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Transcript
Blood
Complex Transport Mixture
• Connective Tissue (4-6 liters/person)
• Maintains Homeostasis
– Water / Electrolyte Balance
– Ph Balance
– Temperature Regulation
• Transport Medium
– Nutrients/ Wastes
– Gases: Oxygen/Carbon dioxide
– Hormones, Antibodies
– Red Blood Cells, White Blood Cells
– Clotting Factors and Platelets
Figure 37-7 Blood
Blood Section
Components:
Red Blood Cells, White Blood Cells
37-2
Platelets and Plasma
Plasma
Platelets
White blood
cells
Red blood
cells
Whole Blood
Sample
Sample Placed in
Centrifuge
Spin to separate plasma
from cellular components
Blood Sample
That Has Been
Centrifuged
Blood Composition
Red Blood Cells / White Blood Cells
Plasma: Liquid Portion
Together= Blood
Platelets: cell fragements
Necessary for normal blood
clotting
Blood Components
•
Plasma (55%) Liquid
portion
–
–
–
–
–
–
–
90% Water
Proteins
Salts (Electrolytes)
Nutrients (glucose,
amino acids, fats,
vitamins)
Hormones
Antibodies
Cellular Wastes
(Carbon dioxide,
Urea)
•
Cellular Elements
–
Red Blood Cells
(erythrocytes)
• Contain Hemoglobin,
carry oxygen
–
White Blood Cells
(leukocytes)
•
–
Defend body from
infection/disease
• Phagocytes (eat
invaders)
• Lymphocytes
• (B ) Make antibodies
and “Killer” Ts
Platelets (cell fragments)
•
Blood Clotting
Plasma: Liquid Portion
• Straw-colored liquid (90% water)
• 10% Dissolved substances
– Salts
– Nutrients: Sugars, dissolved fats, amino
acids
– Plasma proteins: clotting factors,
transport proteins
– Hormones (chemical messengers)
– Antibodies (immune response)
– Cellular Wastes
Red Blood Cells (Erythrocytes)
• Contain Hemoglobin (red pigment) that
binds with Oxygen (250 million/RBC)
• Delivers Oxygen
to All body cells
• Biconcave Disks
• No nucleus
• Most abundant of
all blood cells
• Made in Bone Marrow
Platelets: Tiny cell Fragments
• Formed in the Bone Marrow
• Small pieces of Megakaryocytes break –
off and enter the blood circulation
• Platelets carried by blood to sites of
injury
• Release proteins and clotting factors
• Forming Blood clots
Figure 37-10 Blood Clotting
Platelets go to site of injury, form a fibrin net/ ”plug”
Clot Forms -- prevents blood loss from site
Break in Capillary
Wall
Blood vessels
injured.
Clumping of
Platelets
Platelets clump at the
site and release
thromboplastin.
Thromboplastin
converts prothrombin
into thrombin..
Clot Forms
Thrombin converts
fibrinogen into fibrin,
which causes a clot.
The clot prevents
further loss of blood..
Platelets Form a Fibrin Net to
form Clots
“Fighting the
Enemy
Within”
phagocytic
leukocyte
Immune System
lymphocytes
attacking
cancer cell
lymph
system
Why an immune system?
• Attack from the outside & inside
– lots of organisms want you for lunch!
– we are a tasty vitamin-packed meal
• cells are packages of proteins, carbohydrates & fats
• no cell wall
– animals must defend themselves against invaders
• viruses
– HIV, flu, cold, measles, chicken pox, SARS
• bacteria
– pneumonia, meningitis, tuberculosis
• fungi
– yeast
• protists
– amoeba, Lyme disease, malaria
– cancer cells
• abnormal body cells
What’s for
lunch?!
Pathogens and Disease
Section 40-1
Pathogen
Types
Viruses
Bacteria
Common cold
Influenza
Chicken pox
Agent That Causes
Disease
Rhinovirus
Two types (A, B),
plus subtypes
Varicella
Measles
Paramyxovirus
Tuberculosis
Meningitis
Mycobacterium
tuberculosis
Neisseria meningitidis
Vibrio cholerae
Clostridium tetani
Trypanosoma
Disease
Cholera
Tetanus
African sleeping
Protists
sickness
Malaria
Amoebic dysentery
Worms
Schistosomiasis
Beef tapeworm
Fungi
Athlete’s foot
Ringworm
Plasmodium
Entamoeba histolytica
Schistosom
a
Taenia saginata
Imperfect fungi
Imperfect fungi
Method of
Transmission
Airborne; direct contact with infected person
Airborne; droplet infection; direct contact with
infected person
Airborne; direct contact with infected person
Droplets in air; direct contact with secretions of
infected person
Droplets in air; contaminated milk and dairy products
Direct contact with a carrier
Contaminated drinking water
Contaminated wound; usually puncture wound
Spread by tsetse fly
Spread by Anopheles mosquitoes
Contaminated drinking water
Freshwater streams and rice paddies
Contaminated meat
Contact with infected person
Exchange of hats, combs, or athletic head gear with
infected person
How are invaders recognized?
