BLOOD

River of life
Transport everything that must be carried from one place to another
within the body (nutrients(sugar, protein), hormones, wastes(metabolic)
& body heat) through blood vessels
Only fluid tissue in the body (Tissue group of cells with same function)
Connective Tissue cells, extracellular matrix(plasma)
Has both solid and liquid components

COMPONENTS OF BLOOD

Complex connective tissue in which living blood cells (Formed

elements) are suspended in nonliving matrix (Plasma)
Collagen and elastin fibers are absent but dissolved proteins become
visible fibrin strands in blood clotting
Erythrocytes/RBC

reddish mass at the bottom

formed elements that function in oxygen transport

Buffy Coat

Thin whitish layer at the junction between RBC and plasma

Contains the remaining formed elements, leukocytes (WBC

that protect body) and platelets (cell fragments that stop
bleeding)
Hematocrit percentage/blood fraction of RBC in blood

PHYSICAL REPRESENTATION OF BLOOD

Sticky opaque fluid with a characteristic metallic state
Salty metallic taste because of Iron
Color depends on the amount of oxygen (oxygenation of RBC) it is
carrying

Scarlet oxygen rich

Dull red oxygen poor

Heavier than water and because of its formed elements
5 times thicker (viscous) because of RBCs
Slightly alkaline (pH- 7.35-7.45)
Temperature slightly higher than body temperature (38 C or 100.4 F)
because one of its function is to remove heat
Accounts for approximately 8% of the body weight
5 to 6 liters (6 quarts) healthy man
Plasma
90% water liquid part of blood
Straw-colored due to dissolved substances

Nutrients(glucose, fatty acid, AA, vitamins)

salts(electrolytes Na(osmotic), K(pH buff), Ca, MG, Cl,

bicarbonate(membrane permeability))

respiratory gas (O2 CO2)

hormones(steroid and thyroid hormone)

plasma proteins

waste products of cell metabolism (urea)

Plasma proteins

Most abundant solutes in plasma

Mostly made by the liver (except antibodies & protein based

hormones)

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Cannot be used by cell as source of energy/fuel/metabolic

nutrients (sugar, amino acids can be used as fuel)

Composition of plasma varies continuously (after eating, etc)

Albumin acts as a carrier to shuttle certain molecules

through circulation ;; important blood (ph) buffer ;; contribute
to osmotic pressure of blood (which acts to keep water in
bloodstream)

Clotting proteins(Fibrinogens) help stem blood loss when a

blood vessel is injured

Antibodies(Globulins) help protect body from pathogens

Not taken up by the cells to be used as food fuels/metabolic

nutrients, as are other solutes such as glucose, fatty acids
and oxygen
Composition of plasma varies continuously as cells remove or add
substances to the blood
Composition of plasma is kept relatively constant by various
homeostatic mechanisms of the body

When blood proteins drop to undesirable levels, the liver is

stimulated to make more

When blood starts to become too acid (acidosis) or too basic

(alkalosis), respiratory system and kidneys restores it to
normal slightly alkaline pH
Helps to distribute body heat, a by-product of cellular metabolism

FORMED ELEMENTS
Erythrocytes
Red blood cells
Ferry oxygen to all cells of the body
fit between cell structure and function
Differ from other blood cells (biconcave) because they are
Anucleate(lack nucleus) and contain few organelles
Literally bags of hemoglobin molecules
Hemoglobin

Iron bearing protein

Transport bulk of the oxygen that is carried in the blood

Also binds with a small amount of CO2

A single RBC contains about 250 million hemoglobin

molecules (billion oxygen)

Each hemoglobin molecules can bind 4 oxygen molecules

The more hemoglobin the RBCs contain, the more oxygen

they will be able to carry

Contain to a-chain and 2 b-chain

12-18 grams of hemoglobin per 100 ml of blood

Hemoglobin is slightly higher for men than women

Lack mitochondria and make ATP by anaerobic respiration, they do not
use up any oxygen they are transporting making them efficient oxygen
transporters
Small flexible cells shaped like biconcave discs (flattened sheets with
depressed centers on both sides
Look like miniature donuts because of their thinner centers
Their small size and peculiar shape provide a large surface area
relative to their volume, making them ideally suitable for gas exchange
Outnumbers WBC by 1000 to 1

