Professional Documents
Culture Documents
it may under-react as
with human
immunodeficiency
virus infection (HIV)
OVER-REACTION TO
ANTIGENS
Over-reaction to antigens
Pollen grains
Mast cell
www.DennisKunkel.com
Over-reaction to antigens
a type of antibody called IgE binds to the allergen
causing mast cells to produce chemicals called
histamines.
Common symptoms include:
runny nose and itchy, watery eyes, with repeated exposure
resulting in a more rapid onset of symptoms
treatments
antihistamines are given to counteract the histamines
shots containing low doses of an allergen can help a person to
become desensitized to that specific antigen
Type I reactions
Immediate hypersensitivity reactions
Type II reactions
Cytotoxic hypersensitivity reactions
Type IV reactions
Delayed hypersensitivity reactions, cell-mediated
immunity
Type I reactions
Type II reactions
Type IV reactions
Hypersensitivity reaction
undesirable side effect of immunity manifesting trivial
discomforts such as itching of the skin to potentially fatal
disease such as bronchial asthma.
initiated by the interaction of antigen w/ humoral antibody
or by cell-mediated immune mechanisms.
Hypersensitivity
There are four different types of hypersensitivities that
result from different responses of the immune
system:
14
Process of Allergy
Step 1: Sensitization
Occurs when one develops IgE antibodies against a
substance that is inhaled, ingested, or injected
Newly formed IgE antibodies stick to basophils and
mast cells no s/s yet
Type I:
Immediate hypersensitivity
Etiology
Allergic reactions
Reactions can be elicited by various aeroallergens
(eg, pollen, animal dander), drugs, or insect stings.
Other possible causes are latex, drug, and food
allergy.
histamine
Etiology
Allergens
Allergens can be complete protein antigens or lowmolecularweight proteins capable of eliciting an IgE response.
Pollen and animal dander represent complete protein antigens.
Haptens are lowmolecular-weight (inorganic) antigens that are
not capable of eliciting an allergic response by themselves.
Etiology
Foods
most common food allergens are
peanuts, tree nuts, finned fish, shellfish, eggs, milk, soy, and
wheat.
Etiology
Hymenoptera
Bee, wasp, yellow jacket, hornet, and fire ant stings
can cause IgE-mediated reactions.
While anaphylaxis is the most serious reaction,
localized swelling and inflammation can also occur
and do not by themselves indicate increased risk of a
subsequent life-threatening reaction.
At least 50 Americans die each year from anaphylaxis
caused by a stinging insect.
Systemic reaction
usually IV injection of an antigen to which the
host has already become sensitized
state of shock can be produced within
minutes (may be fatal)
Local reactions
depend on the portal of entry of the allergen.
May take the form of:
localized cutaneous swelling (skin allergy,
hives)
nasal & conjunctival discharge (allergic rhinitis
and conjunctivitis)
hay fever
bronchial asthma
allergic gastroenteritis (food allergy)
cytokines
Mast
cell
Antigens (red dots) from inhaled pollen are ingested and presented by
macrophages to T cells. Activated T cells produce cytokines leading to
the production of IgE, which binds to receptors on mast cells and causes
the release of histamine, which is responsible for allergy symptoms.
Onset is usually within minutes of contact with antigen.
