Download NUR127 Unit 1 Lecture 2 Immunology

The Immune System
The body’s protective
response to invading foreign
organisms
Immune System: Functions

Protects from pathogens and foreign
molecules
 Parasites
 Bacteria
 Viruses
Removes dead/damaged cells
 Attempts to recognize and remove
abnormal cells

Immune System: Pathologies

Incorrect responses
 Autoimmune

disease
Overactive responses
 Allergies

Lack of response
 Immunodeficiency
disease (AIDS)
Body Defenses: Two Lines
 First
line of defense
 Physical
and chemical barriers:
 Skin,
epithelial linings, and cilia
 Acids, mucous, and lysozymes
Second
line of defense
 Innate,
non-specific, immediate response
 Acquired; attack a specific pathogen (antigen)
3 processes needed for
immunity:
Inflammation
Immunity
Cell-mediated
Immunity
Antibodymediated/Humoral
Lymphatic System: Anatomy
Figure 24-2a
Key Cells of the Immune System

Leukocytes (white blood cells)
Cells of the Immune System
Figure 24-4
Cells

Leukocytes: 5 major categories.
 Neutrophils:
Phagocytic cells that wander throughout
the connective tissue destroying bacterias.
 Eosinophils: Phagocytic cells that destroy allergens,
antigen & anti-body complexes, & some inflammatory
chemicals.
 Surround larger parasites & attack them with
enzymes to weaken or destroy them.
 Defend against allergies & parasitic worm
infections.
 Basophils: Helper cells that secrete vasodilators &
anticoagulants in order to speed other leukocytes to
the infected zone.
Cells
 Lymphocytes:
A variety of cells active in the immune
response.
 Natural Killer Cells (NK Cells): Attack any cell
with an unusual plasma membrane, such as cells
that are infected by a virus or have become
cancerous.
Cytolysis: Perforin protein is injected into the cell to
cause it to “explode”.
 Granzymes: Cause the cell to self-destruct.
 Found in the spleen, red bone marrow, & lymph nodes.

 Monocytes:
Wandering cells that eventually turn into
macrophages.
Inflammation (natural immunity)
Inflammation: One of the body’s most
common responses to tissue damage.
Occurs in roughly the same way in any
tissue.
 Four Cardinal signs of Inflammation:

 Redness
 Swelling
 Heat
 Pain
Major cells of inflammation:

Neutrophils:
 1st
line defense against invaders in blood and
ECF.
 Destroy invaders by phagocytosis
 Absolute neutrophil count is used to
determine a person’s risk for infection
Major cells of inflammation:

Macrophages
 Preform
phagocytosis, repair injured tissue
 Stimulate CMI + AMI
 Long life span and plenty of energy to
degrade many foreign proteins.
Cells
Phagocytes
•Cells
under attack
release histamine.
•Purpose is to engulf and
destroy invaders
Major cells of inflammation:

Basophils
 Cause
the manifestation of inflammation
 Contain chemicals that act on b. vessels
Heparin inhibits blood clotting
 Histamine constricts small veins & respiratory
smooth muscle

Major cells of inflammation:

Eosinophils
 Act

against infestations of parasitic larvae
Can inhibit and induce inflammation
 Number
increases during allergic reaction
Immune System

Specific Immune Defenses: Cells
specifically geared toward fighting certain
invaders, and remembering previous
foreign invaders so that they can be
rapidly eliminated in the future.
Immune System

Two Divisions of the Immune System:
1.
Humoral Immunity aka AntibodyMediated Immunity:

2.
Driven by B cells.
Cell-mediated immunity:

Driven by T cells.
What is specific
immunity?



Specific response
Memory for future
reinvasion
Antibody-based
B

cells primary actors
Cell-mediated
T
cells only
Antigens

Antigen:

Typically large molecules, often proteins.
Antigen Processing

Major Histocompatability Complex
(MHC): “Self-antigens” that are unique to
all of your body cells except red blood
cells.
 Help
T-cells recognize which cells are foreign.
 MHC-1s: Cells that posses MHC and are
labeled “you” by the T-cells.
Antibodies
Also known as immunoglobulins
 Some act as labels to identify
antigens for phagocytes
 Some work as antitoxins



Some attach to bacteria making them less
active


i.e. block toxins for e.g. those causing diphtheria and
tetanus
easier for phagocytes to engulf
Some cause agglutination (clumping
together) of bacteria
Humoral Immunity

Humoral Immunity aka AntibodyMediated Immunity

B cells (B-lymphocytes) produce antibodies to
engage in a complex purging process.
 Immunoglobulins

Antibodies made up of glycoproteins called
globulins.
 Antigen-Binding

(Igs)
Site
Tips of each chain are called variable regions &
are areas where the antibody attaches to the
antigen.
B -Lymphocytes

Receptors recognize an antigen on the surface
of the invader, the B-cell divides rapidly.

