Hypothyroidism (Study Outline) For study only—this is not me…
Questions
Hypоthyrоidism (Study Outline) Fоr study only—this is not medicаl аdvice or а substitute for professional care. 1. Background Definition:A clinical syndrome resulting from deficient production of thyroid hormones (T₄ and T₃) or impaired action at the tissue level. Pathophysiology: Primary hypothyroidism (most common): failure of the thyroid gland → ↑ TSH, ↓ free T₄. Secondary (central): pituitary dysfunction → ↓ TSH and ↓ T₄. Tertiary: hypothalamic failure (↓ TRH). Common Causes (Primary): Autoimmune (Hashimoto thyroiditis) – most common in the U.S. Iatrogenic: post-thyroidectomy, radioactive iodine, or antithyroid medications. Iodine deficiency or excess. Congenital hypothyroidism (thyroid dysgenesis, enzyme defects). Drugs: lithium, amiodarone, interferon-α, tyrosine kinase inhibitors. Epidemiology: More common in women and older adults. Hashimoto’s thyroiditis often associated with other autoimmune disorders (e.g., type 1 DM, pernicious anemia). 2. History Symptoms (Gradual Onset): Fatigue, weakness, cold intolerance. Weight gain despite decreased appetite. Constipation. Dry skin, hair loss, brittle nails. Depression, memory impairment, slowed thinking. Menstrual irregularities, infertility. Severe Forms: Myxedema: severe, long-standing hypothyroidism → nonpitting edema, facial puffiness, hoarseness, periorbital swelling. Myxedema coma: life-threatening decompensation with hypothermia, bradycardia, hypotension, and hypoventilation (precipitated by illness or sedatives). Historical Clues: Prior thyroid surgery or radioactive iodine therapy. Family history of autoimmune disease. Recent medication changes (e.g., lithium, amiodarone). 3. Exam Findings General: Fatigued appearance, weight gain, coarse dry hair, pallor. Skin: Cool, dry, thickened skin; nonpitting edema (myxedema). Cardiovascular: Bradycardia, diastolic hypertension, pericardial effusion (severe). Neurologic: Delayed relaxation of deep tendon reflexes (especially Achilles). HEENT: Puffy face, periorbital edema, enlarged or atrophic thyroid. Other: Macroglossia, hoarseness, carpal tunnel syndrome. Pediatric Findings: Growth retardation, delayed bone age, developmental delay if congenital. 4. Making the Diagnosis Initial Test (Gold Standard): Serum TSH — most sensitive screening test. Interpretation: Primary hypothyroidism: ↑ TSH, ↓ free T₄. Secondary (pituitary): ↓ or inappropriately normal TSH, ↓ free T₄. Subclinical hypothyroidism: mildly ↑ TSH with normal free T₄. Autoimmune Confirmation: Positive anti-thyroid peroxidase (anti-TPO) or anti-thyroglobulin antibodies → Hashimoto thyroiditis. Other Findings: Lipid abnormalities: hypercholesterolemia, ↑ LDL. Hyponatremia: due to decreased free water clearance. Anemia: normocytic or macrocytic. Imaging: Thyroid ultrasound: heterogenous or atrophic gland (Hashimoto). MRI of pituitary: indicated if secondary hypothyroidism suspected. 5. Management (Exam Concepts) (Conceptual overview only—no dosing or treatment directives.) General Principles: Thyroid hormone replacement (e.g., levothyroxine) is standard. Primary hypothyroidism: lifelong replacement and regular TSH monitoring. Secondary hypothyroidism: monitor free T₄, not TSH, for adjustment. Special Situations (Conceptual): Myxedema coma: medical emergency—requires ICU care and supportive management. Pregnancy: increased thyroid hormone requirement; check TSH each trimester. Exam Tip: Drug-induced hypothyroidism → lithium, amiodarone. Most sensitive test: serum TSH. Hashimoto thyroiditis: firm, irregular, painless goiter + positive anti-TPO antibodies. Monitoring: Reassess TSH every 