Allergy and Immunology Board Review

Taylor Doherty M.D.

Contributors Drew White, M.D. and Mark Tuker, M.D.

Pearls
• • • • • • • Pregnancy B inhaled steroid: budesonide Asthma with mononeuritis multiplex: CSS ABPA: central bronchiectasis, high IgE Asthma symptoms with insp loop plateau:VCD Nasal polyps + Asthma: Aspirin sensitivity Allergic rhinitis: 1st line=nasal steroid Eczema in adult: biopsy to r/o cutaneous lymphoma

Pearls
• Chronic urticaria: assoc with thyroid abs and IgE receptor antibodies (FcER1) • Hereditary Angioedema: no hives, low C1 esterase inhibitor, low C2/C4, normal C1Q • Aquired Angioedema: above but low C1Q • Anaphylaxis after eating fish: consider scromboid (high histidine fish) vs IgE mediated • Urticarial vasculitis:lesions last >24hr , leave a hyperpigmented spot, and can be painful

Pearls
Insect anaphylaxis: refer for testing and IT Anapylaxis: serum tryptase within hours PCN cephalospoin xreactivity: 2-5% Abacavir hypersensitivity:HLA-B5701 Redman syndrome with Vancomycin-slow infusion rate if not severe • Vaccines with Egg: Influenza (both), yellow fever. MMR negligible • • • • •

Pearls
• Adult onset recurrent/chronic sinusitis, bronchiectasis, giardia, autoimmunity, lymphomas- Common Variable (CVID), check QIGS/specific titers • IgA deficient: can anaphylaxis to IgA containing products • Recurrent/sever Neisserial infections- complement deficiency (check CH50) usually late pathway. • Dysphagia, male, allergic: biopsy for EE • Hypereosinophilia: >1500 AEC, check strongyloides (O+P and ELISA)

Gell and Coombs Classification
• I – IgE on Mast cells – anaphylaxis • II – antigens on cell surface lead to cell destruction (IgG) – PCN binds to RBC, IgG binds to PCN/RBC and RBC destroyed • III – soluble antigen  Ag:Ab aggregates (immune complexes) deposit in tissues (serum sickness) • IV – T cell mediated, delayed hypersensitivity. Direct T cell toxicity (PPD, Poison Ivy)

Two ways to fire a Mast Cell
• Cross link specific IgE on the surface • Directly disrupt the Mast Cell
– Physically (think dermatographism) – Pharmacology (think morphine) – Chemically (RCM?)

Asthma Diagnosis
• FEV1 improvement of 12% and 200mL after betaagonist is evidence for asthma according to ATS • Decreased FEV1/FVC ratio
– 20-39yr 85% – 40-59yr 80% – 60-80yr 70%

• Methacholine challenge –
– + with 20% decrease FEV1 with <8-16mg/mL – True benefit is in negative predictive value

Asthma Statistics
 7% of US population  300 million worldwide  Every day in America 40,000 people miss school or work, 30,000 people have an asthma attack, 5, 000 people visit the emergency room, 1,000 people are admitted to the hospital and 11 people die.
American Academy of Allergy, Asthma, and Immunology –asthma statistics http://www.aaaai.org/media/resources/media_kit/asthma_statistics.st

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Adult asthma phenotypes

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AERD: Aspirin exacerbated respiratory disease
• Asthma (moderate-severe), nasal polyposis, ASA and NSAID (naso-ocular and bronchial) reactions (can be severe and delayed) • Usually adult onset, female>male, many have atopy as well • NSAIDS (Cox-1) and ASA reactions are only a marker of a progressive disease • Refer to allergy

Differential Dx for adult asthma
• • • • • • Vocal cord dysfunction (VCD) COPD (overlap?) Parenchymal lung disease LV failure Panic Attacks Don’t forget that asthma is part of other diseases (CSS and ABPA) • Be aware that asthma variants may have expanded differentials (cough, chest tightness predominant)

Vocal Cord Dysfunction
• Female 2:1 • Athletes • Bronchodilator non responsive • Many (up to 1/3) can have coexist asthma • Difficulty getting breath in

