Allergy and Immunology Flashcards
First Aid and NEJM Knowledge+
Differentiate epidermal vs intradermal tests for allergen skin testing
Both are used to test for presence of allergen-specific IgE antibody
Epidermal skin test- some antigen extract put on skin then punctured into epidermis to see if IgE mediated response
-adequate for most things
Intradermal test of injected antigen into dermis for drug reactions
-use for venom and penicillin testing
Both should include histamine and saline controls, look for wheal and flare reaction 15-20 minutes after injection
What is RAST testing used for?
(a) What allergies can it not test for
RAST test = test serology for antigen-specific IgE (basically to see if there is an allergy)
Use when skin testing unavailable or not possible (ex: pt just took benadryl or would cause anaphylaxis)
-more for environmental and food allergens
However RAST alone is not adequate for venom (bee sting) or drug allergy (need intradermal skin test)
Candida and PPD purified antigens injected into skin- what is this a test of?
Both test for cell-mediated immunity
Lack of response to injection indicates inadequate cell-mediated immunity or anergy
Buzzword: otherwise healthy pt p/w recurrent neisseria meningitis
Recurrent neisserial infections c/w terminal complement deficiency (C5-C9 which makes the MAC complex)
What can be used as a screening test for the classic complement pathway?
CH50 can be used as a screening test for the classic complement pathway (triggered by immune complexes)
B/c all elements C1-C9 are needed to make normal CH50
Mnemonic for hypersensitivity type I-IV reactions
‘ACID’
Type I- anaphylactic
Type II- cytotoxic (antibodies directed at self cells)
type III- immune complex mediated
type IV- delayed hypersensitivity (T- cell mediated)
Describe the mechanism of type I hypersensitivity reaction
Type I = anaphylactic
Antigen exposure causes cross-linking of IgE on mast cells or basophils => release of histamine, leukotrienes, PGEs, and tryptase => symptoms
Give clinical examples of type II hypersensitivity
ACID- anaphylactic, cytotoxic (Ab mediated), immune complex, delayed hypersensitivity (T-cell)
Examples of antibody mediated hypersensitivity reaction:
- drug-induced (ex: PCN) autoimmune hemolytic anemia
- autoimmune thyroiditis
- Goodpasture’s syndrome
- ABO incompatibility
Describe the mechanism of type II hypersensitivity reaction
IgM or IgG antibodies produced that attack self- cell surface or tissue antigens
These IgM/G antibodies destroy cells by
- opsonization (coating for phagocytosis)
- complement-mediated lysis
- antibody-dependent cellular toxicity
Describe the mechanism of type III hypersensitivity reaction
‘ACID’: anaphylaxis, cytotoxic (auto-immunity), immune complex, delayed (T-cell)
Exposure to antigen in genetically predisposed individuals cause antigen-antibody complex formation, these immune complexes activate complement and neutrophil invasion => tissue inflammation
Prototypical type III hypersensitivity rxn
Serum sickness- where exposure to certain drugs (most frequently beta-lactam abx) causes symptoms 10-14 days after exposure due to immune complex deposition (causing inflammation and neutrophil invasion) into tissues
=>
rash pruritus arthralgia fever lymphadenopathy malaise hypotension
Most common type of type IV hypersensitivity rxn
Allergic contact dermatitis such as poison ivy (diagnosed by skin patch testing)
Describe the mechanism of type IV hypersensitivity reaction
Antigen (ex: poison ivy) directly activates already sensitized T cells (usually CD4+ cells)
CD4 activation => tissue inflammation 48-96 hrs after exposure
Best diagnostic test for allergic contact dermaitits
Allergen patch test- substance covered by adhesive x48 hrs- then watch for erythema, edema, vesiculation
Which to test for the following deficiencies
(a) Humoral immunity deficiency
(b) NK cell deficiency
(a) Test CD19 for B cell immunity
(b) Test CD16 and CD56 for natural killer cell immunity
19 y/oM w/ asthma- taking ICS BID and albuterol as needed
Persistent wheeze and cough day and night 2x per week
Next step in management?
