First Aid for the® Internal Medicine Boards Second Edition ppt

As of August 2006, the ABIM exam is a one-day computer-based test CBT.The exam is divided into four two-hour sections with 60 questions in eachsection, for a total of 240 questions.. Ple

FIRST AID

INTERNAL MEDICINE

BOARDS

Second Edition

TAO LE, MD, MHS

Assistant Clinical Professor of Medicine and Pediatrics

Chief, Section of Allergy and Immunology

University of California at San Francisco

San Francisco, California

THOMAS E BAUDENDISTEL, MD, FACP

Associate Director, Internal Medicine Residency

Department of Medicine

California Pacific Medical Center

San Francisco, California

New York / Chicago / San Francisco / Lisbon / London / Madrid / Mexico City

FOR

McGraw-Hill’s prior consent You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited Your right to use the work may be terminated if you fail to comply with these terms

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DOI: 10.1036/007149913X

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Chapter 1 Allergy and Immunology 1

Chapter 11 Infectious Diseases 421

University of California, San Francisco

SCOTT W BIGGINS, MD, MAS

Assistant Professor, Division of Gastroenterology

Department of Medicine

University of California, San Francisco

THOMAS CHEN, MD, PhD

Staff Physician

Associated Medical Specialists

San Mateo Medical Center

Medical Director, Center for Diabetes Services

Department of Internal Medicine

California Pacific Medical Center

ROBERT L TROWBRIDGE, MD

Assistant Professor University of Vermont College of Medicine Maine Hospitalist Service

Maine Medical Center

SIEGRID S YU, MD

Assistant Professor Department of Dermatology University of California, San Francisco

SENIOR REVIEWERS

䡲 Updated summaries of thousands of board-testable topics

䡲 Hundreds of revised high-yield tables, diagrams, and illustrations

䡲 Key facts in the margins highlighting “must know” information for theboards

䡲 Mnemonics throughout, making learning memorable and fun

We invite you to share your thoughts and ideas to help us improve First Aid for the®Internal Medicine Boards See How to Contribute, p xiii.

San Francisco Peter Chin-Hong

San Francisco Thomas Baudendistel

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Franklin

Thanks to our publisher, McGraw-Hill, for the valuable assistance of theirstaff For enthusiasm, support, and commitment to this challenging project,thanks to our editor, Catherine Johnson For outstanding editorial support, wethank Andrea Fellows A special thanks to Rainbow Graphics, especiallyDavid Hommel and Susan Cooper, for remarkable editorial and productionwork

San Francisco Peter Chin-Hong

San Francisco Thomas Baudendistel

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ABIM—The Basics xvi

In this chapter we talk more about the ABIM and provide you with proven proaches to conquering the exam For a detailed description of the ABIM,

ap-visit www.abim.org or refer to the Certification Examination in Internal

Medi-cine Information Booklet, which can also be found on the ABIM Web site.

A B I M — T H E BA S I C S

How Do I Register to Take the Exam?

You can register for the exam online by going to “On-Line Services” atwww.abim.org The registration fee is currently about $1135 If you miss theapplication deadline, a $400 nonrefundable late fee is tacked on Check theABIM Web site for the latest registration deadlines, fees, and policies

What If I Need to Cancel the Exam or Change Test Centers?

The ABIM currently provides partial refunds if a written cancellation is ceived before certain deadlines You can also change your test center with awritten request for a specific deadline Check the ABIM Web site for the latestinformation on its refund and cancellation policy as well as procedures

re-How Is the ABIM Test Structured?

As of August 2006, the ABIM exam is a one-day computer-based test (CBT).The exam is divided into four two-hour sections with 60 questions in eachsection, for a total of 240 questions Images (blood smears, x-rays, ECGs, pa-tient photos) are embedded in certain questions During the time allotted foreach block, examinees can answer test questions in any order as well as reviewresponses and change answers However, examinees cannot go back andchange answers from previous blocks The CBT format (see Figure 1) allowsyou to make your own notes on each question using a pop-up box, and it alsopermits you to click a box to designate which questions you might wish to re-view before the end of the session (time permitting)

Please check the ABIM Web site to check for Web demos, updates, and tails about the new format, as well as to identify testing centers nearest to you

de-What Types of Questions Are Asked?

All questions are single-best-answer types only You will be presented with a

scenario and a question followed by four to six options Virtually all questions

on the ABIM are vignette based A substantial amount of extraneous

informa-Register early to avoid an

extra $400 late fee.