Asthma Pharmacotherapy
 Rescue medicine
 SABA (short acting β agonists)  Anticholinergics

 Controller medicine
     ICS (inhaled corticosteroids) LABA (long acting β agonists) LTRA (leukotriene receptor antagonists) Anti-IgE Others

Risk Factors for Asthma Death
• Previous life-threatening asthma, respiratory arrest • Hospitalization or ED visit for asthma within the last year • Use of 2 or more canisters of rescue inhaler/month • Poor perception of hypoxia or airway obstruction • Psychosocial disturbance

Pregnancy and Asthma
• 1/3 worsen, 1/3 improve, 1/3 no change • Treatment – short answer, better to treat asthma than not to. Inhaled steroids and beta agonists generally felt to be safe.
– Pulmicort is class B, other ICS class C

• Avoid decongestants, epinephrine

Things to consider in the out of control asthmatic
• Vocal cord dysfunction – episodes of dyspnea, inspiratory stridor, dysphonia • GERD • Sinusitis • Churg-Strauss syndrome • ABPA • Compliance/technique

Hypersensitivity Pneumonitis
• • • • • Also known as “extrinsic allergic alveolitis” Acute, subacute, chronic Fevers, chills, malaise, cough CXR/CT scan abnl Chronic  pulmonary fibrosis

Hypersensitivity Pneumonitis (High yield)
• Farmer’s lung – moldy hay – Saccharopolyspora rectivirgula • Pigeon Breeder’s disease – parakeets, parrots, pigeons – avian proteins • Malt workers lung – Moldy barley – aspergillus fumigatus and clavis

Hypersensitivity Pneumonitis
• Hot tub lung – mycobacterium avium complex

• Cigarette smoking DECREASES risk of HP

Occupational Asthma
• Basically, asthma occurring because of exposure at work. • Testing difficult, so sometimes need to do pulmonary evaluation at the workplace. (Start with peak flows at work versus home). • Earlier you diagnose the better, because may lead to permanent asthma even when removed from environment.

Occupational Asthma

Tends to lead to persistent asthma

Eosinophilic pulmonary disease

Defining Characteristics
• Peripheral Blood Eosinophilia with pulmonary abnormalities (peripheral Blood eosinophilia is not uniformly increased in many types of eosinophilic lung disease). • Lung tissue eosinophilia by biopsy • Increased eosinophils in BAL

Differential Dx - ID
• Loffler’s syndrome=transpulmonary passage of larvae – migratory infiltrates • Helminth infections
– Ascaris – Hookworms – Strongyloides

ID-Eosinophilic lung dz
• Coccidiodal infection – up to 25% with eosinophilia • TB, though less likely than cocci • Lung fluke/echinococosis/cysticercosis

Meds/Tox –Eosinophilic lung dz
• Meds – NSAIDS, minocycline, nitrofurantoin, ampicillin • Toxins- Aluminum silicate, Sulfite exposed grape workers, scorpion stings, crack inhalation, dust, smoke, rubber manufactering

Pulm – Eosinophilic lung dz
• AEP – acute eosinophilc pneumonia
– – – – – Less than 3 weeks Hyoxemic respiratory failure BAL eos >25% Evaluate for other causes Responsive to steroids

Pulm –Eosinophilic lung dz
• Chronic Eosinophilic PNA
– Asthma precedes in 50% – Peripheral infiltrates “photo negative” of pulmonary edema – Peripheral eos, high esr, Fe def anemia – Rx: steroids but relapse occur

Rheum – Eosinophilic lung dz
• Churg-Strauss
– – – – – – – Small vessel vasculitis Sinsusitis, asthma, and eosinophilia Transient pulm infiltrates Neuropathies MPO- ab/P-ANCA (only about 50%+) Steroids (cyclophosmamide/azathioprine in severe) ? relationship to LTRA

Heme –Eosinophilic lung dz
• Lymphoma/Leukemias • Hypereosinophilic syndromes
– Lung involved about 50% – Thrombotic events – Steroids/Gleevac/anti-IL-5

Others – pulm eos
• • • • Sarcoid Hypersensitivity pneumonitis Other connective tissue diseases UIP/BOOP

