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USMLE Step 2 (Fach) / Muskuloskeletal/Rheumatology (Lektion)

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• "Nightstick fracture" Ulnar shaft fracture from direct trauma often in self-defense against a blunt object. Treatment: ORIF if significantly displaced.
• Osteosarcoma Malignant, osteoid and bone-forming tumor arising from mesenchymal stem cells (osteoblasts) located in the periosteum.- Most common primary bone malignancy- Incidence: bimodal distribution- Increased incidence in patients with retinoblastoma and Li-Fraumeni syndrome Localization: - Metaphyses of long bones (particularly distal femur and proximal tibia)- Metastases to lung Etiology:- Primary osteosarcoma (children, adolescents): unknown- Secondary osteosarcoma (elderly): Paget's disease of bone, radiation injury, bone infarction Clinical features:- Progressive pain that worsens at night- Tender to palpation and accompanied by erythema- Limping and decreased range of motion- B symptoms such as fever, night sweats, weight loss Diagnosis:- X-ray:→ Signs of osteolysis adjacent to osteosclerosis (moth eaten appearance)→ Codman triangle: periosteal new-bone formation at the diaphyseal end of the lesion)→ “Sunburst pattern”(In contrast to the multilayered “onion skinning” that is classic for Ewing sarcoma and the “soap bubble” appearance of giant cell tumor of bone.)- Biopsy: always feature woven bone matrix → distinction from chondrosarcomas and fibrosarcomas- Laboratory: ↑ alkaline phosphatase, ↑ LDH, ↑ ESR Treatment:- Surgery (definitive resection) with neoadjuvant and adjuvant polychemotherapy (e.g., combination of methotrexate, doxorubicin, cisplatin, and ifosfamide)- Amputation may be necessary.
• Osteoarthritis Disabling joint disease characterized by a noninflammatory degeneration of the joint complex (articular cartilage, subchondral bone, and synovium) that occurs with old age or from overuse. Risk factors:- Obesity, joint overuse, age (> 55 years), familial history, history of joint injury, anatomic factors Presentation:- Pain on exertion, which is relieved with rest- Pain in both complete flexion and extension- Crepitus on joint movement- Morning stiffness < 30 minutes Subtypes and variants :- Heberden's nodes: Pain and nodular thickening on the dorsal sides of the distal interphalangeal joints (DIP)- Bouchard's nodes: Pain and nodular thickening on the dorsal sides of the proximal interphalangeal joints (PIP)- Hallux rigidus: Arthrosis of the first metatarsophalangeal joint  Diagnosis:- Radiological signs: Irregular joint space narrowing, subchondral sclerosis, osteophytes, subchondral cysts- Synovial fluid: normal viscosity, WBC count < 2000 cells/L- Laboratory tests, including inflammatory markers, are typically normal Treatment: 1. Nonpharmacologic treatment (e.g., exercise, weight reduction)2. NSAIDs3. Topical agents (eg, NSAIDs, capsaicin, intra-articular glucocorticoids, intraarticular hyaluronic acid)4. Surgery
• Gout Inflammatory arthropathy characterized by painful and swollen joints resulting from precipitating uric acid crystals. Risk factors: - Nonmodifiable: Male gender, African American race- Decreased uric acid secretion: thiazides, aspirin, niacin, chronic renal insufficiency- Increased uric acid production: tumor lysis syndrome, hemolytic anemias, Lesch-Nyhan syndrome, high-protein diet, obesity, postmenopasual status in women- Both: Alcohol consumption Clinical features: - Acute severe pain with overlying erythema, swelling, and warmth; possible fever- More likely to occur at night, typically waking the patient- Symptoms peak after 12-24 hours; regression may take days to weeks.- Most commonly affects the first MTP joint (podagra) and the midfoot, knees, ankles, and wrists.- Tophi (urate crystal deposits in soft tissue) can be seen with chronic disease. Tophi can ulcerate and drain a chalky white material.- Uric acid kidney stones are seen with chronic disease. Diagnosis:- Arthrocentesis:→ Joint fluid aspirate shows needle-shaped, negatively birefringent crystals→ Synovial fluid: WBC > 2000/μL with > 50% neutrophils- Serum uric acid is usually ↑ (≥ 7.5 mg/dL), but patients may have normal levels.- Ultrasound: "Double-contour" sign- MRI: Method of choice to detect spinal involvement Treatment:Acute attacks:- High-dose NSAIDsare first line. - Colchicine: patients who cannot tolerate NSAIDs (e.g., patients with chronic kidney disease or gastrointestinal ulcers)- Steroids are used when NSAIDs are ineffective or contraindicated, as in renal disease. Maintenance therapy:- General measures: → Weight loss (if applicable)→ Purine-restricted diet (e.g., low-protein diet)→ Reduce alcohol consumption→ Sufficient/high fluid intake→ Close management of diabetes and blood pressure→ Consuming dairy products, vitamin C, and coffee can lower levels of uric acids and therefore prevent gout.- Allopurinol: Xanthine oxidase inhibitor (contraindicated in kidney disease; febuxostat is alternative)- Probenecid: Inhibits uric acid reabsorption (contraindicated in kidney disease, nephrolithiasis)- Rasburicase: Catalyzes the breakdown of uric acid into allantoin 
• Rheumatoid arthritis Systemic inflammatory autoimmune disorder characterized by symmetric joint pain, swelling, and synovial destruction. Etiology: - Sex: ♀ > ♂ (3:1)- Peak incidence: 50-75 years- Genetic disposition: HLA-DR4- Environmental triggers: smoking, infection Pathophysiology:- Inflammatory joint effusion and synovial hypertrophy- Pannus formation along the synovial tissue → destroy cartilage extracellular matrix- Patients with positive rheumatoid factor (RF) are more likely to develop extra-articular manifestations of rheumatoid arthritis.  Clinical features:- Symmetrical pain and swelling of joints; commonly small joints (MCPs, PIPs, wrists, ankles knees; not DIPs)- Morning stiffness > 30 mins, improves with movement- Ulnar deviation, Boutonniere deformity, swan neck deformity, Baker cyst, atlantoaxial subluxation- Constitutional symptoms: low-grade fever, myalgia, malaise, night sweats- Skin: rheumatoid nodules; non-tender, firm, subcutaneous swellings (2 mm-5 cm)- Lungs: causing fibrosis, nodules, pleuritis, and pleural effusions- Eye: keratoconjunctivitis sicca, scleritis, and episcleritis- Endocrine and exocrine glands: secondary Sjögren syndrome- Hematological: anemia of chronic disease- Heart: pericarditis and myocarditis; higher risk of myocardial infarction, stroke, and CHF- Vascular: peripheral vasculitis manifesting as livedo reticularis, Raynaud phenomenon, purpura, necrosing fingertips or rheumatoid neuropathy Subtypes:- RA of the cervical spine- Felty syndrome = Rheumatoid arthritis + Splenomegaly + Granulocytopenia Diagnosis:- Inflammatory arthritis of ≥ 3 joints for > 6 weeks- Rheumatoid factor (RF): Low specificity- Anti-citrullinated peptide antibody (anti-CCP): Specificity > 90%- ↑ ESR, CRP- X-ray: demineralization, narrowing of joint space, erosions of cartilage and bone- Synovial fluid aspirate: turbid, ↓ viscosity, and an ↑ WBC count (3000-50,000 cells/µL)- Exudate effusions marked by very low (< 50 mg/dL) glucose and very high LDH (> 700 U/L) Treatment:- Acute flairs: NSAIDs, glucocorticoids- Disease-modifying anti-rheumatic medications (DMARDs): Methotrexate, hydroxychloroquine, sulfasalazine- Biologicals: Abatacept, rituximab, adalimumab/etanercept/infliximab, anakinra (blocks IL-1)
• Polymyositis Inflammatory myopathy (others: dermatomyositis, inclusion body myositis) affecting the proximal skeletal muscles. Etiology: cell-mediated cytotoxicity against unidentified skeletal muscle antigens, chiefly affecting the endomysium. Presentation:- Proximal muscle weakness affecting both sides of the body (progresses within weeks to months)- The pelvic and shoulder girdle muscles are most commonly affected→ Leads to difficulties combing hair, standing up, and climbing stairs- Muscle tenderness in approx. 33% of cases Diagnosis:- Proximal muscle involvement- Positive laboratory findings (↑ CK, ↑ aldolase, ANA, anti-Mi-2, anti-Jo-1 antibodies)- Electromyogram (EMG) suggestive of inflammatory myopathy- Typical biopsy findings: cell-mediated inflammation, intrafascicular infiltration of cytotoxic CD8+ T cells  Treatment: High-dose corticosteroids with taper after 4–6 weeks to ↓ the maintenance dose.Azathioprine and/or methotrexate can be used as steroid-sparing agents.