The majority of your patients

will be aware of your

certification status.

tion may be given, or a clinical scenario may be followed by a question that

could be answered without actually requiring that you read the case Some

questions require interpretation of photomicrographs, radiology studies,

pho-tographs of physical findings, and the like It is your job to determine which

information is superfluous and which is pertinent to the case at hand

Question content is based on a content “blueprint” developed by the ABIM

(see Table 1) This blueprint may change from year to year, so check the

ABIM Web site for the latest About 75% of the primary content focuses on

traditional subspecialties such as cardiology and gastroenterology The

re-maining 25% pertains to certain outpatient or related specialties and

subspe-cialties such as allergy/immunology, dermatology, and psychiatry There are

also cross-content questions that may integrate information from multiple

pri-mary content areas

How Are the Scores Reported?

The passing scores are set before the exam administration, so your passing is

not influenced by the relative performance of others taking the test with you

Scoring and reporting of test results may take up to three months In

addi-tion, your pass/fail status will be available to you on the ABIM Web site

through the “On-Line Services” within a day of the results being mailed to

you Note that you need to register to access this feature

F I G U R E 1 ABIM CBT format.

Virtually all questions are case based.

pri-tween 20 and 40 questions on the exam do not count toward your final score.

Again, these may be “experimental” questions or questions that are later

disqual-ified Historically, between 85% and 90% of first-time examinees pass on the

first attempt (see Table 2) About 90% of examinees who are recertifying pass onthe first attempt, and about 97% are ultimately successful with multiple at-tempts There is no limit on the number of retakes if an examinee fails

T A B L E 1 ABIM Certification Blueprint

T H E R E C E RT I F C AT I O N E X A M

The recertification exam is given twice per year, typically in the spring (April

or May) and in the fall (October) It is a one-day exam that consists of three

modules lasting two hours each Each module has 60 questions, for a total of

180 questions You get two minutes per question The recertification exam is

currently administered as a CBT at a Pearson VUE testing site Performance

on the recertification exam is similar to that of the certification exam;

how-ever, pass rates have been trending downward over the last few years (see

Table 3)

T E ST P R E PA R AT I O N A DV I C E

The good news about the ABIM is that it tends to focus on the diagnosis and

management of diseases and conditions that you have likely seen as a resident

and that you should expect to see as an internal medicine specialist Assuming

that you have performed well as a resident, First Aid and a good source of

practice questions may be all you need However, consider using First Aid as a

guide and using multiple resources, including a standard textbook, journal

re-view articles, MKSAP, or a concise electronic text such as UpToDate, as part

Ideally, you should start your preparation early in your last year of residency,

especially if you are starting a demanding job or fellowship right after dency Cramming in the period between end of residency and the exam is

Other High-Yield Areas

Focus on topic areas that are typically not emphasized during residency ing but are board favorites These include the following:

train-■ Topics in outpatient specialties (e.g., allergy, dermatology, ENT, mology)

ophthal-■ Formulas that are needed for quick recall (e.g., alveolar gas, anion gap,creatinine clearance)

■ Basic biostatistics (e.g., sensitivity, specificity, positive predictive value,negative predictive value)

■ Adverse effects of drugs

T E ST-TA K I N G A DV I C E

By this point in your life, you have probably gained more test-taking expertisethan you care to admit Nevertheless, here are a few tips to keep in mindwhen taking the exam:

■ For long vignette questions, read the question stem and scan the options;

then go back and read the case You may get your answer without having

to read through the whole case

■ There’s no penalty for guessing, so you should never leave a question

blank

■ Good pacing is key You need to leave adequate time to get to all the tions Even though you have two minutes per question on average, youshould aim for a pace of 90 to 100 seconds per question If you don’t knowthe answer within a short period, make an educated guess and move on

ques-■ It’s okay to second guess yourself Research shows that our “second

hunches” tend to be better than our first guesses

■ Don’t panic with “impossible” questions They may be experimental

questions that won’t count Again, take your best guess and move on.

■ Note the age and race of the patient in each clinical scenario When nicity is given, it is often relevant Know these well, especially for morecommon diagnoses

eth-The ABIM tends to focus on

the horses, not the zebras.

Use a combination of First Aid,

textbooks, journal reviews,

and practice questions.

Never, ever leave a question

blank! There’s no penalty for

guessing.