6–8 weeks after dose adjustment. Evaluate for improvement in symptoms, energy, and metabolic parameters. QUESTION A 45-year-old woman presents with fatigue, weight gain, and constipation. Physical exam shows dry skin, bradycardia, and delayed relaxation of deep tendon reflexes. Laboratory results reveal TSH 9.8 mIU/L (elevated) and free T₄ below normal. Which of the following additional findings is most likely? A. Elevated anti-thyroid peroxidase (anti-TPO) antibodiesB. Elevated free T₃ and suppressed TSHC. Elevated serum calcium and decreased phosphateD. Decreased LDL cholesterol
Hemоrrhоids 1. Bаckgrоund Definition: Dilаted аnd symptomatic venous cushions of the hemorrhoidal plexus in the anal canal. Anatomy: Internal hemorrhoids: Above the dentate line; covered by columnar mucosa; visceral innervation → painless. External hemorrhoids: Below the dentate line; covered by squamous epithelium; somatic innervation → painful when thrombosed. Pathophysiology: Increased venous pressure from straining, constipation, prolonged sitting, pregnancy, portal hypertension, or obesity causes engorgement and prolapse of venous plexus. Epidemiology: Common in adults 45–65 years; prevalence rises with age and constipation. 2. History Internal hemorrhoids: Painless bright red rectal bleeding (on toilet paper or dripping after defecation). Mucosal prolapse or soiling in advanced grades. External hemorrhoids: Painful perianal lump (thrombosis) with acute onset after straining or prolonged sitting. May have pruritus or swelling but typically no bleeding unless ulcerated. Risk factors: Chronic constipation, prolonged sitting, low-fiber diet, pregnancy, portal hypertension, or frequent heavy lifting. 3. Exam Findings Inspection: External: Visible bluish perianal mass if thrombosed. Internal: Not always visible unless prolapsed (use anoscopy). Digital rectal exam: May reveal soft compressible masses or exclude other causes (fissure, abscess, tumor). Anoscopy: Confirms diagnosis and grades internal hemorrhoids: Grade I: No prolapse, bleeds only Grade II: Prolapse with straining, reduces spontaneously Grade III: Prolapse requires manual reduction Grade IV: Irreducible, may thrombose or ulcerate 4. Making the Diagnosis Clinical diagnosis: Based on history and physical exam (inspection, DRE, anoscopy). Exclude other causes of bleeding: Colonoscopy indicated in: Age ≥45 or risk factors for colorectal cancer Iron-deficiency anemia or melena Atypical bleeding (dark stool, mixed blood, systemic symptoms) Laboratory: CBC if chronic bleeding suspected. 5. Management A. Conservative (First-line for most) Dietary fiber supplementation and increased fluids. Avoid prolonged straining; use stool softeners (docusate). Topical therapies: Witch hazel, hydrocortisone, or anesthetic creams for short-term relief. Sitz baths for comfort. B. Office Procedures (Persistent Grade I–III) Rubber band ligation (most effective for internal hemorrhoids). Sclerotherapy or infrared coagulation if not surgical candidates. C. Surgical Management Excisional hemorrhoidectomy: For large Grade III–IV internal hemorrhoids or recurrent thrombosed external hemorrhoids. Thrombosed external hemorrhoid: Excision within 72 hours provides rapid pain relief. D. Prevention High-fiber diet, hydration, prompt defecation, and avoidance of prolonged sitting or straining. Question A 42-year-old man presents with severe anal pain that began suddenly after straining during a bowel movement this morning. He reports mild swelling but no rectal bleeding. Physical examination reveals a tender, bluish perianal nodule below the dentate line. Which of the following is the most appropriate management?
