LinkedIn emplea cookies para mejorar la funcionalidad y el rendimiento de nuestro sitio web, así como para ofrecer publicidad relevante. Si continúas navegando por ese sitio web, aceptas el uso de cookies. Consulta nuestras Condiciones de uso y nuestra Política de privacidad para más información.
LinkedIn emplea cookies para mejorar la funcionalidad y el rendimiento de nuestro sitio web, así como para ofrecer publicidad relevante. Si continúas navegando por ese sitio web, aceptas el uso de cookies. Consulta nuestra Política de privacidad y nuestras Condiciones de uso para más información.
Histamine – potent vasodilator, causes smooth mus contraction and bronchial constriction, PARASYM. Neurotransmitter acetylcholine dilatation of blood vessles and smooth mus contraction. Kinins inflammatory peptides requires activation to produce the same thing.
Sensitization-priming stageProstaglandins and leukotrienes are derived from their cell membrane
Prepared by: Mae Michelle F. Aguilar RN
USI-Graduate School MAN-MS
• The excessive or
inappropriate activation of
the immune system.
• Disorders caused by the
immune responses are
collectively referred to as
• IgE mediated, occurs rapidly within minuites
of antigen challenge.
• Referred to as allergic reactions and the
antigens causing the response as allergens.
T cells of the
TH2 type and
Mast Cells or
• CD4+ T cell of TH2 cells differentiate in
response to allergens and helminthes
• Cytokines of TH2 stimulate differentiation of
B cells into IgE producing plasma cells, acts as
growth factor for mast cells and recruit and
• MAST CELLS are tissue cells while BASOPHILS
are blood cells.
• Distributed throughout connective
tissue, beneath the skin and mucous
membranes of the respiratory tract, GIT, GUT
and adjacent to blood and vessles.
• With subsequent exposure, the sensitizing
allergen binds to the cell associated IgE
• Degranulation of sensitized mast cells occur
(Release of their performed mediators)
Initial or Early Response
• 5 to 30 mins of exposure to antigen and
subsides within 60 mins.
• Mediators: Histamine, Acetylcholine,
enzymes such as trypsin and chymase that
lead to generation of kinins
• Vasodilation, vascular damage, smooth muscle
Secondary or Late Phase
• 2 to 8 hours later and lasts for several days.
• Results from lipid mediators and cytokines
involved in the inflammatory response.
• Mast cell membrane phospholipids which
broken down to form Archidonic Acid where
leukotrienes and prostaglandins are
• Similar effects with histamine and
acetylcholine though effects are delayed and
prolonged by comparison.
• Mast cells also produce cytokines and
chemotactic factors that attract eosinophils
and leukocytes to the site of allergen contact.
• Systemic anaphylactic shock occurs with the
activation of mast cells in the vascular system.
• Local or atopic reactions occur if confined to a
particular site by virtue of exposure.
OF DISEASE 6th ed
• Systemic, life-threatening hypersensitivity
reaction characterized by vasodilation.
• Fall in blood pressure, airway
constriction, vascular swelling, obstruction of
• MILD SYSTEMIC
– Peripheral tingling
– Sensation of warmth
– Fullness of mouth and
– Nasal congestion
– Periorbital swelling
– Tearing of the eyes
• MODERATE SYSTEMIC REACTIONS
– Itching in addition to above symptoms
– Dyspnea, coughing, wheezing, bronchospasm, edema of
• SEVERE SYSTEMIC
– Laryngeal edema
– Severe dyspnea
– Abdominal Cramping
– Cardiac arrest and coma
Common medications that cause
• Antibiotics (Penicillin and sulfa antibiotics)
• Radio contrast agents
• Anesthetic agents (lidocaine, procaine)
• Avoidance of
• Screening for
• Wear medical alert
• Carry an Emergency
• Intravenous infusion (NSS), volume expanders
• Antihistamines and corticosteroids to treat
urticaria and angioedema
• Aminophylline and corticosteroids
• Assess the airway, breathing pattern and other
• Emergency measures (
intubation, administration of emergency
medications, insertion of intravenous
lines, fluid administration, oxygen
• Health Teaching!