• Dermatomyositis Inflammatory myopathy (others: polymyositis, inclusion body myositis) that presents similarly to polymyositis, with the addition of skin involvement. Etiology: - Idiopathic or paraneoplastic antibody-mediated vasculopathy- Associated with malignancies (non-Hodgkin lymphoma; lung, stomach, colorectal, or ovarian cancer) Clinical features:- Symptoms of polymyositis + cutaneous manifestations- Gottron papules: Prominent erythematous papules, symmetrically distributed on the extensor surface of the hands- Heliotrope rash: erythematous rash on the upper eyelids, sometimes accompanied by edema- Shawl sign: erythema of the upper back, posterior neck, and shoulders- V sign: erythema of the upper chest and neck- Holster sign: erythema of the lateral thighs Diagnosis:- Proximal muscle involvement- Anti-Jo-1 (antisynthetase antibody) and anti-Mi-2 (against helicase)- Electromyogram (EMG) suggestive of inflammatory myopathy- Biopsy: antibody-mediated inflammation involving parafascicular and perivascular infiltration with plasmacytoid dendritic cells and B lymphocytes- DM is diagnosed if additional cutaneous manifestations are present.All patients diagnosed with DM should be tested for possible malignancies! Treatment:- High-dose corticosteroids with taper after 4-6 weeks to ↓ the maintenance dose.- Azathioprine and/or methotrexate can be used as steroid-sparing agents.
• Ankylosing spondylitis A chronic inflammatory disease of the axial skeleton that leads to partial or even fusion and rigidity of the spine.- ♂ > ♀ (3:1)- Age: 15-40 years- 90-95% of patients are HLA-B27 positive Clinical features:- Fatigue, intermittent hip pain, lower back pain that worsens with inactivity and in the mornings.- Limited mobility of the spine, especially reduced forward lumbar flexion (⊕ Schober test)- Inflammatory enthesitis (e.g., of the Achilles tendon, iliac crests, tibial tuberosities): Painful at insertion site- Arthritis outside the spine: hip, shoulder, and knee joint- Acute, unilateral anterior uveitis (∼ 25% of cases)- Gastrointestinal symptoms: associated with chronic inflammatory bowel disease- Restrictive pulmonary disease due to decreased mobility of the spine and thorax- Cardiac (rare): aortic valve insufficiency, atrioventricular blocks Must be ruled out: Reactive arthritis, psoriatic arthritis, enteropathic spondylitis Diagnostic approach:1. Physical examination, patient history, and pelvic x-ray: If results are conclusive, no additional testing is required!2. If inconclusive → HLA-B27 testing3. If still inconclusive → pelvic MRI- X-ray: Fused sacroiliac joints, vertical syndesmophytes, sclerotic ligaments, and bamboo spine- Labs: ESR or CRP is ↑ in 75% of cases; ⊝ RF; ⊝ antinuclear antibody (ANA)- Chest expansion measurement: < 2 cm is pathological- Spine mobility tests- Examination of the hip→ Mennell sign: tenderness to percussion and pain on displacement of the sacroiliac joints→ FABER test: Flexion, ABduction, and External Rotation provokes pain in the ipsilateral hip Treatment:- NSAIDs (eg, indomethacin) for pain; exercise to improve posture and breathing- TNF-α inhibitors or sulfasalazine can be used in refractory cases
• Systemic sclerosis (scleroderma) Chronic disease caused by abnormal growth of connective tissue, which leads to diffuse thickening and hardening of the skin and often the inner organs.- F > M (3:1)- Higher incidence in African Americans- Age 35-50 years Clinical presentation:- Systemic: Fatigue, weakness- Skin: Teleangiectasia, sclerodactyly, digital ulcers, calcinosis cutis, thickening and hardening - Extremities: Arthralgias, contractures, myalgias- Gastrointestinal: Esophageal dysmotility, dysphagia, dyspepsia- Vascular: Raynaud's phenomenon 1. Limited cutaneous systemic sclerosis- In 90% of cases, Raynaud's phenomenon precedes the onset of other symptoms.- Skin manifestations are usually restricted to the hands, fingers, and face- Often manifests as CREST syndrome: C → Calcinosis cutis R → Raynaud's phenomenonE → Esophageal hypomotilityS → SclerodactylyT → Telangiectasia 2. Diffuse cutaneous systemic sclerosis- GI dysmobility- Pulmonary disease: pulmonary hypertension and interstitial lung disease- Cardiac disease: fibrosis, myocarditis, pericarditis- Renal disease Diagnostics:- Auto-antibodies: Antinuclear antibodies (ANA) present in about 90% of cases→ Limited SSc: anticentromere antibodies (ACA)→ Diffuse SSc: Anti-Scl-70 (anti-topoisomerase I antibody), anti-RNA polymerase III- Serum protein electrophoresis: ↑ γ-globulins- Complete blood count and differential- Chest x-ray: detects possible pulmonary involvement Treatment:- General measures: Physical therapy, prevent dry skin, phototherapy- Immunosuppressive therapy: eg, methotrexate- Organ-specific therapy: eg, PPIs in cases of GERD, Ca2+ channel blockers in cases of Raynaud phenomenon