Lаctоse Intоlerаnce 1. Bаckgrоund Definition: Inability to digest lactose, the main carbohydrate in milk and dairy products, due to lactase enzyme deficiency in the brush border of the small intestine. Pathophysiology: Undigested lactose remains in the intestinal lumen → osmotic diarrhea and bacterial fermentation → gas, bloating, and cramping. Types: Primary (genetic): Gradual loss of lactase after childhood (most common worldwide). Secondary (acquired): Due to mucosal injury (celiac disease, gastroenteritis, Crohn disease). Congenital: Rare, autosomal recessive, presents in infancy. Epidemiology: Very common globally; affects up to 90% of Asian, African, and Native American populations; less common in Northern Europeans. 2. History Symptoms: Bloating, flatulence, crampy abdominal pain, and watery diarrhea after ingestion of milk or dairy products. Symptoms occur 30 minutes to 2 hours after lactose ingestion. Risk factors: Increasing age, certain ethnic backgrounds, recent intestinal infection, or small bowel disease. Relief: Avoidance of dairy eliminates symptoms. 3. Exam Findings Usually benign; may show mild abdominal distension or hyperactive bowel sounds. Signs of dehydration if diarrhea severe. Otherwise normal physical exam. 4. Making the Diagnosis Gold standard: Hydrogen breath test — elevated breath hydrogen after lactose load indicates malabsorption. Common alternative: Lactose elimination and re-challenge — symptom resolution after lactose avoidance confirms diagnosis. Supportive tests: Stool acidity test (infants): Low stool pH due to fermentation. Small bowel biopsy: Rarely needed; shows decreased lactase activity (used to rule out secondary causes). 5. Management A. Dietary Lactose restriction or use of lactose-free dairy products. Many patients tolerate small amounts of milk with meals. B. Supplements Lactase enzyme replacement before dairy intake (e.g., Lactaid). Calcium and vitamin D supplementation to prevent deficiency in those avoiding dairy. C. Treat underlying cause (if secondary) Address intestinal mucosal disease (e.g., celiac disease, Crohn disease, gastroenteritis recovery). A 23-year-old woman reports several months of bloating, flatulence, and crampy abdominal pain that occur about 1 hour after drinking milk or eating ice cream. She denies fever, weight loss, or blood in her stool. Physical examination is normal. Which of the following is the most appropriate diagnostic test to confirm lactose intolerance?
Alcоhоl-Assоciаted Liver Diseаse (ALD) 1. Bаckground Definition: Spectrum of liver injury due to chronic alcohol use — fatty liver → alcoholic hepatitis → cirrhosis. Pathophysiology: Alcohol → ↑NADH/NAD⁺ ratio → impaired fatty acid oxidation → steatosis. Acetaldehyde causes oxidative stress, mitochondrial injury, and inflammation. Chronic exposure leads to fibrosis and portal hypertension. Epidemiology: Second most common cause of cirrhosis in the U.S. Risk rises with intake >40–60 g/day in men, >20–40 g/day in women. Synergistic injury with obesity or viral hepatitis. 2. History Symptoms: Early: fatigue, anorexia, nausea, or vague RUQ pain. Advanced: jaundice, pruritus, edema, abdominal distension, confusion (encephalopathy). Risk factors: Long-term heavy alcohol use, poor nutrition (especially folate, thiamine). Coexistent hepatitis C or metabolic syndrome accelerates damage. Alcohol timeline: Steatosis can appear after weeks of heavy intake; hepatitis requires sustained use; cirrhosis follows years of abuse. 3. Exam Findings General: Fever (alcoholic hepatitis), cachexia, jaundice. Skin: Spider angiomas, palmar erythema, ecchymoses. Abdomen: Hepatomegaly (early), splenomegaly, ascites, caput medusae. Neurologic: Asterixis, confusion, tremor (encephalopathy). Endocrine: Gynecomastia, testicular atrophy, menstrual irregularities. 