• Inflammation of the nasal mucosa.
• hay fever; chronic allergic rhinitis, pollinosis
• Most common form of respiratory allergy.
• Often occurs with other conditions such as allergic
conjunctivitis, sinusitis and asthma.
• Induced by airborne pollen or molds.
• Histamine is the major mediator of allergic
reactions in the nasal mucosa.
• Upon inhalation or ingestion of the antigen,
nasal mucosa reacts by slowing the ciliary
action, edema formation and leukocyte
• Complications may result to allergic asthma,
chronic nasal obstruction, chronic otitis media
with hearing loss, anosomia (absence of the
sense of smell)
Assessment and Diagnostic Findings
• Nasal smears
• Peripheral blood counts
• Total serum IgE
• Epicutaneos and intradermal screening
• Food elimination and challenge
• Nasal provocation test
GOAL: RELIEF from symptoms!
– H1 receptor antagonist (H1 blockers)
– H1 blockers selectively bind to H1 receptors
preventing actions of histamines at these sites
– Oral antihistamines – limited to certain patients
with hay fever, vasomotor rhinitis, urticaria (hives)
and mild asthma
–Major side effect : SEDATION
• Nervousness, tremors, dizziness, dry mouth,
palpitations, anorexia, nausea and vomiting.
• Contraindicated: Third trimester of pregnancy,
nursing mothers and newborns, in children
and elderly people and in patients with
conditions that can be aggravated by
• 2nd generation or non-sedating H1 receptor
– Does not cross the blood brain barrier and do not
bind to the cholinergic, serotonin, or alpha-
– Binds to the peripheral nervous system H1
receptors causing less sedation.
– Ethanolamine : Diphenhydramine (Benadryl)
•MAJOR SIDE EFFECTS NURSING IMPLICATIONS:
•drowsiness, and confusion Teach patient to avoid alcohol,
driving or engaging in hazardous
•dry mouth, nausea,
Sucking on hard candy or ice
chips for relief of dry mouth,
•Photosensitivity Encourage use of sunscreen and
hat while outdoors
•urinary retention Assess for urinary retention,
monitor urinary output
– Vasoconstrictors of
mucosal vessels, are
used topically (nasal
and ophthalmic) in
addition to the oral
– Drops or spray has
used for a few days
to avoid rebound
• MAST CELL STABILIZERS
– Intranasal cromolyn sodium (Nasalcrom)
– A spray that acts by stabilizing the mast cell
membrane thus reducing histamine and other
mediators of the allergic response.
– Used prophilactically before exposure to allergens.
– Benefits may take a week or so to occur.
– For more severe cases that cannot be controlled
by conventional medications.
– Dexamethasone, budesonide, fluticasone,
– Suppress host defenses so they must be used with
caution for patients with tuberculosis, untreated
bacterial infections of the lungs.
• Side Effects: Fluid retention, weight
gain, hypertension, gastric irritation, glucose
intolerance, and adrenal suppression.
– Used to treat IgE mediated diseases by injections
of allergen extracts.
– Patient is at risk for general and potentially
• Improving Breathing Pattern
• Promoting understanding of allergy control
• Coping with a chronic disorder
• Monitor and manage potential complications.
• Family history is common.
• Highest incidence in infants and children
• Significant elevations of
serum IgE and peripheral
• Pruritus and
hyperirritability of the skin.
• Large amounts of
histamine in the skin.
• Chronic condition with
• Tendency to recur with
adolescence to age 20
• Skin rashes induced by
• Common causes are
g ampicillin, semi
• Primary target of food
allergy may be the
gastrointestinal tract or
the respiratory system.
• Occur at any age but
• Allergic reaction to
natural rubber proteins.
• Type II (Cytotoxic) hypersensitivity are
mediated by IgG and IgM antibodies directed
against target antigens on the surface of cells
or other tissue components.
• Complement-mediated or antibody-mediated
• Antigens are endogenous or exogenous
Source: Robbins PATHOLOGIC
BASIS OF DISEASE 6th ed.
