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ALLERGY
- An altered state of reactivity tocommon environmental
antigens.
FEATURES OF ALLERGIC DISEASES :
Allergens
- refers to an antigen that triggers an Ig E response in genetically
predisposed individuals.
Type 2 Helper T cells
- Secrete cytokines favoring Ig and E synthesis and are involved
in host defense against extracellular organisms such as
parasites.
Eosinophils
- Allergic diseases are characterized by peripheral blood and
tissue eosinophilia.
- Contains intracellular granules that are sources of inflammatory
proteins.
Mast Cells
- Derived from CD 34 hematopoietic progenitor cells that arise
from the bone marrow.
- Contains histamine, serine proteases and proteoglycans.
Note:
• The most important mass cell-derived lipid mediators are the
cyclo-oxigenase and lipoxygenase metabolites of Arachidonic
Acid.
• The major Cyclo-oxygenase product of mass cells is
Prostaglandin D2.
• The major lypoxygenase products are the
sulfidopeptideleukotrienes : LTC4 and its peptidodytic
derivatives LTD4 and LTE4.
MECHANISMS OF ALLERGIC TISSUE INFLAMMATION
Classification of Ig E – mediated immune responses:
1. Early phase response.
2. Late phase response.
3. Chronic Allergy diseases.
Early Phase Response
- Immediate response after introduction of allergen into target
organs.
- Within 10 minutes after allergen exposure and resolving within
1-3 hrs.
- e.g. leakage of plasma proteins tissue swelling increased blood
flow.
- Ex. Itching, sneezing, wheezing, acute abdominal cramps in the
skin, nose, lung, and GIT.
Late Phase Response
- Can occur within hrs of allergen, exposure, reaching a
maximum at 6-12 hrs and resolving by 24 hrs.
Clinically – cutaneous LPRs
- Characterized by edema, redness, and induration; sustained
nasal blockage, wheezing.
Chronic Allergic disease
- Tissue inflammation can persist for days to years.
- Risk Factors: recurrent exposure to the allergens and microbial
agents.
- Ex. Asthma – remodeling involves thickening of the airway.
Atopic dermatitis – lichenification
DIAGNOSIS OF ALLERGIC DISEASE
• Allergy History
• Risk of allergic disease in a child whose parent is allergic-50%
• Both parents 66%
CHARACTERISTIC BEHAVIOR OFTEN SEEN IN ALLERGIC CHILDREN :
Allergic Salute
- rubbing their nose upward with the palm of their hand because
of the nasal pruritus and rhinorrhea .
Nasal Crease
- a horizontal skin fold over the bridge of the nose.
Allergic Cluck
- is produced when the tongue is place the roof of the mouth to
the form to form a seal and withdraw rapidly in an effort to
scratch the palate.
Aeroallergens
- pollens or fungal spores are prominent causes of allergic
disease whose concentration in outdoor air fluctuates
seasonally.
PHYSICAL EXAMINATION
Allergic shiners
- blue gray to the purple discoloration beneath the lower eyelids
attributed to venous stasis.
Dennie lines
- Prominent symmetric skin folds that extent in an arc from the
inner canthus beneath and parallel to the lower lid margin.
Conjuctival Injection and edema
- in allergic conjunctivitis
External Ear
- eczematoid changes in Atopic Dermatitis.
Nasal Patency
- should be assessed, examine for septal deviation, turbinate
hypertrophy, septal spurs, or nasal polyps.
Pale to purple nasal mucosa
- suggest allergic rhinitis.
Lips
- Reveal cheilitis cause by drying of the lips from continuous
mouth breathing and repeated licking of the lips
Post pharynx
- Presence of post nasal drip and post pharyngeal lymphoid
hyperplasia.
Xerosis
- Dry skin in the most common skin abnormality of allergic
children.
Keratosis Pilaris
- Found on the extensor surfaces of the upper arms and tight,
characterized by roughness of the skin caused by keratin plugs
logged in the openings of hair follicles.
Atopic Dermatitis
- A chronic, heritable, cutaneous inflammatory disease
characterize by early age of onset of intense pruritus.
- Skin lesions maybe dry, easily irritated, weeping
Atopic Dermatitis
- Atopic Eczema
- Genetic predisposition
- Relapsing course
- Increase serum Ig E
CLINICAL MANIFESTATIONS :2 STAGES
I. Infantile stage
- begins during the 4th-6th months
- Erythematous, pruritic, weeping dermatitis in the cheeks which
spread to the forehead and extensor surface of the arms and
legs.
- Cradle cap
- Disappears between 3rd – 5thyear of life.
II. Childhood stage
- May disappear before 10 years of age or continue to adulthood.
- “Mark of atopic dermatitis” where there is whitish hue of the
face.
Stigmas of atopic dermatitis pruritus
- Characterized all phases of atopic dermatitis, intense during
infancy.
Lichenification
- A dramatic increase in the visibility of the normal geometric
skin markings pruritic on the sides of the neck and in the
popliteal and antecubital fossa.