• Systemic lupus erythematosus A multisystem autoimmune disorder related to antibody-mediated cellular attack and deposition of antigen-antibody complexes.- F >> M (10:1)- Women aged 20-40 years- Highest prevalence in African-American- Genetic predisposition: HLA-DR2 and HLA-DR3 Diagnostic criteria (according to the American college of rheumatology (ACR))Requirements: at least 4 of the 11 criteria must be met:1. Dermatological- Malar rash ("butterfly rash") with sparing of the nasolabial folds- Discoid rash- Photosensitivity- Oral or nasopharyngeal ulcers2. Internal organs- Nonerosive arthritis: involving at least two peripheral joints; rarely deforming (normal x-ray)- Pleuritis or pericarditis (possibly with effusion)- Renal disorder: lupus nephritis with proteinuria- Neurologic disorder: seizures, psychosis, and/or personality changes3. Laboratory tests- Hematologic disorders: autoimmune hemolytic anemia, thrombocytopenia, leukopenia, lymphopenia- Immunological findings: anti-dsDNA, anti-Sm, or antiphospholipid antibodies- Antinuclear antibodies (ANA)- ↓ C3 and C4 Drug-induced SLE: antihistone antibodies are seen in 100% of cases but are nonspecific.Neonatal SLE: Associated with anti-Ro antibodies transmitted from mother to neonate. Treatment:- Induction therapy: Corticosteroids- Basic therapy: Hydroxychloroquine - Severe symptoms: Azathioprine, mycophenolate, cyclophosphamide (renal)
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• Complex regional pain syndrome (CRPS) A pain syndrome accompanied by loss of function and autonomic dysfunction, usually occurring after trauma. Etiology:- Trauma- Medical conditions→ Carpal tunnel syndrome→ Acute MI: The form of CRPS that can follow MI is sometimes referred to as shoulder-hand syndrome.→ Malignancy: e.g., lung cancer, breast cancer, ovarian cancer, brain tumors→ CNS disorders: e.g., traumatic brain injury, stroke, tumor Clinical presentation:- Symptoms usually develop within 4-6 weeks following a trauma- Pain excessive in duration or severity given the inciting event- Sensory: hyperesthesia and/or allodynia- Vasomotor: hypo-/hyperthermia and/or hypo-/hyperpigmentation of the skin- Sudomotor/edema: hypo-/hyperhidrosis and/or edema- Motor/trophic: ↓ range of motion and/or strength, tremors, and/or changes in nail and hair growth Diagnosis: Clinical- X-ray: patchy demineralization- Bone scintigraphy: ↑ uptake in the affected limb Treatment:- Physical and occupational therapy: first-line therapy→ Ensuring daily function and motion of the affected limb→ Desensitization techniques→ Lymph drainage for the treatment of edema→ Hot/cold contrast therapy- NSAIDs, corticosteroids, low-dose TCAs, gabapentin, pregabalin, and calcitonin
• Fibromyalgia A chronic pain disorder characterized by soft tissue and axial skeletal pain in the absence of joint pain.- F > M (9:1)- Age range: 20-50 years Etiology: Unknown. - Associated with ↓ serotonin and ↑ substance P/nerve growth factor levels → hypersensitivity to pain- Associated with depression, anxiety, sleep disorders, inflammatory bowel syndrome, and cognitive disorders (“fibro fog”) Clinical features:- Chronic, widespread pain, primarily at points where muscles and tendons attach to bone (tender points)- Headache- Fatigue- Morning stiffness- Unrefreshing sleep- Cognitive dysfunction (“fibro fog”)- Paresthesias- Further symptoms of autonomic dysfunction: digestive problems, weight fluctuation, palpitations, sexual dysfunction, night sweats Diagnostic criteria:- Tender points: ≥ 11 of 18 - Pain-affected areas: all four regions of the body and the axial skeleton- Duration: ≥ 3 months- Laboratory values and imaging are normal (helpful for excluding other causes or comorbidities). The presence of <11 of 18 painful areas or non-fibromyalgia-associated painful areas is known as myofascial pain syndrome. Treatment:- Patient education- Lifestyle changes: dietary recommendations, sleep hygiene, regular physical activity- Medication: Initially monotherapy: low-dose tricyclic antidepressants (TCA, e.g., amitriptyline), selective serotonin-norepinephrine reuptake inhibitors (SSNRIs) (eg, duloxetine), or anticonvulsants (eg, pregabalin)- Avoid narcotic medications (eg, opioids)
• Sjögren syndrome Sex: F > M (∼ 9:1)Age of onset: 40-60 years Etiology:- Primary Sjögren syndrome: idiopathic (association with HLA-DR52)- Secondary Sjögren syndrome: rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, polymyositis, primary biliary cirrhosis (PBC) Clinical presentation:- Xerostomia (dry mouth)- Parotitis- Xerophthalmia (dry eyes) → keratoconjunctivitis sicca- Sicca syndrome: combination of dry mouth and dry eyes- General symptoms: fatigue and arthralgias (∼ 70% of cases)- Xerosis, Raynaud's phenomenon (∼15-30% of cases)- Vasculitis (∼ 10% of cases): Palpable purpura of the legs, recurrent urticaria, skin ulcerations- Neurological and psychiatric manifestations Diagnosis:- ↑ ESR- Anti-Ro/SSA antibody and anti-La/SSB antibody (∼70% of cases): target ribonucleoprotein antigens- Antinuclear antibodies (ANAs; positive in up to 97% of cases)- Rheumatoid factor (RF; positive in > 90% of cases of secondary Sjögren syndrome)- Urinalysis: possible signs of glomerulonephritis or interstitial nephritis- Schirmer's test: shows decreased tear production < 5 mm of moisture on the filter paper after 5 minutes - Slit lamp examination- Biopsy: Sialadenitis with dense lymphocytic infiltrations, parenchymal atrophy Treatment:- For dry mouth: Hydration, muscarinic agonists- For dry eyes: Artificial tears, topical immunosuppression (e.g., cyclosporine), lubricants Complications: - Risk of developing associated conditions (e.g., systemic lupus erythematosus, rheumatoid arthritis)- Corneal scarring, ulcer, rupture, and infection- Pregnancy: fetal loss, infant with neonatal lupus syndrome and associated complete heart block- Increased risk of lymphomas (B-cell lymphoma, MALT lymphoma)!