27
Initial response
vasodilation
vascular leakage
smooth muscle spasms
Allergen
Histamine
Increased capillary
permeability
Edema, facial
puffiness
Increased mucus
secretion
Primary Phase
Pruritus and
erythema
Secondary Phase
DX TESTS
Laboratory
CBC
Increased WBC eosinophil
count
Radioallergosorbent Test
(RAST)
Determines the blood
concentration of IgE directed
against a specific antigen and
thus can determine specific
antigen
Allergy testing
Scratch test
Intradermal test
Oral food challenge
In vitro testing
Allergy Testing
Skin Testing
Scratch Test
Results in an immediate hypersensitivity reaction to an
allergen
Discontinue antihistamines for 5 days before the test
Allergens are introduced through a superficial scratch or prick
cause a localized reaction (wheal) when the test result is
positive
Serious reactions are rare
Skin test
Intradermal Testing
Reserved for substances that are strongly suspected
of causing allergy but did not test positive during
scratch test
Greater risk for anaphylaxis occurs
In Vitro Testing
Drawing blood from a
client and exposing it to
different panels containing
food and mold allergens
After incubation the cells
are checked
Positive reaction
Increase WBC size by 12 %
Increased platelet
aggregation
COLLABORATIVE
MANAGEMENT
Collaborative Management
Avoidance
Therapy
Medications
Decongestants
vasoconstriction in the inflamed tissue thereby
reducing the edema
Caution in patients with HPN, glaucoma
Antihistamines
blocks histamine from binding with its receptor
preventing vasodilation and capillary permeability
Sedation
Corticosteroids
decrease inflammation by preventing the synthesis of
mediators
Nasal
Beclomethasone
Fluticasone
Oral
Prednisolone
Prednisone
Leukotriene Inhibitors
Zileuton
Zafirlukast
Desensitization
The most common form of desensitization
involves subcutaneous injections of small
amount of the allergen
An increasing dose is usually given weekly until
the patient is receiving a 0.5ml dose
Recommended course of treatment is
approximately 5 years
Desensitization
The mechanism of action to reduce allergic
responses by desensitization is thought to be
competition.
Instead of IgE , IgG is produced and binds with
the allergens so as not to cause degranulation of
mast cells or basophils.
ALLERGIC RHINITIS
Allergic rhinoconjunctivitis
s/s
Congestion
Sneezing
Itchy , runny nose and eyes;
Itching of the palate and inner ear.
postnasal drip, which can cause sore throat,
coughing, or throat clearing.
Rhinoconjunctivitis
usually results from exposure to aeroallergens
can be seasonal or perennial.
Airborne allergens typically also cause ocular
symptoms consisting of itchy eyes, tearing,
swelling or redness of the eyes.
Repeated exposure to the allergen can result in
chronic allergic inflammation, which causes
chronic nasal congestion that can be further
complicated by sinusitis.
s/s
Patients may sneeze, be congested, have a runny nose,
or have frequent throat clearing and/or cough from
postnasal drip.
Sclera may be injected, and patients may have dark
rings under the eyes (ie, allergic shiners).
Nasal mucosa can be boggy and pale, usually with clear
drainage.
The pharynx may have a cobblestone appearance
reflecting lymphoid hyperplasia from postnasal mucus
drainage.
The patient may have frontal or maxillary sinus
tenderness from chronic sinus congestion or infection.
allergic shiners
Mgmt
Avoid the offending allergen, if possible.
Oral H1-receptor blockers
helpful for controlling itchiness, rhinorrhea, and
lacrimation but most have little effect on nasal
congestion.
intranasal glucocorticosteroid
control nasal symptoms, including nasal congestion.
need to be used regularly to be effective
patients may need to use them for a week or more
before maximum effect is seen.
Mgmt
Other topical nasal agents include
azelastine
olopatadine (H1-receptor blockers)
cromolyn (a mast cell stabilizer).
Mgmt
Topical nasal decongestants can provide
immediate relief of nasal congestion and can be
used temporarily and as needed.
Note: Patients should be cautioned not to use
them for more than a few days, however, as they
can cause rebound congestion (rhinitis
medicamentosa).
Mgmt
ocular symptoms
Topical decongestants, mast cell stabilizers, or
antihistamines
artificial tears - can be refrigerated for an extra
cooling effect.
Cold compresses can also be used.
Antigen-injection immunotherapy
AKA: subcutaneous immunotherapy (SCIT)
very effective in treating inhalant allergies and
can be considered in patients whose symptoms
do not respond well to medications or in patients
who cannot avoid the allergen in question (eg,
cat owner allergic to cats).
The mechanism of action of immunotherapy is
not yet fully elucidated.
