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IMMUNE SYSTEM

Immune system
Composed of many
interdependent cell types that
collectively protect the body
from bacterial, parasitic, fungal,
or viral infections, and from the
growth of some tumor cells.
Definition of terms:
Immune system
- Group of cells, molecules,
and organs that act
together to defend the body
against foreign invaders
that may cause disease
such as bacterial, viruses of
fungi.
Immunology
- Study of our protection from
foreign macromolecules or
invading microorganism and
our responses to them.
Immunity
- Ability to resist damage
from foreign substances.
Antigen
- Molecules that trigger an
immune response, a protein
that stimulates an immune
reaction, causing the
production of antibodies.
Antibodies
- Proteins that fight
infections, a globulin
produced by B cells as a
defense mechanism against
foreign materials.
Epidemiology
- Study of how disease is
produced, and its
distribution in a given
population.
Pathogens
- Microorganism or
proteinaceous substances
capable of producing
disease.

Virulence
- Ability to cause damage.
Nosocomial infections
- Acquired in health care
setting.
Immune competent
- Client whose immune
system is able to identify
antigens and effectively
destroy or remove them.
Immune compromised
- Whose immune system is
unable to effectively destroy
or remove antigens
Mast cells
- Tissue cells that resemble a
peripheral blood basophil
and that contain granules
with chemical mediators.

Functions of immune system


Defend and protect the body
from infection by bacteria,
viruses, fungi, and parasites
Removing and destroying
damaged or dead cells
Identifying and destroying
malignant cells, thereby
preventing their further
development into tumors.
Development of cells in the
immune system

Types of T-cells
1. Helper T (CD4 + TH) cells
have central role in immune
response, these activate
macrophage and help form
cytotoxic T-cells.
2. Cytotoxic T (CD8 + CTLs)
destroys target cells on contact
by producing perforin that lysis
an infected cells
3. Delayed hypersensitivity T (TD)
cells: mostly T helper and a few
cytotoxic T cells that are
involved in some allergic
reactions (poison ivy) and
rejection of transplanted tissue
4. Suppressor T (TS) cells inhibit
the production of CTL cells to
shut down immune response
once they are unneeded, least
they cause more damage than
necessary
(N.C regulatory T cells)

Innate or natural or Non-specific


immunity
Immunity an organism is born with.
Genetically determined, effective from
birth present before exposure to
pathogens
Non-specific responses to pathogens
Acquired or specific immunity:
Immunity that an organism develops
during lifetime.
Not genetically determined

Develops after exposure to antigens


(microbes, toxins, or other foreign
substances)
Very specific responses to pathogens
maybe acquired naturally or artificially
Specific immune response
- a type of immunity effective
against specific harmful
agents entering the body.
Types:
a. Inborn immunity
- Inherited immunity of
species, races, and
individuals to certain
diseases
b. Acquired immunity
- Immunity that develops as
an individual encounters
specific harmful agents
a. Natural
- Activated by affected
individuals
a. Active contact with the
disease
b. Passive placenta,
breast milk
b. Artificial
- Activated by vaccine
a. Active vaccine killed
attenuated, toxoid
b. Passive immune serum
Non-specific inflammatory response
- Mechanical barriers that
cover the body surfaces and
to cells and chemicals that
act on the initial battle
fronts to protect the body
from invading pathogens
o Surface membrane barriers
- The 1st line of defense of the
body is an intact skin and
mucous membranes
o Chemical barriers
- Acidic gastric juices,
enzymes in tears and saliva,
sebaceous and sweat
secretion.
o Biologic response modifiers
- Interferon, viricidal
substance, counters viruses
and activates other

components of the immune


system.
o Natural killer (NK) cells
- Lymphocytes responsible for
immune surveillance and
host resistance to infection.
Inflammation
3 stages of immune response
Vascular response
characterized by vasodilation
and increased permeability of
blood
Cellular response and
phagocytosis
Tissue repair
Types of acquired immunity
Naturally acquired immunity
- Obtained in the course of
daily life
Naturally acquired active
immunity
Antigens or pathogens enter
body naturally
Persons contract disease;
generates specific immune
response to the antigen
Immunity may be lifelong
(chickenpox or mumps) or
temporary (influenza or
intestinal infections)
Naturally acquired passive
immunity
Antibodies pass from mother to
fetus via placenta or
breastfeeding (colostrum). No
immune response to antigens.
Develops immediately
immunity and is usually shortlived (weeks or months)
Affects all antigens to which the
mother has immunity.
Protection until childs immune
system develops
Artificial acquired immunity
Obtained by receiving a vaccine
or immune serum
Artificial acquired active immunity
Involves production of antibody
following exposure of specially
prepared antigen