• Inclusion body myopathy Inflammatory myopathy affecting both the proximal and distal skeletal muscles. Clinical features:- Progresses slowly over years- Selective and asymmetric muscle involvement of both proximal and distal muscle groups→ Quadriceps muscle weakness: knees lack support → frequent falling→ Finger flexors: difficulties gripping, e.g., shopping bags or a briefcase Diagnosis:- ↑ Creatinine kinase- EMG: Abnormal electrical signal conduction- Biopsy: Inflammation, vacuoles of abnormal proteins Treatment: Exercise and physical therapy- Immunosuppressants aren't effective
• Pseudogout (CPPD) Paroxysmal joint inflammation due to calcium pyrophosphate crystal deposition (calcium pyrophosphate dihydrate). Epidemiology:- Age of onset: > 50 years Etiology:- Mostly idiopathic (primary form)- Secondary form: joint trauma, familial chondrocalcinosis, hyperparathyroidism, hemochromatosis, gout, hypophosphatemia Clinical presentation:- Often asymptomatic- Acute (pseudogout attack): monoarthritis (rarely oligoarthritis), mostly affecting the knees and other large joints (e.g., hips, wrists, and ankles)- Chronic (can affect multiple joints): Progressive joint degeneration with episodes of acute inflammatory arthritis typical of pseudogout attacks Diagnosis:- Arthrocentesis should be performed, especially in acute cases.→ Polarized light microscopy: detection of rhomboid-shaped, positively birefringent CPPD crystals→ Synovial fluid findings: 10,000-50,000 WBCs/μL with > 90% neutrophils- X-ray findings: cartilage calcification of the affected joint (chondrocalcinosis)- Test for hypercalcemia (esp. hyperparathyroidism)- Serum uric acid levels are normal Treatment:- Asymptomatic cases do not require treatment unless there is an underlying condition (e.g., hyperparathyroidism).- Best initial treatment: NSAIDs- Alternatives: colchicine or intra-articular corticosteroids- Arthroscopic lavage may also be considered- Possible joint replacement
• Septic arthritis Etiology:- From a distant site (e.g., abscesses, wound infection, septicemia)- Disseminated infection (e.g., gonorrhea)- Iatrogenic (e.g., joint injection, arthrocentesis, arthroscopy)- Trauma (e.g., open wounds around the joint, penetrating trauma) Risk factors:- Prosthetic implant- Interventions (e.g., intra-articular injections)- Underlying joint disease, especially rheumatoid arthritis- Immunosuppressed state- Diabetes mellitus- Age > 80 years- Chronic skin infections- IV drug use Causative organisms- Staphylococcus aureus - most common, in adults and children > 2 years and arthritis caused by invasive procedures - Streptococci, S. epidermidis- N. gonorrhea - Gram-negative rods esp. E. coli and P. aeruginosa- M. tuberculosis and atypical mycobacteria- B. burgdorferi (Lyme disease) Clinical features:- Acute onset- Usually monoarticular- Most commonly affected joints: knees; followed by hip, wrists, shoulders, and ankles- Classical triad of fever, joint pain, and restricted range of motion- Joint may be swollen, red, and warm Diagnostics:- Ultrasound-guided arthrocentesis→ Cell count: > 50,000 WBC/μl (neutrophil predominant)→ Fluid appears yellowish-green and turbid→ Synovial fluid culture and gram stain- Laboratory tests: ↑ CRP/ESR- Imaging: to look for signs of underlying osteomyelitis Treatment: Empiric- Gram-positive cocci: Vancomycin- Gram-negative cocci: Ceftriaxone- Gram-negative bacilli: 3rd generation cephalosporin (e.g., ceftazidime), cefepime, piperacillin-tazobactam- No organism on gram stain but strong suspicion for bacterial septic arthritis: IV vancomycin plus either ceftazidime, cefepime, or an aminoglycoside- Start serial drainage with lavage- Sometimes debridement (arthroscopic or open approach) is necessary
• Reactive arthritis Epidemiology:- Genetic predisposition and association with HLA-B27 (see seronegative spondyloarthritis)- Commonly affects young men Etiology:- Post-urethritis: mostly after chlamydial infection- Post-enteritis: after infection with Shigella, Yersinia, Salmonella, or Campylobacter Clinical features:- Latency period: 1-4 weeks- Polyarthritis→ Often asymmetrical with a migratory character→ Occurs predominantly in the lower extremities- Sacroiliitis- Enthesitis- Dactylitis- Conjunctivitis or iritis- Oral ulcers- Skin lesions of the glans resembling psoriasis (balanitis circinata); hyperkeratinization of the palms and soles (keratoderma blenorrhagicum) - Symptoms from preceding infection: Diarrhea; Urogenital tract symptoms (dysuria, pelvic pain, urethritis, prostatitis) Diagnostics:- ↑ ESR and CRP- Test for potentially positive HLA-B27- Arthrocentesis: may be performed to rule out differentials:→ ↑ WBC count: 10,000-40,000/μL→ Mostly polymorphonuclear leukocytes predominate→ Gram stain and cultures are negative Treatment: Usually self-limiting- First line: NSAIDs- Local treatment: cryotherapy and physiotherapy- If NSAIDs are not effective: glucocorticoids (intraarticular or oral)- In chronic cases: DMARDs, e.g., sulfasalazine or MTX
• Psoriatic arthritis Inflammation of joints (primarily on hands, feet, spine) that may occur with psoriasis Epidemiology: 5-30% of psoriasis patients affected Clinical features:- Psoriasis and psoriatic arthritis may occur independently or together - Oligoarthritis (most common, accounting for 70% of cases): typically with involvement of both the distal and proximal interphalangeal joints- Spinal involvement (up to 40% of cases)- Enthesitis- Tenosynovitis- Dactylitis: inflammation and swelling of fingers or toes (“sausage digit”)- Nail pitting & oncholysis- Swelling of the hands or feet with pitting edema Diagnostics:- The Classification Criteria for Psoriatic Arthritis (CASPAR) is helpful for diagnosing psoriatic arthritis (≥ 3 out of the 5 following points required).1. Evidence of psoriasis2. Psoriatic nail dystrophy3. Negative rheumatoid factor (RF)4. Dactylitis5. Radiologic signs- Imaging studies: joint destruction, ankylosis→ Fingers: pencil-in-cup deformity→ Spine: syndesmophytes, and in particular asymmetric paravertebral ossification Treatment:- Mild disease: NSAIDs- Moderate to severe disease: disease-modifying antirheumatic drugs (DMARDs)- Physical therapy
• Giant cell arteritis Type of vasculitis, which causes chronic inflammation of large and medium-sized arteries.- Peak incidence: 70-79 years- 40-50% of patients with giant cell arteritis also have polymyalgia rheumatica Clinical features:- Constitutional symptoms: Fever, weight loss, night sweats- New onset pulse-synchronous, throbbing, dull headache, typically located over the temples- Hardened and tender temporal artery- Tenderness of the temples or the scalp- Jaw claudication: jaw pain when chewing- Amaurosis fugax or permanent loss of vision - Diplopia Diagnostics: ACR criteria (3 of the 5 criteria are required)1. Age at disease onset ≥ 50 years2. Headaches3. Abnormalities of the temporal artery4. Elevated ESR (≥ 50 mm/h)5. Histopathological abnormalities in the temporal artery- Temporal artery biopsy (gold standard): mandatory in all patients- Fundoscopy: Swollen and pale disc with blurred margins Treatment:- Ischemic organ damage (e.g., impaired vision): high dose of IV glucocorticoids - Uncomplicated disease: medium dose of oral glucocorticoids- After symptoms have resolved (usually after 2-4 weeks), slowly taper glucocorticoids to the lowest dose that is needed to control symptoms- Low-dose aspirin to prevent ischemic complications
• Takayasu arteritis Granulomatous inflammation of the aorta and its major branches, resulting in stenosis of involved blood vessels and subsequent vascular symptoms. Epidemiology:- Peak incidence: 15-45 years of age- Asian heritage- F > M = 3:1 Clinical features:- Fever, malaise, arthralgia- Decreased bilateral brachial and radial pulses → “pulseless disease”- Syncope, angina pectoris- Impaired vision- Movement-induced muscular pain in one or more limbs- Bilateral carotid bruits- Raynaud syndrome- Skin manifestations: Erythema nodosum, urticaria Diagnostics:- Laboratory findings: ↑ ESR- Angiography (gold standard): detects vascular stenosis- Biopsy of affected vessel: granulomatous thickening of aortic arch; plasma cells and lymphocytes in media and adventitia; vascular fibrosis Treatment:- Corticosteroids; if necessary, MTX or cyclophosphamide may be administered- Surgical intervention (e.g., bypass) may be required if critical stenosis of the aortic arch or its branches occurs.
