This document provides an overview of allergies and hypersensitivity reactions. It defines allergies as conditions caused by an exaggerated immune response, classified them into 4 main types (Type I-IV). Common allergens that cause reactions are discussed, along with risk factors like heredity and environmental exposures. The pathophysiology of allergic reactions is described, involving the release of histamine from mast cells leading to symptoms. Diagnosis involves clinical evaluation, skin testing, and serum testing. Management focuses on medications that block mediators or prevent activation of immune cells, including antihistamines, epinephrine, and corticosteroids.

1. Pbl 4 –HD
asem shadid
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2. Introduction
• allergy is number of conditions caused by hypersensitivity of the
immune system to something in the environment that usually
causes little problem in most people.
• Hypersensitivity (also called hypersensitivity reaction or
intolerance) is a set of undesirable reactions produced by the
normal immune system, including allergies and autoimmunity.
• Allergic disease is estimated to affect around 15-20% of the
population of the western world, with a two- to three-fold increase
being seen in the past 20-30 years (Royal College of Physicians,
2003).
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3. • Allergens By definition, an allergen induces type I IgE-mediated
or type IV T-cell–mediated immune responses. Allergic triggers
are almost always low molecular weight proteins; many of them
can become attached to airborne particles.
• People who have allergies often are sensitive to more than one
thing. Substances that often cause reactions are
• Pollen -Dust
• Mold spores
• Pet dander
• Food
• Insect stings
• Medicines
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4. Classification of Hypersensitivity Reactions
• Coombs and Gell classification It divides the hypersensitivity
reactions into the following 4 types:
• Hypersensitivity disorders often involve more than 1 type.
• Type I reactionsType I reactions (ie, immediate hypersensitivity reactions)
involve immunoglobulin E (IgE)–mediated release of histamine and
other mediators from mast cells and basophils. [2] Examples include
anaphylaxis and allergic rhinoconjunctivitis.
• Type II reactionsType II reactions (ie, cytotoxic hypersensitivity reactions)
involve immunoglobulin G or immunoglobulin M antibodies bound
to cell surface antigens, with subsequent complement fixation. An
example is drug-induced hemolytic anemia.
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5. Con .
• Type III reactionsType III reactions (ie, immune-complex reactions)
involve circulating antigen-antibody immune complexes
that deposit in postcapillary venules, with subsequent
complement fixation. An example is serum sickness.
• Type IV reactionsType IV reactions (ie, delayed hypersensitivity reactions,
cell-mediated immunity) are mediated by T cells rather
than by antibodies. An example is contact dermatitis from
poison ivy or nickel allergy.
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6. • Some authors believe this classification system may be too
general and favor a more recent classification system
proposed by Sell et al.[3]
This system divides
immunopathologic responses into the following 7
categories:
• Inactivation/activation antibody reactions
• Cytotoxic or cytolytic antibody reactions
• Immune-complex reactions
• Allergic reactions
• T-cell cytotoxic reactions
• Delayed hypersensitivity reactions
• Granulomatous reactions
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7. Atopic and Allergic Disorders
• The terms atopy and allergy are often used interchangeably but are
different:
• Atopy is an exaggerated IgE-mediated immune response; all
atopic disorders are type I hypersensitivity disorders.
• Allergy is any exaggerated immune response to a foreign antigen
regardless of mechanism.
• Thus, all atopic disorders are considered allergic, but many
allergic disorders (eg, hypersensitivity pneumonitis) are not
atopic.
• Type I hypersensitivity reactions underlie all atopic and many
allergic disorders.
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8. Cause - Etiology
• Risk factors for allergy can be placed in two general
categories, namely host and environmental factors.
• Host factors include heredity, sex, race, and age, with
heredity being by far the most significant.
• Four major environmental candidates are alterations in
exposure to infectious diseases during early childhood,
environmental pollution, allergen levels, and dietary
changes.
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9. Etiology - Genetic factors
• Genetic factors may be involved, as suggested by familial
inheritance of disease, association between atopy and
specific HLA loci, and polymorphisms of several genes,
including those for the high-affinity IgE receptor β-chain,
IL-4 receptor α-chain, IL-4, IL-13, CD14, dipeptidyl-
peptidase 10 (DPP10), and a disintegrin and
metalloprotease domain 33 ( ADAM33 ).
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10. Environmental factors
• Environmental factors interact with genetic factors to maintain type 2
helper T (T H 2) cell–directed immune responses.
• T H 2 cells activate eosinophils, promote IgE production, and are
proallergic.
• Early childhood exposure to bacterial and viral infections and
endotoxins (eg, lipopolysaccharide) may normally shift native T H 2-
cell responses to type 1 helper T (T H 1)–cell responses, which
suppress T H 2 cells and therefore discourage allergic responses.
• Other factors thought to contribute to allergy development include
chronic allergen exposure and sensitization, diet, and environmental
pollutants.