Dennie’s line
- A prominent fold on the lower eyelid
Atopic palms
- Increase fine palmar and digital creases and lines which are
presumed to be a manifestation of dry skin.
Buffed Nails
- produced by chronic scratching and rubbing
Abnormal Vascular reactions
- Studying of the skin of AD patient produces an initial
erythematous line that is quickly replace by whitish blanch –
“white demographism”
Dryness xerosis
- Seen on the extensor surface of the extremities where there is
also keratosis pilaris
- Deficient sweating
Atopic Personality
- Reactive , active aggressive and somewhat hostile
Atopic foot
- erythematous scaling eczema involving dorsal and ventral
Aspect of the big toes
TREATMENT:
• Avoidance of the triggers
• Food allergens: peanut, milk, eggs, and seafood, inhalants
(houses dust mites , mold spores)
• Extreme change of temperature
• Good hydration - bathing or soaking the affected area for 15
mins in tepid water
• Use of oatmeal to the bath water for soothing
• Moisturizer / Creams
• Avoid soap and detergents, wool, silk, nylon, and other
synthetic fabrics- physical irritants.
ASTHMA
- A chronic inflammatory disorder of the airways in which cell
play a role, including mast cells and eosinophils.
- Etiopathogenesis:
• Hyperresponsive of the airway muscles Activated by:
autonomic
• Immunologic
• Infectious- Viral agents
• Endocrine
• Physiologic
- VIP (vasoactive Intestinal peptide)
Smooth muscle relaxation
- Local hormonal factors (histamine and leukotriene)
produces bronchoconstriction
Increase IgE
- Endocrine Factors
• worsens asthma during pregnancy menstruation and
onset of menopause
• At puberty – improves Thyrotoxicosis worsens the
severity of asthma
- Emotional factors
• Abnormal behavioral characters- affects child’s self
confidence
- Pathophysiology
Triad:
Smooth muscle spasm with hypertrophy
Mucosal edema
Plugging with tenacious albumin, epithelial cells
and eosinophilic leukocytes
- Lung Hyperinflation:
• Increase Residual Vol. and FRC
• Decrease VC, IC-ERC
• Decrease Lung compliance
• Ventilation- perfusion mismatch
- Clinical Presentation
• Wheezing ( High pitched or squeaking expiatory
sound)
• Cough- prolonged expiatory phase
• Tachypnea and dyspnea with used of accessory
muscles of respiration
• Hyperinflation of the chest
• Tachycardia
• Abdominal pain with vomiting
• Excessive sweating
• Fatigue and low grade fever from increase work of
breathing
• Hunched-over sitting position
- Laboratory
• Chest X-Ray – Hyperinflation with peribronchial
thickening
- Allergy skin test or RAST
“not all that wheezes is asthma”
- DDx:
• Congenital malformations of the respiratory tract
• Cardiovascular and GI systems, FB, Croup,
bronchiototis, endobronchial TB, etc.
- Children over 5y/o
o Spirometry
o Peak flow measurements
- Management:
1. Bronchodilator – β2 agonists, theophylline, anticholinergic
(ipatropium bromide)
2. Anti-inflamatory Agents – nedocromil sodium, sodium
cromoglycate, costicosteroids)
STATUS ASTHMATICUS
- severe acute asthma
- progression of the attack unresponsive to the usual appropriate
therapy
- Characteristics:
1. Hx of frequent repeated attacks, excessive daily use of
bronchodilator, corticosteroids
2. Use of accessory muscles
3. Pulses paradoxus
4. Change in consciousness
5. Cyanosis
6. Pneumothorax and pneumonediastinum
7. Hypoxemia with a paCO2 less than 60mmHg
8. Hypercapnea
9. Metabolic acidosis
10. FEV1 less than 20% predicted value
11. EKG abnormalities like p PulmonaleR vent. R Strain,
bundle branch blocks, R axis deviation
- Adverse Drug Reaction
• Type I – Drug Reaction
Urticaria , pruritus, Ig E
• Type II – Cytotoxic Reactions
The antigenic determinants of the drug will
interact with Ig G or Ig M or both antibodies will
bind with the lymphocyte, leukocyte a platelets of
the drug sensitive patients.
Activation is the destruction of the target cells
Ex. Quinidine – induced hemolytic anemia
• Type II – toxic complex syndrome or Arthus phenomenon
prototype of serum sickness
Symptoms are due to tissue damage brought
about by the action of proteolytic enzymes
liberated from neutrophils.
Clinical Features : Urticaria with or without
angioedema erythmatous, maculopapular
rashes, erythema multiforme, arthralgia
• Type IV-V- cell – mediated
Allergic reaction involves the lymphoid cells and
not the hormonal antibodies
Prototype: contact dermatitis (drug induced) –
reaction to topical creams and lotion
ATOPIC DERMATITIS
- Definition
• Atopic Dermatitis – eczema- itchy skin
• Greek – meaning
o (cc-) over
o (-ze) out
o (-ma) boiling
- Infants &small children (affects 1 in 7)
- Atopic dermatitis of childhood may reappear at different site
later in life.