• Polymyalgia rheumatica Systemic vasculitis of the small and medium-sized vessels, which leads to tissue ischemia; most commonly involving skin, peripheral nerves, muscles, joints, gastrointestinal tract, and kidneys. Epidemiology:- Peak incidence: ∼ 45-65 years- Sex: M > F- Often associated with hepatitis B infection Clinical features:- Constitutional symptoms: fever, weight loss, night sweats- Fatigue and malaise- Depressed mood- Symptoms of anemia- New onset, symmetric pain in the shoulder and pelvic girdle, neck- Morning stiffness (> 45 min)- ∼ 10–20% of patients with polymyalgia rheumatica also develop typical symptoms of giant cell arteritis Diagnostics:- ↑↑ ESR, anemia, leukocytosis- ANCA-negative- Normal creatine kinase, negative rheumatoid factors and no autoantibodies Treatment:- Low-dose of oral glucocorticoids- If symptoms improve (usually within 2-4 weeks): slowly taper and eventually stop glucocorticoids- No improvement after 2 weeks or relapse: increase dose
• Eosinophilic granulomatosis with polyangiitis A multisystem disease characterized by a necrotizing granulomatous vasculitis with eosinophilia, which most commonly involves the lungs and the skin, but can also affect the renal, cardiovascular, gastrointestinal, central, and peripheral nervous systems. Clinical features:- Severe allergic asthma attacks (chief complaint)- Allergic rhinitis/sinusitis- Skin nodules, palpable purpura- Gastrointestinal involvement: bleeding, ischemia, perforation- Pauci-immune glomerulonephritis- CNS: impaired mental status, mononeuritis multiplex (loss of motor and sensory function) Diagnostics:- Peripheral blood eosinophilia- ↑ IgE level- Circulating MPO-ANCA/pANCA (∼ 40% of cases)- Biopsy (confirmatory test): tissue eosinophilia with granulomatous reactions Treatment: immunosuppression with glucocorticoids; possible in combination with cyclophosphamide
• Microscopic polyangiitis Necrotizing vasculitis of small vessels, typically with renal and pulmonary involvement; however, multiple organ systems may be affected. Clinical features:- Similar to that of granulomatosis with polyangiitis, but without involvement of the nasopharynx!- Renal: Glomerulonephritis with hypertension has a poor prognosis- Lungs: pulmonary vasculitis with hemoptysis- Skin: palpable purpura, nodules, necrosis Diagnostics:- Biopsy of involved organ: fibrinoid necrosis with infiltration of neutrophils; no granulomas- Laboratory findings: MPO-ANCA/pANCA (∼ 70% of cases) Treatment: immunosuppression with corticosteroids and cyclophosphamide
• Granulomatosis with polyangiitis Systemic vasculitis that affects both small and medium-sized vessels. Clinical features:- Constitutional symptoms: fever, night sweats, weight loss, arthralgias- ENT involvement (∼ 90% of cases)→ Chronic rhinitis/sinusitis: nasopharyngeal ulcerations → nasal septum perforation → saddle nose deformity→ Oral ulcers- Lower respiratory tract (∼ 95% of cases): → Treatment-resistant, pneumonia-like symptoms with cough, dyspnea, hemoptysis, wheezing, hoarseness, or pleuritic pain→ Clinical features of pulmonary fibrosis, pulmonary hypertension, or pulmonary hemorrhage may occur.- Renal involvement (∼ 80% of cases)→ Pauci-immune glomerulonephritis → rapidly progressive (crescentic) glomerulonephritis (RPGN)- Skin lesions (∼ 45% of cases): Papules, vesicles, ulcers, purpura of the lower extremities- Ocular involvement (∼ 45% of cases): Conjunctivitis, episcleritis, retinal vasculitis, corneal ulcerations- Cardiac involvement (∼ 33% of cases): Pericarditis, myocarditis, vasculitis of the coronary arteries; may lead to myocardial infarction and death Diagnositcs:- Blood tests: ↑ Creatinine and ↑ BUN, ↑↑ ESR and ↑ CRP, PR3-ANCA/c-ANCA (anti-proteinase 3)- Urinalysis: microscopic hematuria, proteinuria- Chest x-ray/CT: multiple bilateral cavitating nodular lesions Treatment:- If mild disease → glucocorticoids + methotrexate (MTX)- If moderate to severe disease → glucocorticoids + either cyclophosphamide or rituximab- Remission maintenance: immunosuppressive drugs (e.g., azathioprine, rituximab or methotrexate)
• Cryoglobulinemic vasculitis Characterized by temperature dependent deposition of immune complexes in blood vessel walls and subsequent inflammation of involved vessels and surrounding tissue. Etiology: type II and III cryoglobulinemia (mixed cryoglobulinemia)- > 90% association with hepatitis C infection- Formation of hepatitis C IgG and IgM rheumatoid factor → immune complex formation with hepatitis C antigen → complement activation and inflammation of blood vessels. Clinical features:- Nonspecific systemic symptoms: fatigue, malaise, myalgia, arthralgia- Skin lesions (nearly 100% of cases): palpable purpura, ulceration, necrosis- Vasomotor symptoms: Raynaud's phenomenon, acrocyanosis- Polyneuropathy- Hepatosplenomegaly- Glomerulonephritis (severe cases or late complication) Diagnostics:- Cryoglobulinemia: cold-precipitable immune complexes (slow precipitation after 72 hours)- ↑ Rheumatoid factor (in almost all cases)- Hypocomplementemia (90% of cases)- ↑ serum concentration of polyclonal IgG and IgM- Hepatitis C diagnostics: Hepatitis C RNA and anti-hepatitis C antibodies; ↑ Liver transaminases- Skin or renal biopsy: evaluate inflammatory vascular changes and renal damage; cryoglobulin deposits may be detected in glomeruli. Treatment- Treatment of underlying diseases: hepatitis C infection (IFN-α, ribavirin)- Immunosuppression
• Behçet disease Systemic vasculitis that can affect arteries and veins of all sizes Epidemiology - Most common from the Mediterranean region to eastern Asia- Peak incidence: 20-40 years Clinical features:- Recurrent painful aphthous ulcers- Recurrent genital ulceration- Ocular disease: uveitis (iridocyclitis, chorioretinitis), and/or retinal vasculitis - Skin lesions: erythema nodosum, and/or papulopustular lesions- Arthritis of knees, ankles, hands, and/or wrists- Gastrointestinal disease: ileocecal ulceration- Vasculopathy: → Superficial thrombophlebitis→ Thrombosis of large veins (e.g., deep vein thrombosis, Budd-Chiari syndrome)→ Aneurysms (e.g., pulmonary artery aneurysms)Behçet disease is the only systemic vasculitis known to cause pulmonary artery aneurysms!Behçet disease triad: oral ulcers, genital ulcers, and uveitis! Diagnostics:- Positive pathergy skin test: erythematous papule or pustule 24-48 hours after a needle prick- Non-specific markers of inflammation may be present during flares (e.g., ↑ ESR, ↑ CRP).- Autoantibodies (e.g., ANA, ANCA, rheumatoid factor) are usually absent Diagnostic criteria (International Study Group criteria):- Recurrent oral ulceration at least three times within a 12 month periodAND≥ 2 of the following1. Recurrent genital ulceration2. Eye lesions3. Skin lesions4. Positive pathergy test Treatment:- Oral ulcers and/or genital ulcers: topical corticosteroids ± topical lidocaine for pain relief- Erythema nodosum: colchicine- Arthritis: colchicine- Ocular disease and/or vasculopathy: Systemic corticosteroids + immunosuppressant therapy (e.g., azathioprine)
