Skin & Subcutaneous Tissue
Psoriatic arthritis: recognition and screening
— Adult with known psoriasis reporting new joint pain, morning stiffness >30 minutes, or heel pain
— Asymmetric oligoarthritis (≤4 joints), particularly involving DIP joints
— Dactylitis ("sausage digit") of a finger or toe
— Enthesitis at Achilles or plantar fascia insertion
— Inflammatory low back pain (improves with activity, worsens with rest) in a young/middle-aged adult
— New nail pitting, onycholysis, or oil-drop discoloration with joint symptoms
— Unexplained uveitis or IBD in a patient with skin plaques
Board pearl: Any patient with psoriasis plus inflammatory musculoskeletal symptoms (stiffness >30 min, improves with activity, swelling, nail changes, or enthesitis) should be screened with a tool like PEST and referred to rheumatology — do not wait for radiographic erosions to act.

— Asymmetric oligoarthritis (~30–50%): few large/small joints, often lower extremity
— Symmetric polyarthritis (~30–40%): mimics RA but typically RF/CCP negative and includes DIPs
— Distal interphalangeal (DIP)–predominant (~5–10%): strongly linked to nail disease
— Axial/spondylitic (~5–20%): inflammatory back pain, sacroiliitis, often asymmetric
— Arthritis mutilans (<5%): destructive "pencil-in-cup," telescoping digits
— Inflammatory rhythm: morning stiffness >30 min, improves with movement, nocturnal awakening (especially second half of night for axial disease)
— Dactylitis history: "whole finger or toe swelled up like a sausage for weeks"
— Enthesitis: heel pain on first steps in the morning, lateral epicondyle, iliac crest pain
— Skin/nail review: scalp itch, gluteal cleft rash, umbilical plaques, nail changes (pitting, onycholysis, ridging)
— Family history: psoriasis, PsA, IBD, uveitis, AS in first-degree relatives (strong genetic component, HLA-B27, HLA-Cw6)
— Extra-articular ROS: anterior uveitis (red painful eye, photophobia), IBD symptoms, fatigue
— Triggers/risks: obesity, smoking, trauma (Koebner-like joint phenomenon), recent strep, HIV (severe PsA flare)
— PEST (Psoriasis Epidemiology Screening Tool): 5 items, score ≥3 → refer
— PsA Screen, ToPAS, EARP: alternatives
Step 3 management: In a psoriasis follow-up visit, administer PEST annually; a score ≥3 plus any swollen joint or dactylitis warrants rheumatology referral within 4–6 weeks, not a "watch and wait" approach.

— Uniform swelling of an entire digit ("sausage digit"), often with violaceous hue
— Palpate flexor tendon sheath — tenderness reflects tenosynovitis
— Leeds Dactylitis Index can quantify
— Achilles tendon insertion and plantar fascia at calcaneus
— Lateral epicondyle, medial femoral condyle, tibial tuberosity
— Iliac crest, greater trochanter
— FABER (Patrick) test, Gaenslen, direct SI palpation
— Schober test: <5 cm lumbar excursion suggests reduced spinal mobility
— Chest expansion <2.5 cm suggests costovertebral involvement
— Inspect scalp, retroauricular area, umbilicus, gluteal cleft, palms/soles, intergluteal area — common hidden sites
— Nail signs: pitting (>20 pits highly specific), onycholysis, oil-drop sign, subungual hyperkeratosis, splinter hemorrhages
Key distinction: RA produces symmetric MCP/PIP synovitis sparing DIPs, no dactylitis, no enthesitis, and no nail disease; PsA frequently involves DIPs with adjacent nail dystrophy, dactylitis, and enthesitis — a focused exam separates them before any lab returns.

