Passmedicine Review With Key Concepts of Passmedicine (4th Edition) 7 Volume Set 2026 Edition

Publisher: Banglame Publication

Language: English

ISBN:9789843945921

Year:2026

Edition:18th

Pages:5048

Author: GENESIS Expert Panel

Product Type: Paperback

Condition: New

Price: ₹24,950/-

Delivery Time:7-8 days

Description

The presence of an elevated prolactin level along with secondary hypothyroidism and hypogonadism is indicative of stalk compression is consistent with a non-functioning pituitary adenoma Non-functioning pituitary adenoma (NFPA) is correct. This patient presents with secondary hypothyroidism (low TSH and free T4), hypogonadotropic hypogonadism (low FSH/LH), and a modestly elevated prolactin (650 mU/L), consistent with hypopituitarism due to a non-functioning pituitary adenoma. The prolactin elevation is attributable to the 'stalk effect,' where pituitary stalk compression disrupts dopamine inhibition, unlike prolactinomas which typically cause markedly higher levels (> 1000 mU/L). Headaches and visual disturbances suggest a macroadenoma compressing the optic chiasm. Premature ovarian insufficiency is unlikely given the low gonadotropins, and hypothalamic amenorrhoea does not explain the panhypopituitarism or mass effect symptoms. Hypothalamic amenorrhoea is incorrect. While both this condition and NFPA cause hypogonadotropic hypogonadism (low FSH/LH), hypothalamic amenorrhoea does not lead to secondary hypothyroidism, elevated prolactin, or neurological symptoms. This patient's headaches, visual disturbances, and multiple pituitary hormone deficiencies point to a structural lesion rather than functional hypothalamic dysfunction. Hypothalamic amenorrhoea would be plausible if there were a history of excessive exercise, low body weight, or stress, with isolated gonadotropin suppression and no other pituitary axis involvement none of which are present here. Premature ovarian insufficiency (POI) is incorrect. POI typically causes hypergonadotropic hypogonadism (elevated FSH/LH) due to ovarian failure, whereas this patient has low gonadotropins indicative of central hypogonadism. Additionally, the secondary hypothyroidism and modest prolactin elevation suggest pituitary dysfunction, not primary ovarian failure. POI could be considered if FSH/LH were elevated with amenorrhoea and hot flushes, but the hormonal profile here is inconsistent with ovarian failure. Prolactinoma is incorrect. Although prolactin is elevated, the level (650 mU/L) is too low for a prolactinoma, which typically exceeds 1000 mU/L. Moreover, prolactinomas rarely cause secondary hypothyroidism or visual field defects early in their course, whereas this patient exhibits panhypopituitarism and mass effect symptoms. A prolactinoma would be plausible if prolactin levels were markedly elevated without other pituitary deficiencies, but the clinical picture here favours a non-functioning adenoma with stalk effect. Sheehan's syndrome is incorrect. This condition follows postpartum haemorrhage, leading to pituitary infarction, but this patient has no history of obstetric complications. While both Sheehan's syndrome and NFPA can cause hypopituitarism, Sheehan's syndrome manifests shortly after childbirth with lactation failure and hypotension, neither of which is reported here. The absence of peripartum haemorrhage and the presence of mass effect symptoms make NFPA the more likely diagnosis.