• Juvenile idiopathic arthritis Broad term for childhood rheumatic diseases that begin before the age of 16 and involve joint inflammation lasting more than six weeks. Epidemiology:- Sex: ♀ > ♂- Age of onset: < 16 years Clinical features:- Red, swollen joints, early morning stiffness, limited or painful joint movement- Synovial thickening- Fever and other extra-articular manifestations (e.g., uveitis, rashes, nail changes, lymphadenopathy, hepatosplenomegaly) may be present depending on the type of JIA  Subtypes:- Oligoarticular JIA (≤ 4 joints within 6 months of onset)- Seropositive polyarticular JIA- Seronegative polyarticular JIA- Systemic JIA (Still's disease) Diagnostics:- Rheumatoid factor (RF) is absent in most cases of JIA except seropositive polyarticular JIA.- ↑ ESR in all forms of JIA.- ↑ Acute phase reactants (e.g., CRP, ferritin) and leukocytosis are usually associated with systemic JIA.- ↑ ANA (antinuclear antigen) levels may be seen with oligoarticular, polyarticular, and psoriatic JIA.- Anti-CCP antibodies indicate a poor prognosis. - CBC: Anemia, thrombocytosis, and/or leukocytosis are seen in the case of systemic JIA. - Imaging (e.g., X-ray, ultrasound) of the affected joint - Regular ophthalmological screening using slit lamp examination for anterior uveitis Treatment:- First-line: NSAIDs; Local intra-articular steroids (e.g., triamcinolone) are indicated in the case of active arthritis.- Second-line: Disease-modifying antirheumatic drugs (DMARDs); Biologic agents; Systemic glucocorticoid therapy (oral, IV)
• Osteopetrosis Inherited, diffuse bone disease that results in increased sclerotic appearance of the skeleton on radiological examination (from Latin: "petrosus" = stony). Type I osteopetrosis (malignant osteopetrosis):- Age of onset: infancy- Clinical course: severeType II osteopetrosis (benign osteopetrosis, Albers-Schonberg disease):- Age of onset: early adulthood- Clinical course: mild Pathophysiology: impaired osteoclastic resorption of bone with preserved osteoblastic function Clinical features:- Pathological fractures- Cranial nerve disorders: as a result of hyperostosis and stenosis of the cranial nerve foramina- Pancytopenia: due to decreased bone marrow activity as a result of decreased marrow space- Hepatosplenomegaly: due to extramedullary hematopoiesis Diagnostics:- Imaging (X-ray): homogenous, marbled thickening of both cortical and trabecular bone- Laboratory findings: Hypocalcemia- ↑ Tartrate-resistant acid phosphatase (TRAP) Therapy: Bone marrow transplantation may be successful in the case of pancytopenia.
• Paget disease of bone (Osteitis deformans) A slowly progressive monostotic or polyostotic skeletal disease characterized by increased bone turnover, which causes normal lamellar bone to be replaced by weak woven bone. Epidemiology: - Second most prevalent skeletal disease after osteoporosis- Sex: ♂ > ♀ - Age of onset: > 55 years Pathophysiology: - High rate of bone remodeling- ↑ RANKL-RANK activity → ↑ NF-κB signaling → ↑ osteoclast activity → ↑ osteoblast activity → formation of disorganized (woven) bone1. Lytic phase2. Mixed lytic and blastic phase3. Sclerotic phase Clinical features: - Approximately 70-90% of cases are asymptomatic. - Bone pain, which may be associated with erythema and elevated skin temperature over the affected bones- Bony deformities; e.g., bowing of legs (saber shin; also seen in congenital syphilis and severe rickets)- Skull involvement (in ∼ 40% of cases)→ Skull enlargement (increasing hat size)→ Cranial nerve deficits→ Impaired hearing→ Headache- Pathological fractures: Chalk-stick fractures of long bones Diagnostics:- Normal calcium, phosphate, and parathyroid hormone (PTH) levels- ↑↑ Serum alkaline phosphatase (ALP)- ↑ Markers of collagen degradation (in urine): deoxypyridinoline, N-telopeptide, C-telopeptide, hydroxyproline- Conventional x-ray: → Deformed bones with both sclerotic and osteolytic lesions→ Thickened cortical bone→ Coarsened trabeculae; expansion or enlargement of a region of the bone.→ Skull x-ray: thickening of the diploe; osteoporosis circumscripta (cotton wool appearance).→ Vertebral x-ray: thickening of the upper and lower plates of the vertebral body gives rise to a “picture frame” appearance; diffuse enlargement of the vertebrae (ivory vertebra)→ Pelvic x-ray: disruption/fusion of sacroiliac joints; thickened iliopectineal line (brim sign)- Bone scan: focal increase in uptake of 99TcPaget disease should be considered in an asymptomatic patient who presents with isolated ALP elevation that cannot be explained by any other means (e.g., cholestasis or bone metastases)! Treatment:- First-line: bisphosphonates (induce apoptosis of osteoclasts)- Second-line: calcitonin therapy - Supportive therapy: Vitamin D3 (cholecalciferol) and calcium- NSAIDs may be used in addition to bisphosphonates to treat pain Complications:- High-output heart failure- Osteosarcoma
• Popliteal (Baker) cyst Swelling in the popliteal fossa between the medial head of the gastrocnemius muscle and the semimembranosus muscle that contains synovial fluid Risk factors:- Trauma (e.g., meniscal tear)- Underlying joint disease (e.g., osteoarthritis, rheumatoid arthritis) Clinical features:- Asymptomatic bulge behind knee that diminishes with flexion- Posterior knee pain, swelling, stiffness Complications:- Venous compression (leg/ankle swelling)- Dissection into calf (erythema, edema, positive Hoan sign)- Cyst rupture (acute calf pain, warmth, erythema, ecchymosis) Treatment:- Asymptomatic cysts do not require treatment. The majority resolve spontaneously.- Symptomatic cysts:→ Treat underlying pathology of the knee joint→ If symptoms persist, intra-articular injection of glucocorticoids can control inflammation→ Surgical resection for symptomatic cysts that persist despite treatment
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• Indications for imaging in low back pain X-ray:- Osteoporosis/compression fracture- Suspected malignancy- Ankylosing spondylitis (eg, insidious onset, nocturnal pain, better with movement) MRI:- Sensory/motor deficits- Cauda equina syndrome (eg, urine retention, saddle anesthesia)- Suspected epidural abscess/infection (eg, fever, intravenous drug abuse, concurrent infection, hemodialysis) Radionuclide bone scan or CT scan:- Indications for, but patient not able to have, MRI