5 million per mm3 (cubic millimeter)

Number of RBC/mm3 increases, viscosity increases

Number of RBC decreases, blood thins and flows more

rapidly
More hemoglobin molecules the RBCs contain, the more oxygen they
will be able to carry
Destined to die (3-4 months life span) because they dont have any
nucleus so no proteins (also doesnt have ER and mitochondria)

Homeostatic Imbalance
Anemia - decrease in the oxygen carrying ability of the blood

May be a result of:

Lower than normal number of RBCs

Hemorrhagic anemia losing blood because of

external/internal cut ;; gatric ulcer

Hemolytic anemia - RBCs are rupturing

Pernicious anemia secondary to lack of particular

nutrient(iron, folic acid, vit B 12) that would be needed
in production to RBC

Aplastic anemia reduction of production of RBC in

bone marrow bec cancer(leukemia)

Abnormal or deficient hemoglobin content in the RBCs

Sickle cell anemia

Iron deficiency anemia iron binds oxygen to

hemoglobin
Sickle Cell Anemia

The abnormal hemoglobin formed becomes spiky and sharp when

the RBCs unload oxygen molecules or when the oxygen content of
the blood is lower than normal, as during vigorous exercise, anxiety
or other stressful situation

The stiff, deformed erythrocyte rupture easily and dam up in small

blood vessels (interfere with oxygen delivery and can cause
extreme pain)

Single nucleotide GAG(Glutamine) GTG (Valine)

Havoc results from a change in just 1 AA in 2-4 polypeptide chains

Sickle cell trait sickling gene that can be passed on

Polycythemia

Excessive or abnormal increase in number of RBC

May result from bone marrow disease/cancer(polycythemia vera)

May be normal physiologic response to living at high altitudes

where air is thinner and less oxygen I available (secondary
polycythemia)

Causes blood to flow sluggishly and impairs circulation

Blood becomes more viscous/thicker

Leukocytes
White blood cells
Crucial to body defense against disease
4000 to 11000 WBC/mm3 (in book 4800-10800)
Account for less than 1% of total blood volume
Only complete cells in blood (contain nuclei and usual organelles)
Form a protective, movable army that helps defend the body against
damage by bacteria, viruses, parasites and tumor cells
Diapedesis ability of WBC to slip in and out of blood vessels where
there is infection (unlike RBCs are confined in bloodstream)
Circulatory system is simply their means of transportation to areas of
the body where their services are needed for inflammatory and immune
response
Positive Chemotaxis ability to locate areas of tissue damage and
infection in the body by responding to certain chemicals that diffuse
from damaged cells
Once they have caught the scent the WBCs move through tissue
spaces by AMOEBOID MOTION (they form flowing cytoplasmic
extensions that help them move along)
Leukocytosis

Total WBC count is above 11000 cells/mm3

Indicates that a bacterial/viral infections is stewing in the

body
Leukopenia

Abnormally low WBC count

Caused by certain drug (corticosteroids and anticancer

agents)
Classified into 2 major groups

Granulocytes

Agranulocytes

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Granulocytes
Granule-containing WBCs
Have lobed nuclei (which typically consist of several rounded nuclear
areas connected by thin strands of nuclear malt)
Granules stain with Wrights stain
Neutrophils both red and blue

Most numerous of the WBCs

Multilobed nucleus

Fine granules respond to both acidic and basic stains

Cytoplasm stains pink, has fine granules that are difficult to

see, deep purple nucleus has 3-7 lobes connected by thin
strands of nucleoplasm

Avid phagocytes at sites of acute infections

Particularly partial to bacteria and fungi (which they kill

during a respiratory burst that deluges the phagocyte
invaders with a potent brew of oxidizing substances (bleach,
hydrogen peroxide and others))
Eosinophils - red

blue-red nucleus that resembles an old fashioned telephone

receiver (figure 8 or bilobed)

sport coarse, lysosome-like, brick red cytoplasmic granules

number increases during allergies and infections by parasitic

worms(flatworms, tapeworms) ingested in food(raw fish) or
entering via skin
Basophils - blue