4. Diagnosis A. Laboratory Findings Stage Typical Findings Steatosis Mild ↑AST/ALT (2 : 1 (values 100 fL) common due to folate deficiency. AST > ALT hallmark due to mitochondrial damage. B. Imaging Ultrasound: Fatty infiltration, nodular liver, splenomegaly, ascites. Elastography: Estimates fibrosis. CT/MRI: Excludes alternate causes or HCC. C. Severity Scoring (Alcoholic Hepatitis) Maddrey Discriminant Function (MDF): ≥32 → severe disease. MELD or Lille score guide prognosis and treatment response. D. Differential Diagnosis Viral hepatitis, drug-induced injury, hemochromatosis, MAFLD, autoimmune hepatitis. 5. Management A. Alcohol Cessation (Essential) Abstinence halts progression and can reverse steatosis. Refer to counseling, behavioral therapy, and pharmacologic support (acamprosate, naltrexone, disulfiram). B. Nutritional Support High-protein, high-calorie diet; supplement thiamine, folate, and zinc. Correct electrolyte abnormalities. C. Specific Therapy (Alcoholic Hepatitis) Corticosteroids (prednisolone 40 mg/day × 28 days) if MDF ≥ 32 or MELD ≥ 20 and no infection. Pentoxifylline if steroids contraindicated. Treat concurrent infections before starting steroids. D. Cirrhosis Management Complication Key Treatment Ascites Sodium restriction, spironolactone ± furosemide, paracentesis Varices Nonselective β-blockers, endoscopic band ligation Encephalopathy Lactulose ± rifaximin HCC screening Ultrasound ± AFP every 6 months E. Advanced Disease Liver transplant for end-stage cirrhosis; many centers require ≥6 months sobriety. F. Prevention Routine screening for alcohol misuse. Vaccinate against HAV and HBV. Address comorbid obesity, diabetes, and viral hepatitis. A 54-year-old man presents with two weeks of fatigue, jaundice, and right upper quadrant discomfort. He drinks approximately six beers daily and has done so for 20 years. Laboratory results: Test Result Reference Range AST 180 U/L (10–40 U/L) ALT 75 U/L (7–56 U/L) Alkaline phosphatase 130 U/L (44–147 U/L) Total bilirubin 4.2 mg/dL (0.2–1.2 mg/dL) INR 1.8 (0.8–1.2) MCV 104 fL (80–96 fL) Which of the following findings is most characteristic of this patient’s condition?
Mesenteric Ischemiа 1. Bаckgrоund Definitiоn: Intestinаl hypоperfusion leading to ischemia and necrosis of the bowel wall; can be acute or chronic. Pathophysiology: Acute mesenteric ischemia (AMI): Sudden loss of blood flow to small intestine. Causes: Arterial embolism (most common; often from atrial fibrillation or MI). Arterial thrombosis (atherosclerotic plaque). Venous thrombosis (hypercoagulable states). Nonocclusive ischemia (low flow states—shock, vasopressors). Chronic mesenteric ischemia (CMI): Atherosclerotic narrowing of mesenteric arteries leading to postprandial pain (“intestinal angina”) and weight loss. Epidemiology: AMI is uncommon but carries high mortality (~60%). CMI seen in older adults with diffuse atherosclerosis. 2. History Acute: Severe, sudden-onset abdominal pain that is disproportionate to physical findings. Nausea, vomiting, diarrhea, or occult GI bleeding. May have atrial fibrillation, recent MI, or heart failure. Chronic: Recurrent, dull epigastric pain occurring 30–60 minutes after meals. Fear of eating → weight loss. Risk factors: Embolic disease (A-fib, valvular disease). Atherosclerosis (coronary, carotid, peripheral). Hypotension, dehydration, hypercoagulable disorders. 3. Exam Findings Acute: Abdomen may be soft or mildly tender early, with pain out of proportion to findings. Later: peritonitis (guarding, rebound) if infarction occurs. Possible tachycardia, hypotension, or signs of shock. Chronic: Bruit over epigastrium or abdomen. Weight loss, signs of malnutrition. 4. Making the Diagnosis Gold standard: CT angiography (CTA) — best initial and confirmatory test; shows arterial occlusion, bowel wall thickening, or pneumatosis intestinalis. Laboratory clues: Elevated lactate (due to anaerobic metabolism). Leukocytosis, metabolic acidosis. Other modalities: Mesenteric angiography (definitive but invasive). Duplex ultrasound for chronic disease (shows stenosis). Plain X-ray: May show thumbprinting or pneumatosis intestinalis (late finding). 