— CBC, CMP (baseline before DMARDs/biologics; assess renal/hepatic function)
— ESR and CRP — elevated in ~40–60% of active PsA; normal values do not exclude diagnosis (a common pitfall)
— Rheumatoid factor (RF) and anti-CCP — typically negative; positivity does not exclude PsA but lowers CASPAR points
— HLA-B27 — supports axial PsA; not diagnostic
— Uric acid — to evaluate gout in podagra-like presentations
— Hepatitis B, hepatitis C, HIV, TB (IGRA or PPD) — required before initiating biologics or methotrexate
— Lipid panel, HbA1c — cardiometabolic screening (PsA confers elevated CV risk)
— Plain radiographs of symptomatic joints, hands, feet, pelvis (SI joints), and lumbar spine
— Early disease: often normal or soft tissue swelling
— Established: erosions with adjacent new bone formation, "fluffy" periostitis, pencil-in-cup deformity, ankylosis, asymmetric sacroiliitis, syndesmophytes that are chunky and asymmetric (vs. thin marginal in AS)
Board pearl: A normal CRP/ESR does not rule out PsA — up to half of patients have normal acute-phase reactants despite active synovitis. Diagnose using clinical features + imaging, not labs alone.

— Current psoriasis (2 points), personal/family history of psoriasis (1)
— Typical psoriatic nail dystrophy (1)
— Negative RF (1)
— Current or history of dactylitis (1)
— Radiographic juxta-articular new bone formation on hand/foot films (1)
— Sensitivity ~91%, specificity ~99%
— Hand/foot MRI: bone marrow edema, synovitis, tenosynovitis, erosions before plain film changes
— Sacroiliac joint MRI (STIR/T2 fat-suppressed): bone marrow edema → diagnoses early axial PsA when radiographs are normal
— Particularly useful in young patients with inflammatory back pain and negative X-rays
— Quantifies synovitis, identifies subclinical enthesitis
— Distinguishes dactylitis (flexor tenosynovitis + soft tissue edema) from cellulitis
Step 3 management: A 35-year-old with psoriasis, 4 months of inflammatory low back pain, normal lumbar X-ray, and HLA-B27 positive → order MRI of SI joints with STIR sequences to detect active sacroiliitis; do not stop the workup at a normal radiograph.

— TJC ≤1, SJC ≤1, PASI ≤1 or BSA ≤3%, patient pain VAS ≤15, patient global VAS ≤20, HAQ ≤0.5, tender entheseal points ≤1
— Peripheral arthritis
— Axial disease
— Enthesitis
— Dactylitis
— Skin and nail psoriasis
— Associated conditions (uveitis, IBD)
— Poor prognostic features: ≥5 active joints, elevated CRP, radiographic damage at baseline, dactylitis, nail involvement, prior glucocorticoid need, functional limitation
— Comorbidities that alter drug choice: latent TB, hepatitis B/C, HF, demyelinating disease, recurrent infections, malignancy history
— Mild/oligoarticular without poor prognostic markers: NSAIDs + intra-articular steroid injections for monoarthritis; reassess in 4–6 weeks
— Persistent or polyarticular: start csDMARD (methotrexate preferred)
— Inadequate response or poor prognostic features: advance to biologic DMARD (TNFi first-line) or targeted synthetic DMARD
Board pearl: Methotrexate does NOT treat axial PsA or enthesitis effectively — if these are the dominant domain, skip MTX and initiate a TNF inhibitor or IL-17 inhibitor as first-line systemic therapy.

— Methotrexate 15–25 mg PO/SC weekly + folic acid 1 mg daily
· Best for peripheral arthritis and skin
· Limited efficacy for axial/enthesitis
· Monitor CBC, LFTs, creatinine every 4–8 weeks initially, then every 12 weeks
· Avoid in pregnancy, ETOH abuse, hepatic disease
— Sulfasalazine, leflunomide, cyclosporine — alternatives; less commonly used
— TNF inhibitors (adalimumab, etanercept, infliximab, golimumab, certolizumab): first-line biologic, effective across all domains including axial; certolizumab preferred in pregnancy (minimal placental transfer)
— IL-17 inhibitors (secukinumab, ixekizumab, bimekizumab): excellent for skin and axial; avoid in IBD (can worsen Crohn's)
— IL-23 inhibitors (guselkumab, risankizumab): strong skin efficacy; emerging joint data; not effective for axial as monotherapy
— IL-12/23 (ustekinumab): moderate joint efficacy, strong skin
— T-cell costimulation (abatacept): modest joint response
— JAK inhibitors (tofacitinib, upadacitinib): oral, effective; black box warnings — MACE, VTE, malignancy, serious infection; reserve for patients failing TNFi, especially age >65 or CV risk factors
— PDE4 inhibitor (apremilast): oral, modest efficacy, no required lab monitoring — useful in mild disease or when biologics contraindicated
Step 3 management: Before starting any biologic or JAKi, screen for latent TB (IGRA), HBV (HBsAg, anti-HBc), HCV, and HIV; update vaccines (avoid live vaccines after initiation).

