Allergy & Immunology Flashcards
Asthma Pathophysiology
After an episode: airways fill w/ mucus,muscles around the airway contract, airways swell
Obstruction- partially reversible w/ bronchodilator therapy
Hyperresponsiveness- abnormal response to external stimuli
Chronic inflammation
mast cell activation → inflammatory cell infiltration: eosinophils, helper T-cells lymphocytes, neutrophils
Asthma Predictive Index
Criteria utilized to predict a diagnosis of asthma for ages 3 or younger w/ 4 + wheezing episodes within the past year:
Major (need 1)
- Parent w/ asthma
- Diagnosis of eczema
- Sensitivity to aeroallergens
Minor (need 2)
- Food allergy
- >4% eosinophils in blood
- Wheezing not associated w/ URI
Asthma classification: symptoms
Intermittent: </= 2 days/week
Persistent: mild, moderate, severe
- Mild > 2 days/ week, but not daily
- Moderate- daily
- Severe- throughout the day
Asthma classification: severity
Impairment
- nighttime awakenings
- SABA use
- interference with normal activity
- lung function
Risk
-exacerbation requiring oral steroid use
Asthma classification: control
3 categories:
- Well controlled - little to no use of rescue inhaler
- Not well controlled- increasing use of rescue inhaler
- Very poorly controlled- excessively using rescue
Assessed as often as every 1-6 mts
Therapy adjustments made based on asthma classification + level of control
Asthma Diagnostic Criteria
Current episodic symptoms of airflow obstruction
- Cough, wheezing, SOB, chest tightness
Airway flow obstruction or airflow limitations that is partially reversible with bronchodilator
- Younger children with positive clinical response to bronchodilator
- Older children with evidence of improvement measured by spirometry
Alternative diagnosis excluded
Quick Relief Medications
SABA- albuterol MDI or nebulized
Oral corticosteroid- prednisone, methylprednisolone, dexamethasone
Anticholinergic- ipratropium bromide MDI or nebulized
Short acting beta agonist (SABA)
quick relief
albuterol - metered dose inhaler (MDI) or nebulized
Anticholinergic (asthma)
quick relief
ipratroprium bromide (MDI or nebulized)
Oral steroids (asthma)
quick relief
prednisone, prednisolone methylprednisolone (1-2 mg/kg/day; max 60mg/day)
dexamethasone (0.3-0.6 mg/kg/day; max 12-16 mg/day)
Long term controllers
Inhaled corticosteroid (ICS)- Budesonide, fluticasone, beclomethasone,mometasone
SABA+ICS
LABA- salmeterol, formoterol
LABA+ICD-Fluticasone+Salmeterol, Budesonide+Formoterol, Mometasone+Formoterol (dulera)
Leukotriene receptor antagnonists (LRA)- montelukast
Inhaled corticostroids (ICS)
long term controller
Budesonide, fluticasone, beclomethasone, mometasone
LABA
long term controller
salmeterol, formoterol
LABA + ICS
long term controller
Fluticasone+Salmeterol (advair, airduo)
Budesonide+Formoterol (symbicort)
Mometasone+Formoterol (dulera)
Leukotriene receptor antagonist (LRA)
long term controller
Montelukast
Asthma differentials
Allergic rhinosinusitis
Sinusitis
Adenoid or tonsillar hypertrophy
Foreign body
Vocal cord dysfunction
Tracheobronchomalacia
Cystic fibrosis
Bronchiolitis
Pneumonia
Bronchiectasis
Gastroesophageal reflux
Adverse reaction to ACE inhibitor meds
Increased risk of asthma death
History of sudden, severe exacerbation
Prior ICU admission
Prior intubation for asthma
2 or > hospitalizations or > 3 ED visits
Using >1 canister of SABA in short period of time
Chronic oral steroid use
Inability / difficulty perceiving severity of asthma
Status Asthmaticus
Severe asthma exacerbation
Risks include:
-multiple hospitalizations
-prior intubation
-prior attack with severe, unexpected & rapid deterioration
-frequent beta agonist use
-abrupt cessation of ICS
Manifestations:
coughing, wheezing, difficulty breathing, retractions, complaint of chest pain, nasal flaring, grunting, head bobbing, difficulty speaking in sentences, anxious
Signs of impending respiratory failure
Altered mental status
Cyanosis
Decreased breath sounds
Difficult to speak more than a few words in a single breath
Status asthmaticus PE/management
PE: tachycardia, tachypnea, pulsus paradoxus (decrease in SBP of >10 mmHg during inspiratory phase), hypoxemia
Observe LOC, hydration status, peripheral perfusion (check cap refill)
Management - hospitilization
Oxygen if hypoxic
IVF for rehydration
Bronchodilator therapy, anticholinergics, magnesium sulfate IV