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Diagnostic Testing in Allergy 2

Gell and Coombs Classification of Immunologic Reactions 4

T YPE IV: D ELAYED H YPERSENSITIVITY R EACTIONS (T-C ELL M EDIATED ) 4

Allergy Skin Testing

■ A confirmatory test for the presence of allergen-specific IgE antibody.

■ Prick-puncture skin testing: Adequate for most purposes A drop of

al-lergen extract is placed on the skin surface, and epidermal puncture isperformed with a specialized needle

■ Intradermal skin testing: Used for venom and penicillin testing; 0.02 mL

of allergen is injected intracutaneously using a 26- to 27-gauge needle

■ All skin testing should use (histamine) and (saline) controls

■ Skin-testing wheal-and-flare reactions are measured 15–20 minutes after

placement

Laboratory Allergy Testing

■ Radioallergosorbent (RAST) serologic testing is performed to confirm the presence of allergen-specific IgE antibody.

■ Results are comparable to skin testing for pollen- and food-specific IgE

■ Recommended when the subject has anaphylactic sensitivity to the gen; useful when skin testing is either not available or not possible owing

anti-to skin conditions or interfering medications (e.g., antihistamine use)

■ RAST testing alone is generally not adequate for venom or drug allergy

testing

Delayed-Type Hypersensitivity Skin Testing

■ An effective screening test for functional cell-mediated immunity.

■ Involves intradermal injection of 0.1 mL of purified antigen The

stan-dard panel includes Candida, mumps, tetanus toxoid, and PPD.

■ The injection site is examined for induration 48 hours after injection.

■ Approximately 95% of normal subjects will respond to one of the mentioned antigens

above-■ The absence of a response suggests deficient cell-mediated immunity oranergy

Allergen Patch Testing

■ The appropriate diagnostic test for allergic contact dermatitis.

■ Suspected substances are applied to the skin with adhesive test strips for 48hours

■ The skin site is examined 48 and 72 hours after application for evidence oferythema, edema, and vesiculation (reproduction of contact dermatitis)

D I AG N O ST I C T E ST I N G I N I M M U N O LO G Y

Complement Deficiency Testing

■ The complement pathway consists of the classic, alternative, and nose-binding lectin pathways (see Figure 1.1).

man-■ CH50 is a screening test for the classic complement pathway.

■ All nine elements of C1–C9 are required to produce a normal CH50.

■ A normal CH50 does not exclude the possibility of low C3 or C4

■ Deficiencies that lead to disease include the following:

■ C1, C2, C4: Recurrent sinopulmonary infections (encapsulated

bacte-ria)

■ C3: Pyogenic bacterial infections.

■ C5–C9: Neisserial infections.

Humoral (B-Cell) and Cellular (T-Cell) Deficiency Testing

Testing for B- and T-cell deficiency is as follows:

■ IgG, IgM, IgA, IgD, IgE: For antibody.

■ CD16, CD56: For natural killer cell immunity.

F I G U R E 1 1 The complement reaction sequence.

(Reproduced, with permission, from Brooks GF et al Jawetz, Melnick, & Adelberg’s Medical

Microbiology, 24th ed New York: McGraw-Hill, 2004, Fig 8-9.)

Membrane attack complex C5b–C9

Cell lysis

C5b C6,C7,C8,C9

C5 convertases [C4b2b3b] [C3bBbC3b] Anaphylatoxins

C3b

C3a C3

C5a C5

Think of terminal complement deficiency (C5–C9) in an otherwise healthy patient presenting with recurrent Neisseria meningitis.

reac-Type I: Immediate Reactions (IgE Mediated)

■ Specific antigen exposure causes cross-linking of IgE on mast cell/basophil

surfaces, leading to the release of histamine, leukotrienes, prostaglandins,

and tryptase.

■ Mediator release leads to symptoms of urticaria, rhinitis, wheezing,

diar-rhea, vomiting, hypotension, and anaphylaxis, usually within minutes of

antigen exposure

■ Late-phase type I reactions may cause recurrent symptoms 4–8 hours

af-ter exposure

Type II: Cytotoxic Reactions

■ Mediated by antibodies, primarily IgG and IgM, directed at cell surface

or tissue antigens Antigens may be native, foreign, or haptens (small

for-eign particles attached to larger native molecules)

■ Antibodies destroy cells by opsonization (coating for phagocytosis),

com-plement-mediated lysis, or antibody-dependent cellular cytotoxicity.

■ Clinical examples include penicillin-induced autoimmune hemolytic

anemia and certain forms of autoimmune thyroiditis.