- Cause :
• Inborn skin defects that tends to run in families, e.g.
asthma or hay fever
• 85% with high serum IgE and + skin tests food &
inhalant
- Distribution:
• In infants , the face is often affected first, then the
hands and feet; dry red patches may appear all over
the body
• In older children , the skin folds are most often
affected, especially the elbow creases and behind the
knees.
• In adults , the face and hands are more likely to be
involved.
- Associated features
• the skin is usually dry, itchy & easily irritated by:
- soap
- detergents
- wool clothing
• May worsen in hot weather & emotional stress.
• May worsen with exposure to dust and cats.
- Associated findings:
• Xerosis
• Keratosis Pilaris
• Itchythyosis
• Hyperlinear Palmar Creases
- Diagnosis:
• Major Characteristics
o Pruritus with or without excoriation
o Typical morphology and distribution
o Chronic relapsing dermatitis
o Personal or family history of atopy (asthma,
allergy, atopic derm, contact urticaria)
• Other characteristics
o Xerosis/Itchythysis/palmarhyper/kerat. pilaris
o Early age of onset
o Cutaneous colonization and/or overt infections
o Hand/foot/nipple/contact dermatitis, cheilitis,
conjunctivitis, erythroderma, subcapsular
cataracts
- Differential Diagnosis
• Seborrheic dermatitis
• Drugs
• Scabies
• Drugs
• Psoriasis
• Allergic contact dermatitis
• Cutaneous T-cell lymphoma
- Treatment:
1. reduces contact with irritants (soap substitutes)
2. reduce exposure to allergens
3. emollients
4. topical steroids
5. antihistamines
6. antibiotics
7. Steroid sparing
8. other (herbals, soaps)
- Reduce contact with irritants
• avoid overheating lukewarm, baths, 100% cotton
clothes, & keep bedding to minimum
• Avoid direct skin contact with rough fibers,
particularly wool, & limit/eliminate detergents
• Avoid dusty conditions & low humidity
• Avoid cosmetics (make-ups, perfumes) as all can
irritate
• Avoid soap-use soap substitute
• Use gloves to handle chemicals and detergents
- Soap Substitute
• Cetaphil-soap substitute – far less drying and irritating
than soap
• Cleansing & moisturizing formulations, all OTC
• Lotion, bar, soap, cream, sunscreen
• Costs about $8-9 for 16oz
- Reduce Exposure to allergens
• Keep home, especially bedroom, free of dust
• Allergic reactions module house dust mute, molds,
grass pollens & animal dander
• Special diets will not help most individuals b/c little
evidence that food is major culprit
• If food allergies exists, most likely d/t dairy products,
eggs, wheat, nuts, shellfish, certain fruits of food
additives
- Emollients
• Emollients soften the skin soft and reduce itching
• Moisture Trapping effective4s
o Best: Oils (e.g. Petroleum Jelly)
o Moderate creams
o Least Lotions
• Apply emollients after bat5hing and times when the
skin is usually dry (e.g winter months)
• Large variety (e.g. Vanicream, Eucerin, Luubriderm,
moistured, curel, neutrogerm)
• Inexpensive emollients include vegetable shortening
(Snowdrift by Martin White) and petroleum jelly
(Vaseline)
• Urea Creams
• Oils
- Emollients: Alpha – Hydroxy acid
• Creams are excellent for relieving dryness, but can
sting & sometimes aggravate eczema
• Useful for maintenance when no longer inflamed
• Forces epidermal cells to produce keratin that is
softer more flexible and less likely to crack
• Preparations
o Glycelic Acid (8%)
o Lactic Acid or Lac-Hydrin (5-12%)
o Urea (3-6%)
• Use IX/day
- Emollients: Oils
• Consider using bath oil or mineral oil-based lotions in
lukewarm bath water
• Add to tub 15 minutes into bath
• Bath oil preparation
o Alpha-keri
o Aveeno bath
o Jeri-bath
• Colloidal oatmeal (Aveeno) reduces itching
- Corticosteroids
• Topical steroids very effective
• Ointments for dry or lichenified skin
• Creams for weeping skin body folds
• Lotions or scalp applications
• Hydrocortisone 1-2.5%appliead to all skin
• Quite safe used even for months
• Use intermittently thin areas-(e.g.-face & genitals)
• Stronger potency topical steroids for non-facial
genital regions.
• Avoid potent ultra potent topical steroid preparations
on face, armpits, grains & bottom
• Once under control, intermittent use of topical
corticosteroid may prevent relapse
• Systemic ateroids may bring under rapid control, but
may precipitate rebound
• Once daily probably most cost effective
- Steroids and Young children
• Fluticasongproprionate cream 0.05%
• Moderate – severe atopic derm>3months
• Applied bid 3-4 weeks –mean 64% BSA
• No HPA suppression
- Corticosteroids: Pearls
• Different preparations prescribed for different parts
of the body for different situations
• Educate on
o Potencies & proper usage
o Write down directions
• Bring all topicals each appointment to clarify use