• Osteogenesis imperfecta Rare, autosomal dominant mutation in COL1A1 or COL1A2 genes; decreased formation of hydrogen and disulfide bonds between type 1 preprocollagen molecules → decreased triple helix formation → defective type I collagen synthesis → impaired bone matrix formation (osteogenesis) Clinical features:- Growth retardation- Skeletal deformities, brittle bones, and recurrent fractures from minimal trauma- Blue sclerae- Progressive hearing loss- Loose joints- Brittle, opalescent teeth- Type II: most severe form; lethal perinatally or within the first year→ Multiple fractures, short femur, hypoplastic thoracic cavity, fetal growth restriction Diagnostics:- DNA test- Ultrasound before birth and radiographic skeletal survey afterwards (fractures, callus, deformities)- Bone or skin biopsy to examine collagen Therapy:- IV bisphosphonates to increase cortical thickness- Surgery for functional improvement
• Langerhans cell histiocytosis A rare disorder caused by clonal proliferation of Langerhans cells (antigen-presenting cells) Peak incidence: 5-10 years Clinical findings:- Osseous lesion (90%): pain and/or swelling→ Localization: skull (most common site), femur, vertebra, mandible, ilium, ribs→ Can cause recurrent otitis media if the mastoid bone is involved- Skin rash: brown to purple papules, eczematous rash- Hepatosplenomegaly, lymphadenopathy- Hypopituitarism that typically manifests as central diabetes insipidus Diagnostics:- X-ray: osteolytic lesions with or without marginal sclerosis- Biopsy (confirmatory test): proliferation of Langerhans cells (S100, CD1a, and/or CD207 positive polygonal cells with coffee-bean shaped nuclei, eosinophilic cytoplasm, and Birbeck granules) Treatment:- Solitary bone lesions in a low-risk anatomical region→ Asymptomatic lesion: a wait-and-watch approach may be appropriate→ Symptomatic lesion: curettage and/or excision (as a part of biopsy)- Bone lesion in a high-risk anatomical region, multifocal bone involvement, or systemic manifestation → Vinblastine and prednisone
• Joint fluid characteristics Normal: Clear, < 200 WBCs (mm3), < 25% PMNs Noninflammatory (e.g., osteoarthritis): Clear, 200-2,000 WBCs, 25% PMNs Inflammatory (e.g., crystals, rheumatoid arthritis): Translucent or opaque, 2,000-100,000 WBCs, often >50% PMNs Septic joint: Opaque, 50,000-150,000 WBCs, >80-90% PMNs
• Patellofemoral pain syndrome One of the most common causes of chronic, poorly localized anterior knee pain.- F > M Etiology:- Overuse (e.g., change in exercise habits)- Malalignment- Structural damage of the patellofemoral joint Clinical features:- Pain provoked by running, squatting, ascending/descending stairs, prolonged sitting- Atrophy or weakness of the quadriceps or hip abductors Management:- Strengthening exercise for the quadriceps and hip abductors- NSAIDs
• Insertional tendinopathies Lateral epicondylitis (tennis elbow) = Overuse injury of the hand and finger extensor tendons that originate in the alteral humeral epicondyle. Etiology: Repeated or excessive pronation/supination and extension of the wrist (eg, in racquet sports) Clinical features:- Pain and tenderness over the lateral epicondyl and along extensor muscles- Thickening of the tendons- Test: The examiner holds the patient's hand with the thumb placed over the lateral epicondlye → The patient makes a fist, supinates the forearm, deviates radially, and extends the fist against the examiner's resistance → pain over the lateral epicondyle Medial epicondylitis (golfer's elbow) = Overload injury of the hand and finger flexor tendons that originate in the medial humoral epicondyle Etiology: Repeated wrist flexion and forearm pronation (eg, while playing golf) Clinical features:- Pain over the medial epicondyle and along flexor muscles, increases with activity; thickening of the tendons- Test: Pain is elicited on asking the patient to flex the wrist against resistance, with the elbow held in extension
• Avascular necrosis of the femoral head Etiology:- Steroid use- Alcohol abuse- SLE- Antiphospholipid syndrome- Hemoglobinopathies (eg, sickle cell)- Infections (eg, osteomyelititis, HIV)- Renal transplantation- Decompression sickness- Gaucher disease Clinical features:- Groin pain on weight bearing- May radiate to the knee or ipsilateral buttock- Pain on hip abduction & internal rotation- Limited active and passive range of motion at the hip- No erythema, swelling, or point tenderness- Bilateral in 50% Lab findings: Normal WBC count, normal ESR & CRP Diagnostics:1. X-ray (best initial test)- Cystic and sclerotic changes in the femoral head- Subchondral collapse- Flattening of the femoral head- Crescent sign seen in advanced stage2. MRI (best confirmatory test) Treatment:- Reduce risk factors (smoking cessation, alcohol abstinence, reduce corticosteroid use if possible)- Conservative treatment: indicated in early stages of disease to the reduce risk of femoral head collapse→ Decreased weight bearing→ Statins and bisphosphonates- Surgery: indicated in later stages of disease when bone structure is compromised
• Charcot joint (neurogenic arthropathy) Risk factors:- Diabetic neuropathy- Other peripheral neuropathy (eg, vitamin B12 deficiency)- Spinal cord injury- Syringomyelia- Tabes dorsalis (tertiary syphilis) Pathogenesis:- Impaired sensation & proprioception- Altered weight bearing & recurrent trauma- Acute inflammatory response Clinical features:- Acute: swelling, warmth, erythema- Chronic: painless bony deformities, midfoot collapse, osteolysis, risk of fractures- X-ray: bone & joint destruction, fragmentation, subluxation/dislocation Treatment: Mechanical offloading & correction of joint mechanics (eg, casting, orthotics)
• Common causes of myopathy Connective tissue diseases:- Polymyositis/dermatomyositis- Inclusion body myositis- Vasculitis- Overlap syndrome (mixed connective tissue disease) Endocrine/metabolic:- Hypothyroidism, thyrotoxicosis- Cushing syndrome- Electrolytes (↓ potassium, calcium, phosphorus) Drugs/toxins:- Corticosteroids, statins- Zidovudine, colchicine- Alcohol, cocaine, heroin Miscellaneous: Infections, trauma, hyperthermia
• Vertebral compression fracture Etiology:- Trauma- Osteoporosis, osteomalacia- Infection (eg, osteomyelitis)- Bone metastases- Metabolic (eg, hyperparathyroidism)- Paget disease Clinical features:- Chronic/gradual VCF: Painless, progressive kyphosis, loss of stature- Low back pain & decreased spinal mobility- Pain increasing with standing, walking, lying on back- Tenderness at affected level Complications:- Increased risk for future fractures- Hyperkyphosis, possibly leading to protuberant abdomen, early satiety, weight loss, decreased respiratory capacity