Type III: Immune Complex Reactions

■ Exposure to antigen in genetically predisposed individuals causes

antigen-antibody complex formation.

■ Antigen-antibody complexes activate complement and neutrophil

infil-tration, leading to tissue inflammation that most commonly affects the

skin, kidneys, joints, and lymphoreticular system.

■ Clinically presents with symptoms of “serum sickness” 10–14 days after

exposure; most frequently caused by β-lactam antibiotics or nonhuman

antiserum (antithymocyte globulin, antivenoms)

Type IV: Delayed Hypersensitivity Reactions (T-Cell Mediated)

■ Exposure to antigen causes direct activation of sensitized T cells, usually

CD4+ cells

■ T-cell activation causes tissue inflammation 48–96 hours after exposure.

■ The most common clinical reaction is allergic contact dermatitis such as that resulting from poison ivy.

A ST H M A

A chronic inflammatory disorder of the airway resulting in airway

hyper-responsiveness, airflow limitation, and respiratory symptoms Often begins

in childhood, but may have adult onset Atopy is a strong identifiable risk

■ Severe exacerbations: Pulsus paradoxus, cyanosis, lethargy, use of

acces-sory muscles of respiration, silent chest (absence of wheezing due to lack

of air movement)

wheezing Signs of allergic rhinosinusitis (boggy nasal mucosa, posterior

oropharynx cobblestoning, suborbital edema) are commonly found Exam

may be normal between exacerbations.

D IFFERENTIAL

■ Upper airway obstruction: Foreign body, tracheal compression, tracheal

stenosis, vocal cord dysfunction

■ Other lung disease: Emphysema, chronic bronchitis, CF, allergic

bron-chopulmonary aspergillosis, Churg-Strauss syndrome, chronic eosinophilic

pneumonia, obstructive sleep apnea, restrictive lung disease, pulmonary

embolism

■ Cardiovascular disease: CHF, ischemic heart disease.

■ Respiratory infection: Bacterial or viral pneumonia, bronchiectasis,

si-nusitis

D IAGNOSIS

Diagnosed by the history and objective evidence of obstructive lung disease.

■ PFTs: Show a ↓ FEV1/FVC ratio with reversible obstruction (> 12% ↑ in

FEV1after bronchodilator use) and normal diffusing capacity.

■ Methacholine challenge: Useful if baseline lung function is normal but

clinical symptoms are suggestive of asthma A methacholine challenge

test is not diagnostic of asthma, but a  test indicates that asthma is

un-likely (high sensitivity; lower specificity).

T REATMENT

Acute exacerbations are treated as follows:

■ Initial treatment: Inhaled rapid-acting β2 -agonists (albuterol), one dose

q 20 min × 1 hour; O2to keep saturation > 90%

■ Good response: With a peak expiratory flow (PEF) > 80% of predicted

or personal best after albuterol, continue albuterol q 3–4 h and

insti-tute appropriate chronic therapy (see below)

best, consider systemic corticosteroids; continue inhaled albuterol q 60

min × 1–3 hours if continued improvement is seen

The role of a methacholine

challenge is to exclude the

diagnosis of asthma A

 challenge can be 2° to numerous etiologies and thus may not be definitive.

■ Patients with improved symptoms, a PEF > 70%, and O2saturation> 90%for 60 minutes after the last treatment may be discharged home with ap-propriate outpatient therapy and follow-up Oral corticosteroids are appro-priate in most cases.

■ Patients with incomplete responses after the initial two hours of treatment

(persistent moderate symptoms, PEF < 70%, O2saturation< 90%) should

be admitted for inpatient therapy and monitoring with inhaled albuterol,

O 2 , and systemic corticosteroids.

■ Patients with a poor response to initial therapy (severe symptoms, lethargy,

confusion, PEF < 30%, PO2 < 60, PCO2 > 45) should be admitted to the

ICU for treatment with inhaled albuterol, O 2 , IV corticosteroids, and possible intubation and mechanical ventilation.

Chronic asthma therapy is based on asthma severity as defined by the

Na-tional Asthma Education and Prevention Program (NAEPP) guidelines (see

Table 1.1) The treatment regimen should be reviewed every 1–6 months,

with changes made depending on symptom severity and clinical course

T A B L E 1 1 NAEPP Guidelines for the Treatment of Chronic Asthma

A STHMA

Mild intermittent ≤ 2 days per week, ≤ 2 nights PEF ≥ 80% Bronchodilator 2–4 puffs q 4 h

necessary.

