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PA31.1-10 | Endocrine System — Practice Quiz

Practice 15 questions · Untimed · Unlimited attempts

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Q1 PA31.1 1 pt

A 45-year-old woman from a coastal iodine-deficient region presents with a painless, diffuse goiter of 3 years duration. She is euthyroid on examination. TSH is mildly elevated, T4 is low-normal. Histology shows follicles distended with colloid and flat lining cells. What is the most likely underlying mechanism of goiter formation?

A Compensatory follicular hyperplasia due to impaired T4 synthesis from iodine deficiency
B Autoimmune destruction of thyroid follicles
C Autonomous TSH-independent follicular proliferation
D Infiltration of follicles by inflammatory lymphocytes

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Q2 PA31.2 1 pt

A 28-year-old woman presents with weight loss, palpitations, heat intolerance, and exophthalmos. TSH is undetectable; free T4 and T3 are markedly elevated. Radioactive iodine uptake (RAIU) scan shows diffusely increased uptake throughout an enlarged gland. What is the most likely pathogenesis?

A TSH-secreting pituitary adenoma stimulating thyroid growth
B IgG autoantibodies (TSI) that activate the TSH receptor
C Subacute granulomatous thyroiditis releasing preformed thyroid hormone
D Autonomous hyperfunctioning nodule secreting T3/T4 independently

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Q3 PA31.3 1 pt

A 40-year-old woman presents with fatigue, weight gain, cold intolerance, constipation, and a firm, rubbery goiter. TSH is elevated; anti-TPO antibodies are strongly positive. Biopsy shows follicular atrophy, Hürthle cell (oxyphilic) metaplasia, lymphocytic infiltration, and germinal centre formation. Which of the following best characterises the underlying immune mechanism?

A Type I hypersensitivity mediated by IgE antibodies against thyroid peroxidase
B Immune complex deposition in follicular basement membranes (Type III)
C Stimulatory IgG antibodies activating the TSH receptor
D CD8+ T-cell–mediated follicular destruction and anti-TPO/anti-Tg autoantibodies

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Q4 PA31.3 1 pt

A 35-year-old woman presents with acute anterior neck pain radiating to the jaw, fever (38.8 °C), and a tender, firm thyroid. ESR is markedly elevated. She had an upper respiratory tract infection 3 weeks ago. Thyroid function shows low TSH and elevated free T4. RAIU is nearly zero. What is the most likely diagnosis?

A Hashimoto thyroiditis
B Graves disease
C De Quervain (subacute granulomatous) thyroiditis
D Riedel thyroiditis

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Q5 PA31.4 1 pt

A 32-year-old woman undergoes hemithyroidectomy for a 2.5 cm solitary thyroid nodule. Histology shows follicular cells with enlarged, ground-glass (Orphan Annie eye) nuclei, nuclear grooves, pseudoinclusions, and psammoma bodies. There is no capsular or vascular invasion. What is the most likely diagnosis and the most reliable prognostic marker?

A Medullary carcinoma; prognosis determined by serum calcitonin levels
B Follicular carcinoma; prognosis determined by capsular and vascular invasion
C Papillary thyroid carcinoma; diagnosed by characteristic nuclear features regardless of invasion
D Anaplastic carcinoma; universal poor prognosis irrespective of histology

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Q6 PA31.4 1 pt

A 55-year-old man presents with a thyroid mass, neck lymphadenopathy, and chronic diarrhoea. Serum calcitonin is markedly elevated (>2000 pg/mL). Fine-needle aspiration shows polygonal cells in a hyalinised stroma that stains positive with Congo red under polarised light. Genetic testing reveals a germline RET proto-oncogene mutation. What additional workup is most immediately necessary?

A Serum thyroglobulin to assess differentiated thyroid cancer burden
B Serum PTH and calcium to establish primary hyperparathyroidism
C RAIU scan to plan radioiodine ablation therapy
D Urine catecholamines/metanephrines to exclude pheochromocytoma before surgery

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Q7 PA31.4 1 pt

A 60-year-old woman with a long-standing multinodular goiter presents with rapidly progressive dysphagia and hoarseness over 6 weeks. Examination reveals a rock-hard neck mass fixed to surrounding structures. CT shows tracheal deviation and local invasion. Biopsy shows highly pleomorphic giant cells and spindle cells with frequent mitoses and necrosis. What is the prognosis and primary treatment modality?

A Excellent prognosis; total thyroidectomy followed by radioiodine ablation is curative
B Intermediate prognosis; managed by total thyroidectomy and lifelong TSH suppression
C Good prognosis with external beam radiotherapy alone; 5-year survival >80%
D Universally fatal within months; palliative chemoradiation with airway preservation

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Q8 PA31.5 1 pt

A 38-year-old woman with known Type 1 diabetes mellitus presents to the emergency department with nausea, vomiting, and deep rapid (Kussmaul) breathing. Blood glucose is 28 mmol/L, blood pH is 7.18, bicarbonate is 10 mEq/L, and urine dipstick shows 3+ ketones. What is the primary pathophysiological defect leading to this presentation?