— Switching to a second TNFi (especially if primary loss of response)
— Class switch to IL-17i, IL-23i, or JAKi (better if primary nonresponse)
— Predominant axial disease: TNFi or IL-17i (NOT MTX, NOT IL-23i monotherapy)
— Severe skin + joints: IL-17i or IL-23i
— Concurrent IBD: TNFi (infliximab, adalimumab) — avoid IL-17 inhibitors and etanercept (ineffective/worsens IBD)
— Concurrent uveitis: monoclonal TNFi (adalimumab, infliximab) — avoid etanercept
— Pregnancy planning: certolizumab pegol
— Before biologics: inactivated influenza, pneumococcal (PCV20 or PCV15→PPSV23), hepatitis B, Tdap, recombinant zoster (Shingrix), HPV
— Avoid live vaccines (MMR, varicella, yellow fever, live attenuated influenza, oral typhoid) once immunosuppressed
— CBC, CMP every 3 months
— Annual TB screening if ongoing risk
— Skin exam annually (increased non-melanoma skin cancer risk)
— Lipids 4–8 weeks after JAKi or IL-6 pathway start
Board pearl: In PsA + Crohn's disease, avoid secukinumab/ixekizumab — IL-17 blockade can worsen IBD. Choose infliximab or adalimumab, which treat both diseases.

— Higher baseline CV, infection, malignancy, and fall risk
— JAK inhibitors carry a black-box warning for patients ≥50 with ≥1 CV risk factor (MACE, VTE, malignancy, mortality vs. TNFi from ORAL Surveillance) — avoid as first-line in this group
— NSAIDs: increased GI bleed, AKI, HF exacerbation, hypertension — use lowest dose and shortest duration; add PPI if needed
— Glucocorticoids: heightened risk of osteoporosis, hyperglycemia, delirium, infection — minimize
— Methotrexate: reduce dose, monitor renal clearance closely
— Methotrexate contraindicated if CrCl <30 mL/min; reduce dose if CrCl 30–60 (risk of cytopenias, mucositis)
— NSAIDs avoided if CrCl <30; cautious if 30–60
— TNF inhibitors and IL-17/IL-23 inhibitors: no renal dose adjustment; generally preferred in CKD
— Apremilast: reduce dose to 30 mg daily if CrCl <30
— JAK inhibitors: dose-adjust per agent (tofacitinib reduce to 5 mg daily if moderate–severe renal impairment)
— MTX contraindicated in significant liver disease, active hepatitis, ETOH use disorder; obtain FibroScan or hepatology consult in suspected steatohepatitis (common with PsA + metabolic syndrome)
— Leflunomide also hepatotoxic
— Screen and treat HBV before biologics; chronic HBV requires antiviral prophylaxis (entecavir/tenofovir) during therapy
— HCV: prefer non-MTX agents; coordinate with hepatology for DAA treatment
Step 3 management: A 72-year-old with PsA, CKD stage 3b, and prior MI → avoid JAK inhibitors and NSAIDs; start a TNF inhibitor (after TB/hepatitis screen) and refer to cardiology for ASCVD risk optimization.