Is on meds for mild persistent (ICS and SABA PRN) but now meets criteria for moderate persistent (given more than 2 nights a month) =>
Increase to medium dose ICS
Add LABA
Use of methacholine challenge in diagnosing asthma
Methacoline challenge alone is not diagnostic for asthma- negative test rules out asthma (sensitive) but not very specific (positive test can be from other things)
So sensitive but not specific
Numeric datapoint useful in helping when to use systemic corticosteroids in asthma exacerbation
Consider systemic ‘roids when PEF (peak expiratory flow) remains under 80% of personal best after albuterol
Which asthma related med, when used as mono therapy, is associated w/ asthma-related deaths
LABA (salmeterolol, formoterol) mono therapy associated w/ asthma-related death => hence why always used in combo w/ ICS
ex: symbicort = budesonde (ICS) + formoterol (LABA)
Distinguish mild persistent and moderate persistent asthma
Mild persistent: more than 2 days per week but less than 1 time/day or more than 2 nights per month
PEF is still 80 or above
While moderate persistent is daily symptoms or more than one night per week, PEF 60-80%
For asthma treatment
(a) When to add LABA
(b) When to add ICS
Asthma step up treatment
(a) Add LABA when moving from mild persistent (2 days a week, 2 or fewer nights per month) to moderate persistent (every day or more than 2 nights/month)
Define mild intermittent asthma
(a) Tx
Symptoms 2 or fewer days per week, 2 or fewer nights per month
(a) SABA PRN, doesn’t require daily meds
Mechanism of drug
(a) Ipratropium
(b) Formoterol
(c) Salmeterolol
(d) Tiotropium
(a) Anticholinergic
(b) LABA
(c) LABA
(d) LAMA
Name the typical
(a) SABA
(b) LABA
(c) ICS
(d) LAMA
(a) SABA- albuterol, levalbuterol
(b) LABA- formoterol, salmeterolol
(c) ICS- budesonide, fluticasone, mometasone
(d) LAMA- tiotropium
Advair vs. Symbicort
Both ICS/LAMA combos
Adair = fluticasone + salmeterol
Symbicort = budesonide + formoterol
Most effective treatment for allergic rhinitis
(a) Only tx that modifies long-term course of disease
Intranasal corticosteroids
(a) Allergen immunotherapy which dampens the response to allergens
What is hypersensitivity pneumonitis?
(a) Symptoms of acute vs. chronic disease
Hypersensitivity pneumonitis = complex immune reaction to repeated inhalation exposure to a variety of organic dusts
(a) Acute easily confused w/ viral/bacterial PNA as acute onset (6-12 hrs of exposure) of fever, SOB, cough
While chronic- gradual onset of dyspnea, productive cough, fatigue, weight loss
53 y/oM p/w acute cough, SOB, fever a few hours after getting out of his hot tub.
CXR w/ interstitial infiltrates
CT w/ centrilobular nodules and GGOs
(a) Most likely dx
(b) Tx
(a) Acute hypersensitivity pneumonitis to MAC
Immune reaction to inhalation exposure to organic dust
(b) Tx- PO steroids w/ taper
PFTs findings of hypersensitivity pneumonitis
(a) Acute
(b) Chronic
PFTs in HP: DLCO reduced in both acute and chronic
(a) Mainly restrictive
(b) Mixed restrictive and obstructive pattern
Contrast CT chest findings in acute vs. chronic hypersensitivity pneumonitis
Acute- diffuse GGOs c/w pneumonitis
Chronic- patchy GGOs with centrilobular nodules, traction bronchiectasis, honeycombing
Prototypical causes of HP
- Farmer’s lung due to moldy hay
2. Bird/pigeon breeder lung from bird feces
Treatment of HP
HP tx- it’s an immune reaction to inhalation of organic dusts => tx w/ steroids!
PO prednisone 40-80mg daily then taper once see clinical improvement
Poorly controlled asthmatic p/w wheezing, bronchial breath sounds
CXR w/ new infiltrates
Serum IgE 2000
(a) Most likely dx
(b) Tx
(a) ABPA = allergic bronchopulmonary aspergillosis = immunologic reaction to antigens of aspergillus in the bronchial tree
(b) Steroids
4 diagnostic criteria for ABPA
- presence of asthma
- immediate kin tests to aspergillus
- Elevated Serum IgE (over 1,000)
- Elevated aspergillus IgG or IgM
18 y/oM p/w recurrent abdominal pain, episodes self-resolve slowly and are associated w/ b/l arm swelling
(a) Most likely Dx
Think hereditary angioedema- abdominal pain 2/2 gut edema, 2/2 C1-INH (complement 1 inhibitor) deficiency
Hereditary angioedema
(a) Typical presenting features
(b) Diagnostic test
(b) Tx
(a) Recurrent abdominal pain 2/2 gut edema
(b) Serum C1-INH (C1 inhibitor) levels, should be low
(c) Tx by replacing C1-INH typically w/ concentrate or FFP
Distinguish angioedema associated w/ anaphylaxis from hereditary angioedema
(a) Clinical features
(b) Response to tx
Angioedema seen in anaphylaxis
(a) Typical edema in airway, associated w/ urticarial hives.
