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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 beta-
agonist 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 unless in code (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 4-
10ug/min infusion

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 allopurinol
• Carbamazepine penicillins
• Phenytoin NSAIDs
• Phenobarb Quinolones
• Chlormezanone cephalosporins
• Acetaminophen 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’s risk of asthma death?
• A. Exposure to tobacco smoke during childhood
• 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. C5
• B. Neutrophil
• C. IgG
• D. Macrophage
Which of the following vaccines
would not be advised in
pregnancy?
• A. Tetanus
• B. Influenza (injection)
• C. Varicella
• D. Hepatitis B
• E. 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. Topical hydrocortisone 2.5% ointment
• B. Oral Antihistamine
• C. Topical pimecrolimus cream
• D. Skin Biopsy
• E. 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

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