Which оf the fоllоwing would be considered а severe reаction to contrаst media?
Eоsinоphilic Esоphаgitis (EoE) 1. Bаckground Definition: Chronic, immune-mediаted inflammation of the esophagus characterized by ≥15 eosinophils per high-power field on biopsy. Pathophysiology: Triggered by food or environmental allergens causing Th2-driven eosinophilic infiltration, fibrosis, and stricture formation. Epidemiology: Increasing prevalence; most common in young to middle-aged men and individuals with atopic conditions (asthma, eczema, allergic rhinitis). Key associations: Atopy, food allergies (milk, egg, soy, wheat, nuts, seafood). 2. History Symptoms: Solid-food dysphagia, food impaction, chest pain or heartburn refractory to PPIs. Children: Feeding difficulty, vomiting, or failure to thrive. Risk factors: Personal/family atopy, male sex, chronic GERD-like symptoms unresponsive to therapy. 3. Exam Findings Physical exam: Usually normal; may see skin or nasal signs of allergy. Endoscopy findings: Concentric rings (“trachealization”) Linear furrows White exudates or plaques Fragile, narrowed lumen 4. Making the Diagnosis Gold standard: Upper endoscopy with biopsy showing ≥15 eosinophils/HPF. Note: Diagnosis requires persistence of eosinophilia after an adequate PPI trial to exclude PPI-responsive esophageal eosinophilia. Other testing: Allergy evaluation may help identify food triggers but is not required for diagnosis. 5. Management A. Lifestyle/Diet Eliminate common food allergens (empiric 6-food elimination: milk, egg, soy, wheat, nuts, seafood). Consider dietitian referral. B. Medication First line: Topical corticosteroids (swallowed fluticasone or budesonide). PPIs may reduce inflammation in some cases. C. Procedures Endoscopic dilation for fixed strictures causing significant dysphagia. Repeat endoscopy to assess response if symptoms persist. Question A 25-year-old man with a history of asthma and seasonal allergies presents with several months of intermittent solid-food dysphagia and two recent episodes of food impaction. He reports no odynophagia, weight loss, or hematemesis. A trial of omeprazole for 8 weeks provided no relief. Upper endoscopy reveals concentric rings and linear furrows in the mid-esophagus. Biopsies show 25 eosinophils per high-power field. Which of the following is the most appropriate initial treatment for this patient’s condition?
Hepаtitis B Virus (HBV) 1. Bаckgrоund Definitiоn: A DNA virus (Hepаdnaviridae family) that infects hepatоcytes, leading to acute or chronic hepatitis. Transmission: Parenteral: Needle sticks, transfusions, IV drug use. Sexual: Unprotected intercourse, especially MSM. Perinatal: Mother-to-child during birth (most common global route). Virology: Partially double-stranded DNA virus; replicates via reverse transcription. Surface antigen (HBsAg), core antigen (HBcAg), and e antigen (HBeAg) are key serologic markers. Epidemiology: Worldwide prevalence ~250 million chronic carriers. High endemicity in Asia and sub-Saharan Africa. In the U.S., declining due to universal vaccination. 2. History Acute infection: Incubation: 6 weeks to 6 months. Symptoms: Fatigue, malaise, anorexia, nausea, RUQ pain, jaundice, dark urine, clay-colored stool. May be subclinical in many adults. Chronic infection: Persistent infection >6 months. Often asymptomatic initially; may progress to cirrhosis or hepatocellular carcinoma (HCC). Risk factors: Unvaccinated individuals, multiple sexual partners, IV drug use, healthcare workers, infants of infected mothers. 3. Exam Findings Acute infection: Jaundice, hepatomegaly, RUQ tenderness. Chronic infection: Spider angiomas, palmar erythema, ascites, hepatosplenomegaly (signs of cirrhosis). Fulminant hepatitis (rare): Encephalopathy, coagulopathy, asterixis. 4. Making the Diagnosis A. Serologic Markers Marker Meaning HBsAg Active infection (acute or chronic) Anti-HBs Immunity (recovery or vaccination) Anti-HBc IgM Acute or recent infection Anti-HBc IgG Past or chronic infection HBeAg Active viral replication, high infectivity Anti-HBe Declining replication, lower infectivity HBV DNA Quantifies viral load; monitors treatment response B. Interpretation Examples Serology Pattern Interpretation HBsAg (+), Anti-HBc IgM (+), HBeAg (+) Acute infection HBsAg (+), Anti-HBc IgG (+), HBeAg (+ or -)** >6 mo** Chronic infection Anti-HBs (+) only Vaccinated Anti-HBs (+), Anti-HBc IgG (+) Recovered (immune after infection) C. Additional Testing LFTs: Elevated AST/ALT (ALT > AST). HBV DNA PCR: Quantifies viral load for treatment decisions. Ultrasound / AFP: Surveillance for HCC in chronic carriers. 5. Management A. Acute Hepatitis B Usually supportive (hydration, rest, avoid alcohol and hepatotoxic meds). Antivirals not routinely indicated unless severe or fulminant disease. >95% of immunocompetent adults recover spontaneously. B. Chronic Hepatitis B Goal: Suppress viral replication and prevent cirrhosis/HCC. Indications for antiviral therapy: Elevated ALT with HBV DNA >2,000 IU/mL. Evidence of liver damage or cirrhosis. Preferred agents: Tenofovir, entecavir (first-line). Monitor: ALT, HBV DNA, HBeAg, and AFP every 6–12 months. C. Prevention Vaccine: Recombinant HBsAg vaccine (3 doses at 0, 1, 6 months). Postexposure prophylaxis: Unvaccinated exposure: HBV vaccine + hepatitis B immune globulin (HBIG) within 24 hours. Newborn of infected mother: HBIG + vaccine at birth. Screening: Pregnant women, high-risk groups, and all blood donors. Question A 26-year-old man presents for evaluation after recovering from fatigue, nausea, and jaundice that developed six weeks ago. His symptoms have resolved, but laboratory testing is repeated to assess his hepatitis B status. The following serologic results are obtained: HBsAg: negative Anti-HBs: negative Anti-HBc IgM: positive Which of the following best explains this serologic pattern?