IV corticosteroid - Methylprednisolone 2-4mg/kg/day given every 6-12 hrs (max 60 mg/day)
PICU if requires positive pressure ventilation (PPV), sedation or IV bronchodilator infusion
Asthma Control Test (ACT)
Score of 19 or less - asthma may not be controlled
Asthma Action Plan
Green zone- doing well
Yellow zone-
- cough, wheeze, chest tightness, or SOB or
- Waking at night d/t asthma or
- Can do some, but not all, usual activities
- Add on quick relief, If not in green zone after 1 hr of treatment, add something else
Red zone
- Very short of breath, or
- Quick relief medicines have not helped
- Cannot do usual activities
- Symptoms are same or get worse after 24 hrs in yellow zone
Allergic Rhinitis
Exposure to allergen → IgE production →binds to mast cells of upper airway
Allergen exposure triggers release of:
- histamines (rhinorrhea, congestion, sneezing)
- leukotrienes
- prostaglandins
- cytokines (eosinophilic reaction- edema)
Common triggers: dust mites, roaches, pollen, animals, molds
Clinical manifestations: runny nose, sneeze, itchy eyes, headache
Allergic Rhinitis exam features/sequelae/diagnostics
Exam features: nasal crease, allergic shiners, allergic salute
Concerning sequelae:
Chronic OME; frequent AOM
Sinusitis
Nasal speech
Mouth breathing secondary to enlarged tonsils and adenoids; high arched palate, malocclusion
Snoring, poor sleep
Nasal polyps- rare in children except CF pts
Diagnostics:
Clinical diagnosis - usually need 1-2 seasons of exposure
Serum labs can be normal in children w/ AR
Cytology testing of nasal secretions is available, not routinely done in primary care
Skin testing or serum IgE testing can identify environmental factors to help guide mitigation strategies
AR treatment guidelines
**Environmental control **
Frequent laundering of bed linen, limiting stuffed animals & pets in the bedroom; pest control
Utilize air filters, dehumidifiers to combat mold
Avoidance of triggers when possible
Less outdoor play during high pollen times
Immediate removal of clothing and showering after outdoor exposures
Pharmacologic
- Antihistamines- cetirizine, loratadine, fexofenadine
- Nasal steroids (pt should fully evacuate nose prior to use)-
Fluticasone propionate (4 yrs+), mometasone, triamcinolone (2 yrs +)
- Leukotriene receptor antagonist- montelukast
- Decongestants- short term use, ensure age appropriate dosing
Long term use can lead to rebound congestion, can cause hyperactivity and irritability in children
Not recommended under 6 yrs
If first line treatment fails or effects wane- referral may be necessary for skin testing
Atopic Dermatitis
IgE mediated type I & cell mediated type IV reaction → results in inflammatory changes in epidermis
Mutation of filaggrin gene (FLG) → results in loss of function leading to entry of allergens and transepidermal water loss
Triggers: airborne allergens, food, contact allergens, infectious agents
Atopic Dermatitis Diagnostic Criteria
(Criteria for diagnosis by Hanifin & Lobitz)
Essential features:
- Pruritus, eczematous dermatitis in age specific pattern
- Chronic or relapsing
Important features:
- Early age at onset, atopy, xerosis
Common associated features
- Atypical vascular response; keratosis pilaris, ocular changes, lichenification
AD: age specific distribution
Infants and toddlers
May appear as a rash on the scalp, face or arms and legs
Children
May begin inside creases of the elbow or knees, the neck, wrists, ankles, and/or the crease between the buttocks/legs
Adults
Often shows on the inner creases of the elbows or knees, hand, and/or nape of the neck
AD differentials/diagnostics
Differentials:
Scabies
Seborrheic dermatitis
Psoriasis
Histiocytosis X
Severe combined immunodeficiency
Acrodermatitis enteropathica
Diagnostics:
Not necessary for diagnosis, can be considered if there is coinciding asthma or allergic rhinitis and you want to identity triggers
Refractory cases may require testing to identify underlying genetic conditions
Skin culture if secondarily infected- impetigo, mrsa
Biopsy rare but can be useful
AD treatment
Dry skin
Moisturizers
Emollients in either cream or ointment form
Shortened bath times, use of mild soaps
Inflammation
Topical corticosteroids creams or ointments
Nonsteroidal immunomodulators
Pruritus- consider oral antihistamine- mixed data on effectiveness
Hydroxyzine or diphenhydramine at bed time