Rarest

U or S shaped nucleus with constrictions, dark blue

Large histamine-containing granules that stain dark blue

Histamine inflammatory chemical that makes blood

vessels leaky and attracts other WBCs to inflammatory site
Agranulocytes
Lack visible cytoplasmic granules
Nucleus closer to norm (spherical, oval or kidney shaped)
Lymphocytes

Large, dark purple nucleus that occupies most cell volume

(spherical/slightly dented)

Cytoplasm pale blue and appears as thin rim around

nucleus

Produces ANTIBODIES

Only slightly larger than RBCs

Tend to take up residence in lymphatic tissues

Not phagocytic
Monocytes

Largest of the WBCs

More abundant gray-blue cytoplasm and blue purple

distinctive U/kidney shaped nucleus (resemble lymphocytes)

When they migrate into the tissues, they change into

macrophages with huge appetites

Macrophages important in fighting chronic infections

(tuberculosis) ;; phagocytic cells

**** most abundant to least Never Let Monkeys Eat Bananas

Homeostatic Imbalance
Leukemia excessive production of abnormal WBCs

Literally white blood

Bone marrow becomes cancerous and huge number of WBCs are

turned out rapidly

Severe anemia and bleeding problems might result

Platelets
Thrombocyte
Not cells in strict sense
Fragments of multinucleated cells called MEGAKARYOCYTE (pinch off
thousands of anucleate platelet pieces that quickly seal themselves
off from the surrounding fluids)
Appear as dark staining irregularly shaped bodies scattered among
other blood cells
Normal platelet count: 300,000/mm
Needed for the blood clotting process that occurs in plasma when blood
vessels are ruptures/broken
HEMATOPEOSIS
Blood cell formation
Occurs in red bone marrow/myeloid tissue from a common stem cell
(HEMOCYTOBLAST)

Forms 2 descendants

Lymphoid stem cell: lymphocytes

Myeloid stem cell: all other classes of formed

elements
Adult tissue is found on flat bones of skull and pelvis, ribs, sternum
and proximal epiphyses of humerus and femur
Each type of blood cell is produced in different numbers in response to
changing body needs and different stimuli (hormones)

Formation of Red blood Cells

Hemocytoblast Proerythroblast Erythroblast
Stimulated by hormones
RBCs- anucleate so they are unable to synthesize proteins, grow or
divide
RBCs fall apart/fragment in 100-120 days
Remains are eliminated by phagocytes in spleen, liver and other body
tissues
Lost cells are replaced continuously by division of hemocytoblasts in
the red bone marrow (flat bones, skull, sternum, ribs, pelvic bone,
proximal epiphysis)
Developing RBCs divide many times then begin synthesizing huge
amounts of hemoglobin
Mag-ipon muna ng hemoglobin which is a protein yung nucleus
When enough hemoglobin has been accumulated, nucleus and most
organelles are ejected out (cell collapses inward) producing the young

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RBC called RETICULOCYTE (bec it still contains ER) (usually found in

bone marrow but sometimes blood hemorrhagic anemia)
Reticulocyte enter the bloodstream to begin their task of transporting
oxygen. Within 2 days, they ejected ER and become fully functioning
erythrocytes (mature)
3-5 days entire developmental process from hemocytoblasts to
mature RBS
Erythropoietin

Hormone that controls rate of production of erythrocyte

(normally small amount of it circulates in the blood and
RBCs are formed at a fairly constant rate)

produced in the kidneys (sometimes liver) step up their

release of it when blood levels of O2 begin to decline

targets bone marrow, prodding it to high gear to turn out

more RBCs
Overabundance of erythrocytes/excessive amount of oxygen
depresses erythpoietin release and RBC production
It is not the number of RBCs in blood that controls RBC production
Control is based on their ability to transport enough oxygen to meet the
bodys demands

Formation of White Blood Cells and Platelets

Stimulated by hormones
Colony Stimulating Factors (CSFs) & interleukins

Prompt red bone marrow to turn out leukocytes

Marshall up an army of WBCs to ward off attacks by

enhancing the ability of mature leukocytes to protect body

Released in response to specific chemical signals in

environment (inflammatory chemicals & certain bacteria and
their toxins)
Thrombopoietin

hormone that accelerates the production of platelets from

megakaryocytes
Flat bones of Ilium/Sternum injection for blood marrow
Bone Marrow Biopsy microscopic examination