A Absolute insulin deficiency causing unrestrained lipolysis and hepatic ketogenesis with consequent metabolic acidosis
B Severe insulin resistance in peripheral tissues with relative insulin deficiency and lactic acidosis
C Hyperosmolar hyperglycaemic state with pseudohyponatraemia and absence of ketonaemia
D Glucagonoma causing excess glucagon secretion and secondary ketosis

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Q9 PA31.5 1 pt

A 58-year-old man with Type 2 diabetes mellitus of 15 years duration is found to have proteinuria (3.2 g/24 h) and a serum creatinine of 210 µmol/L. Kidney biopsy shows nodular glomerulosclerosis at the periphery of the glomerular tuft with thickened basement membranes. PAS stain highlights the nodules. What is the name of this lesion and its pathological basis?

A Wire-loop lesions; subendothelial immune-complex deposition in lupus nephritis
B Focal segmental glomerulosclerosis; podocyte injury from lipid-mediated toxicity
C Kimmelstiel-Wilson nodules; nodular accumulation of mesangial matrix from non-enzymatic glycation and hyperfiltration injury
D Amyloid deposits; misfolded serum amyloid A protein in AA amyloidosis

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Q10 PA31.6 1 pt

A 50-year-old man presents with fatigue, weight loss, abdominal pain, and a serum calcium of 3.1 mmol/L (elevated). Intact PTH is markedly elevated at 180 pg/mL (normal 10–65). Imaging shows a 2.5 cm mass in the superior parathyroid gland. Bone X-rays reveal subperiosteal resorption of the radial aspect of the middle phalanges and a 'salt-and-pepper' skull. What is the diagnosis and most likely cause?

A Secondary hyperparathyroidism due to chronic kidney disease causing compensatory PTH elevation
B Tertiary hyperparathyroidism after successful renal transplantation
C Humoral hypercalcaemia of malignancy due to PTHrP secretion from a lung carcinoma
D Primary hyperparathyroidism due to a parathyroid adenoma causing autonomous PTH secretion

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Q11 PA31.7 1 pt

A 62-year-old man presents with painless jaundice, weight loss of 8 kg over 3 months, and a palpable, non-tender gallbladder (Courvoisier sign). CT abdomen shows a 3.5 cm mass in the head of the pancreas obstructing the common bile duct. CA 19-9 is markedly elevated. What is the most likely histological type and its characteristic growth pattern?

A Pancreatic neuroendocrine tumour; well-differentiated islet cells in trabecular/nested pattern
B Mucinous cystic neoplasm; mucin-filled cysts with ovarian-type stroma
C Pancreatic ductal adenocarcinoma; invasive glands in a desmoplastic stroma with perineural invasion
D Acinar cell carcinoma; cells with granular cytoplasm and lipase/amylase secretion causing fat necrosis

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Q12 PA31.8 1 pt

A 35-year-old woman presents with progressive fatigue, weight loss, hyperpigmentation of skin creases and buccal mucosa, postural hypotension, and hyponatraemia with hyperkalaemia. Serum cortisol is low and does not rise with synthetic ACTH (Synacthen) stimulation. ACTH level is markedly elevated. What is the underlying pathology in the most common cause of this condition in resource-rich settings?

A Bilateral adrenal cortical destruction by metastatic lung carcinoma
B Autoimmune destruction of the adrenal cortex (autoimmune Addison disease)
C Bilateral adrenal cortical destruction by Mycobacterium tuberculosis
D Suppression of HPA axis by long-term exogenous glucocorticoid use

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Q13 PA31.9 1 pt

A 42-year-old man presents with central obesity, moon face, buffalo hump, purple abdominal striae, and hypertension. Serum cortisol is elevated with loss of diurnal variation. Overnight low-dose dexamethasone suppression test is abnormal (cortisol not suppressed). ACTH is elevated. High-dose dexamethasone (8 mg overnight) suppresses cortisol by >50%. What is the most likely cause of Cushing syndrome in this patient?

A Pituitary corticotroph adenoma (ACTH-dependent; Cushing disease)
B Adrenal cortical adenoma (ACTH-independent Cushing syndrome)
C Ectopic ACTH syndrome from small-cell lung carcinoma
D Iatrogenic Cushing syndrome from exogenous glucocorticoids

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Q14 PA31.10 1 pt

A 28-year-old woman presents with episodic hypertension (BP 220/130 mmHg during attacks), palpitations, severe headache, sweating, and pallor. Between attacks, blood pressure is normal. 24-hour urine shows markedly elevated metanephrines and vanillylmandelic acid (VMA). CT adrenal shows a 4 cm right adrenal mass. Which of the following statements about this tumour is most accurate?

A Approximately 90% are malignant and metastasise to liver and lungs
B It follows the 'rule of 10s': ~10% malignant, ~10% bilateral, ~10% extra-adrenal, ~10% familial
C It arises from adrenal cortical cells and secretes cortisol and aldosterone
D Surgical resection should proceed immediately without preoperative alpha-blockade

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Q15 PA31.10 1 pt

A 3-year-old child presents with an abdominal mass that crosses the midline, periorbital ecchymosis ('raccoon eyes'), and proptosis. Urine HVA (homovanillic acid) and VMA (vanillylmandelic acid) are markedly elevated. CT shows a suprarenal mass with calcifications. Bone marrow biopsy reveals small blue round cells. N-MYC gene amplification is detected. Which of the following best describes this tumour's biological behaviour related to N-MYC amplification?

A N-MYC amplification predicts spontaneous regression and excellent prognosis in children <18 months
B N-MYC amplification is only seen in Stage 1 localised neuroblastoma and has no prognostic value
C N-MYC amplification (>10 copies) confers high-risk status with rapid progression and poor prognosis
D N-MYC amplification indicates transformation to pheochromocytoma, requiring alpha-blockade before surgery

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