Mild persistent > 2 days per week but < 1 time PEF ≥ 80% Add low-dose inhaled

per day or > 2 nights per month corticosteroids.

Leukotriene modifiers, theophylline, and cromolyn may also be added.

Moderate Daily symptoms or > 1 night per PEF 60–80% ↑ to medium-dose inhaled

long-acting inhaled β 2 -agonist Leukotriene modifiers or theophylline may also be added.

Severe persistent Continuous symptoms PEF < 60% ↑ to high-dose inhaled

corticosteroids.

Daily oral corticosteroids may

be added if necessary (60 mg QD).

a Dyspnea (at rest or with exertion), cough, wheezing, mucus hypersecretion, chest tightness, and nocturnal awakenings with ratory symptoms.

respi-haledβ2-agonists are preferred.

■ Alternative therapy involves inhaled corticosteroids and leukotriene

modifiers or theophylline

■ Severe persistent asthma (continuous symptoms; PEF < 60%):

-agonists.

■ Oral corticosteroids at a dosage of up to 60 mg QD may be necessary.

Additional treatment considerations include the following:

■ Recognize the exacerbating effects of environmental factors such as

aller-gens, air pollution, smoking, and weather (cold and humidity)

■ Use potentially exacerbating medications with caution (aspirin, NSAIDs,

β-blockers)

■ Always consider medication compliance and technique as possible

com-plicating factors in poorly controlled asthma

■ Treatment of coexisting conditions (e.g., rhinitis, sinusitis, GERD) may

improve asthma

C OMPLICATIONS

■ Hypoxemia, respiratory failure, pneumothorax or pneumomediastinum

■ Frequent hospitalization and previous intubation are warning signs of

po-tentially fatal asthma

■ A subset of patients with chronic asthma develop airway remodeling,

lead-ing to accelerated, irreversible loss of lung function

A L L E R G I C R H I N I T I S

The most common cause of chronic rhinitis Allergic factors are present in

75% of rhinitis cases May be seasonal or perennial; incidence is greatest in

adolescence and ↓ with advancing age Usually persistent, with occasional

spontaneous remission

S YMPTOMS

■ Sneezing, nasal itching, rhinorrhea, nasal congestion, sore throat, throat

clearing, itching of the throat and palate

■ Sleep disturbance; association with obstructive sleep apnea

■ Concomitant conjunctivitis with ocular itching, lacrimation, and

puffi-ness

D IFFERENTIAL

■ Nonallergic rhinitis: Vasomotor or gustatory rhinitis.

■ Rhinitis medicamentosa: Overuse of vasoconstricting nasal sprays, leading

to rebound nasal congestion and associated symptoms

■ Hormonal rhinitis: Associated with pregnancy, use of OCPs, and

■ Nasal obstruction due to a structural abnormality: Septal deviation,

nasal polyposis, nasal tumor, foreign body

D IAGNOSIS

Based on the history and  skin testing to common aeroallergens (e.g.,

grass/tree/weed pollen, house dust mites, cockroaches, dog and cat dander,mold)

T REATMENT

■ Allergen avoidance measures: Most effective for house dust mites

(in-volves the use of allergen-impermeable bed and pillow casings and ing of bedding in hot water) Indoor pollen exposure can be reduced bykeeping windows closed and using air conditioners

wash-■ Antihistamines: Reduce sneezing, rhinorrhea, and pruritus Less effective

for nasal congestion; most effective if used regularly Not effective for allergic rhinitis Nonsedating antihistamines are preferable

non-■ Oral decongestants: Effectively reduce nasal congestion in allergic and

nonallergic rhinitis May cause insomnia and exacerbate hypertension orarrhythmia

■ Intranasal steroids: The most effective medication for allergic and

nonal-lergic rhinitis Have no significant systemic side effects; most beneficialwhen used regularly

■ Allergen immunotherapy: Indicated as an alternative or adjunct to

med-ications The only effective therapy that has been demonstrated to modifythe long-term course of the disease

C OMPLICATIONS

Chronic sinusitis and otitis; exacerbation of asthma

H Y P E R S E N S I T I V I T Y P N E U M O N I T I S

A complex immune-mediated lung disease resulting from repeated

inhala-tional exposure to a wide variety of organic dusts (see Table 1.2) Presents in

acute, subacute, and chronic forms

Intranasal steroids are the

most effective treatment for

allergic rhinitis.