Antigens are introduced as


vaccines (immunization)
Body generates an immune
response slowly and is specific
to the antigen for which the
immunization was given
Immunity can be lifelong (oral
polio vaccine) or temporary
(tetanus toxoid and diphtheria
toxoid)

Artificial acquired passive


immunity
Transfer of immunity from the
immunized person to a nonimmunized person by
transferring sensitized cells
E.g. snake ant venom injection
from horses or rabbits
Used in the treatment of
tetanus, diphtheria and mumps
Immunity is immediate, but
short lived (half life 3 weeks)
Affects all antigen to which the
donor has the immunity
Host immune system does not
respond to antigens
Types of acquired immunity
1. Natural acquired active
immunity
2. Natural acquired passively
3. Artificially acquired active
immunity
4. Artificially passive immunity

Immune response:
- Third line of defense
involves production of
antibodies and generation
of specialized lymphocytes
against specific antigens.
Immune system components
1. Leukocytes
1. Engulf and destroy
pathogens (bacteria)
2. Suppress inflammation
3. Fight parasitic infection
4. Produce antibodies and
provide immunity
A. Granulocytes immediate and provide
immunity
Neutrophils
- Phagocytic response to cell
injury
Eosinophil
- Hypersensitivity reaction
Basophil
- Inflammatory response
B. Agranulocytes fight infection
Monocytes
- Phagocytosis
Lymphocytes
- Production of
immunoglobulin

Organs of the immune system


Lymph nodes
Spleen
Bone marrow
Liver
GALT (gut associated lymphoid
tissues)

Lymphocytes
- Lymphocytes mount a dual
defense
2 kinds of (B and T) lymphocytes carry
out the immune responses
1. Humoral immunity
- (Antibody mediated)
involves the production of
antibody by the B cells
which attack Ag
2. Cell mediated immunity
- Is governed by Tlymphocytes. T cells attack
cells infected with
pathogens

3. NK cells
- Neither T/B in killing tumor

Humoral immunity
Apoptosis
Programmed cell death (falling
away)
Human body makes 100 million
lymphocytes everyday. If an
equivalent number doesnt die,
will develop leukemia.
B cells do not encounter
stimulating antigen will selfdestruct and send signals to
phagocytes to dispose of their
remains.
Many virus infected cells will
undergo apoptosis, to prevent
spread of the infection

3 major groups of mature lymphocytes


1. T- cells
- Programmed in the thymus
are the basis of cellmediated immune response
that defends against
intracellular pathogens,
fungi, and viruses.
2. B cells
- Programmed in the bone
marrow
- The basis of antibody
mediated response helping
the body to defend against
invasive types of bacteria,
bacterial toxins and viruses

Immunological memory
Antibody titer
- The amount of antibody in
the serum

Pattern of antibody levels during


infection
Primary response
After initial exposure to antigen,
no antibodies are found in
serum for several days.
A gradual increase in titer, first
of IgM and then IgG is observed
after
3 - 6 days
Most B cells become plasma
cells, but some B cells become
long living memory cells

Peak levels of plasma antibody are


achieved in 10 days gradual decline of
antibodies follows
Secondary response
Subsequent exposure to the
same antigen displays a faster
and more intense antibody
response with an hour
It is due to the existence of
memory cells, which rapidly
produce plasma cells upon
antigen stimulation
Antibody level peak in 2 3
days
Antibody levels in the blood can
remain high for weeks to
months
Monoclonal antibodies
Monoclonal antibodies are pure
antibody preparations
Specific for a single antigenic
determinant
Produced from descendent of a
single cell

Hybridomas
- Cell hybrids made from a
fusion of a tumor cells
(easytogrow) and a B cells
(specific for a single
antigenic determinant)

Uses of monoclonal antibodies


Monoclonal antibodies are powerful
tools in the laboratory
Commercially prepared antibodies
are used:
In research and clinical
testing
To provide passive immunity
These cells are useful in
medical diagnosis
They are also useful in the
treatment of certain cancers
Have desirable properties of
both parent cell indefinite
proliferation as well as the
ability to produce a single
type of antibody
Cytokines
o Mediators involved in
cellular immunity, including
hormone like glycoproteins
released by activated T
cells and macrophages
Interleukin 1 (1L 1)
released by macrophages
co-stimulates bound T cells
to release 1L2
o

1L - 2 is a key growth
factor, which activates T
cells to divide
Other cytokines amplify
and regulate immune and

non-specific responses.
Examples includes:
Perforin and lymphotoxin
cell toxins
Gamma interferon
enhanced the killing power
of macrophages
Inflammatory factors

Antibody mediated
response (humoral)
produced by B lymphocytes
Cell-mediated response
produced by T
lymphocytes.