— Disease often improves during pregnancy, flares postpartum
— Safe in pregnancy:
· Certolizumab pegol — preferred TNFi (Fc-free, minimal placental transfer); can continue through delivery
· Other TNFi (adalimumab, infliximab, etanercept) typically continued through second trimester, often stopped near term to minimize neonatal immunosuppression
· Sulfasalazine (with folate supplementation)
· Hydroxychloroquine
· Low-dose prednisone if needed
· NSAIDs only in 1st–2nd trimester; stop by 20 weeks (oligohydramnios, premature ductal closure)
— Contraindicated/teratogenic:
· Methotrexate — stop ≥3 months before conception in both partners
· Leflunomide — requires cholestyramine washout
· JAK inhibitors — avoid
— Live vaccines in infants exposed to biologics in utero: delay rotavirus and BCG until 6–12 months
Key distinction: Methotrexate is teratogenic and abortifacient — discontinue ≥3 months before conception in both men and women; certolizumab pegol is the TNFi of choice through pregnancy and lactation.

— Erosive joint damage with "pencil-in-cup" deformity at DIPs/PIPs
— Arthritis mutilans: telescoping fingers, severe disability (<5%)
— Ankylosis of axial spine, reduced spinal mobility, kyphosis
— Secondary osteoarthritis in damaged joints
— Uveitis (~7–25%) — typically anterior, acute, unilateral, can be bilateral/chronic; urgent slit-lamp evaluation
— Inflammatory bowel disease (~3–5%) — Crohn's > UC
— Cardiovascular disease: ~1.5–2× increased MI, stroke, atherosclerosis from systemic inflammation
— Metabolic syndrome: obesity, T2DM, hypertension, dyslipidemia, NAFLD/MASLD
— Osteoporosis — chronic inflammation + steroid use
— Depression and anxiety — both disease- and stigma-driven; impacts adherence
— Fatigue — independent symptom even with controlled inflammation
— Infections: serious bacterial, opportunistic (TB, herpes zoster, fungal), reactivation of HBV
— Malignancy: non-melanoma skin cancer (especially with cyclosporine, PUVA history); lymphoma risk modest
— Hepatotoxicity (MTX, leflunomide)
— Cytopenias (MTX)
— Demyelination (TNFi) — avoid in MS
— Heart failure exacerbation (TNFi in NYHA III–IV)
— MACE, VTE, malignancy (JAK inhibitors)
— Injection-site or infusion reactions
Board pearl: PsA confers a ~50% increased cardiovascular risk, comparable to T2DM — incorporate aggressive lipid management, BP control, smoking cessation, and weight management into every visit; treat the inflammation to reduce CV risk.

— Acute monoarthritis with fever, severe pain — rule out septic arthritis (arthrocentesis required)
— Acute red painful eye with photophobia/visual change — emergent ophthalmology for uveitis
— New neurologic deficit with axial PsA — concern for spinal fracture, cauda equina, or cord compression
— Suspected serious infection on biologic/JAKi (fever, hypotension, focal infection): hold immunosuppression, obtain cultures, broad-spectrum antibiotics
— Severe pustular or erythrodermic psoriasis — dermatology/inpatient admission; fluid/electrolyte risk
— Any newly suspected PsA requiring DMARD initiation
— Inadequate response after 3 months of csDMARD or biologic
— Concurrent IBD or uveitis (multidisciplinary)
— Extensive skin disease (BSA >10%, PASI >10), nail disease, palmoplantar or scalp involvement requiring phototherapy or systemic skin-directed therapy
— Septic joint, necrotizing infection on biologics, severe drug reactions (DRESS from sulfasalazine), MTX pancytopenia
— Severe erythrodermic flare with hemodynamic compromise
CCS pearl: In a CCS case of suspected septic arthritis in a PsA patient on a TNF inhibitor, order arthrocentesis with cell count/differential/Gram stain/culture/crystals before antibiotics if feasible, hold the biologic, and start empiric IV vancomycin + ceftriaxone; consult orthopedics and rheumatology.