Sublingual/swallow immunotherapy
(SLIT)
An alternative to antigen-injection immunotherapy
currently being used with increasing frequency in
Europe.
involves having the patient hold extract under the tongue
for 1-3 minutes before swallowing.
It offers the advantage of a lower likelihood of systemic
adverse effects and has been shown to reduce allergic
rhinitis and asthma symptoms.
may have a more significant impact on these symptoms
than SLIT.
still being evaluated for FDA approval in the United
States.
ASTHMA
Allergic asthma
s/s
Bronchoconstriction
shortness of breath (eg, difficulty getting air out),
wheezing, cough, and/or chest tightness.
Induced sputum:
Sputum induced from the airways can be evaluated for eosinophils, which is a
measure of inflammation seen in asthma.
Mgmt
Avoid the offending allergen, if possible.
A key factor in controlling allergic asthma is
controlling allergic rhinitis symptoms.
Mgmt
Therapy depends on the severity of disease.
albuterol metered-dose inhaler (MDI) (or
nebulizers for young children) to use as needed.
Inhaled glucocorticosteroids should be added if
appropriate.
In general, these medications are used if
symptoms occur more than twice weekly or if
abnormal spirometry findings reverse with the
inhalation of a short-acting bronchodilator.
.
Mgmt
For more refractory symptoms
long-acting beta agonist may be added to the inhaled
glucocorticoid
Mgmt
omalizumab (Xolair)
a humanized monoclonal antibody that prevents
binding of IgE to high-affinity IgE receptors on mast
cells and basophils
In patients refractory to the usual medications and
who have antigen-specific IgE to perennial
environmental aeroallergens (positive skin test or
RAST result)
URTICARIA / ANGIOEDEMA
Urticaria/angioedema
s/s
Diffuse hives or wheals may occur and cause significant
pruritus;
individual wheals resolve after minutes to hours, but new
wheals can continue to form.
Acute urticaria (lasting < 6 wk) can be caused by viral
infections, foods, drugs, or contact allergens.
Chronic urticaria lasts longer than 6 weeks. Although
many causes are possible, often, a cause is not found. In
many cases, this is not due to antigen-IgE mediated
immediate hypersensitivity but to an autoantibody to the
high affinity IgE receptor or to IgE itself.
Angioedema
is localized tissue swelling that can occur in soft
tissues throughout the body.
pain at the site of swelling instead of pruritus, which
occurs with urticaria.
particularly concerning if pharyngeal or laryngeal
tissues are involved.
Mgmt
Avoid the offending allergen if known.
H1-receptor blocker should be added.
If symptoms are not controlled with this alone,
an H2-receptor blocker, leukotriene inhibitor, or oral
glucocorticosteroid can be added.
Most patients require higher than the usual doses;
employing twice daily H1 and H2 antihistamines for
successful control is not uncommon.
ATOPIC DERMATITIS
Atopic dermatitis
is an eczematous cutaneous eruption more
common in children than in adults;
can be exacerbated by allergen exposure,
especially food allergies
(+) pruritus which produces the lesions.
Superinfection with staphylococcal organisms can
occur, particularly in severely excoriated or cracked
lesions.
Mgmt
Avoid the offending allergen if possible, and
properly hydrate and care for the skin.
Topical glucocorticosteroids and topical
immunomodulators (eg, tacrolimus) can be
used.
ANAPHYLAXIS
Anaphylaxis
Most dramatic and life-threatening
Occurs rapidly and systematically
Affects many organs within seconds to minutes
after allergen exposure
Not common
Fatal
s/s
Generalized pruritus and urticaria
Erythema and angioedema
Bronchoconstriction, mucosal edema and
excess mucus production
Wheezes , crackles
Anaphylactic shock
Collaborative Management
Establish and maintain airway
High fowlers position
Apply tourniquet immediately proximal to the
allergen point of entry when possible
O2 by mask
Assess the level of consciousness and vital
signs.
Epipen
Prevention
Avoid the triggering allergen as much as
possible.