• Antigens
– chemical name tags on the surface of
every cell
• “self” vs. “invader”
one of your
own cells
disease-causing
virus
disease-causing
bacteria
antigens say:
“I belong here”
antigens say:
“I am an invader”
antigens say:
“I am an invader”
The Immune System: Lines of
Defense Against Disease
Nonspecific Defenses
1.
2.
3.
First Line of
Defense
Second Line of
Defense
Interferon
Specific Defenses
1.
2.
3.
C.
D.
B- cells
T-Cells
Permanent
Immunity
Active Immunity
Passive Immunity
Nonspecific Defenses: Include
1st and 2nd Lines
• First Line: BARRIERS: Prevent
Pathogens from entering body
– Skin (largest organ)- Physical barrier; oil &
sweat glands create acidic environment –
killing many pathogens
– Mucus in Nose and Throat – traps bacteria
and viruses and using cilia push away from
entering lungs
– Acids and Digestive enzymes in stomach
destroy many pathogens
– Tears, Saliva, sweat contain Lysozymes
37-9 Our
Types Body’s
of White Blood
Cells
White BloodFigure
Cells:
Defenders
When
pathogens get past barriers,
Section 37-2
WBCs “Get Involoved”
Function
Cell Type
Neutrophils
Eosinophils
Basophils
Monocytes
Lymphocytes
Engulf and destroy small bacteria and foreign substances
Attack parasites; limit inflammation associated with allergic reactions
Release histamines that cause inflammation; release anticoagulants, which
prevent blood clots
Give rise to leukocytes that engulf and destroy large bacteria and
substances
Some destroy foreign cells by causing their membranes to rupture; some
develop into cells that produce antibodies, which target specific foreign
substances
Neutrophil
Monocyte Basophil
Lymphocyte
Eosinophil
Phagocytes
macrophage
bacteria
white blood cells that eat
macrophage
yeast
The Inflammatory Response:
Second Line of Defense
Section 40-2
Nonspecific Response to Tissue Damage
Skin
Wound
Phagocytes move into the
area and engulf the bacteria
and cell debris
Bacteria enter
the wound
Capillary
Injured cells signal capillaries to expand, become “leaky”, allowing more
Phagocytic WBCs to arrive along with Platelets to Patch injury
3rd Line/Specific Defenses:
“Immune Response”
• If pathogens get past the 2nd level of
defense, and enter cells or blood, then the
3rd line of defense is alerted!
• Antigens are protein “markers” on cell
surfaces. “Foreign” antigens are
considered a threat
• Note: Antigens are found on all cells and
viruses; our Lymphocytes attack antigens
that are seen as “non-self”
Types of Lymphocytes
• B Lymphs (B-cells)
• Make ANTIBODIES
– “custom made” , Yshaped Proteins that bind
to and help destroy
foreign antigens
(pathogens)
– Mature B-cells reside and
multiply in our lymph
nodes
– Memory B-cells always
remember the pathogen
• T Lymphs (T-cells)
• Helper T;
– Activate B-cells to
produce antibodies
– Activate Killer-T cells
(recognize pathogen and
divide)
• Killer
T;
– Tears open cells
infected with
pathogens; destroying
the cell and pathogens
inside
Structure of an Antibody
Section 40-2
Antigenbinding
sites
Note: An Antibody
“fits” only one specific
Antigen; all antibodies
are “custom made”
Antigen
Antibody
Antibodies
• Proteins made by B cells that tag invaders
in the blood so macrophages can eat them
– tag says “this is an invader”  gotcha!