HEMOSTASIS
Normally, blood flows smoothly past intact lining (endothelium) of blood
vessels
If blood vessel breaks, a series of reactions is set in motion to
accomplish HEMOSTASIS or stoppage of bleeding
Fast and localized
Involves many substances found in plasma, platelets and injured
tissues
Blood loss at the site id permanently prevented when fibrous tissue
grows into the clot and seals the hole in the blood vessel
Three major phases/stages:
1. Vascular Spasms/Vasoconstriction

Immediate response to blood vessel injury is

vasoconstriction (which causes blood vessels to go to
spasms)

Spasms narrow the blood vessel at that point, decreasing

blood loss until clotting can occur

Other factors causing spasms: direct injury to smooth

muscle cells, stimulation of local pain receptors & release of
serotonin by anchored platelets)
2. Platelet plug forms/Platelet Aggregation

Platelets are repelled by intact endothelium, but when it is

broken so that the undelying collagen fibers are exposed,
the platelets become sticky and cling to damage site

Anchored platelets release chemicals that enhance the

vascular spasms and attract more to the site

Platelet plug/White thrombus small mass formed as more

platelets pile up
3. Coagulation/Blood Clotting

Injured tissues are releasing TISSUE FACTOR which

interact with PF3 (phospholipid that coats the surfaces of
platelets)

This combination interacts with other blood protein clotting

factors and Ca2+ to form an activator that leads to formation
of THROMBIN (enzyme)

Thrombin joins soluble FIBRINOGEN proteins into long hairlike molecules of insoluble FIBRIN (meshwork that traps
RBCs and forms the basis for the clot) forms red thrombus ;;
too much fibrinogen means bleeding

Within an hour, the clot begin to retract, squeezing serum

(plasma minus the clotting proteins) from the mass and
pulling the ruptures edges of the blood vessels closer
together
Blood clots in 3-6 minutes
Once clotting cascade has started, the triggering factors are rapidly
inactivated to prevent widespread clotting (Solid blood)
Then endothelium regenerates and clot breaks down
Placing a sterile gauze (provides rough surface to which platelets can
adhere)/applying pressure(fracture cells, increasing release of tissue
factor locally) would speed up clotting process

Disorders of Hemostasis
Undesirable Clotting
Risk factor: High cholesterol level, hypertension
Thrombus

Too much coagulation/excessive clot formation

Clot that develops and persists in in an unbroken blood

vessel

If it is large enough, it may prevent blood from flowing to the

cells beyond the blockage

Coronary Thrombosis blockage in blood vessels serving in

heart, may lead to death of heart muscle or heart attack
Embolus

If thrombus breaks away from the vessel wall and floats

freely in blood stream

Usually no problem unless it lodges a blood vessel too

narrow for it to pass through

Cerebral Embolus (brain) stroke

May be caused by anything that roughens endothelium of a blood
vessel and encourage clinging of platelets (severe burns, physical
blows or accumulation of fatty malt)
Slowly flowing blood/Blood pooling another risk factor especially in
immobilized patients because clotting factors are not washed away as
usual and accumulate so that clot formation becomes possible
Antiplatelet/Anticoagulants used against thrombus prone patients ;;
aspirin, heparin and dicumarol/warfarin(common rat poison internal
bleeding)
Bleeding Disorders
Thrombocytopenia

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Platelet deficiency
Results from an insufficient number of circulating platelets
Petechiae small purplish blotches on the skin
Can arise from any condition that suppresses the bone
marrow cancer, radiation or certain drug
Impaired liver function

Liver unable to synthesize its usual supply of clotting factors,

abnormal/severe bleeding episodes occur

Vitamin K (needed by liver cells to produce the clotting

factor) is deficient vit K supplements

If liver function is severely impaired (hepatitis & cirrhosis)

only whole blood transfusions are helpful (transfusions of
concentrated platelets provide temporary relief from
bleeding)
Hemophilia

Several different hereditary bleeding disorders that result

from lack of any clotting proteins

Bleeders disease

Males are usually the victims (x chromosoms)

