American Board of Internal Medicine Certification (ABIM Board Certification) Infectious Disease, Rheumatology & Immunology Flashcards

24 sample cards from the Infectious Disease, Rheumatology & Immunology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. What is the treatment of choice for early localized Lyme disease (erythema migrans), and the alternative in children/pregnancy?

   Doxycycline (preferred, also treats co-infecting Anaplasma); amoxicillin or cefuroxime are alternatives (e.g., in pregnancy). For Lyme carditis/neuroborreliosis, use IV ceftriaxone.

2. Which tick-borne illness causes fever with a centripetal petechial rash (wrists/ankles spreading inward) and is treated with doxycycline even in children?

   Rocky Mountain spotted fever (Rickettsia rickettsii). Treat empirically with doxycycline; delay increases mortality. Doxycycline is first-line regardless of age.

3. What zoonotic infection is acquired from cat scratches/bites, causes regional lymphadenopathy, and is caused by which organism?

   Cat-scratch disease, caused by Bartonella henselae; usually self-limited, treat with azithromycin if needed.

4. What are the core goals of antimicrobial stewardship, and name two common interventions?

   Goals: optimize clinical outcomes while minimizing resistance, toxicity, C. difficile, and cost. Interventions: prospective audit-and-feedback, formulary restriction/preauthorization, de-escalation/IV-to-PO switch, and dose optimization.

5. What is the difference between ESBL- and carbapenemase (CRE)-producing Enterobacterales, and how does treatment differ?

   ESBL producers hydrolyze penicillins/cephalosporins -> treated with carbapenems. CRE additionally hydrolyze carbapenems -> require agents like ceftazidime-avibactam, meropenem-vaborbactam, or other novel beta-lactam/beta-lactamase inhibitors.

6. What is the recommended chemoprophylaxis and key prevention measures for a traveler to a chloroquine-resistant Plasmodium falciparum malaria region?

   Options: atovaquone-proguanil, doxycycline, or mefloquine, plus mosquito bite avoidance (DEET, permethrin-treated clothing, bed nets).

7. In a returning traveler with fever, what is the most important diagnosis to exclude urgently, and how?

   Malaria (especially P. falciparum). Obtain thick and thin blood smears (or rapid antigen test); repeat smears if initially negative. Falciparum malaria can be rapidly fatal.

8. What classification criteria features and key serologies support a diagnosis of rheumatoid arthritis?

   Symmetric polyarthritis of small joints, morning stiffness >1 hour, RF and anti-CCP (anti-citrullinated peptide) antibodies, elevated ESR/CRP; anti-CCP is more specific. Erosions on imaging support the diagnosis.

9. What is the first-line DMARD for rheumatoid arthritis, and what baseline/monitoring testing is required?

   Methotrexate. Monitor CBC, LFTs, and renal function; supplement folic acid; screen for hepatitis B/C and TB before biologics. Avoid in pregnancy (teratogenic).

10. Which autoantibodies are most specific for systemic lupus erythematosus, and which correlates with disease activity/nephritis?

    Anti-dsDNA and anti-Smith are most specific. Anti-dsDNA titers (and low complement C3/C4) correlate with disease activity, especially lupus nephritis.

11. What are the diagnostic criteria for antiphospholipid syndrome (APS)?

    Clinical: vascular thrombosis or pregnancy morbidity, PLUS persistent (>=12 weeks apart) antiphospholipid antibodies: lupus anticoagulant, anticardiolipin, or anti-beta2-glycoprotein I.

12. How do limited and diffuse cutaneous systemic sclerosis differ, including antibody associations and major organ risks?

    Limited (CREST): anti-centromere antibody, skin distal to elbows/knees, risk of pulmonary arterial hypertension. Diffuse: anti-Scl-70 (topoisomerase I), proximal skin involvement, risk of scleroderma renal crisis and interstitial lung disease.

13. What is the treatment for scleroderma renal crisis, and which class must be avoided?

    ACE inhibitors (e.g., captopril) are the treatment of choice. Avoid corticosteroids (especially high-dose), which can precipitate renal crisis.

14. What distinguishes polymyositis from dermatomyositis, and which antibody/cancer association is important for dermatomyositis?

    Both cause proximal muscle weakness with elevated CK. Dermatomyositis adds skin findings (Gottron papules, heliotrope rash) and carries an increased malignancy risk; anti-Mi-2 and anti-TIF1-gamma (malignancy) antibodies are associated.

15. How are the major vasculitides classified by predominant vessel size, with one example each?

    Large vessel: giant cell arteritis, Takayasu. Medium vessel: polyarteritis nodosa, Kawasaki. Small vessel: ANCA-associated (GPA, MPA, EGPA) and immune complex (IgA vasculitis, cryoglobulinemic).

16. What is the management of suspected giant cell arteritis, and why is prompt treatment critical?

    Start high-dose corticosteroids immediately (do not wait for biopsy) to prevent irreversible vision loss; confirm with temporal artery biopsy. Associated with polymyalgia rheumatica; ESR/CRP usually elevated.

17. Which ANCA pattern/antigen is associated with granulomatosis with polyangiitis (GPA) versus microscopic polyangiitis (MPA)?

    GPA: c-ANCA / anti-PR3. MPA: p-ANCA / anti-MPO. EGPA is usually p-ANCA/anti-MPO with asthma and eosinophilia.

18. What are the classic clinical and HLA associations of ankylosing spondylitis (axial spondyloarthritis)?

    Inflammatory back pain improving with exercise, sacroiliitis, reduced spine mobility; strong HLA-B27 association. Treat with NSAIDs first-line, then TNF or IL-17 inhibitors.

19. What are the hallmark features and autoantibodies of Sjogren syndrome?

    Keratoconjunctivitis sicca (dry eyes) and xerostomia (dry mouth) from lymphocytic infiltration of exocrine glands; anti-Ro/SSA and anti-La/SSB antibodies; increased risk of B-cell (MALT) lymphoma.

20. How do the synovial fluid findings of gout and CPPD (pseudogout) crystals differ under polarized microscopy?

    Gout: monosodium urate, needle-shaped, strongly negatively birefringent (yellow when parallel to axis). CPPD: calcium pyrophosphate, rhomboid-shaped, weakly positively birefringent (blue when parallel).

21. What are first-line treatments for an acute gout flare, and what are urate-lowering therapy options for chronic management?

    Acute: NSAIDs, colchicine, or corticosteroids (oral, intra-articular, or systemic). Chronic urate-lowering: allopurinol (first-line xanthine oxidase inhibitor), febuxostat, or uricosurics; target serum urate <6 mg/dL.

22. What synovial fluid WBC count and other findings suggest septic arthritis, and what is the diagnostic gold standard?

    Synovial WBC typically >50,000/microL (often >100,000) with neutrophil predominance, low glucose. Gold standard is arthrocentesis with Gram stain and culture; S. aureus is the most common pathogen. Urgent drainage plus antibiotics required.

23. What clinical criteria distinguish osteoarthritis from inflammatory arthritis, and what radiographic features are characteristic of OA?

    OA: pain worse with use, brief (<30 min) morning stiffness, bony enlargement (Heberden/Bouchard nodes), no systemic inflammation. X-ray: asymmetric joint-space narrowing, osteophytes, subchondral sclerosis and cysts.

24. What are the diagnostic features and first-line management of fibromyalgia?

    Chronic widespread pain, fatigue, sleep disturbance, and cognitive symptoms without inflammatory markers or joint damage. First-line: patient education, aerobic exercise, and CBT; medications include duloxetine, milnacipran, or pregabalin. ESR/CRP are normal.

What this deck covers

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