5. Management A. Acute Mesenteric Ischemia Immediate resuscitation: IV fluids, broad-spectrum antibiotics, bowel rest, and correction of arrhythmia or hypotension. Definitive treatment: Embolic: Emergent surgical embolectomy or endovascular thrombolysis/stenting. Thrombotic: Surgical revascularization or bypass. Nonocclusive: Treat underlying shock; reduce vasopressors. Necrotic bowel: Resection required. B. Chronic Mesenteric Ischemia Definitive: Endovascular angioplasty/stenting or surgical bypass of affected vessels. Supportive: Risk factor modification (stop smoking, control lipids, manage atherosclerosis). Question A 72-year-old man with a history of atrial fibrillation presents with sudden, severe abdominal pain that began 2 hours ago. He describes the pain as diffuse and constant. On examination, he appears uncomfortable and mildly diaphoretic. His abdomen is soft with minimal tenderness and no rebound or guarding. Laboratory results show: WBC count: 17,000/µL Lactate: 5.2 mmol/L (normal
Chоledоchоlithiаsis 1. Bаckground Definition: Presence of one or more gаllstones in the common bile duct (CBD), leading to biliary obstruction. Pathophysiology: Secondary stones (most common): Migrated from the gallbladder via the cystic duct. Primary stones: Form within the CBD due to stasis or infection. Obstruction → bile stasis → ductal dilation and ↑ pressure → potential cholangitis or pancreatitis. Epidemiology: Occurs in ~10–15% of patients with gallstones. More common in middle-aged women and in patients with a history of cholelithiasis or cholecystectomy. 2. History Symptoms: RUQ or epigastric pain (colicky or steady), often following a fatty meal. Jaundice (fluctuating or progressive). Dark urine and pale stools due to conjugated hyperbilirubinemia. Nausea and vomiting. May be asymptomatic and discovered incidentally (e.g., elevated liver enzymes). Complications: Cholangitis: Fever, jaundice, RUQ pain (Charcot triad). Gallstone pancreatitis: Epigastric pain radiating to back with elevated lipase. 3. Exam Findings RUQ tenderness or mild epigastric tenderness. Jaundice and scleral icterus (key differentiator from uncomplicated cholecystitis). Murphy sign usually negative unless concurrent cholecystitis. Fever or hypotension if cholangitis develops (Charcot triad or Reynolds pentad). 4. Making the Diagnosis A. Laboratory Findings Cholestatic pattern: ↑ ALP and GGT (disproportionate to AST/ALT). ↑ Direct (conjugated) bilirubin. Mild elevation of AST/ALT possible. If pancreatitis: Elevated amylase/lipase. B. Imaging Test Role Ultrasound (first-line) Detects gallstones and dilated CBD (>6 mm); may not visualize CBD stones directly. MRCP (magnetic resonance cholangiopancreatography) Noninvasive, highly sensitive for CBD stones. Endoscopic ultrasound (EUS) Alternative for stone detection if MRCP unavailable or indeterminate. ERCP (endoscopic retrograde cholangiopancreatography) Gold standard for diagnosis and treatment (stone extraction). Used when diagnosis is likely or confirmed. C. Distinguishing Features Condition Key Findings Cholelithiasis Stones confined to gallbladder, no jaundice or LFT elevation Cholecystitis RUQ pain + fever, normal or mildly elevated LFTs, no duct dilation Choledocholithiasis Jaundice, ↑ ALP & bilirubin, dilated CBD Cholangitis Choledocholithiasis + infection (fever, leukocytosis, Charcot triad) 5. Management A. Initial Care NPO, IV fluids, analgesia, and broad-spectrum antibiotics if infection suspected. Correct coagulopathy and fluid/electrolyte imbalances. B. Definitive Therapy ERCP with sphincterotomy and stone extraction (diagnostic and therapeutic). Laparoscopic cholecystectomy after duct clearance to prevent recurrence (unless already removed). C. Alternatives