Chapter 19: The Cardiovascular
System: Blood
Functions of Blood
 ________________
 Oxygen from lungs to cells, CO2 from cells
 Nutrients from GI tract
 Hormones
 Heat and waste
 ___________
 Homeostasis of body fluids
 pH, temperature, osmotic pressure
 _______________- from excessive blood loss & disease
 Clotting
 WBC
 Proteins, Ab, interferon, complement
Components,
Fig 19.1, table 19.1
_____________ - 55% of whole blood
Water, proteins, others
__________________- 45%
RBC = erythrocytes (4.8- 5.4 million/l blood)
WBC = leukocytes, 5 types, (5-10,000/ l blood)
Agranulocytes= Lymphocytes, monocytes
Granulocytes= Neutrophils, eosinophils, basophils
Platelets = thrombocytes; from megakaryocytes;
(150-400,000/l)
Plasma, specific components
Water
Solutes
Proteins- albumin, globulins, clotting factors
Antibodies are _________________- produced
during immune responses against bacteria & viruses
Nutrients- simple sugars, amino acids, fats
Electrolytes- various salts
Gases- oxygen and carbon dioxide
Waste products- byproducts of metabolism:
urea, uric acid, creatinine, ammonia, bilirubin
Normal blood smear
Physical characteristics
Denser, more viscous than water
Temp = 38°C = 100.4°F
Slightly alkaline pH = 7.35 - 7.45
___________________________ is blood
8% body mass
_____________ (1.5 gal) in average male
4-5L (1.2 gal) in avg. ♀
Formation of blood cells Fig 19.3
 ____________- how formed elements are made
 Before birth- in yolk sac of embryo
 In fetus- liver, spleen, thymus and lymph nodes
 Red bone marrow - 1° site last 3 months of fetal
development & continues to be thru out life
 Highly vascularized
 Microscopic spaces in spongy bone
 From pluripotent stem cells
 Rate of production  in adulthood and becomes
predominantly yellow bone marrow
 Marrow  sinusoids (enlarged, leaky capillaries) 
circulation
Red Blood Cells = Erythrocytes
 General Structure: biconcave disk, 7-8 μm
 Function: ____________________
Hemoglobin (Hb) – oxygen carrying protein that gives
blood it’s red color, binds 4 oxygen molecules
 ______________- % of total blood volume that
is occupied by RBC
Normal range adults: ♀ 38-46%, ♂ 40-54%
 Testosterone stimulates erythropoietin- hormone that
stimulates RBC production
 Production – new mature RBC must enter the
bloodstream at least 2 million/ second to = their
rate of destruction
Structural Characteristics
RBC Physiology
 ____________________ for oxygen transport
No nucleus, all space for oxygen storage
Lack mitochondria for ATP generation  do not USE
any of the O2 they transport
Shape facilitates function
 ↑ surface area  ↑ surface for gas diffusion
 280 million Hb / RBC, each Hb can bind 4 O2
 120 day life–wear & tear, no nucleus no repair
Destroyed in spleen and liver & recycled
 ________ on plasma membrane account for
ABO blood types & Rh factor
Hb = 2α, 2β chains; 1 heme with Fe2+ /chain
Figure 19.5 formation & destruction
Erythropoiesis
Figure 19.6
Production of RBC
Start in RB marrow w/ proerythroblast
Divides several times
Ejects nucleus  reticulocyte = immature
Loss of nucleus causes indentation
______________ pass from RB marrow to
bloodstream- squeeze thru endothelial
cells of capillaries called sinusoids
RBC destruction
Fig. 19.5, 6
 If erythropoiesis ≠ destruction, neg. feedback
loop to ↑ RBC production
If cellular oxygen is deficient = _________,
stimulates kidney to release erythropoietin
High altitude – lower O2 content in air
Circulatory problems
________- # RBC or Hb content low (some causes:)
• Lack of iron
• Lack of certain a.a.
• Lack Vitamin B12
 Breakdown & recycling at liver, spleen, or RB
marrow
Erythrocyte Disorders
 ________________ – disorder characterized by >
normal hematocrit (>55%) in which hypertension,
thrombosis (clot in an unbroken vessel), & hemorrahage
(bleeding) can occur
 Anemias- O2 carrying capacity reduced, fatigued,
intolerant to cold, may appear pale:
 Iron deficiency
 Megoblastic- inadequate Vitamin B12 or folic acid
 Pernicious- insufficient hemopoiesis
 Hemorrhagic- excessive loss of RBC
 Hemolytic- RBC rupture prematurely
 Thalassemia- Hb deficiency
 Aplastic- destruction of RB marrow
Erythrocyte disorders (2)
Fig 19.14
 Sickle-Cell Disease (SCD) – RBC contain Hb-S,
an abnormal Hb
Hb-S gives up oxygen to interstitial fluid it forms a
long, rod-like structure,  sickle shape
Some degree of ____________
Mild ____________- yellowness of skin, eyes,
membranes due to build up of bilirubin
Joint, bone pain; breathlessness, rapid h.r., fever,
fatigue due to tissue damage & oxygen debt
__________________
2 defective genes = severe
one gene = minor problems
Leukocytes = WBC
Fig. 19.7, 8
 Types: granular and agranular
 All have nuclei, no Hb
 Functions- each of 5 have specific functions
 See table 19.3
 Far less numerous than RBC
 Avg 5-10,000 cells / μl of blood
 ________________________ > 10,000 cells / μl of blood
• Normal protective response: microbes, strenuous exercise, anesthesia,
surgery
 ________________________ < 5,000 cells / μl of blood
• Never beneficial– caused by radiation, shock, chemotherapy
 Cell life = hours to few days, but T & B memory can live
for many years once established
Granulocytes
fig 19.7, table 19.3
 ______________________= 60-70%
 Phagocytosis
 destruction of bacteria w/ lysozyme, defensins, & strong
oxidants