— Symmetric small-joint polyarthritis at MCPs, PIPs, wrists; spares DIPs
— RF and/or anti-CCP positive in ~70–80%
— No dactylitis, no enthesitis, no nail pitting, no skin psoriasis
— Radiograph: marginal erosions without new bone formation, periarticular osteopenia
— Younger males, inflammatory back pain, symmetric sacroiliitis, bamboo spine with thin marginal syndesmophytes
— Strong HLA-B27 association (~90%)
— Peripheral arthritis less common; no nail or DIP involvement
— PsA axial disease tends to be asymmetric with chunky, non-marginal syndesmophytes and frequent cervical involvement
— Post-infectious (GU: Chlamydia; GI: Salmonella, Shigella, Campylobacter, Yersinia)
— Triad: arthritis, urethritis/cervicitis, conjunctivitis
— Keratoderma blennorrhagicum, circinate balanitis — can mimic psoriasis
— Self-limited (~6 months); HLA-B27 associated
— Peripheral (Type 1 oligoarticular, parallels gut activity; Type 2 polyarticular, independent) or axial
— GI symptoms guide diagnosis
Key distinction: DIP involvement, dactylitis, enthesitis, and adjacent nail dystrophy point to PsA; symmetric MCP/PIP/wrist disease with RF/anti-CCP positivity points to RA — the presence of DIP synovitis plus nail pitting on the same finger is one of the most specific PsA findings on the boards.

— Gout: acute monoarthritis (classic podagra at 1st MTP), tophi may mimic dactylitis; synovial fluid: negatively birefringent needle-shaped urate crystals
— CPPD/pseudogout: older patients, knee/wrist; positively birefringent rhomboid crystals, chondrocalcinosis on X-ray
— DIP/PIP nodes (Heberden/Bouchard); morning stiffness <30 min; gel phenomenon
— Imaging: osteophytes, joint space narrowing, subchondral sclerosis, "gull-wing" erosions in erosive OA
— No dactylitis, no enthesitis, no skin/nail psoriasis
Board pearl: A swollen great toe is not always gout — check for nail pits, scalp/gluteal psoriasis, and inflammatory rhythm; PsA dactylitis of the hallux can be misdiagnosed and treated with allopurinol for years. Aspirate to confirm crystals when feasible.

— Reassess disease activity every 3 months until target (MDA/remission), then every 6 months
— Adjust therapy at each visit if target not met
— Consider tapering biologics (extending interval) only in sustained remission ≥6–12 months, never abrupt discontinuation
— Annual lipid panel, BP, HbA1c, BMI/waist circumference
— EULAR recommends multiplying calculated ASCVD risk by 1.5 in inflammatory arthritis with at-risk features
— Statin therapy per ACC/AHA guidelines; treat hypertension to <130/80 in most patients
— Smoking cessation counseling at every visit (smoking worsens PsA and reduces TNFi response)
— Mediterranean-style diet, weight loss to BMI <25 improves drug response and remission rates
— Aerobic + resistance exercise 150 min/week
— DEXA in patients on chronic glucocorticoids (≥5 mg prednisone ≥3 months) or postmenopausal
— Vitamin D 800–1000 IU + calcium 1000–1200 mg daily
— Influenza (inactivated), pneumococcal (PCV20 or PCV15→PPSV23), Tdap every 10 yr, Shingrix at age ≥19 if immunosuppressed (or ≥50), COVID-19, HBV, HPV
Step 3 management: At every routine PsA follow-up, address the "five Cs": Cardiovascular risk, Cancer screening, Calcium/bone, Cigarettes, and Comorbid mood — these prevent the long-term morbidity that often eclipses joint damage itself.