S YMPTOMS

■ Acute: Nonproductive cough, shortness of breath, fever, diaphoresis,

myal-gias occurring 6–12 hours after intense antigen exposure

■ Chronic: Insidious onset of dyspnea, productive cough, fatigue, anorexia,

weight loss

E XAM

■ Acute: Patients are ill-appearing with fever, respiratory distress, and dry

rales (wheezing is not a prominent symptom) Exam may be normal in

asymptomatic patients between episodes of acute hypersensitivity

pneu-monitis

■ Chronic: Dry rales, ↓ breath sounds, digital clubbing

D IFFERENTIAL

■ Pneumonia: Bacterial, viral, or atypical.

■ Toxic fume bronchiolitis: Sulfur dioxide, ammonia, chlorine.

■ Organic dust toxic syndrome: Inhalation of dusts contaminated with

bacteria and fungi

■ Subacute or chronic: Chronic bronchitis, idiopathic pulmonary fibrosis,

chronic eosinophilic pneumonia, collagen vascular disease, sarcoidosis, 1°

pulmonary histiocytosis, alveolar proteinosis

Bagassosis Thermoactinomyces sacchari Moldy sugar-cane fiber (bagasse).

Mushroom picker’s disease Same as farmer’s lung Moldy compost.

Detergent worker’s lung Bacillus subtilisenzyme Enzyme additives.

Reproduced, with permission, from Tierney LM et al Current Medical Diagnosis & Treatment, 44th ed New York: McGraw-Hill,

2005: 293.

■ Acute: CXR shows transient patchy, peripheral, bilateral interstitial

in-filtrates CT typically shows ground-glass opacifications and diffuseconsolidation

shows centrilobular nodules with areas of ground-glass opacity

■ Chronic: CXR shows fibrotic changes with honeycombing and areas of

emphysema; CT shows honeycombing, fibrosis, traction sis, ground-glass opacities, and small nodules

■ Acute or chronic: High titers of precipitating IgG against the

offend-ing antigen (indicates exposure, not necessarily disease) Double-gelimmunodiffusion is preferred, as ELISA may be too sensitive

■ Bronchoalveolar lavage: Lymphocytosis with a predominance of CD8+ Tcells

■ Lung biopsy: Interstitial and alveolar noncaseating granulomas; “foamy”

macrophages; predominance of lymphocytes

helpful when data are lacking or diagnosis is unclear Performed only withcareful medical monitoring

T REATMENT

■ Avoidance of the offending antigen

■ Oral corticosteroids at a dosage of 40–80 mg QD with tapering after cal improvement has been achieved

clini-C OMPLICATIONS

■ Irreversible loss of lung function

■ Death is uncommon but has been reported

A L L E R G I C B R O N C H O P U L M O N A RY A S P E R G I L LO S I S ( A B PA )

An immunologic reaction to antigens of Aspergillus present in the bronchial tree.

S YMPTOMS

Asthma (may be cough variant or exercise induced); expectoration of golden

brown mucous plugs; fever with acute flare

T REATMENT

■ Prednisone; itraconazole may be used as an adjunctive medication.

■ Chronic inhaled corticosteroids to control asthma

C OMPLICATIONS

Corticosteroid-dependent asthma, irreversible loss of pulmonary function,

chronic bronchitis, pulmonary fibrosis, death due to respiratory failure or cor

pulmonale

A L L E R G I C F U N G A L S I N U S I T I S

An immunologic reaction to fungal aeroallergens (Aspergillus, Bipolaris,

Curvularia, Alternaria, Fusarium) that causes chronic, refractory sinus disease.

S YMPTOMS

Sinus congestion and obstruction that are refractory to antibiotics; thick

mu-coid secretions (“peanut butter” appearance); nasal polyposis; proptosis;

asthma

E XAM

Presents with thickening of the sinus mucosa, allergic mucin on rhinoscopy,

and nasal polyps

D IFFERENTIAL

■ Chronic rhinosinusitis: Bacterial, allergic (nonfungal).

■ Nasal polyposis without allergic fungal sinusitis

■ Invasive fungal disease: Seen in immunocompromised patients (HIV,

dia-betes)

■ Mycetoma (fungus ball)

D IAGNOSIS

■ Diagnostic criteria include the following:

■ Chronic sinusitis for > 6 months

■ Allergic mucin containing many eosinophils and fungal hyphae.

hy-■ Absence of invasive fungal disease.

