osmolarity
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globulins (antibodies)
 provide immune system functions
 alpha, beta and gamma globulins
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fibrinogen
 precursor of fibrin threads that help form blood clots
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Plasma proteins formed by liver
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18-6
except globulins (produced by plasma cells)
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Nitrogenous compounds
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amino acids
 from dietary protein or tissue breakdown
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nitrogenous wastes (urea)
 toxic end products of catabolism
 normally removed by the kidneys
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Nutrients
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O2 and CO2
Electrolytes
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18-7
glucose, vitamins, fats, minerals, etc
Na+ makes up 90% of plasma cations
BUN
Creatinine
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Iron
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ferric (Fe3+) and ferrous (Fe2+)
 stomach acid converts Fe3+ to absorbable Fe2+

gastroferritin binds Fe2+ and transports it to intestine
 absorbed into blood and binds to transferrin for transport
 bone marrow for hemoglobin, muscle for myoglobin and all
cells use for cytochromes in mitochondria
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Vitamin B12 and folic acid
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Vitamin C and copper
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18-8
rapid cell division
cofactors for enzymes synthesizing RBCs
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Disc-shaped cell with thick rim
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18-9
7.5 M diameter and 2.0 m thick at rim
blood type determined by surface glycoprotein and
glycolipids
cytoskeletal proteins give membrane durability
18-10
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Gas transport - major function

increased surface area/volume ratio
 due to loss of organelles during maturation
 increases diffusion rate of substances
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33% of cytoplasm is hemoglobin (Hb)
 O2 delivery to tissue and CO2 transport to lungs
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Carbonic anhydrase (CAH)
produces carbonic acid from CO2 and water
 important role in gas transport and pH balance
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18-11
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Are your red blood cells
Carry oxygen from the
lungs to your tissues
Contain hemoglobin, a
protein molecule that
actually carries the O2
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Anemia is a low amount of hemoglobin in the blood,
sometimes caused by too few RBCs.
Symptoms:
 Pallor
 Weakness
 Tiredness
 Unable to
exercise
without getting
out of breath
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RBC count and hemoglobin concentration
indicate amount of O2 blood can carry
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hematocrit (packed cell volume) - % of blood
composed of cells
 men 42- 52% cells; women 37- 48% cells
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hemoglobin concentration of whole blood
 men 13-18g/dL; women 12-16g/dL
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RBC count
 men 4.6-6.2 million/L; women 4-2-5.4 million/L
18-14
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Adult produces 400 billion platelets, 200 billion RBCs
and 10 billion WBCs every day
Hemopoietic tissues produce blood cells
yolk sac produces stem cells
 liver stops producing blood cells at birth
 spleen remains involved with WBC production
 red bone marrow
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 pluripotent stem cells
 hemopoiesis produces RBCs, WBCs and platelets
18-17

Negative feedback control
drop in RBC count causes
kidney hypoxemia
 EPO production stimulates
bone marrow
 RBC count  in 3 - 4 days
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Stimulus for erythropoiesis
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18-18
low levels O2
increase in exercise
loss of lung tissue in
emphysema
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2.5 million RBCs/sec
Development takes 3-5 days
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First committed cell - erythrocyte colony forming unit
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has receptors for erythropoietin (EPO) from kidneys
Erythroblasts multiply and synthesize hemoglobin
Discard nucleus to form a reticulocyte
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18-19
reduction in cell size, increase in cell number, synthesis of hemoglobin
and loss of nucleus
named for fine network of endoplasmic reticulum
0.5 to 1.5% of circulating RBCs
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RBCs lyse (pop) in narrow channels in spleen
Macrophages in spleen
Globins hydrolyzed into
 digest membrane bits
amino acids
 separate heme from globin
18-20
Iron removed from heme and
converted (stepwise) into
bilirubin
Bilirubin
 is released into blood
plasma (kidneys - yellow
urine)
 liver secretes into bile
 concentrated in gall
bladder: released into small
intestine; bacteria create
urobilinogen (brown feces)
18-21

