This is a real-world medical entrance exam question, please give the true answer based on the question and selection. Topic name: None, Subject name: Pathology
[{'content': 'Biopsy of the parotid gland in Sjogren’s shows: \nSelect and explain. \nA. Neutrophils, B. Eosinophils, C. Basophils, D. Lymphocytes', 'role': 'user'}, {'content': 'Answer: D \nExplanation: "The earliest histologic finding in both the major and the minor salivary glands is periductal and\xa0perivascular lymphocytic infiltration." (Ref: Robbins)\nSjogren Syndrome\n\nIt is an immune-mediated destruction of the lacrimal and salivary glands characterized by dry eyes\xa0{keratoconjunctivitis sicca) and dry mouth (xerostomia)\nIt occurs as an isolated disorder (primary form), also known as the sicca syndrome, or more often in\xa0association with another autoimmune disease (secondary form).\nAssociated diseases\nRheumatoid Arthritis (Me)\nSLE\nPolymyositis\nSystemic sclerosis\nVasculitis\nThyroiditis\nThe ductal epithelial cells of the exocrine glands are the primary target for autoantibodies.\nThere is also systemic B-cell hyperactivity, as evidenced by the presence of ANAs and RF.\nAutoantibodies to the RNP antigens SS-A (Ro) and SS-B (La) (also present in SLE)\nOther secretory glands like nasopharynx, upper airway, and vagina, may also be involved\nInvolved tissues show an intense lymphocyte (primarily activated CD4+ T cells) and plasma cell\xa0infiltrate.\nLacrimal gland destruction results in a lack of tears, leading to drying of the corneal epithelium, with\xa0subsequent inflammation, erosion, and ulceration (keratoconjunctivitis).\nSimilar changes may occur in the oral mucosa as a result of the loss of salivary gland output, giving rise to\xa0mucosal atrophy, with inflammatory Assuring and ulceration (xerostomia).\nDryness and crusting of the nose may lead to ulcerations and even perforation of the nasal septum.\nWhen the respiratory passages are involved, secondary laryngitis, bronchitis, and pneumonitis may\xa0appear.\nApproximately 25% of the patients (especially those with anti-SS-A antibodies) develop extra-glandular\xa0disease affecting the CNS, skin, kidneys, and muscles.\nRenal lesions take the form of mild interstitial nephritis associated with tubular transport defects: Unlike\xa0in SLE. glomerulonephritis is rare.\n90%\xa0of cases occur in women between 35 and 45 years\nExtraglandular manifestations include synovitis, pulmonary fibrosis, and peripheral neuropathy.\nThere is a 40-fold increased risk of developing non-Hodgkin B-cell lymphoma.', 'role': 'assistant'}]