• Scleroderma renal crisis - Occurs in 10-15% of cases of diffuse scleroderma. Life-threatening condition with:- Oliguric renal failure- Malignant hypertension- Encephalopathy- Microangiopathic hemolytic anemia
• Felty syndrome Severe type of seropositive rheumatoid arthritis. Clinical features:- Triad 1. Arthritis2. Splenomegaly3. Neutropenia (↑ risk of recurrent bacterial infections)- Skin ulcers of the lower limbs - Hepatomegaly- Fever- Chest pain (indicating pleuritis or pericarditis)- Associated with increased risk of developing non-Hodgkin lymphoma Diagnostics:- Leukopenia with selective neutropenia- ↑↑ RF- ↑↑ ACPA (Anti-citrullinated peptide antibodies) Treatment:- DMARD: methotrexate- Alternative: cyclophosphamide
• Management of low back pain Acute pain:- Maintain moderate activity- NSAIDs or acetaminophen- Consider: muscle relaxants, spinal manipulation, brief course of opioids Chronic pain:- Intermittent use of NSAIDs or acetaminophen- Exercise therapy (stretching/strengthening, aerobic)- Consider: TCAs, duloxetine
• Morton neuroma Sudden, shooting pain or numbness on the plantar side of the foot between the 3rd and 4th metatarsal Affected areas are innervated by the common plantar digital nerves (of the medial and lateral plantar nerves of the tibial nerve) Mulder sign1. The forefoot is held firmly with one hand in the medial-lateral direction.2. Pressure is applied to the sole of the foot between the metatarsal heads (at the location of symptoms).3. If pain is perceived (especially on the plantar side), it indicates Morton neuroma. This maneuver may also produce a “click” or snapping sensation, which is known as Mulder's click.
• Stress fracture Complete bone fracture caused by repetitive stress without underlying bone pathology or disease affecting the bone Etiology: Increased load or frequency of physical activity can facilitate bone resorption. Risk factors:- Repetitive high intensity physical activity- Improper technique during physical activity- Caloric restriction, especially in patients with anorexia nervosa- Decreased bone density (e.g., bisphosphonate use)- Calcium deficiencies- Female sex Clinical features:- Most common in the lower extremities (metatarsals, also the tibia, fibula, and navicular bones); less common in the upper extremities (humerus, scapula, ribs)- Acute pain with activity (worsens with loading or stress, relieved with rest)- Bone tenderness, erythema, or soft tissue swelling Diagnosis:- Clinical diagnosis- Conventional x-rays can appear normal in the first 2-3 weeks. - MRI for definitive diagnosis: detects fracture line, surrounding tissue damage, and edema Treatment:- Pain control: acetaminophen, ice packs - Rest, physical therapy, and risk factor modification (improved nutrition, calcium, and vitamin D supplementation)
• Rotator cuff impingement Clinical syndrome caused by compression of tissues around the glenohumeral joint (e.g., rotator cuff tendons, subacromial bursa) when the shoulder is elevated. It is a spectrum of clinical findings, and can eventually result in complete rotator cuff tear. Clinical features:- Pain on movement which is worsened by overhead activities.- Subacromial tenderness- Most common symptoms are due to supraspinatus injury or subacromial bursitis→ Painful arc → pain-related restriction of movement and strength with abduction of the arm between 60-120°- Positive impingement tests (eg, Neer, Hawkins) Can progress to rotator cuff tendinitis and rotator cuff tear
• Frozen shoulder (adhesive capsulitis) Inflammation and fibrosis of the joint capsule leading to contracture of the shoulder joint Clinical features:- Severe restriction of both active and passive range of movement of the glenohumeral joint in all planes (especially external rotation)- Dull shoulder pain Self-limiting course; however, improvement may take more than a year
• Rotator cuff tear Etiology:- Chronic degenerative tear seen in older adults (> 50 years)- Acute injury seen mostly in athletes- Inflammatory: complication of rotator cuff tendinitis Clinical features:- Most commonly affects the supraspinatus tendon- Acute ruptures: acute severe pain and loss of strength- Degenerative ruptures: chronic pain; loss of strength less pronounced- Restriction of ROM (depending on which muscle is involved)- Drop arm test: Patient's arm is abducted above the head and patient is asked to lower the arm slowly. With a complete tear, the patient will be unable to lower the arm smoothly and it will drop rapidly around mid-descent Diagnostics:- Clinical examination - X-ray: superior displacement of the humeral head (high-riding humeral head)- Ultrasound and then possibly MRI to evaluate the extent and location of the rupture Treatment:- Treatment of degenerative rupture, especially in elderly, inactive patients, can be conservative - Surgical repair of the rotator cuff is recommended in cases of traumatic rupture, especially in physically active patients, or treatment-refractory cases.
• Biceps tendinitis Tendinitis, tenosynovitis, or tendinosis of the proximal long head of the biceps tendon at its insertion on the glenoid Clinical features:- Anterior shoulder pain that becomes worse with lifting- Tenderness along the anterior humerus- Weakness less common Complications: biceps tendon tear or rupture
• Achondroplasia Etiology:- Activating mutation in fibroblast growth factor receptor 3 gene (FGFR3) → inhibited chondrocyte proliferation → reduced endochondral ossification- New mutations in ∼ 80% of cases; autosomal dominant inheritance in ∼ 20% of cases (homozygosity is lethal) Epidemiology:- Most common type of skeletal dysplasia and disproportionate short stature (1:40,000 children worldwide affected)- The probability of new mutations increases with the father's age at the time of conception. Clinical features:- Average standing height of 4'4″ (131 cm) in males or 4'1″ (124 cm) in females- Average-sized torso; short, plump extremities- Macrocephaly, prominent brow, midface retrusion, flattening of the nose- Normal intelligence Diagnostics: X-ray- Lateral skull: midface hypoplasia, frontal prominence- Spine: abnormally narrow interpedicular distance → spinal canal stenosis; scoliosis- Extremities: bones are short and broad; short fingers Treatment:- Early administration of growth hormone (1-6 years)- Surgical corrections: spinal stenosis, secondary scoliosis, genu varum, foramen magnum decompression

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