Begin early in life

Repeated bleeding

Given a transfusion of fresh plasma or injections of the

purified clotting factor they lack

Victims of blood transmitted viral disease (hepatitis and

AIDS-acquired immune deficiency syndrome is a condition
of depressed immunity)

BLOOD GROUPS AND TRANSFUSIONS

Body can only compensate loss of blood at certain limit
Losses of 15-30% - pallor & weakness
Losses over 30% - severe shock (fatal)
Whole body transfusions are routinely given to replace substantial
blood loss and to treat severe anemia or thrombocytopenia
Blood bank mixes blood and anticoagulant to prevent clotting
Treated blood stored (ref at 4C/39.2F) for 35 days
Human Blood Groups
Antigen

genetically determined proteins in the plasma membrane of

RBC

identify each person as unique

substance that the body recognizes as foreign

it stimulates the immune system to release antibodies or use

other means to mount a defense against it

foreign proteins (part of viruses or bacteria that invaded the

body)

Each of us can tolerate our own antigen

Anothers antigen will be recognized as foreign

antibodies act
Antibodies

recognizers

Present in plasma that attach to RBCs bearing surface

antigens different from those on the patients RBC

Agglutination and/or hemolysis caused by binding of

antibodies causing the foreign RBC to clump ;; leads to
clogging of small blood vessels throughout body

During next few hours, foreign RBCs are lysed (ruptured)

and their hemoglobin released into bloodstream
Most devastating consequence of severe transfusion freed
hemoglobin molecules may block kidney tubules (causing kidney failure
and death)
May also cause: fever, chills, nausea and vomiting

ABO BLOOD GROUP

Blood Group
AB
B
A
O

Prevent kidney damage - infusing fluids to dilute and dissolve the

hemoglobin and diuretics to flush it out of the body in urine

RBC Antigens
(agglutinogens)
A
B
B
A
None

Plasma antibodies
(agglutinins)
None v
Anti A
Anti B
Anti A & Anti B

Blood can receive

A, B, AB, O
Uni. recipient
B, O
A, O
O
Uni. donor

30 common RBC antigens in the body so each persons blood can be

classified into diff blood groups
ABO blood groups based on which antigen a person inherits (type A or
B)

Absence of both: type O (most common)

Presence of both: type AB

Presence of each yield each types: A & B

Antibodies from during infancy against ABO antigens not present in
your won RBCs

RH Blood groups
Named because 1 of the 8 Rh antigens (agglutinogen D) Rhesus
monkeys
Usually were Rh+
Rh+ - their RBCs carry Rh antigen
Unlike ABO antibodies, Anti-Rh antibodies are not automatically formed
and present in the blood of Rh- individuals
If Rh- person receives Rh+, after transfusion his immune system
becomes sensitized and begins production of antibodies (anti-Rh+)
Hemolysis

Rupture of RBCs

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Does not occur with first transfusion because it take time for
body to react and start making antibodies

Second time and after, patients antibodies attack and

rupture the donors Rh+ antibodies
Hemolytic disease of the newborn (erythroblastosis fetalis)
Rh- women carrying Rh+ babies

First is healthy delivery

Then forms anti-Rh+ bodies destroying babies RBC

producing condition called HEMOLYTIC DISEASE OF THE
NEWBORN (baby becomes anemic and hypoxix and
cyanotic)

Treated with RhoGAM immune serum

BLOOD TYPING
Testing blood by mixing it with 2 different types of immune serum (antiA and anti-B)
Person A mixed with anti A serum Agglutination occurs
Person b Agglutination with anti-B serum
No Agglutination at all Type O
Cross matching: testing for agglutination of donor RBCs by the
recipients serum and of the recipients RBC by the donors serum
Developmental Aspects
Before birth blood cell formation liver and spleen
7 months red marrow
Congenital blood defects include various types of hemolytic anemias
and hemophilias
Fetal Hemoglobin has greater ability to pick up O2 that the adult
Hemoglobin
Physiologic jaundice reflects liver immaturity of infants
Excessive leukocytosis may be indicative of malignancy or leukemia
(common in the very young and very old)
Elderly are at risk for pernicious anemia

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