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11. Pathophysiology
• When allergen binds to IgE-sensitized mast cells and basophils,
histamine is released from their intracellular granules.
• Mast cells are widely distributed but are most concentrated in skin,
lungs, and GI mucosa; histamine facilitates inflammation and is the
primary mediator of clinical atopy.
• Physical disruption of tissue and various substances (eg, tissue
irritants, opiates, surface-active agents, complement components
C3a and C5a) can trigger histamine release directly, independent of
IgE.
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12. Con .
• Histamine causes the following:
• Local vasodilation (causing erythema)
• Increased capillary permeability and edema (producing a wheal)
• Vasodilation of surrounding arterioles mediated by neuronal reflex
mechanisms (causing flare—the redness around a wheal)
• Stimulation of sensory nerves (causing itching)
• Smooth muscle contraction in the airways (bronchoconstriction) and
in the GI tract (increasing GI motility)
• Increased nasal, salivary, and bronchial gland secretioson
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13. Con .
• When released systemically, histamine is a potent arteriolar dilator
and can cause extensive peripheral pooling of blood and hypotension;
cerebral vasodilation may be a factor in vascular headache.
• Histamine increases capillary permeability; the resulting loss of
plasma and plasma proteins from the vascular space can worsen
circulatory shock.
• This loss triggers a compensatory catecholamine surge from adrenal
chromaffin cells.
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15. Symptoms and Signs
• Common symptoms include
• Rhinorrhea, sneezing, and nasal congestion (upper respiratory
tract)
• Wheezing and dyspnea (lower respiratory tract)
• Itching (eyes, nose, skin)
• Signs may include nasal turbinate edema, sinus pain during
palpation, wheezing, conjunctival hyperemia and edema,
urticaria, angioedema, dermatitis, and skin lichenification.
Stridor, wheezing, and hypotension are life-threatening signs of
anaphylaxis
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16. • Diagnosis
• Clinical evaluation
• Sometimes CBC and occasionally serum IgE
levels (nonspecific tests)
• Often skin testing and allergen-specific serum
IgE testing (specific tests)
• Rarely provocative testing
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17. Nonspecific tests
• Blood tests (in vitro immunoglobulin E antibody tests) can be useful
for those who shouldn't undergo skin tests.
• Blood tests aren't done as often as skin tests because they can be less
sensitive than skin tests and are more expensive.
• CBC to detect eosinophilia if patients are not taking corticosteroids,
which reduce the eosinophil count.
• However, CBC is of limited value because although eosinophils may
be increased in atopy or other conditions .
• Serum IgE levels are elevated in atopic disorders but are of little help
in diagnosis because they may also be elevated in parasitic infections,
infectious mononucleosis, autoimmune disorders, drug reactions,
immunodeficiency disorders
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18. Allergy skin tests
• During allergy skin tests, your skin is exposed to (allergens) and is then observed
for signs of an allergic reaction.
• Along with your medical history, allergy tests may be able to confirm whether or
not a particular substance you touch, breathe or eat is causing symptoms.
• Allergy skin tests are widely used to help diagnose allergic conditions, including:
• Hay fever (allergic rhinitis)
• Allergic asthma
• Dermatitis (eczema)
• Food allergies
• Penicillin allergy
• Bee venom allergy
• Latex allergy
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( )‫النف‬ ‫حساسية‬ ‫القش‬ ‫حمى‬
‫التحسسي‬ ‫الربو‬
( )‫الكزيما‬ ‫الجلد‬ ‫التهاب‬
‫الطعام‬ ‫حساسية‬
‫البنسلين‬ ‫حساسية‬
‫النحل‬ ‫سم‬ ‫الحساسية‬
‫اللتكس‬ ‫حساسية‬

19. Management
• Several medications maybe used to block the action of allergic
mediators, or to prevent activation of cells and degranulation
processes.
• These include antihistamines, glucocorticoids, epinephrine, mast
cell stabilizers, and antileukotriene agents are common treatments
of allergic diseases.
• Anti-cholinergics, decongestants, and other compounds thought
to impair eosinophil chemotaxis, are also commonly used.
Epinephrine is important in anaphylaxi
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20. epinephrine pen
• Epinephrine auto-injector is an emergency injection ("shot") of epinephrine. It is a
medicine used for life-threatening allergic reactions such as severe swelling,
breathing problems, or loss of blood pressure.
• It is administered by injection into the middle of the outer side of the thigh (upper
leg) and begins working rapidly.3,4
• Remember: Use of epinephrine auto-injector must be followed by emergency
medical care.
• Epinephrine auto-injector is designed for self-administration. The press-and-hold
technique - press hard, hold in the middle of the outer side of the thigh (upper leg)
for 10 seconds - is designed to deliver the full dose of epinephrine.
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21. Thanks
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