 ______________________= 2-4%
 combat histamine effects in allergic rxns
 phagocytize A-Ab complexes
 destroy certain parasitic worms
 _______________ = 0.5-1%
 liberate heparin (prevents clotting)
 histamine (vasodilate, ↑perm of bv, constricts airway)
 serotonin in allergic rxns
Agranulocytes
fig 19.7, table 19.3
 __________________ = 20-25%
mediate immune responses- A-Ab rxns
B cells develop into plasma cells, secrete Ab
T cells attack invading viruses, cancer cells,
transplanted tissue cells
Natural killer cells attack wide range of infectious
microbes & certain spontaneous arising tumor cells
 ___________________ = 3-8%
Phagocytosis
transform into fixed or wandering macrophages
Emigration (aka diapedesis)
Fig 19.8
 How WBC leave bloodstream
Rolling along the endothelium, stick to it, squeeze
between endothelial cells
 Precise signals stimulate, vary for different types
Adhesion molecules- ____________ tether neutrophils
to endothelium & assist in movement to ECF
Neutrophils & macrophages are phagocytic
 _____________ -microbe secretions attract phagocytes
Neutrophils- quick responders:
 Lysozyme, strong oxidants, defensins- proteins that
exhibit broad range antibiotic activity  bacteria & fungi
Phagocytosis (in ch 22)
Inflammation
Immunity
 State of being resistant to injury, particularly by
poisons, foreign proteins, & invading pathogens
______________– due to an individual’s biological
makeup
Antibodies, skin, stomach acid, mucous, coughing,
enzymes in saliva & tears, skin oils
______________ – acquired due to injection of
vaccine, dead or attenuated pathogens or
immunoglobulins
______________ – resistance to disease or infection
due to one’s immune system functioning to produce
antibodies
______________ – acquired by transfer of serum
from another animal produced by sensitized
lymphocyte, or mother to fetus
Antigen - Antibody
 _____________ (A) – substance provoking
immunogenicity and reactivity (react w/Ab or cells that
result from immune response)
 On RBC = agglutinogens = glycoproteins or glycolipids
 Categorized the blood groups: A, B, AB, O; also Rh
 ____________ (Ab) - protein produced by a plasma cell
to specific antigen
 Combine with Antigen to neutralize, inhibit or destroy it
 __________________ – clumping of microorganisms or
blood cells due to A-Ab rxn
MHC Antigens
Major _________________ (MHC)
antigens – surface proteins on WBC &
other nucleated cells that are unique to
each person (except identical twins)
Used for tissue typing
Leukemias
 group of RB marrow cancers, abnormal WBC multiply
uncontrollably
 accumulation of cancerous WBC interferes w/production of RBC,
WBC & platelets
 O2 carrying capacity , more susceptible to infection, abnormal clot
 Cancerous WBC spread to lymph nodes, liver, & spleen causing
enlargement
 Anemia, weight loss, fever, night sweats, excessive bleeding,
recurrent infections
 Cause- unknown, risk factors: radiation, chemotherapy, genetic
disorders, environmental factors, microbes
 Acute- symptoms develop rapidly (adults or children)
 Chronic- take years to develop (usually just adults)
 Treatment- chemotherapy, radiation, stem cell transplant,
interferon, Ab, blood transfusion
Platelet formation
Hemostasis
Fig 19.11
 1. _____________ – smooth muscle contraction in rxn to
damage
 2. ______________________ – platelets adhere,
activate, liberate contents, aggregation forms plug
 3. ___________________ – fibrin threads form
 4. ________________________ - contraction of fibrin
threads to tighten clot, release factors to strengthen
 5. ______________ – enzyme digests clot
 Fibrinolytic system – dissolves small inappropriate clots
 Streptokinase – first thromolytic agent for dissolving clots in
coronary arteries, approved 1982
Coagulation time
 Time required for blood to coagulate, 2-6 min
 Can be prolonged due to the following:
__________________ – X chromosome linked disorder
resulting in deficiency of clotting factor VIII (type A) or
deficiency of factor XI (type B & C)
 Spontaneous or traumatic subcutaneous intramuscular
hemorrahaging, nose bleeds, blood in urine
Obstructive jaundice – obstructing bile flow
Some anemias and leukemias
Some of infectious diseases
Blood typing
Fig 19.12-19.14
Human Blood Groups
ABO Blood Groups
Rh Blood Groups
Transfusion rxns:
Agglutination
Hemolysis
Blood Typing
Table 19.5 - frequency of types
Table 19.6 - group interactions
Transfusion
RBC only or blood plasma only is
transferred into the bloodstream or directly
into red bone marrow
INCOMPATIBLE BLOOD TYPE:
Agglutination rxn – recipient’s
____________bind to the _____________
A-Ab complex activate plasma proteins to the
complement family
Make the plasma membrane of donated cells leaky
_________________ – rupture of cells, loss of Hb
Rh factor
Fig 19.13
 Antigen discovered in Rhesus monkey
 Rh+ have antigen, Rh- do NOT have antigen
 Normally, plasma does not contain anti-Rh Ab
If Rh- person receives Rh+ transfusion immune
system will start to make anti-Rh Ab that will remain
in blood. Problem: _____________ of Rh+ occurs
later, Anti-Rh Ab that have been building can cause
agglutination of donated blood  hemolysis
Hemolytic disease of newborn (HDN)- if fetal blood
(Rh+) leaks across placenta, exposure to Rh-A 
mother (Rh-) making anti-Rh, prob – 2nd baby RH+