ABPA
• Criteria
– – – – Asthma High total IgE (>1000 ng/mL or 417 kU/L) Positive skin test to A. fumigatus Elevated specific IgE to A. fumigatus

• If CT with central bronchiectasis then ABPA-CB, otherwise ABPA-S (seropositive)

Stages
• • • • • Stage I – acute phase Stage II – remission Stage III – exacerbation Stage IV – steroid dependent Stage V – pulmonary fibrosis

Treatment
• Steroids for acute flares • Follow IgE and CXR • Itraconazole as steroid sparing agent, long term studies not yet in

Mimics of Allergic Rhinitis
• Nasal manifestations of systemic disease:
– Diabetes mellitus – mucor – Wegener’s granulomatosis – Midline granuloma – Relapsing polychondritis – Sarcoidosis – Cystic fibrosis – CSF leak – check beta 2 transferrin (very specific) • Vasomotor rhinitis, rhinitis medicamentosa

Allergic Rhinitis
• Increases chances that truly allergic rhinitis
– Longstanding – Seasonal peaks, triggers (pets, grass…) – Nasal pruritus, sneezing, congestion, post nasal drip, rhinorrhea – Eye features (watering, pruritic, injected) – Family history

Lab Evaluation
• Skin testing with highest sens/spec • RAST test – in vitro test ~85-90% sens
– Good for those on antihistamines – Diffuse dermatitis with no normal skin to test

Allergic Rhinitis
• Nasal steroids – first line • Antihistamines and leukotriene receptor antagonists – second line (about equal efficacy as second line agents)

Immunotherapy
• Indicated for severe symptoms, usually not responding to medical management and avoidance of allergen • Duration of 3-5 years • Therapeutic effect after 3-5 years usually permanent • Approved for allergic rhinitis, asthma, venoms. Less effective for things like AD

Nasal Polyps/Chronic Sinusitis
• Anosmia – big tip off • Causes: idiopathic, immunodeficiency, CF • Can be associated with Aspirin Triad:
– Chronic sinusitis/ nasal polyposis – Asthma – Exacerbation with ASA / NSAID product

Treatment
• • • • • Treat underlying disease if present Systemic, topical steroids Leukotriene antagonists Surgical debulking For ASA triad – ASA desensitization is proven to improve outcomes.

Atopic Dermatitis
• Increased susceptibility to
– Staph aureus, HSV(eczema herpeticum), vaccinia

• Usual affected areas – flexural aspects of extremities, hands • Need to rule out cutaneous T – cell lymphoma in an adult presenting with eczematous dermatitis

Treatment
• • • • • Skin hydration/moisturization Topical corticosteroids Oral antibiotics (Staph) Antihistamines (control itch) Topical calcineurin inhibitors (protopic/ elidel)

Urticaria and Angioedema
• <6 weeks – acute, usually find the cause • >6 weeks – chronic, unusual to find cause • Physical urticarias – cold, heat, cholinergic, delayed pressure, dermatographism, solar

Urticaria – Look for
• Pruritic, erythematous lesions that blanch
– Lesion duration <24 hours – Can be papules or plaques

• May have exacerbation with NSAIDs

Urticaria - Treatment
• Daily non-sedating antihistamine is first line therapy • Second line agents are H2 blockers, leukotriene modifiers (Montelukast) • Some may need oral steroid burst • For chronic urticaria, some require oral steroids or other immunomodulators

Chronic Urticaria
• Not usually allergen driven • 30-40% have autoantibodies to high affinity IgE receptor or to IgE • Thyroid autoimmunity higher than controls

Hiveless Angioedema
• Hereditary or Acquired • More likely to have angioedema precipitated by trauma
– Dental visit, surgery

• Visceral attacks – many undergo appy for acute abdomen, but normal appendix.