Behavior modification - rubbing instead of scratching, socks or mittens at bedtime, keep nails trimmed
Nonsteroidal options (after first line of moisturization and second line of mild/medium potency steroid)
Calcineurin inhibitors: Tacrolimus and Pimecrolimus
Black box warning - increased risk of cancer associated with oral, topical has been found safe to date
Safe to apply on body and face for mild-moderate AD
Phosphodiesterase-4 (PDE-4) inhibitor- Crisaborole
Anti inflammatory and anti-itch
Burning or stinging common side effect
Home interventions
Wet wrap therapy- put on layer of lukewarm wet clothing, and put dry layer overtop
Cut fingernails short
Teach to pat/rub and not scratch
Avoid food triggers once identified- hydrolyzed formula for infants w/ mild protein allergy
Moisturize often
Refer if:
→ Dermatology or allergist:
No response to first or second line therapy
If has HPV or Molluscum contagiosum involvement
Severely infected may require hospitalization for IV abx:
- Staphylococcus
- Eczema herpeticum/ kaposi varicelliform eruption
AD topical corticostroid potencies
Low potency:
Desonide 0.05%
Hydrocortisone 0.5-2.5%
Medium potency:
Bethamethasone valerate 0.1%
Triamcinolone acetate 0.1%, 0.5%
Flurandrenolide 0.05%
Flutcasone proprionate 0.05%
High potency:
Betamethasone diproprionate 0.05%
Clobetasol proprionate 0.05%
Halobetasol proprionate 0.05%, 0.25%
Flucinonide 0.05%
generally limit high potency TCS to < 2 weeks duration
gel formulation are highest potency
Urticaria
Rash produced by capillary leak vasodilation & edea of skin
Occurs as a result of histamines, prostaglandins, and leukotrienes being released from epidermal mast cells
Triggers: IgE mechanisms, viral, bacterial, parasitic, and fungal infections, collagen vascular disease, malignancy, endocrine disease, and physical factors like heat, cold, pressure, sun, vibration
Erythematous, popular, coalesce, blanching, last <24 hrs but can recur, itchy
Angioedema
Extension of uritcarial process deeper into the dermis
+/- mucous membrane involvement
tissue swelling, tightness
involvement of abdominal viscera results in colicky abdominal pain
Urticaria & Angioedema management
Eliminate offending agent
Manage underlying infections
Manage underlying condition
Medications
- Antihistamines 1st (diphenhydramine) and 2nd gen (claritin, zyrtec, allegra)
- H2 receptor antagonists- cimetidine, famotidine, ranitidine (helpful for GI manifestations)
- systemic steroids (for angioedema)
Food Allergies
most common: milk, egg, wheat, soy - resolve in childhood
peanut, tree nut, shellfish, fish- can resolve, but more likely to be persistent
Clinical manifestations:
suspect when the following are present within minutes or hours after food ingestion-
- Urticaria
- Edema
- Wheezing
- Mouth itch- children may not verbalize but will rub tongue against top of mouth, or click with tongue
- Cough
- Nausea / vomiting
- Anaphylaxis
Food allergy diagnosis
- based on history & clinical presentation
- medically managed food challenge is the most definitive test for food allergy
- food specific IgE testing (should not be sole source used for diagnosis)
In children w/ moderate to severe eczema that are < 5 yrs, food allergy should be considered for milk, wheat, peanut, egg, and soy if at least 1 of the following are met
- The child has persistent AD in spite of optimized management and topical therapy
- The child has a reliable history of an immediate reaction after ingestion of a specific food
Prevention of peanut allergy
Infant w/ severe eczema, egg allergy, or both- consider eval by IgE and/or skin prick test (SPT), if necessary OFC, based on results, introduce peanu containing food (4-6mts)
Infant w/ mild to moderate eczema- introduce peanut containing food (6 mts)
Infant w/ no eczema or food allergy- introduce peanut containing food at any age appropriate time
Anaphylaxis
Multisystem reaction that occurs suddenly after contact w/ a substance/mechanism
Constellation of symptoms involving multiple organ systems:
Skin (90% of cases)- flushing, pruritus, urticaria, angioedema
GI (30% of cases)- nausea, abdominal pain (colic), vomiting (large amounts of “stringy” mucus), and diarrhea
Respiratory (70% of cases; most common cause of death in children)
- laryngeal: pruritus and “tightness” in the throat, dysphagia, dysphonia and hoarseness, dry “staccato” cough.