■ Other supportive findings include peripheral blood eosinophilia and

im-mediate skin tests to fungus

T REATMENT

■ Surgical removal of allergic mucin.

■ Prednisone 0.5–1.0 mg/kg for weeks with slow tapering.

■ Intranasal corticosteroids; nasal irrigation

S YMPTOMS

Presents with pruritic hives and painful soft tissue swelling on the lips, oral

mucosa, periorbital area, hands, and feet Individual skin lesions resolve in

< 24 hours without residual scarring Angioedema may take longer to fully solve

re-E XAM

Erythematous, blanching skin wheals; soft tissue swelling as described above

No scarring or pigmentary changes can be seen at previously affected sites.Exam may be normal between symptomatic flares

D IFFERENTIAL

■ IgE-mediated allergic reaction: Food, medication, insect stings.

■ Non-IgE reactions: Aspirin, narcotics, radiocontrast media.

■ Physical urticaria: Pressure, vibratory, solar, cholinergic, local heat and

cold

■ Autoimmunity: Vasculitis, associated thyroiditis.

■ Infections: Mononucleosis, viral hepatitis, fungal and parasitic disease.

■ Idiopathic: Accounts for the majority of chronic urticaria cases.

an-gioedema (associated with vasculitis and neoplasms)

■ Other: Dermatographism; cutaneous mastocytosis.

D IAGNOSIS

■ The clinical history suggests diagnostic testing

■ Provocative testing for physical urticarias

■ Labs include ESR, ANA, skin biopsy (if necessary to exclude vasculitis),and antithyroid antibodies if autoimmunity is suspected

■ Order a CBC, viral hepatitis panel, and stool O&P if the history is tive of infection

sugges-■ In the setting of angioedema alone, obtain a C1 inhibitor assay to exclude

In contrast to angioedema

associated with anaphylaxis,

hereditary angioedema does

not respond to epinephrine.

Treat with fresh frozen

plasma.

Think of hereditary angioedema in a patient

presenting with recurrent

episodes of angioedema

without pruritus or urticaria.

Check a C1 inhibitor (C1-INH)

assay, which will be low.

When used regularly at

adequate doses, antihistamines successfully

treat most cases of urticaria.

■ Danazol or stanozolol for chronic treatment of hereditary

angio-edema

C OMPLICATIONS

Laryngeal edema

ATO P I C D E R M AT I T I S

A chronic inflammatory skin disease that is often associated with a personal or

family history of atopy Usually begins in childhood.

S YMPTOMS

Characterized by intense pruritus and an erythematous papular rash typically

occurring in the flexural areas of the elbows, knees, ankles, and neck Pruritus

precedes the rash (“an itch that rashes”) Chronic atopic dermatitis manifests

as thickened nonerythematous plaques of skin (lichenification)

E XAM

Presents with an erythematous papular rash in flexural areas as well as with

excoriations, serous exudate, lichenification (if chronic), and other findings of

atopic disease (boggy nasal mucosa, conjunctival erythema, expiratory

wheez-ing)

D IFFERENTIAL

■ Other dermatitis: Seborrheic, irritant, contact, psoriasis.

■ Infectious: Scabies, candidiasis, tinea versicolor.

■ Hyper-IgE syndrome: Usually diagnosed in childhood.

D IAGNOSIS

Diagnosis is readily made through the history and physical Consider skin

biopsy to rule out cutaneous T-cell lymphoma in new-onset eczema in an

adult

T REATMENT

■ Skin hydration: Lotions, emollients.

■ Topical corticosteroids.

■ Antihistamines to reduce pruritus.

A patient with angioedema and well-controlled hypertension? Think ACEIs.

■ Treat bacterial, fungal, and viral superinfection as necessary.

■ Topical tacrolimus/pimecrolimus and oral corticosteroids for severe

dis-ease

C OMPLICATIONS

■ Chronic skin changes: Scarring, hyperpigmentation.

■ Cutaneous infection: Bacterial (primarily S aureus), viral (primarily

HSV); risk of eczema vaccinatum with smallpox vaccine

A L L E R G I C C O N TAC T D E R M AT I T I S

A lymphocyte-mediated delayed hypersensitivity reaction causing a skin rash

on an antigen-exposed area

S YMPTOMS

Characterized by a pruritic rash that typically appears 5–21 days after the initial

exposure or 12–96 hours after reexposure in sensitized individuals The typical

pattern is erythema leading to papules and then vesicles The rash precedes

pruritus and appears in the distribution of antigen exposure (see Figure 1.2)

E XAM

■ Acute stage: Skin erythema, papules, vesicles.

