NEET SS Endocrinology (DM) Flashcards

24 sample cards from the Endocrinology (DM) deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. What is the management of thyrotoxicosis in pregnancy?

   PTU in first trimester (methimazole teratogenicity), switch to methimazole in second/third trimester; use lowest effective dose to keep free T4 high-normal; avoid radioiodine; beta-blockers short-term.

2. How are thyroid nodules evaluated?

   Measure TSH; if low, do radioiodine scan (hot nodule rarely malignant). If normal/high TSH, do ultrasound; FNA based on TI-RADS/sonographic risk and size. Report cytology by Bethesda system.

3. Name the major types of thyroid cancer and their key features.

   Papillary (most common, lymphatic spread, Orphan-Annie nuclei/psammoma bodies, excellent prognosis); Follicular (hematogenous spread, capsular/vascular invasion); Medullary (parafollicular C-cells, calcitonin, MEN2); Anaplastic (aggressive, elderly, poor prognosis).

4. Which thyroid cancer is associated with MEN2 and what tumor marker is used?

   Medullary thyroid carcinoma (parafollicular C cells); tumor marker calcitonin (and CEA). Associated with RET proto-oncogene mutation. In MEN2A/2B prophylactic thyroidectomy is indicated.

5. What are the sonographic features suggesting thyroid malignancy?

   Marked hypoechogenicity, microcalcifications, irregular margins, taller-than-wide shape, extrathyroidal extension, and suspicious cervical lymphadenopathy.

6. What is the most common functional pituitary adenoma and its presentation?

   Prolactinoma: hyperprolactinemia causing galactorrhea, amenorrhea/oligomenorrhea, infertility (women), and decreased libido/erectile dysfunction (men); mass effect causes bitemporal hemianopia. First-line treatment: dopamine agonists (cabergoline).

7. How do you diagnose acromegaly?

   Elevated IGF-1 for age, and failure to suppress GH (<1 ng/mL) after oral glucose load (OGTT). MRI localizes the GH-secreting pituitary adenoma. Treatment: transsphenoidal surgery, somatostatin analogs, pegvisomant.

8. What is Sheehan syndrome?

   Postpartum pituitary necrosis from hypotension/hemorrhage causing hypopituitarism; failure of lactation (low prolactin), amenorrhea, and other anterior pituitary hormone deficiencies.

9. Differentiate central from nephrogenic diabetes insipidus using the water deprivation/desmopressin test.

   Both: dilute urine despite high serum osmolality. After desmopressin (DDAVP): central DI urine osmolality rises >50% (ADH deficient); nephrogenic DI shows little/no response (renal ADH resistance).

10. What distinguishes Cushing disease from Cushing syndrome?

    Cushing syndrome = any cause of chronic glucocorticoid excess. Cushing disease = Cushing syndrome specifically due to an ACTH-secreting pituitary adenoma (the most common endogenous cause).

11. Outline the diagnostic workup for Cushing syndrome.

    Screen: 24-hr urinary free cortisol, late-night salivary cortisol, low-dose dexamethasone suppression test. Then measure ACTH (low = adrenal; normal/high = ACTH-dependent). High-dose dexamethasone and inferior petrosal sinus sampling differentiate pituitary from ectopic ACTH.

12. What is the most common cause of primary hyperaldosteronism (Conn syndrome) and its biochemical profile?

    Bilateral adrenal hyperplasia or aldosterone-producing adenoma. Profile: hypertension, hypokalemia, metabolic alkalosis, high aldosterone with suppressed renin (high aldosterone-to-renin ratio).

13. What is Addison disease and its biochemical hallmarks?

    Primary adrenal insufficiency (commonly autoimmune): deficiency of cortisol and aldosterone → hyponatremia, hyperkalemia, hypoglycemia, hypotension, hyperpigmentation (high ACTH/MSH). High ACTH; low cortisol failing to rise on ACTH stimulation test.

14. How is congenital adrenal hyperplasia from 21-hydroxylase deficiency characterized?

    Most common CAH: low cortisol and aldosterone, elevated 17-hydroxyprogesterone, and androgen excess → virilization, ambiguous genitalia in females, salt-wasting (hyponatremia/hyperkalemia) in severe forms.

15. What is the classic triad of pheochromocytoma and the best screening test?

    Episodic headache, palpitations, and diaphoresis with paroxysmal hypertension. Best screening: plasma free metanephrines or 24-hr urinary fractionated metanephrines. Tumor of adrenal medulla chromaffin cells.

16. What is the rule of 10s for pheochromocytoma, and preoperative management?

    ~10% extra-adrenal, bilateral, malignant, familial, in children. Preop: alpha-blockade first (phenoxybenzamine) THEN beta-blockade to avoid unopposed alpha-mediated hypertensive crisis; volume expansion.

17. How is an adrenal incidentaloma evaluated?

    Assess for hormone hypersecretion (1-mg dexamethasone suppression test for cortisol, plasma metanephrines for pheo, aldosterone/renin ratio if hypertensive) and for malignancy (imaging: size >4 cm, irregular margins, high unenhanced HU >10, slow washout suggest malignancy).

18. What is the function of PTH and its effects on calcium and phosphate?

    PTH raises serum calcium: increases bone resorption, increases renal calcium reabsorption, decreases phosphate reabsorption (phosphaturia), and stimulates renal 1-alpha-hydroxylase → more calcitriol (gut Ca absorption). Net: high Ca, low phosphate.

19. Differentiate primary, secondary, and tertiary hyperparathyroidism.

    Primary: autonomous PTH (usually adenoma) → high Ca, low phosphate, high PTH. Secondary: compensatory PTH rise (e.g., CKD/vitamin D deficiency) → low/normal Ca, high PTH. Tertiary: autonomous hyperplasia after prolonged secondary → high Ca, very high PTH.

20. What are the causes and management priorities of hypercalcemia?

    Most common: primary hyperparathyroidism (outpatient) and malignancy (inpatient, PTHrP/osteolytic). Acute management: IV normal saline hydration, then bisphosphonates/calcitonin; treat underlying cause. Severe: consider denosumab/dialysis.

21. How is osteoporosis diagnosed by DEXA and what is the WHO T-score classification?

    DEXA T-score: normal ≥−1.0; osteopenia −1.0 to −2.5; osteoporosis ≤−2.5; severe osteoporosis ≤−2.5 with fragility fracture. T-score compares to young adult peak bone mass.

22. What are the components of the MEN syndromes?

    MEN1 (MEN1/menin gene): parathyroid hyperplasia, pancreatic islet tumors (gastrinoma/insulinoma), pituitary adenoma (3 Ps). MEN2A (RET): medullary thyroid cancer, pheochromocytoma, parathyroid hyperplasia. MEN2B (RET): medullary thyroid cancer, pheochromocytoma, mucosal neuromas/marfanoid habitus.

23. What are the diagnostic criteria for PCOS (Rotterdam) and its endocrine features?

    Rotterdam: ≥2 of—oligo/anovulation, clinical/biochemical hyperandrogenism, polycystic ovaries on ultrasound (after excluding other causes). Features: elevated LH:FSH ratio, insulin resistance, hyperandrogenism; managed with lifestyle, OCPs, metformin.

24. How is the cause of male hypogonadism localized using LH/FSH levels?

    Primary (hypergonadotropic) hypogonadism: low testosterone with HIGH LH/FSH (testicular failure, e.g., Klinefelter). Secondary (hypogonadotropic): low testosterone with LOW/normal LH/FSH (hypothalamic-pituitary cause, e.g., Kallmann syndrome with anosmia).

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