- Lung: dyspnea, chest tightness, “deep” cough, and wheezing;
- nose- pruritus, congestion, rhinorrhea, and sneezing
CV (20% of cases)- feeling of faintness, syncope, chest pain, dysrhythmia, hypotension, shock
Anaphylaxis diagnostic criteria
Highly likely when 1 of the following 3 criteria are met
Criterion 1: acute onset (minutes to several hours) with involvement of skin, mucosal tissue, or both, even in the absence of known or suspected trigger and at least* one* of the following:
- Respiratory compromise
- Reduced BP or associated symptoms of end-organ dysfunction (collapse, syncope, incontinence)
Criterion 2:* two or more *of the following occur rapidly (minutes to several hours) after exposure to a likely allergen
- Involvement of the skin or mucosal tissue
- Respiratory compromise
- Reduced BP or associated end-organ dysfunction
- Persistent GI symptoms
Criterion 3: reduced BP rapidly (minutes to several hours) after exposure to known allergen
Anaphylaxis categories
Uniphasic - anaphylactic reaction, treated, and pt improves
Biphasic (up to 14% of cases)
Develop initial symptoms
Appear to recover
Develop symptoms again
Protracted- lasts 1 day-3 weeks
Anaphylaxis management/ discharge
- Assess airway, breathing, circulation, and neuro status - continue to monitor throughout
- Place in recumbent position
- Administer Epinephrine IM
- do not wait for symptoms development
-administer at onset of mild symptoms (pruritus, urticaria, etc.)
- may use epipen or epi vial
Child - 0.1mg/kg/dose IM/SC up to max of 0.5mg/dose q20 min- 4 hrs prn
Adult - 0.1-0.5 mg IM/SC q20min-4 hr prn; may increase to single max dose of 1 mg - Administer supplemental O2 in patients w/ respiratory symptoms
- Bolus of NS (20-40 ml/kg) in patients w/ hypotension
Second line therapies:
- antihistamine (diphenhydramine 1-2mg/kg)
- steroid (oral prednisone or IV methylprednisolone at 1-2 mg/kg/dose)
- inhaled SABA for wheezing
Discharge:
Mild anaphylaxis- 4-6 hrs observation
Moderate anaphylaxis- 6-8 hrs observation
Severe anaphylaxis- admit for at least 24 hrs obs
Diagnostics for unknown cause
Trigger avoidance education
Auto injector epinephrine (AIE) prescription for 2 autoinjectors
- <30kg: 0.15 mg (epipen junior)
-** >/=30kg: 0.3 mg**
Educate to seek immediate medical attention anytime anaphylaxis occurs
Written emergency plan
Erythema Multiforme
Cutaneous and mucosal hypersensitivity reaction w/ characteristic lesions triggered by a stimuli
Lesions appear on the skin favoring the extremities and usually resolve within 7-21 days
Mucous membranes are involved in about 10% of cases
Etiology: HSV (likely to re occur in pts), mycoplasma pneumoniae, other virsues, bacteria, fungi, drugs, heavy metals, herbals, topical therapies, poison ivy
Increased risk: HIV, corticostroid therapy, immunosuppresion, BMT recipient, Lupus
Erythema Multiforme Minor
Typical skin lesions w/ symmetrical acral (peripheral) distribution (limbs)
Mucous membrane involvement is rare, only single mucosa, usually mouth
Healing takes 2-3 weeks
Erythema Multiforme Major
Skin lesions are extensive but less than 10% of body surface area
Typical target lesions present
Mucosal involvement is severe and affects at least 2 mucosal sites
Healing takes 4-6 weeks
Erythema Multiforme clinical presentation
Fever and feeling of unease prior to or accompanying the eruption
Arthralgia, joint swelling
Target lesion is typical- symmetrical, trunk is usually spared, some complain of burning sensation but no itching
