Allergy and Immunology Flashcards
Role for IV epi in anaphylaxis
- after repeated doses of IM epi
- persistent hypotension despite fluid resuscitation wtih 20mL/kg of NS
concentration 0.1mg/mL (1:10,000)
Biphasic reaction
- most are in first 4-6 hrs (range 1-72 hrs)
- higher risk if delayed epi, more than 1 epi doses, more severe sx (b-agonist given, wide pulse pressure)
25kg epipen
0.3mg IM
Skin prick testing pros:
- results within 15 minutes
- more sensitive
- high negative predictive value
- cost effective
Skin prick testing cons:
- false positives
- affected by use of antihistamines and corticosteroids
- low risk of having a systemic reaction
- cannot perform if skin disease at testing site (e.g. eczema)
High risk for food allergy (CPS)
- personal history of atopy
- first degree relative with an allergic condition
Food protein induced proctitis onset
2-8 weeks of age
by age 9 months, 95% tolerate
Food protein induced enterocolitis syndrome onset and features
1-4 weeks after intro of the food
- vomiting 1-3hrs after ingestion
- hypotension in 15%
(generally resolve by 3 yrs)
Test to look for systemic mastocytosis
serum tryptase
Cross-reactivity between penicillin and cephalosporins
2%
Erythema multiforme
- target lesions
- +/- mucosal membrane
- cna be infections OR medications
- tx with topical corticosteroids, antihistamines
SJS/TEN onset and features
1-3 weeks of drug exposure
- fever, sore throat
- mucus membranes
- blistering lesions with skin detachment
DRESS onset and features
1-8 weeks of drug exposure
- rash, eosinophilia, hepatic dysfunction, fever, facial angioedema, lymphadenopahty
Serum sickness onset and features
1-3 weeks of drug exposure
- rash, arthralgia, arthritis, renal disease, fever
- low complement
- e.g. ATG, monoclonal antibodies
Serum sickness -like
1-3 weeks of drug exposure
- rash, fever, arthralgia, arthritis
- NO renal disease
- normal complement
- e.g. cefaclor, penicillin
Treatment for SJS/TEN
- discontinue med
- supportive therapy
- steroids + IVIG = controversial
Treatment for DRESS
- discontinue med
- steroids if severe
Treatment for serum sickness
- discontinue meds
- NSAIDS, analgesics
- steroids, PLEX if severe
Treatment for serum-sickness-like
- discontinue med
- NSAIDS, analgesics
- steroids if severe
Hereditary angioedema
- genetics
- test
- triggers
- autosomal dominant
- C1 esterase inhibitor (will be low)
- triggers by trauma, infection, estrogen
Treatment allergic rhinitis
- allergen avoidance
- 2nd gen oral antihistamines (cetirizine, loratadine)
- intranasal steroids
- leukotriene receptor antagonist
- immunotherapy
Humoral deficiencies (B-cell)
- X linked agammaglobulinemia
- common variable immunodeficiency
Combined immunodeficiencies (T and B cell)
- SCID
- Wiskott-Aldrich
- ataxia - telangiectasia
- DiGeorge
Phagocyte defects
- CGD
- leukocyte adhesion deficiency
B-cell immunodeficiency features
> 6 months
- encapsulated, enterovirus, giardia,
- AOM, sinopulmonary, arthitis, meningoencephalitis
Phagocytic immunodeficiency features
- early onset
- staph, pseudomonas, serratia
- abscesses, gingivitis, osteomyelitis, skin
Complement immunodeficiency features
- any age
- pneumococcus, meningococcus
- septicemia, meningitis
10 warning signs of PID
- 2+ serious sinus infections /yr
- 2+ months on abx
- 2+ pneumonias /yr
- 2+ deep seated infections (e.g. septicemia)
- 4+ AOM/yr
- recurrent deep skin or organ abscesses
- persistent thrush or fungal infection
- FTT
- need for IV abx
- family history of PID
Humoral (B-cell) assessment
Quantitative: IgG, IgA, IgM, IgE, lymphocyte subsets (CD19+cells) by flow cytometry
Qualitative: specific antibodies e.g. diphtheria, tetanus, measles, mumps, rubella, varicella titres, isohemagglutinins,
Cellular assessment (T-cells)
Quantitative: total lymphocyte counts, lymphocyte subsets by flow cytometry
Qualitative: in vitro lymphocyte proliferation in response to mitogens and antigens, enzyme levels, TRECs, Vbeta
Phagocytic assessment
Quantitative: Neutrophil counts
Qualitative: neutrophil oxidative burst index (or nitroblue test) , measumrent of adhesion markers (for LAD)
Complement assessment
Quantitative: C1 esterase inhibitor levels, specfici complement levels
Qualitative: CH50, AH50, C1 esterase inhibitor fxn (for HAE)
SCID
- presents 2-6 months
- most common = X-linked SCID
- die in infancy unless treated
- severe, recurrent, persistent opportunistic infections and failure to thrive
Ataxia telangiectasia features
- AR
- ataxia (cerebellar) starts as toddler and progresses
- progressive neurodegenerations
- telangiectasia (appear at 4-5 yrs)
- immune deficiency
- abnormal DNA repair
- 25% develop malignancy (esp lymphoma)
Ataxia Telangiectasia screen test
- increase alpha fetoprotein
- absent IgA in 80%
CGD susceptibilities
Catalase positive pathogens:
- s. aureus, aspergillus, serratia, nocardia, brukhorderia, salmonella
HyperIgE features
AD
- recurrent abscesses (cold boils)
- scoliosis, fractures,
- eczema
- dealyed shedding of teeth
- facial features
complement infection susceptibilities
- neisseria
4 types hypersensitivity reaction
Type I = IgE (<2hrs)
Type II = cytotoxic e.g. anemia, thrombocytopenia (10hrs to weeks)
Type III = immune complex e.g. serum sickness (1-3 weeks)
Type IV = T-cell mediated e.g. SJS (2-14 days)
When is penicillin drug challenge contraindicated?
If history is consistent with anaphylaxis or systemic, non-immediate immune reaction e.g. serum sickness, SJS, dRESS or drug-induced hemolytic anemia
Stinging allergy and tryptase
- baseline level of tryptase if hx severe anaphylaxis
- high levels means higher risk for systemic reactions and higher failure rate to VIT
- > 20ng/mL may indicate comorbid systemic mastocytosis
IgE reactions to stinging insects
- large local reactions - no epipen
- systemic reaction - carry epipen
(exception = urticaria alone, low risk for anaphylaxis)