3.Autoimmune hemolytic anemia,
agranulocytosis, thrombocytopenia – (+)
antibodies vs own blood cells
4.Pemphigus vulgaris – Ab’s vs. desmosomes
BLOOD TRANSFUSION REACTION
• Cells from an
antibody of the host.
Nursing Interventions when complications
occurs in Blood transfusion
• If blood transfusion reaction occurs. STOP THE TRANSFUSION.
• Start IV line (0.9% NaCl)
• Place the client in fowler’s position if with SOB and administer O2
• The nurse remains with the client, observing signs and symptoms and
monitoring vital signs as often as every 5 minutes.
• Notify the physician immediately.
• The nurse prepares to administer emergency drugs such as
antihistamines, vasopressor, fluids, and steroids as per physician’s
order or protocol.
• Obtain a urine specimen and send to the laboratory to determine
presence of hemoglobin as a result of RBC hemolysis.
• Blood container, tubing, attached label, and transfusion record are
saved and returned to the laboratory for analysis.
• Antigenic difference between mother and
fetus and antibodies from the mother cross
the placenta and cause destruction of fetal
• due to NK activity non-sensitized cells with Fc
• Ab + Ag activation of NK cells bind to Fc
fragment of IgG cell lysis without
• Destruction of targets too large to be
phagocytosed (parasites, tumor cells) + graft
1.Myasthenia gravis – acetylcholine receptors
2.Goodpasture’s syndrome – type IV collagen
3.Pernicious anemia – intrinsic factor
4.Acute rheumatic fever – antibodies vs.
Streptococcal antigens cross-react with heart
• Antibodies directed against cell surface
receptors impair or deregulate function
Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.
• a type of autoimmune
that usually results to
muscle weakness and
fatigue primarily in the
face. This makes the
muscles get tired and
weakened more easily
than what is normal.
(IMMUNE COMPLEX MEDIATED)
Immune Complex Mediated
• Formation of immune complexes in
circulation deposit in various tissues
trigger classical pathway of complement
• Produce damage as they localize within
blood vessel walls or when trapped in
filtering structures (e.g. renal glomeruli)
OF DISEASE 6th ed.
Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.
Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.
• Patient forms antibodies to xenogeneic Ig
administered during passive immune therapy
• Seen when boosters are administered to individuals
who already possess high antibody titers to vaccine
• Localized area to tissue necrosis edema,
• Develop over a few hours
• Initiated by sensitized T lymphocytes
• Principal pattern of immunologic
response to intracellular microbiologic
agents (particularly Mycobacterium
tuberculosis) as well as
viruses, fungi, protozoa
• Mediated by CD4 T cells
• 1st exposure to Ag CD4 T cells + class
II MHC differentiation of naïve CD4 T
cells to TH1 cells release of IL-12, IFN-
, IL-2, TNF & lymphotoxin
• Tuberculin skin test, contact
• Avoidance of offending material
• Burrow’s solution or cool water compress
• Systemic Corticosteroids (Prednisone)
• Topical Corticosteroids
• Oral antihistamines
• Hydrophilic cream or petrolatum
• Antibiotics for infection
T Cell-Mediated Cytotoxicity
• Mediated by CD8+ T cells
• Sensitized CD8+ T cells kill antigen-
bearing target cells
• Graft rejection, virus infections,
• Two mechanisms:
killing cause perforation of
activation of apoptosis
• One of the goals of present day
immunologic research is successful
transplantation of tissues in humans
without immunologic rejection.
Mechanisms in Graft Rejection
• Antigens responsible for
rejection in humans are
those of the Major
antigen (HLA) system
• T cell-Mediated
T cell mediated Reactions
• Activation of the CD8 CTLsand delayed
hypersensitivity reactions triggered by
activated CD4 helper cells seem to be
Increasing Graft Survival
• Immunosuppressive Therapy
– Azathiprine, steroids, cyclosporine,
antilymphocyte globulins, monoclonal anti-T cell
– Cyclosporine suppresses T cells mediated
immunity by inhibiting activation of cytokine
genes, in particular, the gene for IL 2.
• Caused by the breakdown in the ability of the
immune system to differentiate between self
and non self.