— Active disease/treatment initiation: every 4–8 weeks until controlled
— Stable on therapy: every 3–6 months to rheumatology; primary care every 6–12 months
— TJC/SJC (66/68), patient global VAS, physician global VAS
— Dactylitis count, enthesitis count (LEI or SPARCC)
— Skin (BSA, PASI), nail score
— Axial symptoms (BASDAI)
— Function: HAQ-DI
— Composite measures: DAPSA, MDA, PASDAS
— MTX/leflunomide: CBC, CMP every 2–4 weeks initially, then every 8–12 weeks
— TNFi/IL-17/IL-23: CBC, CMP, every 3–6 months; annual TB screen
— JAK inhibitors: CBC, CMP, lipids 4–8 weeks after initiation, then every 3 months; herpes zoster surveillance
— Annual hepatitis serology if risk; HIV if indicated
— Adherence (biologic gaps cause anti-drug antibody formation and loss of response)
— Injection technique, self-injection support
— Signs of infection — when to hold biologic and call (fever ≥38°C, new productive cough, dysuria, cellulitis)
— Avoid live vaccines while on biologics
— Sun protection (increased non-melanoma skin cancer risk)
— Alcohol limits with MTX (≤4 drinks/week is a common practical guidance; avoid binge use)
— Contraception counseling on teratogenic agents
CCS pearl: When advancing the clock on a PsA case, after initiating MTX, schedule "return visit in 6 weeks" with CBC, CMP, and clinical reassessment; do not jump to 3 months without interim labs.

— Discuss infection risk (including opportunistic and TB reactivation), malignancy risk, MACE/VTE risk (JAKi), demyelination, infusion reactions, cost
— Document baseline TB/HBV/HCV/HIV screening and shared decision-making
— JAK inhibitor: explicit discussion of black-box warnings in older patients or those with CV risk
— Document contraception use in patients on MTX or leflunomide
— Discuss 3-month preconception washout for MTX in both men and women; cholestyramine washout for leflunomide
— Pregnancy planning is a shared decision — coordinate with maternal-fetal medicine when appropriate
— Patients on biologics transitioning between insurers or pharmacies may face gaps in therapy → loss of response, immunogenicity
— Hospital discharge after surgery: clear plan for when to restart biologic (typically after wound healed, ~14 days, no infection)
— Communicate immunosuppression status to all providers (e.g., dental procedures, endoscopy, vaccinations)
— Document live vaccine avoidance in chart; counsel household contacts
— Infant exposed to TNFi in utero: alert pediatrician — delay live rotavirus and BCG
Board pearl: Before initiating any biologic, document four items: TB screen, HBV/HCV/HIV screen, vaccination status update, and informed consent including infection/malignancy risks — omission is a frequent malpractice and Step 3 stem trap.

— Dactylitis
— DIP involvement
— Dystrophic nails (pitting, onycholysis, oil drop)
— Destructive arthropathy (pencil-in-cup)
— Diffuse enthesitis
— Skin → MTX, IL-17i, IL-23i
— Peripheral arthritis → MTX, TNFi
— Axial → TNFi or IL-17i (NOT MTX)
— Enthesitis/dactylitis → TNFi, IL-17i, JAKi
— IBD overlap → TNFi (infliximab/adalimumab); avoid IL-17i
— Pregnancy → certolizumab pegol
Board pearl: A young adult with psoriasis + sausage digit + heel pain + nail pitting = PsA until proven otherwise — start workup with hand/foot/SI joint imaging, CRP, hepatitis screen, TB screen, and refer to rheumatology.

— PsA + Crohn's: choose infliximab or adalimumab (avoid IL-17i, etanercept)
— PsA + pregnancy: certolizumab pegol
— PsA + multiple sclerosis: avoid TNFi → choose IL-17i or IL-23i
— PsA + recurrent infections/CHF: avoid TNFi → IL-17i/IL-23i or apremilast
— PsA + age >65 with CV risk: avoid JAK inhibitors
Step 3 management: When two biologics seem equally appropriate, the comorbidity sidebar (IBD, uveitis, pregnancy, MS, infection, CV risk) is the deciding factor — Step 3 questions almost always hide the answer in the patient's other diagnoses.

Psoriatic arthritis is a seronegative inflammatory arthritis suspected in any psoriasis patient with morning stiffness, dactylitis, enthesitis, DIP synovitis, or nail dystrophy — diagnosed clinically by CASPAR criteria, screened annually with PEST, and treated to target with domain-tailored therapy that also reduces the elevated cardiovascular and metabolic risk that accompanies the disease.
Board pearl: The Step 3 PsA question is rarely "what is the diagnosis?" — it is "what is the next best step, given this comorbidity?" Master the comorbidity-to-biologic matching and the pre-biologic safety checklist and the topic is solved.