Hereditary Angioedema
• Autosomal Dominant • Type 1 – low C1 esterase inhibitor level • Type 2 – low C1 esterase FUNCTION (15%)

Acquired Angioedema
• Associated with lymphoproliferative disorders:
– Low C1q (due to autoactivation and consumption)

• Anti – C1 esterase inhibitor antibodies have been described as well

Test for Hereditary/acquired angioedema
• C4 – low in all, great screening test!! • C1 esterase inhibitor level AND function • C1q (low in acQuired)

Treatment
• Acutely – airway protection
– Steroids/epi/antihistamines – ineffective – FFP may be effective – Various drugs recently or close to FDA approval
• C1 esterase inhibitor concentrate, bradykinin 2 receptor antagonists, plasma kallikrein inhibitors

• Chronic
– C1 inhibitor – Danazol (attenuated androgen) – Aminocaproic acid

Anaphylaxis
• Serious allergic reaction that is rapid in onset and may cause death.
– IgE mediated – Non IgE mediated (“Anaphylactoid”)
• Direct mast cell degranulation
– Radiocontrast – Opiates

• Complement mediated

JACI, March 2005

Biphasic “late” reactions
• Can occur in up to 20% of patients with anaphylaxis and have variable severity (fatalities have occurred) • 1-78 hours after resolution of initial event • Exact mechanism unknown • Associated with delayed or inadequate epinephrine use and no/little corticosteroids.

Anaphylaxis
• Most common causes are peanut/nut ingestion (and other foods), insect stings, drug allergy
– Don’t forget latex, especially in medical spaces

• No obvious trigger- think mastocytosis (check serum baseline tryptase) or idiopathic

Laboratory Evaluations
• Serum tryptase - levels peak 60-90min after onset of anaphylaxis and persist to 6 hours. Ideally to be obtained within 2 hours of onset of symptoms. Can be low in food related anaphylaxis. • Skin testing for medications - other than penicillin, no standardization. Remember metabolism-hapten model. Skin testing/RAST for foods and venoms very useful.

Early Management
• Hypotension - supine, IV (NS) • Respiratory distress - oxygen and albuterol, intubation • EPI, EPI, EPI!!!
– 1:1000 .3-.5cc IM for adults (note this is NOT the 1:10,000 dilution - (1mg/10ml) mistakes have been made) – Can repeat in 5 minutes – If on beta blocker and not responsive to epi, consider glucagon 1mg IM, IV, SC – Can start epi infusion if not responsive to IM epi
• (1:10,000) 1-3 mg over 3 min, then 3-5mg over 3 minutes, then 410ug/min infusion

unless in code

Anaphylaxis Updated Practice Parameter, JACI 200

Epinephrine absorption in adults: Intramuscular versus subcutaneous injection Journal of Allergy and Clinical Immunology November 2001 Volume 108 • p871
to p873 F. Estelle R. Simons, MD, FRCPCa, Xiaochen Gu, PhDb, Keith J. Simons, PhDa,b

Other management
• Antihistamine (supportive)- Cetirizine 10mg po or Diphenhydramine 50mg po, IM, IV • H2 blockers- ranitidine 1mg/kg IV • Corticosteroids (?prevent biphasic)- prednisone po or methylprednisolone IV, 1mg/kg • Follow up allergy clinic if needed (definitely in venom, food, or unknown)

Management
• Observation with monitoring and epi nearby. Length individualized for severity of reaction with consideration of biphasic reactions. • Assess need for epipen - unless obvious etiology such as a specific medication, teach use and prescribe • Patient and family members should be made aware of previous reactions

Venom Allergy
• 40 deaths per year • 15-25% of Americans sensitized at one time in their life • Systemic reactions in 3% of adults • Large local reactions in 10-15%

Venom Allergy
• Apids (honeybee, bumblebees) • Vespids (wasps, yellow jacket, hornets) • Formicids – Fire ants

Possible Reactions
• Large Local – swelling that can extend adjacent to area stung. Lasts 2-7 days. May be dramatic. Should be no concurrent systemic symptoms • Systemic reaction –
– Systemic hives – anaphylaxis

Why Important?
• Venom skin testing only for those who would benefit from immunotherapy • For systemic reactions, immunotherapy decreases re-sting anaphylaxis rate from 60% to ~1%. • Large local reactions basically have the same rate of anaphylaxis as normals