• The ability of the immune system to differentiate self
from non-self is called SELF TOLERANCE.
• Maintained through central and peripheral mechanisms
that delete auto reactive B or T cells or suppress or
inactivate immune responses that would be destructive
to host tissues.
• Defects on these mechanisms could impair
self-tolerance and predispose one to
Mechanisms of Autoimmune Disease
• Genetic Susceptibility
– Increase incidence and severity of autoimmune
diseases is shown in familial clustering of several
autoimmune diseases and the observation that a
certain inherited HLA genotypes occur
more frequently with a variety of autoimmune
– 90% of people with Ankylosing Spondylitis carry
the HLA-B27 antigen
– Rheumatoid Arthritis (HLA-DR4)
– SLE (HLA-DR3)
• Environmental Factors
– Breakdown of T cell Anergy
– Release of Sequestered Antigens
– Molecular Mimicry
in the synovial
antigen to T cells
T and B cell proliferation.
Angiogenesis in synovial
in synovial fluid. Cell
proliferation. No cartilage
Early pannus invasion.
Degredation of cartilage by
Subchondral bone erosion
Pannus invation of cartilage.
Laxity of ligaments
Swelling of small joints,
pain, stiffness, fatigue
effusions, pain, poss.
Increase in severity of
signs and symptoms Joint instability,
• Medications that treat pain and inflammation.
– DMARDs (disease modifying anti rheumatic drugs)
• condition characterized by chronic inflammation
of body tissues caused by autoimmune disease
• abnormal antibodies produced in blood target
tissues within own body rather than foreign
• antibodies & accompanying cells of inflammation
can involve tissues anywhere in the body has
potential to affect a variety of areas of the body
• can cause disease of the skin, heart, lungs,
kidneys, joints, and/or nervous system
• only the skin involved discoid lupus
• internal organs involved SLE
• shape referred to as the "butterfly rash" of SLE
• painless, does not itch
• worsened by exposure to sunlight (photosensitivity)
• no permanent cure for SLE
• goal of treatment - to relieve symptoms & protect
organs by decreasing inflammation and/or the
level of autoimmune activity in the body
• mild symptoms - need no treatment or only
intermittent courses of antiinflammatory
• serious illness (damage to internal organ) -
require high doses of corticosteroids with other
medications that suppress the body's immune
• Topical corticosteroid creams
• Anti-Malarials to treat joint pain, skin rashes,
mouth ulcers, fatigue and fever
• Systemic corticosteroids
• Cytotoxic therapy to treat diffuse proliferative
• Methotrexate (anti inflammatory and
BITS OF HISTORY
HIV came from a similar virus found in chimpanzees - SIV.
HIV probably entered the United States around 1970
CDC in 1981 noticed unusual clusters of Kaposi’s sarcoma in
gay men in NY and San Francisco, which led to the disease
to be called GRID (Gay Related Immune Deficiency).
By 1982 the disease was apparent in heterosexuals and was
renamed AIDS (Acquired Immune Deficiency).
1984- Scientists(Dr. Luc Montagnier, Dr. Robert Gallo)
identify HIV (initially called LAV or HTLV-III) as the cause of
1987- AZT is the first drug approved for treating AIDS
Who is at risk?
The following are behaviors that increase chances of getting HIV:
• Injecting drugs or steroids or shared equipment (such as
needles, syringes, works) with others
• Unprotected vaginal, anal, or oral sex, multiple partners, or anonymous
• Diagnosed with or treated for hepatitis, tuberculosis (TB), or a sexually
transmitted disease (STD)
• Had unprotected sex with someone who could answer yes to any of the
criteria as listed above.
HIV LIFE CYCLE
• Binding- HIV searches for cells that have CD4 surface receptors. Main
target is the T4-lymphocyte. The T4-cell is responsible for warning your
immune system that there are invaders in the system.
• Reverse Transcription- Makes a DNA copy of the virus’s RNA. Can be
blocked by Nucleoside Reverse Transcriptase Inhibitors (NRTIs) and Non-
Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
• Integration-The HIV DNA is then carried to the cell’s nucleus. When the cell
makes new proteins, it accidentally makes new HIVs. Integration can be
blocked by integrase inhibitors, a new class of drugs that are in the earliest
stage of research.