(b) Responds to epinephrine
Hereditary angioedema
(a) Not always hives, involves more of face (eyes, tongue)
(b) Doesn’t respond to epi, need FFP or C1-INH concentrate
Location of atopic dermatitis vs. psoriasis
Atopic dermatitis on flexor surfaces (popliteal fossa, antecubital fossa)
While psoriasis is typically on extensor surfaces- back of elbow, front of knee
Treatment for eczema
- Skin emollients/lotions- keep it hydrated
- then topical corticosteroids
- can use topical antihistamines for the pruritus
- for severe can use tacrolimus (immunosuppressant)
2 drugs aside from epi to give in anaphylaxis
Anaphylaxis
- epi
- benadryl
- systemic steroids to blunt delayed phase of reaction
Dose of epi used in anaphylaxis vs PEA arrest
Epipen = .3mg (.3ml of 1:1,000)
Epi push in code = 1 mg q3-5 minutes
Differentiate ‘allergic’ reaction to PCN vs. vanc/radiocontrast
Anaphylactic reaction to PCN, bee sting, peanuts = IgE mediated
No use of pre-medication
AnaphylacTOID reaction = clinically indistinguishable, but this is non-IgE mediated
Pretreatment can avoid reaction
Lab test to confirm type I-IV drug hypersensitivities
‘ACID’
Type I = anaphylactic- skin testing, RAST testing, serum tryptase
Type II = cellular (Ab)- direct/indirect Coomb’s test for drug-induced autoimmune hemolytic anemia
Type III = Immune complex- tissue biopsy w/ stains, ESR/CRP, complement levels
Type IV = Delayed hypersensitivity- allergic contact dermatitis- allergen patch test
Explain how rubbing/stroking hyper pigmented skin in pt w/ mastocytosis causes pruritis
Mastocytosis = kit (tyrosine kinase) mutation causing overabundance of mast cells, cutaneous regions w/ too many mast cells that release vasoactive substances with mechanical disruption
So pigmented macular skin rash that urticates (starts itching) when stroked is typical of mastocytosis
IgA deficiency
(a) Screen for what other complications
(b) Tx
(a) Monitor for lymphoproliferative diseases and celiac disease
For unknown reasons ppl w/ IgA deficiency are 10-20 times more likely to develop autoimmune response to gluten
(b) Tx- vaccinations and abx as needed
Differentiate treatment for CVID and IgA deficiency
CVID- tx w/ monthly IVIG
then same as IgA deficiency: vaccines and antibiotics for treatment/ppx as needed
IgA deficiency- vaccines and antibiotics as needed IVIG contraindicated due to risk of anti-IgA IgE antibody
Lab tests to distinguish CVID from IGA deficiency
CVID- low levels of IgG (diagnostic below 500 mg/dl), usually with also low IgA and IgM but doesn’t have to be
IgA deficiency- absent IgA (under 7 mg/dl? w/ normal IgG and IgM
Most common primary immunodeficiency
IgA deficiency: 1 in 500 ppl
Other etiology of hypogammaglobulinemia that must be ruled out before diagnosing CVID
Other causes of protein loss: nephrotic syndrome, protein-losing enteropathy, meds, lymphopenia
Special transfusion needs for its w/ IgA deficiency
Washed blood products- ‘wash’ the product of plasma to get rid of all antibodies
Given risk of anaphylaxis due to exposure to IgA (b/c ppl w/ deficiency presumed to have anti-IgA)
Expect IgA deficiency in pt who gets blood transfusion and develops anaphylaxis within seconds to minutes
Typical clinical presentation of primary immunodeficiency
Recurrent sinopulmonary infections (sinus infection, otitis media, pneumonias), typically presents in 20-30s