Percutaneous transhepatic cholangiography (PTC): For patients not candidates for ERCP. Intraoperative cholangiography: Detects stones during cholecystectomy. D. Complications Acute cholangitis Gallstone pancreatitis Biliary cirrhosis (from chronic obstruction) E. Prevention Removal of gallbladder if source of recurrent stones. Adequate hydration and healthy diet to reduce stone formation risk. Question A 52-year-old woman presents with right upper quadrant abdominal pain, jaundice, and nausea for the past two days. She had a laparoscopic cholecystectomy 3 years ago. Her temperature is 99.9°F (37.7°C), blood pressure 118/72 mm Hg, and pulse 88/min. Physical exam reveals scleral icterus and mild right upper quadrant tenderness without guarding. Laboratory studies: AST: 96 U/L ALT: 112 U/L ALP: 480 U/L Total bilirubin: 5.2 mg/dL (direct 4.7 mg/dL) Ultrasound shows a dilated common bile duct (9 mm) without gallbladder. Which of the following is the most appropriate next step in management?
Osteоsаrcоmа Bаckgrоund Most common primary malignant bone tumor in children and adolescents (peaks at ages 10–20 years). Associated with rapid growth and metaphyseal regions of long bones (commonly distal femur, proximal tibia, proximal humerus). Risk factors: Paget disease of bone, radiation exposure, familial syndromes (e.g., Li-Fraumeni, hereditary retinoblastoma). Symptoms Progressive localized bone pain, often worse at night and not relieved by rest. Swelling or palpable mass at the site. May present after minor trauma, which brings attention to the lesion. Physical Exam Findings Tenderness and swelling at the metaphyseal region of the affected bone. Limited range of motion if near a joint. Possible palpable firm mass fixed to bone. Making the Diagnosis X-ray: “Sunburst” periosteal reaction, Codman’s triangle (periosteal elevation). MRI: defines local extent of tumor and relationship to soft tissue. Chest CT: screens for lung metastasis (most common site). Biopsy: confirms diagnosis (malignant osteoid-producing cells). Management Neoadjuvant chemotherapy followed by surgical resection (limb-sparing surgery when possible; amputation if needed for local control). Postoperative chemotherapy to reduce recurrence. Prognosis improved significantly with multi-agent chemotherapy; 5-year survival ~60–70% in localized disease.
Clаvicle Frаctures Bаckgrоund The clavicle is the mоst cоmmonly fractured bone, especially in children and adolescents, after a fall on an outstretched hand or direct blow to the shoulder. Pathophysiology involves the disruption of the bone shaft, typically at the midshaft, where forces are concentrated. Accounts for a large percentage of pediatric fractures, typically in healthy, active children and teens. Symptoms Acute pain localized to the shoulder/clavicle. Swelling, bruising, and decreased shoulder range of motion. Sometimes a “crunch” or popping sound at the time of injury. Physical Exam Findings Visible deformity or step-off at the midshaft. Tenting of skin may suggest risk for open fracture. Tenderness over the clavicle; guarding of arm. Neurovascular exam usually normal but must be checked carefully. Making the Diagnosis Diagnosis is confirmed with plain X-ray (AP view of clavicle). Imaging may show midshaft fracture with or without displacement. Always check for pneumothorax or vascular injury in high-energy trauma. Management Lifestyle/Activity: Sling or figure-8 brace for 4–6 weeks, gradual return to activity. Procedures: Surgical fixation only if open, severely displaced, or associated with neurovascular injury. Medications: NSAIDs for pain control. Education: Encourage early ROM exercises after immobilization; watch for nonunion, especially in older teens/adults. Question A 35-year-old cyclist presents with an open midshaft clavicle fracture with exposed bone after a high-speed crash. What is the most appropriate next step in management?