Patients should be given a prescription for at
least 2 autoinjectable epinephrine doses (eg, 2
EpiPens or 1 Twinject) and instructed in their
proper use. Importantly, patients must carry
them at all times.
Patients can also be instructed to carry both an
H1 and an H2 antihistamine with them.
http://emedicine.medscape.com/article/136217-treatment#showall
Anaphylactoid reactions
NonIgE-mediated mast cell and basophil degranulation
can occur from a variety of substances.
Although the mechanisms are different, the clinical
manifestations can appear the same.
Causes can include
radiocontrast dye, opiates, and vancomycin (eg, red man syndrome).
Anaphylactoid reactions
Mgmt
glucocorticosteroids and both H1 and H2
antihistamines
LATEX ALLERGY
Latex Allergy
GI ALLERGIES
GI allergies s/s
Patients may report nausea, vomiting,
abdominal cramping, and diarrhea after
ingestion of the offending food.
Note that other mechanisms (eg, lactose
intolerance) commonly cause these symptoms.
Eosinophilic esophagitis and gastritis are newly
recognized syndromes that may be allergic in
nature.
Type II:
Cytotoxic hypersensitivity
Type II examples
1. Transfusion reactions
cells from an incompatible donor react w/ the hosts antibody
2. Erythroblastosis fetalis
there is an antigenic difference between the mother & the fetus,
and antibodies (IgG) cross the placenta & cause destruction of
fetal red cells.
4. Drug reactions
antibodies are produced that react w/ the drug.
Collaborative Management
Discontinue the offending agent
Plasmapheresis
Filtration of the plasma to remove specific substances
like autoantibodies
Symptomatic Treatment
RH INCOMPATIBILITY
Rh incompatibility
Rh incompatibility occurs when the mother's
blood type is Rh negative and her fetus' blood
type is Rh positive.
Symptoms
Rh incompatibility can cause symptoms ranging
from very mild to deadly.
In its mildest form, Rh incompatibility causes the
destruction of red blood cells.
After birth, the infant may have:
Yellowing of the skin and whites of the eyes
(jaundice)
Low muscle tone (hypotonia) and lethargy
Complications
Possible complications include:
Brain damage due to high levels of bilirubin
(kernicterus)
Fluid buildup and swelling in the baby (hydrops
fetalis)
Problems with mental function, movement, hearing,
speech, and seizures
Treatment
Because Rh incompatibility is preventable with
the use of RhoGAM, prevention remains the
best treatment.
Treatment of an infant who is already affected
depends on the severity of the condition.
Infants with mild Rh incompatibility may be
treated with:
Feeding and fluids (hydration)
Phototherapy using bilirubin lights
Prevention
Rh incompatibility is almost completely preventable.
Rh-negative mothers should be followed closely by their
obstetricians during pregnancy.
Special immune globulins, called RhoGAM, are now
used to prevent RH incompatibility in mothers who are
Rh-negative.
If the father of the infant is Rh-positive or if his blood type
cannot be confirmed, the mother is given an injection of
RhoGAM during the second trimester. If the baby is Rhpositive, the mother will get a second injection within a
few days after delivery.
Prevention
These injections prevent the development of
antibodies against Rh-positive blood. However,
women with Rh-negative blood type must
receive injections:
During every pregnancy
If they have a miscarriage or abortion
After prenatal tests such as amniocentesis and chorionic villus
biopsy
After injury to the abdomen during pregnancy
http://www.ncbi.nlm.nih.gov/pubmedhealth/
PMH0002567/
ABO INCOMPATIBILITY
Symptoms
The following are symptoms of ABO
incompatible transfusion reactions:
Back pain
Hematuria
Feeling of "impending doom"
Fever
jaundice
Treatment
http://www.ncbi.nlm.nih.gov/pubmedhealth/
PMH0002283/
Expectations (prognosis)
ABO incompatibility can be a very serious
problem that can even result in death. With the
right treatment, a full recovery is likely.