Skin testing
• Only for those with systemic symptoms from sting (including just hives) • If skin test negative, do RAST (about 15% with false negative skin test)

Mastocytosis
• Cutaneous Mastocytosis
– Urticaria pigmentosa – reddish brown or tan macules. Darier’s sign – Indolent, benign course

Systemic Mastocytosis
• Major
– Multifocal dense infiltrates of mast cells in bone marrow or extracutaneous organ

• Minor
– – – – >25% mast cells are spindle-shaped or atypical Presence of c-kit point mutation Mast cells co-express Kit and CD2 Persistent serum tryptase >20ng/mL

• Need one major and one minor, or 3 minor

Mastocytosis
• Skin involvement has good prognosis • Common organs involved
– – – – Bone marrow Liver Spleen Lymphatic system

Hypereosinophilic Syndrome
• Peripheral blood eos count >1500 µL for at least 6 months • Absence of any other known cause of eosinophilia • Presumptive signs/symptoms of organ involvement • 9:1 male:female

Organs involved
• Heart • Skin, Lungs, GI tract, Nervous System • Treatment
– Interferon α – Gleevac (imatinib) - for FIP1L1-PDGFRα gene rearrangement – Steroids

Food Allergy
• Oral Allergy Syndrome
– Pollen cross reactivity – Ragweed – melons, banana – Birch – apple, peach, plum, cherry, almond, potato, carrot – Mugwort – celery

• Oral itching only, no anaphylaxis

Food Allergy
• Peanut, tree nut, fish, shellfish most common • Skin test or RAST test for diagnosis • Treatment – avoidance
– No role for immunotherapy

Drug Allergy
• Beta – lactam
– – – – Cross reactivity to cephalosporins - ~2-5% More common with first generation cephalosporins Carbapenams highly cross reactive with PCNs Monobactams (aztreonam) – not cross reactive with PCNs – Aztreonam and ceftazidime share side chain and may cross react

Vancomycin
• “red man syndrome” – pruritis and erythema of face, neck, upper torso, occasionally with hypotension • Non-immunologic release of histamine • Not IgE mediated • Tx: slow the infusion and pre-treat

Sulfa
• Most common rxn – maculopapular eruption with fever beginning 7-12 days after treatment in HIV. • Fever and urticaria may be present • Anaphylaxis is rare
– IgE mediated reactions to sulfa antibiotic are not cross reactive with non-antibiotic sulfa drugs.

• Can usually still desensitize

Drug desensitization
• Universally successful for IgE mediated reactions • Nearly always successful for non-IgE reactions • Contraindicated in Stevens Johnson Syndrome, TEN, and serum sickness reactions

Local anesthetics
• In general IgE hypersensitivity does not occur. • Reactions are either Toxic or vasovagal

Anticonvulsant Hypersensitivity
• Deficiency of epoxide hydrolase • Fever, maculopapular rash, generalized lymphadenopathy • Resembles serum-sickness reaction • LN bx resembles Hodgkin’s • Phenytoin, carbamazepine, phenobarb

Radiocontrast
• Anaphylactoid
– Non-IgE mediated mast cell histamine degranulation

• No sensitivity to seafood or iodine • Pretreatment with steroid/antihistamine effective • Lower osmolar contrasts have lowered risk

NSAIDs
• • • • Isolated NSAID – can cause anaphylaxis Class effect – worsen pre-existing urticaria Class effect – urticaria/angioedema Class effect – Asthma exacerbation, sinusitis, polyps (triad)

ACEI
• Cough in 1-30% • Resolves with switch to ARB • Angioedema 0.1-0.2% • Does not always resolve with switch to ARB

EM, SJS, TEN
• EM – target lesions, usually caused by HSV, mild self limited. Oral lesions • SJS – diffuse, severe mucocutaneous eruption (<10% of skin detached)
– Usually drug induced – Fever/malaise – 2 mucosal surfaces involved

TEN
• >30% BSA has epidermal detachment • >90% linked to causative drug • Treatment for SJS, TEN – supportive, burn unit. (lots or meds studied, none proven) • Pathophysiology – CD8+ mediated keratinocyte destruction through fas ligand