Antigens are presented to the B-cells by
macrophages
B -Lymphocytes
Type
Number of
ag binding
sites
Site of action
Functions
IgG
2
•Blood
•Tissue fluid
•CAN CROSS
PLACENTA
•Increase
macrophage activity
•Antitoxins
•Agglutination
IgM
10
•Blood
•Tissue fluid
Agglutination
IgA
2 or 4
•Secretions (saliva,
tears, small intestine,
vaginal, prostate,
nasal, breast milk)
•Stop bacteria
adhering to host
cells
•Prevents bacteria
forming colonies on
mucous membranes
IgE
2
Tissues
•Activate mast cells
 HISTAMINE
•Worm response
When help arrives . . .
The T-helper cell receptor “docks” with the
B cell’s MHComplex
 B cells proliferate . . .

Antigen & T-helper cell
Naïve cell
Proliferation of cell
line
B cells differentiate into . . .
 Antibody
producing cells [attack mode]
 Memory cells [remembers & future
protection]
Antigen & T-helper cell
antibodies
memory
AMI in summary

An invaders attacks…
 Antigen

is phagocytized by the B cell
Broken into non-infective pieces & attached to MHC
which is placed on the cell membrane surface here it is
recognized by the helper T cell…
Cell Mediated Immunity

Cellular Immunity:
 Lymphocytes
directly attack & destroy foreign
cells & infected host cells.

T-Cells or T-lymphocytes activated by a specific
antigen.
Cellular Immunity

Types of T-Cells involved in Cell-mediated
Response:
 Cytotoxic
T-Cells: Responsible for actual
attacking of the foreign body or infected cell.
 Helper T-Cells: Stimulate other helper Tcells, cytotoxic T-cells, and B cells.
 Suppressor T-Cells: Help regulate the attack
& prevent tissue destruction.
 Memory T-Cells: Remain as an immune
response and stimulate faster responses if the
same antigen invades again.
T Lymphocytes: Cell-Mediated
Roles of T lymphocytes and NK cells in cellmediated immunity
Figure 24-16
What happens in a cellmediated response?

The key events:
 Surveillance
 Attack
 Memory
and recognition
Types of Immunity

Active Immunity: You encountered the
pathogen yourself and developed your own
antibodies to it.

Passive Immunity: You received antibodies
directly introduced into the body.

Naturally Acquired: Antibodies are received
through natural means.

Artificially Aquired: Antibodies are received
through artificial (scientific) methods.
Vaccination
A preparation containing antigenic
material:
 Whole live microorganism
 Dead microorganism
 Attenuated (harmless) microorganism
 Toxoid (harmless form of toxin)
 Preparation of harmless ags
Disorders of the Immune System

Hypersensitivity Disorders
Allergy
 Anaphylaxis
 Transfusion reactions, transplant rejection


Immunodeficiency Disorders


HIV/AIDS
Autoimmune

Systemic lupus erythematosus, rheumatoid
arthritis etc.
Hypersensitivity

Excessive reaction to
an antigen (allergen)
to which most people
do not react
 Includes
 Allergies
 Transplant reaction
 Transfusion
Hypersensitivity Disorders
 Reaction may be Local (gastrointestinal, skin, resp,
conjuctaval) or systemic (anaphylactic)

Q: What factors affect the severity of a
hypersensitivity reaction?
 Host response
 Exposure amount
 Nature of the allergen
 Route of allergen entry
 Repeated
Exposure (
Hypersensitivity Assessment

Subjective Information
 Pruritus,

nausea and uneasiness
History of present illness
 Onset,
frequency and duration of symptoms
 Nature and progression of s/s
 Possible exposures of known
allergens/common allergens
 Chronic, seasonal or single episode
 Aggravating & alleviating factors
Hypersensitivity Assessment

Physical Assessment

Respiratory



Cardiovascular



S/Sx caused by Vasodilation—Flushing, Hypotension, Edema
Shock followed by cardiovascular collapse and respiratory arrest
GI


S/Sx caused by Bronchoconstriction—SOB, difficulty breathing,
wheezing, & coughing
Sneezing, excessive nasal secretions, inflamed nasal
membranes
Nauses, vomiting, diarrhea
Skin

Rash, areas of raised inflammation (urticaria/hives)
Hypersensitivity Studies & Medical
Management

Studies—CBC, Total serum IgE levels, skin
testing

Medical Management
 Immediate
intervention
 Symptom management & long term control
 Environmental control
Hypersensitivity—Medications


Oxygen—if respiratory assistance needed
Bronchodilators


Antihistamines—symptom management & long term
control



First Generation—Prototype Diphenhydramine
Second Generation—Prototype Fexofenadine
Leukotriene inhibitors—Inhibits the release of leukotrienes from mast cells & basophils)


Emergency bronchodilator—Epinephrine 1:1,000 SQ–
Anaphylactic reactions (may need to following with IV Epi)
Prototype—montelukast (Singulair)
Steroids—symptom management & long term control

Systemic—Prototype Prednisone
Allergies
When the immune system responds to
harmless substances
 Allergens – antigenic substances
 Allergens include house dust, animal skin,
pollen, house dust mite and its faeces

Immunoglobulins and Allergic
Response

Allergen triggers the B cell to make IgE
antibody, which attaches to the mast cell;
when that allergen reappears, it binds to the
IgE and triggers the mast cell to release its
chemicals
Allergic Responses

First exposure
 Sensitization
 Activation,
clone B cells, form antibodies and
memory cells

Re-exposure
 Many
antibodies, activated T cells, intensified
response, inflammation
Allergies
Histamine causes blood vessels to widen and
become leaky.
 Fluid and white blood cells leave capillaries.
 The area of leakage becomes hot, red and
inflamed

Hypersensitivity—Latex
Allergies

Latex products in health care—Gloves,
tourniquets, electrode pads, tape, urinary catheters, B/P cuffs,
stethoscopes, IV tubing & syringes, O2 masks, etc.