2 Major Classes of T cells


Effector Cells
- Cytotoxic cells (killer T
cells)
Regulator Cells
- Helper T cells (Majority)amplify activity of killer
T cells
- Suppressor T cells
Hypersensitivity Reaction
Altered immune response
to an antigen that results in
harm to the client

Immune response
Recognition of self and nonself
Antigens

CLASSIFICATIONS
Immediate
- Type I (anaphylactic )
reactions- mediated by
IgE antibody, which
promotes the release of
histamine and other
reactive mediators
- Type II (cytotoxic)
reactions mediated by
IgM and IgG antibodies,
which attach to cells
and cause cell lysis
- Type III (immune
complex) reactions(rheumatoid arthritis)
mediated by antigenantibody complexes
that deposit in the lining
of blood vessels or on
tissue surfaces
Delayed response
- Type IV (delayed
hypersensitivity)
reactions (transplant
rejection) are mediated
by lymphokines
released from sensitized
T lymphocytes
Chemical Mediators of Immediate
Hypersensitivity reactions
Histamine

Leukotrienes- potent
bronchoconstrictor, cause
increased venous
permeability
Prostaglandins- potent
vasodilators and potent
bronchoconstrictors
Cytokines- control and/or
regulate immunologic
functions
Platelet-activating
Factor- causes platelet
aggregation

Effects of Chemical Mediators


1. Generalized
vasodilation,
hypotension, flushing.
2. Increased permeability
a. Capillaries of the
skin
b. Mucous membrane
3. Smooth muscle
contraction
a. Bronchioles
b. Intestines
4. Increased secretions
a. Nasal mucous
glands
b. Bronchioles
c. GI
d. Lacrimal
e. Salivary
5. Pruritus
a. Skin
b. Mucous membrane

Pharmacology
Acetaminophen (Tylenol)
reduces fever and pain
- has no anti-inflammatory
effect.
Anti-inflammatory Meds
3 GROUPS
Salicylates
NSAID ex. Diclofenac Na
(Voltaren), Ibuprofen
(Advil), Indomethacin
(Indocin), Ketorolac
Tromethamine (Toradol)
for pain management only,
Naproxen (Naprosyn)
Corticosteroids

Incubation period period


begins with active replication but
with no symptoms
Prodromal stage Symptoms
first appear
Acute phase proliferation and
dissemination of pathogens
Convalescent stagecontainment of infection and
pathogens are eliminated
Resolution total elimination of
pathogens without residual
manifestation

Nosocomial infection
Infection acquired in a health care
setting.
Typically manifest after 48 hrs.
UTI most common type
Gerontologic Consideration
Cardiovascular changes
Respiratory system changes
Loss of muscle tone
Gastrointestinal system changes
Skin and subcutaneous changes
Slowed or impaired healing
process.
FACTORS THAT MAY CONTRIBUTE TO
INCREASED RISK FOR INFECTIOUS
DISEASE:
Decreased activity level
Poor nutrition
Chronic disease
Hospitalization
Presence of invasive device
Standard precautions
Blood
All body fluids, secretions,
excretions,
Non-intact skin
Mucous membranes
Essential elements
Use barrier protection
Prevent inadvertent percutaneous
exposure, dispose of needles
Immediate and thorough hand
washing

Stages of Infectious Process

Pharmacology
check for:
History of hypersensitivity.
Age and childbearing status of the
client.
Renal function
Hepatic function
Site of infection
Classification of antimicrobial
preparations:
Bacteriostatic
Bactericidal
Five Basic Mechanisms of antimicrobial
agents
Impairing cell wall synthesis,
leading to lysis and cell
destruction.
Protein synthesis inhibition,
impairing microbial function
Altering the permeability of the
cell membrane, causing
intracellular contents to leak.
Inhibiting the synthesis of nucleic
acids
Inhibiting other specific
biochemical pathways of the
organism.