• biological “handcuffs”
– antibody attaches to antigen on invader
B cells
releasing antibodies
Y
Y
Y
Y
Y
Y
Y
invading germs tagged
with antibodies
Y
Y
Y Y
Y
Y
macrophage
eating tagged invaders
The Lymphatic System: Network of thin-walled vessels
that collect and filter the fluid seeping out of our
Blood vessels. Lymph nodes, swellings in lymphatic
vessels, contain lymphocytes
Superior
vena cava
Thymus
Heart
Thoracic
duct
Spleen
Lymph nodes
Lymph
vessels
B- Lymphs: Immune Response
Section 40-2
Bacteria With Antigens
on Surface
Bacterial antigens
also stimulate B cells
A large
phagocyte called
a macrophage
engulfs a
bacterium
T cell
Macrophage
Antigens are
displayed on
surface of
macrofage after
digestion of
bacterium
B cell
T cell binds
to activated
macrophage
Helper T cell
assists the
activated B
cell to develop
into an
antibodyproducing
plasma cell
T cell, activated
by
macrophage,
becomes a
helper T cell
Active B cells
proliferate to
produce clones
of memory cells
Plasma cell produces
large amounts of
antibody proteins,
released into
the bloodstream
Circulating antibodies bind to bacterial
antigens, helping other immune cells to
identify and destroy bacteria
Humoral Immunity
Section 40-2
Macrophage
T-Cell
Immune Response
T cell binds to
activated
macrophage
Helper T cell activates
killer T cells and B cells
Helper
T Cell
Killer
T Cell
T Cell
Antigens are displayed
on surface of
macrophage
T cell, activated by
macrophage, becomes a
helper T cell
Cell-Mediated Immunity
Infected Cell
Killer T cells bind to infected
cells, disrupting their cell
membranes and destroying
them
Antibody Concentration
Section 40-2
Primary and Secondary
Immune Responses
Interval
between
exposures
First
exposure
Second
exposure
Provides Permanent
Immunity to pathogen
Time
Memory B-cells respond quickly if re-exposed to a pathogen by
Producing large numbers of antibodies (protecting us from disease)
How Can We Avoid Diseases?
•In the United States, babies and small
children are usually given a series of
vaccines, which protect them from many
infectious diseases.
• A vaccine is an injection of a weakened
or mild form of a pathogen. People may
also receive vaccines against certain
diseases later in their lives.
Vaccination results in Active
Immunity without the Risk
• Receiving dead, weakened or parts of a
pathogen stimulates our immune system
• B lymphocytes ACTIVELY produce
antibodies and MEMORY CELLS
• When ever WE make our own antibodies
and memory cells (for future
protection), it’s called ACTIVE
IMMUNITY
Vaccinations
• Exposure to harmless version of germ
(pathogen)
– stimulates immune system to produce
antibodies to invader
– rapid response if
future exposure
• Most successful
against viral diseases
Passive Immunity: Antibodies
Given to Us Don’t Last Long
• Mothers provide
passive immunity to
their babies
• Antibodies made by
mom are passed to
babies in breast
milk
• The baby will only
be protected while
receiving milk
(short-term)
• Injected antibodies
made by others will
provide only short
term protection
• Borrowed antibodies
are destroyed
within weeks
• Considered passive
because our immune
system did not
make them
Immune System Disorders
•
Allergies: Exaggerated response to
–
non pathogenic Antigens (pollen, food, etc)
Histamines cause
•
•
•
running nose, eyes
Itching and swelling
Anaphylactic Shock
B. Autoimmune Disease: Immune system
mistakenly attacks own body cells
–
–
–
–
MS (Multiple Sclerosis)-destruction of
myelin sheathing of nerves
Myasthenia gravis – antibodies attack
nerve receptors of the muscles
Juvenile-onset diabetes- antibodies
attack insulin-producing cells of
pancreas
Rheumatoid Arthritis
Immune system malfunctions
• Allergies
– over-reaction to harmless compounds
• allergens
– proteins on pollen
– proteins from dust
mites
– proteins in animal
saliva
• body mistakenly
thinks they are
attackers
Immune system malfunctions
• Auto-immune diseases
– immune system attacks own cells
• lupus
– antibodies attack many different body cells
• rheumatoid arthritis
– antibodies causing damage to
cartilage & bone
• diabetes
– beta-islet cells of pancreas
attacked & destroyed
• multiple sclerosis
– T cells attack myelin sheath of
brain & spinal cord nerves
Autoimmune Disease
• Rheumatoid Arthritis
Immunodeficiency Diseases
• People lack one or more parts of the
immune system or it is defective
• Rendering them susceptible to infections
that ordinarily cause no problems
– SCID (Severe Combined Immunodeficiency)deficit in both B and T cells
– AIDS (Acquired immunodeficiency Syndrome)
caused by HIV, a virus that occupies and
suppresses Helper T-cell function
• Death results from the inability to fight other infections
Stages of HIV Infection
As T-cell concentration goes down, HIV concentration goes up
Infection;
Immune
system
eliminates
most of HIV
Symptoms, such as
swollen lymph
nodes, are few
Loss of immune
function more
Almost
apparent; appearance total loss
of characteristic
of cellular
diseases such as
immunity;
yeast infections
AIDS
Relative HIV
concentration
T cell
concentration
Years
HIV interferes with normal Helper-T function (does
not recognize HIV as an Invader) In turn, does not
activate B-cells and Killer T-cells
Blood Transfusions
Section 37-2
Blood
Transfusion: Applying Our knowledge of
Antigen-Antibody interaction to Medicine
Blood Type
of Donor
Antigens on Cells
Blood Type of Recipient
Antigens on Recipient’s cells
A
B
AB
O
A
B
AB
O
Unsuccessful transfusion
Successful transfusion
Recall: We will make antibodies AGAINST Non-Self
Antigens