Drugs and SJS/TEN (usually predates symptoms by 2-3 weeks)
• • • • • • Sulfonamides Carbamazepine Phenytoin Phenobarb Chlormezanone Acetaminophen allopurinol penicillins NSAIDs Quinolones cephalosporins valproic acid

Serum Sickness
• Pruritic (sometimes more burning) hive-like rash. May last longer than hives. • Fever • Rheumatic symptoms (MCP, knee, wrist, ankles) • Some swelling can occur of extremities or around joints • Neutropenia with reactive lymphocytes • +/- thrombocytopenia and eosinophilia • High ESR/CRP

Serum sickness
• Ceclor (kids), penicillins, sulfa • Any animal protein (antisera, monoclonal abs) • Very long list of uncommon drugs that cause serum sickness • Treatment – remove antigen, antihistamines +/- steroids • Avoid culprit in future

Immunodeficiency
• T- cell (cellular) – virus, fungi, protozoa, mycobacteria • Humoral (antibody) – extracellular pyogenic organisms
– Haemophilus – Pneumococcus – Streptococcus

Immunodeficiency
• • • • • • Increased infections Recurrent respiratory infections Multiple systems involved Unusual organisms Malabsorption Big LNs or absent LNs

Common Variable Immunodeficiency
• • • • • Various immune and genetic defects Lymph tissue present or enlarged High incidence of autoimmune disease (22%) Increased risk of adenocarcinoma and lymphomas In addition to encapsulated organisms
– Giardia, yersinia, H. pylori, and H. jejuni are common

IgA deficiency
• Most common of primary immunodeficiency (1:333) • Need IgA <5mg/dL (VERY LOW) • Most patients with IgA def. are NORMAL • Have increased risk of infections, collagen vascular dz, allergic dz, GI dz, and malignancy

IgA deficiency
• Can make anti-IgA antibodies
– Leads to anaphylaxis with IgA containing blood products

Specific Antibody Deficiency
• Normal QIGs, but do not appropriately respond to infection or vaccination with appropriate rise in antibody titer. • To diagnose, check pre-post vaccination titers. • i.e. check strep ab level, vaccinate with pneumovax, recheck ab level in 4-6 weeks. Should increase >4x.

IVIG
• Indicated for CVID and specific antibody deficiency • NOT indicated for IgA deficiency • Best ONE SCREENING TEST FOR HUMORAL IMMUNODEFICIENCY • IgA

IVIG
• Side effects
– – – – Never been transmission of HIV Fever, chills, HA, muscle pain. Aseptic meningitis Renal failure (was due to osmotic load, not as common now), Stroke, MI

Complement Deficiency
• C2 deficiency (most common) – sepsis, pneumonia, meningitis, pyogenic arthritis with Strep pneumo • C2 deficiency – increased risk of rheumatoid arthritis • Terminal Complement Components – Neisseria sp infections
– Think about if recurrent meningitis or if unusual strand

Nutritional Immunodeficiency
• Severe protein calorie malnutrition – profound B and T cell defects • Autosomal recessive inability to absorb zinc – acrodermatitis enteropathica • Eczema around mouth and rectum • Chronic diarrhea, malabsorption • Recurrent sinopulmonary infections

Vaccine
• Live Viral Vaccines –
– – – – – – – – Measles Mumps Oral Polio Rubella Varicella MMR Smallpox (vaccinia) Flumist

Egg allergy and Vaccines
• Influenza and Yellow fever

• A 56 year old man comes to your office for evaluation of scrotal swelling and abdominal cramping of recent onset. He has no other pain or pruritus. Two months ago, he noted swelling of the right hand. The rest of the findings are unremarkable, except for a recent onset of night sweats. • Which of the following laboratory findings is most likely? • A. Low serum levels of C3 and C4 • B. Low serum levels of C1q • C. Elevated serum tryptase level • D. Normal serum levels of C1q and decreased serum levels of C2 and C4.