• Transcription-Once HIV’s genetic material is inside the cell’s nucleus, it
directs the cell to produce new HIV. The strands of viral DNA nucleus
separate and special enzymes create messenger RNA (mRNA). This can
be blocked by antisense antiviral or transcription inhibitors (Tis) new classes
of drugs that are in the earliest of research.
• Translation-The mRNA carries instructions for making new viral proteins
from the nucleus.
• Viral Assembly and Maturation-The virus becomes an infection and each
infected cell can produce lots of new viruses. Viral assembly can be blocked
by Protease Inhibitors (PIs).
• Helper T-Cells (also called T4 or CD4)- help other cells destroy infective
• Suppressor T-Cells (also called T8 or CD8)-suppress the activity of other
lymphocytes so they don’t destroy normal tissue.
• Killer T-Cells (also called cytotoxic T lymphocytes, or CTLs, and are
another kind of T8 or CD8 cell)- recognize and destroy abnormal or infected
How long after exposure?
• It can take some time for the immune system to produce enough antibodies for
the antibody test to detect, and this time period can vary from person to person.
This time period is commonly referred to as the “window period.”
• Most people will develop detectable antibodies within 2 to 8 weeks (the average is
25 days). Even so, there is a chance that some individuals will take longer to
develop detectable antibodies.
• Therefore, if the initial negative HIV test was conducted within the first 3 months
after possible exposure, repeat testing should be considered >3 months after the
exposure occurred to account for the possibility of a false-negative result. Ninety-
seven percent of persons will develop antibodies in the first 3 months following the
time of their infection. In very rare cases, it can take up to 6 months to develop
antibodies to HIV.
TESTING FOR THE VIRUS
• EIA (enzyme immunoassay) used on blood drawn from a vein, is the most
common screening test used to look for antibodies to HIV. A positive (reactive)
EIA must be used with a follow-up (confirmatory) test such as the Western blot
to make a positive diagnosis. There are EIA tests that use other body fluids to
look for antibodies to HIV. These include:
Oral Fluid Tests – use oral fluid (not saliva) that is collected from the
mouth using a special collection device. This is an EIA antibody
test similar to the standard blood EIA test. A follow-up confirmatory
Western Blot uses the same oral fluid sample.
Urine Tests – use urine instead of blood. The sensitivity and
specificity (accuracy) are somewhat less than that of the blood and oral
fluid tests. This is also an EIA antibody test similar to blood EIA tests
and requires a follow-up confirmatory Western Blot using the same
• Rapid Tests:
A rapid test is a screening test that produces very quick results, in approximately 20
minutes. Rapid tests use blood from a vein or from a finger stick, or oral fluid to look for the
presence of antibodies to HIV. As is true for all screening tests, a reactive rapid HIV test
result must be confirmed with a follow-up confirmatory test before a final diagnosis of
infection can be made.
• Home Testing Kits
The testing procedure involves pricking a finger with a special device, placing drops of
blood on a specially treated card, and then mailing the card in to be tested at a licensed
laboratory. Customers are given an identification number to use when phoning in for the
results. All individuals receiving a positive test result are provided referrals for a follow-up
confirmatory test, as well as information and resources on treatment and support services.
• RNA Tests
RNA tests look for genetic material of the virus and can be used in screening the blood
supply and for detection of very early infection rare cases when antibody tests are unable
to detect antibodies to HIV.
From mother to child
• HIV stands for human immunodeficiency virus. This is
the virus that causes AIDS. HIV is different from most
other viruses because it attacks the immune system. The
immune system gives our bodies the ability to fight
infections. HIV finds and destroys a type of white blood
cell (T cells or CD4 cells) that the immune system must
have to fight disease.
Symptoms of HIV
HIV can cause any symptoms of illness, since infections can occur
throughout the body. Special symptoms relating to HIV infection include:
• Frequent vaginal yeast infections
• Mouth sores, including candidal infection
• Muscular stiffness or aching
• Rash of various types, including seborrheic dermatitis
• Sore throat
• Swollen lymph glands
• AIDS stands for acquired immunodeficiency syndrome.
