Whаt is the best single chоice tо imprоve the performаnce of the "15 second rule":
Hаshimоtо Thyrоiditis (Chronic Lymphocytic Thyroiditis) (Study Outline) For study only—this is not medicаl аdvice or a substitute for professional care. 1. Background Definition:Autoimmune destruction of the thyroid gland leading to chronic hypothyroidism.It is the most common cause of primary hypothyroidism in iodine-sufficient regions (e.g., the U.S.). Pathophysiology: Autoantibodies target thyroid antigens, primarily thyroid peroxidase (anti-TPO) and thyroglobulin (anti-Tg). Lymphocytic infiltration with formation of germinal centers leads to gradual destruction of thyroid tissue. Over time → decreased T₄/T₃ synthesis, elevated TSH, and permanent thyroid failure. Early in disease, transient thyrotoxicosis (“Hashitoxicosis”) can occur due to release of preformed thyroid hormones. Epidemiology: Most common in middle-aged women (30–60 years). Associated with other autoimmune disorders: type 1 diabetes, Addison disease, pernicious anemia, celiac disease, vitiligo. Genetic predisposition: linked to HLA-DR3 and HLA-DR5. 2. History Typical Symptoms (Gradual Onset): Fatigue, weight gain, cold intolerance. Constipation, dry skin, hair loss, brittle nails. Depression, slowed thinking, memory issues. Menstrual irregularities, infertility. Voice changes, neck fullness, dysphagia (from goiter). Early “Hashitoxicosis” Phase: Transient symptoms of hyperthyroidism (anxiety, heat intolerance, palpitations) due to hormone leakage from damaged follicles. Historical Clues: Family history of autoimmune thyroid disease. Previous thyroid enlargement (“goiter”) followed by gradual slowing of metabolism. 3. Exam Findings General: Tired appearance, weight gain, dry coarse hair and skin. Thyroid Exam: Firm, rubbery, non-tender, diffusely enlarged thyroid in early stages. May become atrophic over time due to fibrosis. Skin: Cool, pale, dry. Cardiovascular: Bradycardia, diastolic hypertension. Neurologic: Delayed relaxation of deep tendon reflexes. HEENT: Puffy face, periorbital edema, hoarse voice (from myxedema). Late Stage: Myxedema signs, macroglossia, and generalized slowing of activity. 4. Making the Diagnosis Initial Test (Gold Standard): Serum TSH — elevated (primary hypothyroidism). Confirmatory Findings: ↓ Free T₄, sometimes ↓ T₃. Positive anti-thyroid peroxidase (anti-TPO) and/or anti-thyroglobulin (anti-Tg) antibodies → diagnostic hallmark. Additional Laboratory Findings: Mild hypercholesterolemia (due to reduced LDL clearance). Normocytic or macrocytic anemia. Hyponatremia possible due to impaired free water excretion. Imaging (if indicated): Thyroid ultrasound: diffuse heterogeneity and hypoechogenicity (“moth-eaten” appearance). Fine-needle aspiration (FNA): lymphocytic infiltration, Hurthle cells (oncocytic metaplasia). Diagnostic Pattern: ↑ TSH + ↓ T₄ + positive anti-TPO antibodies = Hashimoto thyroiditis. 5. Management (Exam Concepts) (Conceptual overview only—no dosing or treatment regimens.) General Principle: Thyroid hormone replacement (levothyroxine) for symptomatic or overt hypothyroidism. Monitoring: Reassess TSH every 6–8 weeks after initiating or adjusting therapy. Once stable, check annually. Complications: Myxedema coma: life-threatening hypothyroid crisis in severe, untreated disease. Goiter enlargement may cause local compressive symptoms. Increased risk of thyroid lymphoma (especially if longstanding Hashimoto’s). Exam Tips: Firm, painless goiter + anti-TPO antibodies → classic for Hashimoto thyroiditis. Thyroiditis progression: transient thyrotoxic phase → euthyroid → permanent hypothyroid. Differentiate from subacute thyroiditis: Hashimoto is painless and chronic; subacute is painful and self-limited. QUESTION A 42-year-old woman presents with fatigue, weight gain, and cold intolerance. Physical exam reveals a firm, non-tender, diffusely enlarged thyroid gland. Laboratory results show TSH 11.2 mIU/L (elevated) and free T₄ below normal. Which of the following findings would most likely confirm the diagnosis? A. Positive thyroid-stimulating immunoglobulins (TSI)B. Positive anti–thyroid peroxidase (anti-TPO) antibodiesC. Decreased serum thyroglobulin concentrationD. Diffuse increased radioactive iodine uptake