Polycythemia - an excess of RBCs
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primary polycythemia
 myeloproliferative disorder
 erythropoietic cell line in red bone marrow
 hematocrit as high as 80%!!
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secondary polycythemia
 from dehydration, emphysema, high altitude, or physical
conditioning
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Dangers of polycythemia
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increased blood volume, pressure, viscosity
 can lead to embolism, stroke or heart failure
18-22
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Inadequate erythropoiesis or hemoglobin synthesis
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inadequate vitamin B12 from poor nutrition or lack of
intrinsic factor (pernicious anemia)
Don’t make
iron-deficiency anemia
enough
kidney failure and insufficient erythropoietin
aplastic anemia - complete cessation
Hemorrhagic anemias
Hemolytic anemias
18-23
Lose cells
faster than
you can
make them
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Tissue hypoxia and necrosis (short of breath and
lethargic)
Low blood osmolarity (tissue edema)
Low blood viscosity (heart races and pressure drops)
18-24
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Hereditary Hb ‘defect’ of African Americans
 recessive allele modifies hemoglobin structure
 sickle-cell trait - heterozygous for HbS
 individual has resistance to malaria
 HbS indigestible to malaria parasites
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sickle-cell disease - homozygous for HbS
 individual has shortened life
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18-25
in low O2 concentrations HbS causes cell elongation and sickle shape
cell stickiness causes agglutination and blocked vessels
intense pain; kidney and heart failure; paralysis; stroke
chronic hypoxemia reactivates hemopoietic tissue
 enlarging spleen and bones of cranium
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1 in 500 African
Americans have the
disease
1 in 1000 to 1400
Hispanic-Americans
18-26
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Platelets (thrombocytes)
Fibrinogen
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Small fragments of megakaryocyte cytoplasm
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Functions
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18-28
2-4 m diameter; contain “granules”
amoeboid movement and phagocytosis
secrete vasoconstrictors
stick together to form temporaryplatelet plugs
secrete clotting factors
initiate formation of clot-dissolving enzyme
phagocytize bacteria
chemically attract neutrophils and monocytes to sites of
inflammation
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All 3 steps involve platelets
18-29
pain receptors
 smooth muscle injury
 platelets release serotonin (vasoconstrictor)
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18-30
broken vessel exposes collagen
platelet pseudopods stick to damaged vessel and other
platelets
 pseudopods contract and draw walls of vessel together
forming a platelet plug
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18-31
Platelets degranulate releasing substances that initiate
fibrin clot
 Fibrinogen (in plasma) is converted into fibrin threads
which form the clot
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18-32
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Most of the clotting factors are made in the liver
Liver diseases compromise clotting
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Clot retraction occurs within 30 minutes
Platelet-derived growth factor secreted by platelets
and endothelial cells
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Fibrinolysis (dissolution of a clot)
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18-34
repair damaged vessel
plasmin, a fibrin-dissolving enzyme (clot buster)
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Genetic lack of any clotting factor affects coagulation
Sex-linked recessive (on X chromosome)
hemophilia A missing factor VIII (83% of cases)
 hemophilia B missing factor IX (15% of cases)
note: hemophilia C missing factor XI (autosomal)
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Physical exertion causes bleeding and excruciating
pain
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18-35
transfusion of plasma or purified clotting factors
factor VIII produced by transgenic bacteria
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Embolism - clot traveling in a vessel
Thrombosis - abnormal clotting in unbroken vessel
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most likely to occur in leg veins of inactive people
pulmonary embolism - clot may break free, travel from veins
to lungs
Infarction may occur if clot blocks blood supply to an
organ (MI or stroke)
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18-36
650,000 Americans die annually of thromboembolism
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18-38
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Conspicuous nucleus
Travel in blood before migrating
to connective tissue
Protect against pathogens
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Granulocytes
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neutrophils (60-70%)
 fine granules in cytoplasm; 3 to 5 lobed nucleus
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eosinophils (2-4%)
 large rosy-orange granules; bilobed nucleus
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basophils (<1%)
 large, abundant, violet granules (obscure a large S-shaped nucleus)
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Agranulocytes
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lymphocytes (25-33%)
 variable amounts of bluish cytoplasm (scanty to abundant);
ovoid/round, uniform dark violet nucleus
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monocytes (3-8%)
 largest WBC; ovoid, kidney-, or horseshoe- shaped nucleus
18-39
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Neutrophils ( in bacterial infections)
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Eosinophils ( in parasitic infections or allergies)
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phagocytosis of antigen-antibody complexes,
allergens and inflammatory chemicals
release enzymes to destroy parasites
Basophils ( in chicken pox, sinusitis, diabetes)
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18-40
phagocytosis of bacteria
release antimicrobial chemicals
secrete histamine (vasodilator)
secrete heparin (anticoagulant)
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Lymphocytes ( in diverse infections and
immune responses)
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destroy cells (cancer, foreign, and virally infected cells)
“present” antigens to activate other immune cells
coordinate actions of other immune cells
secrete antibodies and provide immune memory
Monocytes ( in viral infections and inflammation)
differentiate into macrophages
 phagocytize pathogens and debris
 “present” antigens to activate other immune cells

18-41
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Hematocrit
Hemoglobin concentration
Total count for RBCs, reticulocytes, WBCs, and platelets
Differential WBC count
RBC size and hemoglobin concentration per RBC
18-42
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Leukopoiesis
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pluripotent stem cells – most WBCs develop in the bone
marrow
T lymphocytes complete development in thymus
Red bone marrow stores and releases granulocytes
and monocytes
Circulating WBCs do not stay in bloodstream
granulocytes leave in 8 hours and live 5 days longer
 monocytes leave in 20 hours, transform into macrophages
and live for several years
 WBCs provide long-term immunity (decades)

18-43
Fig. 18.18
18-44