Mucosal lesions are most common in the mouth
- Bullous then painful erosion
- May note white coating
Pulmonary system may be involved with cough, dyspnea (particularly w/ mycoplasma pna if that is trigger)
Multiforme Erythema differentials/ diagnostics
Differentials:
Pityriasis rosea
Urticaria
Viral exanthems
Stevens johnson syndrome
Hypersensitivity reaction
Diagnostics:
Diagnosis is clinical
Skin biopsy of lesion center
Look for current HSV outbreak (oral and genital or other parts of the body)
Consider CXR with cough, respiratory symptoms (M. pneumoniae)
CBC/D
- Mild leukocytosis
- Neutropenia
- Mild anemia
Chemistry if concern for dehydration (d/t mouth lesions)
Multiforme Erythema treatment
Topical treatment
-antiseptics for bullous lesions
- antiseptic mouthwash
- anesthetic
- topical steroid
Ocular involvement- refer to ophtha
M. Pneumoniae- azitrhomycin
HSV- acyclovir
Hospitalize for
- dehydration
- pain control
- extensive lesions w/ burn like qualities- to decrease likelihood of secondary infection
Stevens-Johnson Syndrome (SJS)
Rare, acute, serious and potentially fatal skin reaction
Characterized by sheet-like skin and mucosal loss accompanied by systemic symptoms
Medications are the cause in over 80% of cases: anticonvulsants, allopurinol, sulfonamides, antibiotics, APAP, nevirapine, NSAIDs, contrast media
SJS Clinical Manifestations
Begins w/ nonspecific symptoms like fever, malaise, URI symptoms
Blistering rash and erosions appear to the face, trunk, limbs, and mucosal surfaces
- erythematous, target like, annular, or purpuric macules
- bullae
- large painful erosions
- Nikolsky positive- lateral pressure on the skin results in shedding of the epidermis
Mucosal ulcerations involving the lips, mouth, pharynx, esophagus, GI tract, eyes, genitals, upper respiratory tract
Patient is ill appearing and in pain
Liver, kidneys, lungs, bone marrow, joints may be involved
SJS management/prognosis
Treatment/ management:
Hospitalization- preferably burn care unit
Cessation of causative drug
Fluid replacement
Nutritional support
Temp control, pain control
Supplemental O2 and ven support if needed
Skin care
Abx to treat secondary infections
Prognosis:
at risk for secondary infections & organ failure
more common complicationsL blindness, scarring, renal scarring
mortality up to 20%
IgA Vasculitis
IgA collects in small blood vessels → becomes inflamed & leaks blood
Most common vasculitis in children (<10 yrs, males> females)
Clinical findings:
- may be proceeded by URI (likely trigger)
- skin rash (palpable purpura to buttocks and LE)
- arthritis (60-80%)
- colicky abdominal pain (50-70%), may proceed rash
- renal involvement (20-60%)
IgA diagnostic criteria
based on clinical presentation
2 or more of the following:
-palpable purpura (usually to the LEs)
-initial presentation at 20 yrs or younger
-bowel angina (manifests as colicky abdominal pain)
-typical renal biopsy findings
IgA diagnostics/management
Diagnostics:
UA and BP- monitor for renal involvement (baseline, then q month x 6 mts)
Consider
Stool guaiac for occult blood
Abdominal CT (if obstruction suspected)
Renal biopsy if
-proteinuria > 1 mt
-renal insufficiency
-HTN
-nephrotic syndrome
Management
-symptomatic , analgesics for mild joint pain
- monitor for hematuria & proteinuria
- monitor BP
- refer/consult for GI, renal, significiant joint involvement
usually runs its course within 3-4 wks, rash may recur for up to 1 yr