Complications
Kidney failure
Hypotension
Death
Immune complexes of
antigen (red dots) and
antibody form in
target organ
Immune complexes
activate complement
(green dots- C3a, C4a,
and C5a), and mast cells
(yellow cell) degranulate.
Inflammation and
edema occur, and
organ is damaged
134
138
small blood vessels of the skin if the complexes are formed and
deposited locally (local Arthus reaction)
Arthus reaction
A dermal inflammatory
reaction produced under
conditions of antibody
excess, when a second
injection of antigen
produces intravascular
antigen-antibody
complexes which bind
complement, causing cell
clumping, endothelial
damage, and
vascular necrosis
Rheumatoid arthritis
Systemic Lupus Erythematosus
Serum sickness
SERUM SICKNESS
Serum sickness
a condition that may develop when a patient is
injected with a large amount of e.g. antitoxin that
was produced in an animal or other drugs
After about 10 days, anti-antitoxin antibodies
react with the antitoxin forming immune
complexes that deposit in tissues, walls of the
blood vessels, skin, joints, kidney
Most common cause is penicillin and animal
serum antitoxins
s/s
Fever
Arthralgia
Rash
Lymphadenopathy
Malaise
Polyarthritis and nephritis
Collaborative Management
Usually Self limiting
Symptomatic treatment
Aspirin for pain
Antihistimines for pruritus
Steroids - prednisone
Type IV hypersensitivity
the only type that is not antibody-mediated.
contact hypersensitivity (poison ivy, reactions to
metals in jewelry);
tuberculin-type hypersensitivity (the tuberculosis skin
test);
granulomatous hypersensitivity (leprosy, tuberculosis,
schistosomiasis and Crohns disease).
Self limiting
Inflammatory
response causes
tissue injury.
155
Inflammatory
response causes
tissue injury.
Type IV hypersensitivity
antigen presented by APCs activates antigenspecific memory T cells (which have been
sensitized by prior exposure),
causing them to release cytokines that activate
and attract other T cells and phagocytic cells to
the area.
Where the source of antigen is at the skin
surface, the APC migrates from the dermis,
through lymphatic vessels to a lymph node in
order to present antigen to a T cell.
1. Tuberculin reaction
- the best known example
of delayed-type
hypersensitivity
- produced by
intracutaneous injection of
tuberculin
- In previously sensitized
individual: reddening and
induration of the site(8-12
hours), peaks in 24-72 hours,
and thereafter slowly subside.
2. Transplant rejection
3. Contact dermatitis
4. Poison Ivy skin rashes
5. Local response to insect stings
Patch Testing
Used to identify the allergen
Skin contact with substances
to which the client is
potentially allergic
Contact with a specific
allergen results in a delayed
reaction that develops in 4896 hours
Substances applied under
occlusive tapes
Localized erythema, blister,
swelling
Collaborative Management
Removal of the offending antigen
Monitor reaction site and sites distal to the
reaction for circulation adequacy
Antihistamines minimal benefit
Steroids
TYPE V. STIMULATORY
REACTIONS
Collaborative Management
If one organ is involved like in Graves disease
,surgical removal or radiation can be done
If more than one organ is involved then
immunosuppresion is warranted
167
168
Diet
Environment
Exposure to certain things in their environment may
activate the immune systems of some people
Chemicals
dioxin
pesticides
solvents
Viruses
Bacteria
Sunlight
Medication
Food
170
171
SARCOIDOSIS
Erythema nodosum
associated with sarcoidosis
This picture shows reddishpurple, hard (indurated),
painful nodules (Erythema
nodosum) that occur most
commonly on the shins. These
lesions may be anywhere on
the body and may be
associated with tuberculosis
(TB), sarcoidosis,
coccidioidomycosis, systemic
lupus erythematosis (SLE),
fungal infections, or in
response to medications
Sarcoidosis - close-up
Typical sarcoid
lesions consist of red,
raised lesions
(papules) and
patches (plaques)
with minimal
surrounding skin
change.
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001140/