Type I anaphylactic hypersensitivity
reaction from rubber latex proteins
 Exposure—skin,
mucous membranes,
inhalation or blood
 Reaction—ranges from erythema, urticaria,
rhinitis, conjuctivitis to asthma & full blown
anaphylactic shock
Latex Allergy

Risk factors for latex allergies


Long term exposure
Hx of hay fever, asthma & allergies to certain foods



Fruits/vegetables—avocado, guava, kiwi, bananas, tomatoes,
peaches, grapes, apricots, potatoes
Nuts—water chestnuts, hazelnuts, peanuts
NIOSH Recommendations—National Institute of Occupational Safety &
Health

Gloves—powder free, non-latex when unlikely to be in
contact with infectious materials, avoid oil-based hand lotions
when wearing glove, hand wash w/ soap after removal
 Frequent cleaning of areas with latex-containing dust
 Know s/sx of latex allergy—if symptoms develop avoid direct
contact with latex gloves and products
 Medical-alert bracelet & Epi pen
Hypersensitivity—Anaphylaxis

Most severe IgE-mediated allergic reaction

Potentially fatal

Symptoms are often severe with a rapid onset

Fall in B/P, laryngeal edema, bronchospasms leading to
CV collapse, MI and Resp. failure
 First sign may be an “uneasiness” or “sense of impending
doom” or nausea followed quickly by respiratory difficulty
and a drop in B/P
 Signs—wheezing/stridor, severe dyspnea, congestion,
tachycardia, hypotension, cyanosis, pallor, N/V, diarrhea
Anaphylaxis
Decision tree for patient with anaphylactic
reaction
Hypersensitivity—Anaphylaxis
Patient education
 Avoidance of allergen
 S/Sx requiring immediate medical intervention
 Medication management
 Self
administration of subcut epinephrine (Epi-pen)
 Importance of Benadryl in addition to epinephrine
 Prevention—taking preventive medications as
ordered

Medic-alert identification
Hypersensitivity—Transfusion
Reactions

Mild to moderate hypersensitivity reactions
 S/Sx—Low
grade fever, possible chills, urticaria,
diarrhea, cough
 Stop the transfusion, administer NS IV, Benadryl,
Tylenol, diuretic and a possible steroid
 Restart transfusion after symptoms subside at a
slower rate

Hemolytic reactions
 S/Sx—Fever,
chills/rigors, urticaria, wheezing,
hypotension
 Stop the transfusion, O2, NS IV, epinephrine
(severe), antihistamines
Hypersensitivity—Transplant
Rejection

“Graft versus Host Disease” GVHD
 Reaction
occurs approx 7-10 days after
transplant once blood supply to new tissue
has developed

Sensitized lymphocytes cause sloughing at the
graft site
 Long-term
immunosuppressive therapy—
Corticosteroids (Prednisone), cyclosporin
(Sandimmune) & azathioprine (Imuran)
Immunodeficiency Disorders

Primary
 Genetic
 May affect phagocytic function, B cells and/or T cells,
or the complement system

Secondary
 Acquired
 Contributing causes: Burns, malnutrition, chronic
stress, diabetes
Primary Immunodeficiency's

Usually seen in infants and young children
 Manifestations:
vary according to type; severe or
recurrent infections; failure to thrive or poor
growth; and positive family history

Potential complications: recurrent, severe,
potentially fatal infections

Treatment: varies by type; treatment of
infection; pooled plasma or immunoglobulin;
GM-CSF or GCSF; thymus graft, stem cell,
or bone marrow transplant
Immunodeficiency—Nursing
Management & Patient Teaching
Monitor for S/Sx of infection
 Monitor lab values
 Dietary support
 Management of stress & anxiety
 Reduce risk of infection—hand washing,
hygiene, avoiding crowds
 Medication management

Autoimmune Disorders





Development of a cellular and/or humoral response to one’s own
tissue
Disorders tend to cluster—many individuals have more than one
autoimmune disorder
Genetic predisposition likely
Examples—rheumatoid arthritis (RA), systemic lupus
erythematosus, ulcerative colitis, multiple sclerosis (MS), psoriasis,
type 1 diabetes, etc
Treatment


Symptom management
Plasmapheresis/plasma exchange—removal of plasma
(immunoglobuin—IgG, antigen-antibody complexes, & inflammatory
mediators) and replacement with NS, LR, FFP or albumin
 Immunosuppressive therapy to prevent recovery of IgG production
Autoimmune Diseases