Gigаntism (Study Outline) Fоr study оnly—this is nоt medicаl аdvice or a substitute for professional care. 1. Background Definition:Gigantism is excessive growth hormone (GH) secretion before epiphyseal plate closure in children/adolescents, leading to abnormally accelerated linear growth and tall stature.After epiphyseal fusion, the same process manifests as acromegaly. Pathophysiology: GH excess → ↑ hepatic IGF-1, promoting growth of bone, cartilage, and soft tissues. Because epiphyseal plates remain open, longitudinal bone growth increases dramatically. Excess GH/IGF-1 also causes organomegaly, metabolic dysfunction, and pituitary mass effects. Etiology: Pituitary somatotroph adenoma (most common). Rare: ectopic GHRH-producing tumors (pancreatic, bronchial). Genetic syndromes: McCune–Albright, Carney complex, MEN 1. Epidemiology: Very rare; typically presents in adolescence. 2. History Key Presentation: Rapid growth velocity above expected percentiles. Extreme height compared with peers or family norms. Associated Symptoms: Headaches, visual changes (bitemporal hemianopsia) from pituitary mass. Excessive sweating, fatigue, heat intolerance. Joint pain, rapid shoe and clothing size changes. Metabolic: weight gain, insulin resistance, possible diabetes. Reproductive: delayed puberty, menstrual irregularities. Organ/System Effects: Enlargement of hands, feet, facial features (may resemble acromegaly features). Cardiomegaly, sleep apnea. Historical Clues: Growth acceleration charted on pediatric growth curves. Symptoms of pituitary mass (headache, visual deficits). 3. Exam Findings Growth/Anthropometrics: Tall stature with accelerated growth velocity. Arm span often exceeds height. Craniofacial Features: Frontal bossing, prognathism (jaw protrusion), nasal enlargement. Spaced teeth, macroglossia. Musculoskeletal: Large hands/feet, joint laxity or pain. Neurologic: Visual field defects (classically bitemporal hemianopsia). Skin: Oily skin, acne, skin tags. Cardiovascular: Hypertension, signs of cardiomyopathy in advanced cases. 4. Making the Diagnosis Step 1 – Screening: Serum IGF-1: elevated; most reliable initial test (stable marker of GH activity). Step 2 – Confirmatory Testing: Oral glucose tolerance test (OGTT) with GH measurement: Normal response: glucose suppresses GH. Gigantism: GH fails to suppress after glucose load. Step 3 – Identify Source: MRI of the pituitary gland: Detects pituitary adenoma (micro or macroadenoma). If MRI negative → evaluate for ectopic GHRH via serum GHRH level; CT/MRI of chest/abdomen. Additional Labs: Fasting glucose/insulin (insulin resistance). Other pituitary hormones (possible compression effects). Gold Standard: Elevated IGF-1 + failure of GH suppression on OGTT + pituitary adenoma on MRI. 5. Management (Exam Concepts) (Conceptual overview only—no dosing or treatment regimens.) 1. First-Line Therapy Transsphenoidal resection of pituitary adenoma. 2. Medical Therapy Somatostatin analogs (octreotide, lanreotide) — suppress GH secretion. GH receptor antagonist (pegvisomant) — blocks IGF-1 production. Dopamine agonists (cabergoline) — used in some GH/prolactin co-secreting tumors. 3. Radiation Therapy For residual tumor or persistent disease not controlled with surgery/medications. 4. Long-Term Monitoring Serial IGF-1 measurements. Periodic pituitary imaging. Screen for cardiomyopathy, sleep apnea, and metabolic complications. QUESTION NBME-Style Practice Question A 14-year-old boy is brought to clinic for rapid growth over the past year. His height increased from the 75th to >99th percentile. He reports headaches and needing larger shoes every few months. Exam shows frontal bossing, enlarged hands, and visual field deficits. Labs reveal markedly elevated IGF-1. After an oral glucose load, GH levels remain high. Which of the following is the most appropriate next step to determine the underlying cause? A. Serum GHRH levelB. MRI of the pituitary glandC. Bone age radiographD. Abdominal CT scan
in humаns, blооd type shоws which of the following