■ Subacute or chronic stage: Crusting, scaling, lichenification, and

thick-ening of the skin

F I G U R E 1 2 Contact dermatitis.

Erythematous papules, vesicles, and serous weeping localized to areas of contact with the

of-fending agent are characteristic (Reproduced, with permission, from Hurwitz RM Pathology

of the Skin: Atlas of Clinical-Pathological Correlation Stamford, CT: Appleton & Lange,

1991: 3.)

C OMPLICATIONS

2° infection from scratching affected skin

A N A P H Y L A X I S

A systemic type I (IgE-mediated) hypersensitivity reaction that is often

life-threatening Requires previous exposure (known or unknown) for

sensitiza-tion Risk factors include parenteral antigen exposure and repeated

inter-rupted antigen exposure Common causes are foods (especially peanuts and

shellfish), drugs (especially penicillin), latex, stinging insects, and blood

products.

S YMPTOMS

■ Symptoms include skin erythema, pruritus, urticaria, angioedema,

laryn-geal edema, wheezing, chest tightness, cramping abdominal pain, nausea,

vomiting, diarrhea, diaphoresis, dizziness, a sense of “impending doom,”

hypotension, syncope, and shock

■ Symptoms most frequently appear seconds to minutes after exposure but

may be delayed several hours for ingested agents

E XAM

Urticaria, angioedema, flushing, wheezing, stridor, diaphoresis, hypotension,

tachycardia

D IFFERENTIAL

■ Other types of shock: Cardiogenic, endotoxic, hemorrhagic.

■ Cardiovascular disease: Arrhythmia, MI.

■ Scombroid: Histamine poisoning from spoiled fish.

■ Anaphylactoid reaction: Nonspecific mast cell activation (not IgE).

vasovagal reaction, systemic mastocytosis, panic attack

D IAGNOSIS

■ Elevated serum tryptase drawn 30 minutes to three hours after onset can

help confirm the diagnosis

■ Presence of allergen-specific IgE antibody by skin or RAST testing (best

performed one month after event)

■ Epinephrine 1:1000 0.3 mL IM: Repeat every 15 minutes as needed.

■ Maintain airway: O2; inhaled bronchodilators; intubation if necessary

■ Rapid IV fluids if the patient is hypotensive

■ Corticosteroids (prednisone 60 mg or equivalent) IV/IM/PO: Reduce

late-phase recurrence of symptoms 4–8 hours later

■ Vasopressor medications in the presence of persistent hypotension

■ IV epinephrine 1:10,000 0.3 mL should be given only in terminal tients

pa-■ Consider glucagon and/or atropine for patients on β-blockers whose

symptoms are refractory to therapy

■ Monitor patients for 8–12 hours after reaction

■ Ensure that patients have access to injectable epinephrine and mines on discharge

antihista-C OMPLICATIONS

Respiratory obstruction, cardiovascular collapse, death

A N A P H Y L AC TO I D R E AC T I O N S

Clinically indistinguishable from anaphylactic reactions, but caused by

non-specific mast cell activation (not IgE mediated) May occur with initial

expo-sure to medication Common causes include radiocontrast media, comycin, amphotericin, opiates, and general anesthetics (induction agentsand muscle relaxants)

van-D IAGNOSIS

■ Elevated serum tryptase drawn 30 minutes to three hours after onset helps

confirm mast cell release

■ Absence of allergen-specific IgE antibody to suspected antigens by skin or

RAST testing (best performed one month after event)

T REATMENT

■ The same as that for anaphylaxis

■ Vancomycin: Slow infusion rate.

■ Radiocontrast media: Use low-osmolality forms.

■ Anaphylactoid reactions are generally preventable with pretreatment

through use of corticosteroids and antihistamines Pretreatment is mended for patients with a history of reactions to radiocontrast media

recom-F O O D A L L E R G Y

True (IgE-mediated) food allergy in adults is most commonly caused by

peanuts, crustaceans, tree nuts, and fish Sensitivities to these foods tend to

be lifelong Multiple food allergies are rare in adults Anaphylactic signs and

symptoms occur minutes to two hours after ingestion.

D IFFERENTIAL

■ Nonallergic food intolerance (lactase deficiency, celiac disease, symptomsdue to vasoactive amines)

The treatment of anaphylaxis

consists of the prompt