Stress Frаctures Bаckgrоund Overuse injuries cаused by repetitive lоw-intensity fоrces applied over time, leading to microfractures in bone. Common sites: tibia (“shin splints”), metatarsals (2nd metatarsal “march fracture”), femur, navicular. Risk factors: sudden increase in activity, endurance sports, military training, poor footwear, female athlete triad (amenorrhea, disordered eating, osteoporosis). Symptoms Gradual onset of localized pain, worse with activity and relieved by rest. Pain returns earlier and with less activity as injury progresses. Physical Exam Findings Point tenderness directly over the fracture site. Minimal swelling or deformity (unlike acute fractures). Pain reproduced by weight-bearing or hopping on the affected limb. Making the Diagnosis X-rays often normal early; changes may not appear for weeks. Later findings: cortical lucency, periosteal reaction, callus formation. MRI or bone scan: most sensitive for early detection. Management Conservative treatment is mainstay: Activity modification/rest (“if it hurts, don’t do it”). Immobilization if needed for pain control. High-risk sites (femoral neck, navicular, 5th metatarsal) may require orthopedic referral or surgical fixation due to risk of nonunion. Address contributing factors: footwear, training errors, nutrition. QuestionAn 18-year-old female collegiate distance runner presents with 2 months of progressive shin pain that worsens with activity and is now present at rest. Exam shows focal tenderness along the mid-tibia. Radiographs are normal. She reports a recent increase in weekly mileage, low dietary calcium intake, and irregular menses. Which of the following factors most directly predisposes her to stress fracture?
Ankylоsing Spоndylitis (AS) Bаckgrоund A chronic seronegаtive spondyloаrthropathy primarily affecting the axial skeleton. Strongly associated with HLA-B27. Onset usually in young men (late teens to 30s). Part of the spondyloarthritis family (includes psoriatic arthritis, reactive arthritis, IBD-associated arthritis). Symptoms Chronic low back pain and stiffness with insidious onset. Symptoms worse in the morning and with rest, improve with activity. May also have peripheral arthritis (hips, shoulders). Extra-articular manifestations: anterior uveitis, aortic regurgitation, restrictive lung disease (due to decreased chest wall expansion). Physical Exam Findings Reduced spinal mobility and loss of lumbar lordosis. Decreased chest expansion. Positive Schober test (reduced lumbar flexion). Tenderness over sacroiliac joints. Making the Diagnosis X-ray of sacroiliac joints: sacroiliitis with erosions and sclerosis. Spine imaging: “bamboo spine” due to syndesmophyte formation. Labs: ESR/CRP elevated; RF and anti-CCP negative. Diagnosis is clinical + imaging. Management First-line: NSAIDs (indomethacin often used). Physical therapy/exercise to maintain posture and mobility. Biologic therapy (TNF inhibitors, IL-17 inhibitors) for refractory disease or axial disease not controlled with NSAIDs. Surgery (hip replacement, spinal osteotomy) for severe deformity. Monitor and treat extra-articular complications (uveitis, cardiac, pulmonary). Question A 26-year-old man presents with progressive low back pain and stiffness for the past 18 months. His symptoms are worst in the morning and improve after exercise. On exam, he has tenderness over both sacroiliac joints and limited forward flexion of the lumbar spine. Radiographs show bilateral sacroiliitis. Which of the following additional findings is most likely to be seen in this patient?