• A 22 year old woman comes to your office with hives. For the past 4 months, she has had recurrent pruritic lesions that occur on various areas of her body and last for several hours. Extensive review does not indicate any physical or other specific triggers. Review of systems is unremarkable. Examination shows several raised erythematous lesions on the trunk.

Which of the following statements about this patient is true?
• A. She has an autosomal dominant disease • B. The skin lesions are probably associated with exposure to allergens • C. The serum complement level will be low. • D. She may have histamine-releasing autoantibodies that bind the alpha chain of the high affinity IgE antibody receptor on mast cells

• A 32 year old woman who lives in a suburban neighborhood and recently was admitted to the ICU for asthma tells you that her asthma is under control, although you can hear wheezing from across the room. She states that she takes her medications exactly as prescribed, without missing a dose. You notice a pack of cigarettes in her open purse.

Which of the following factors most significantly increases this patient’sto tobacco smoke during childhood risk of asthma death? • A. Exposure
• • • • B. Recent admission to the ICU C. Female gender D. Non-compliance with her medication regimen E. Wheezing that is audible form across the room

B. Recent Admission to ICU
• Recent admission to hospital, ED or particularly to ICU • 2 or more short acting beta agonist canisters/month • Poor perception of asthma symptoms • Psychosocial disturbance

Which of the following is/are NOT part of the innate immune system
• • • • A. B. C. D. C5 Neutrophil IgG Macrophage

Which of the following vaccines would not be advised in pregnancy?
• • • • • A. B. C. D. E. Tetanus Influenza (injection) Varicella Hepatitis B Pneumovax

Varicella
• Live virus which is thus contraindicated in pregnancy due to the increased risk of congenital varicella syndrome

A 35 yo male with a history of mild persistent asthma, presents with the following pruritic rash. The most appropriate next step would be?

• • • • •

A. B. C. D. E.

Topical hydrocortisone 2.5% ointment Oral Antihistamine Topical pimecrolimus cream Skin Biopsy Solumedrol oral taper.

A 19 yo college student survives meningitis which was culture positive for N. meningitidis
• • • • • • Which test is the most appropriate? A. C5 level B. Quantitative immunoglobulins C. IgA level D. CH50 E. N. meningitidis antibody titer

A 28 yo female presents after her 3rd X-ray proven pneumonia. An IgA level was drawn and was 60 mg/dL (80-350)
• What is the next best course of action?

• A. Start IVIG therapy at 0.5 gm/kg q month • B. Place an anergy panel to assess T cell function • C. Get Chest CT to eval for bronchiectasis • D. Check CH50 • E. Check anti-pneumococcal IgG titers, administer pneumovax and recheck in 4 weeks • F. Place on antibiotic prophylaxis

• During a urologic surgical procedure, a 62 year old man has sudden hypotension and cardiac dysrhythmia. The anesthesiologist believes that she saw some raised wheals on the patient’s trunk, but is unsure whether he was having an anaphylactic reaction or an acute cardiac event. Which of the following would be most helpful in identifying intraoperative anaphylaxis?

• A. Measurement of the serum tryptase level within 4 hours of the incident. • B. A 24- hour urine collection to detect leukotriene C4 beginning immediately after the procedure. • C. An in vitro serologic test to detect specific IgE to natural rubber latex. • D. Measurement of plasma levels to detect histamine and its metabolites within 4 hours of the incident.

• A 21 year old woman with persistent asthma and allergic rhinitis is in her 6th week of pregnancy. She is using an albuterol inhaler and budesonide inhaler for her asthma. She uses Claritin-D for her rhinitis. • What do you recommend?

• A. Stop budesonide and use albuterol as needed for wheezing. Switch to pseudophed for nasal symptoms. • B. Continue budesonide and albuterol, use plan pseudophe for nasal symptoms • C. Continue budesonide and albuterol, avoid Claritin-D during the first trimester. • D. Stop all drugs and initiate immunotherapy • E. Stop budesonide and use albuterol and benadryl prn.

Which of the following would be the medicine most likely to be effective in treating allergic rhinitis from dust mites?
• • • • • A. Cetirizine B. Montelukast C. Diphenydramine D. Fluticasone nasal spray E. Ipratroprium 0.06% nasal spray