AIDS is the final stage of HIV infection. It can take years
for a person infected with HIV, even without treatment, to
reach this stage. Having AIDS means that the virus has
weakened the immune system to the point at which the
body has a difficult time fighting infections. When
someone has one or more of these infections and a low
number of T cells, he or she has AIDS.
Symptoms of AIDS
• The following is a list of AIDS-related infections and
cancers that people with AIDS acquire as their CD4
count decreases. Previously, having AIDS was defined
as having HIV infection and getting one of these
additional diseases. Now it is additionally defined as a
CD4 count below 200, even without an opportunistic
infection. Many other illnesses and corresponding
symptoms may develop in addition to those listed here.
Absolute CD4 Count
• Normal Values- in a healthy adult, a normal CD4 count can vary a great
deal but is typically 600-1200 cells per cubic millimeter of blood
• Between 600 and 350 – in an HIV+ person, this range is considered “very
good”. HIV medications are typically not indicated.
• Between 350-200-the immune system is weakened and therefore the HIV+
person may be at increased risk for infection and illness. May start taking
• Less than 200 – The immune system is severely weakened and the HIV+
person is at much greater risk of opportunistic infections. HIV medications
and prophylactic antibiotics will be prescribed to help prevent illnesses and
infections. The patient be classified as having AIDS.
CD4 count below 200 cells/ml
• Pneumocystis carinii pneumonia, "PCP pneumonia," now called
Pneumocystic jiroveci pneumonia
• Candida esophagitis -- painful yeast infection of the esophagus
• Bacillary angiomatosis -- Skin lesions caused by a bacteria called
Bartonella, which is usually acquired from cat scratches
CD4 count below 100 cells/ml
• Cryptococcal meningitis -- infection of the lining of the brain by a yeast
• AIDS dementia -- worsening and slowing of mental function, caused by HIV
• Toxoplasmosis encephalitis -- infection of the brain by a parasite, which is
frequently found in cat feces; causes discrete lesions in the brain
• Progressive multifocal leukoencephalopathy -- a viral disease of the brain
caused by a virus (called the JC virus) that results in a severe decline in
cognitive and motor functions
• Wasting syndrome -- extreme weight loss and loss of appetite, caused by
• Cryptosporidium diarrhea -- Extreme diarrhea caused by one of several
• Asymptomatic HIV infection is a phase of chronic infection with human
immunodeficiency virus (HIV) during which there are no symptoms of HIV infection.
• The length of this phase varies from person to person. It depends on how quickly
the HIV virus is copying itself and the genetic differences that affect the way the
immune system handles the virus.
• Some people can go 10 years or longer without symptoms, while others may have
symptoms and worsening immune function within a few years after the original
• People with asymptomatic infection can progress to symptomatic HIV infection and
develop opportunistic infections associated with HIV. In addition, pregnant women
with asymptomatic HIV infection can still transmit HIV to their fetus.
• People who are asymptomatic but who have CD4 lymphocyte counts of less than
200 should be on therapy.
• Persons infected with HIV-2, immunodeficiency seems to develop more slowly
and to be milder. Compared with persons infected with HIV-1, those with HIV-2
are less infectious early in the course of infection.
• Both HIV-1 and HIV-2 have the same modes of transmission and are associated
with similar opportunistic infections and AIDS.
• As the disease advances, HIV-2 infectiousness seems to increase; however,
compared with HIV-1, the duration of this increased infectiousness is shorter.
HIV-1 and HIV-2 also differ in geographic patterns of infection; the United States
has few reported cases.
• HIV-2 is highly concentrated in West Africa countries such as Senegal, Nigeria,
Ghana, and the Ivory Coast. HIV-2 also spreads to other parts of the world but
predominantly to those countries having strong ties to West Africa.
Guarda las diapositivas más importantes con los recortes.
Los recortes son una forma práctica de recopilar y organizar las diapositivas más importantes de una presentación. Puedes guardar tus magníficos descubrimientos en tableros de recortes organizados por temas.