American Board of Internal Medicine Certification (ABIM Board Certification) Endocrinology, Diabetes & Metabolism Syllabus

How should levothyroxine be managed in pregnancy for a woman with hypothyroidism?

Increase dose ~30% (e.g., two extra tablets/week) as soon as pregnancy confirmed; target trimester-specific TSH (generally <2.5 mIU/L) and recheck TSH every 4 weeks in the first half.

What is thyroid storm and how is it treated (drug sequence)?

Life-threatening thyrotoxicosis with fever, tachycardia/arrhythmia, CNS and GI dysfunction. Treat with beta-blocker (propranolol), thionamide (PTU preferred), iodine (SSKI) given >=1 hr AFTER thionamide, and glucocorticoids; treat precipitant.

Which antithyroid drug is preferred in the first trimester of pregnancy and which is preferred afterward, and why?

PTU in the first trimester (methimazole is teratogenic-aplasia cutis, embryopathy); switch to methimazole after the first trimester (PTU carries hepatotoxicity risk).

What is the recommended first step in evaluating a thyroid nodule when TSH is normal or high?

Thyroid ultrasound to characterize the nodule; if TSH is low, obtain a radionuclide scan first (hot/autonomous nodules rarely malignant and are not biopsied).

What ultrasound features and size thresholds prompt fine-needle aspiration of a thyroid nodule?

FNA based on sonographic risk (TI-RADS/ATA): high-suspicion (hypoechoic, microcalcifications, irregular margins, taller-than-wide) at >=1 cm; intermediate at >=1-1.5 cm; spongiform/cystic generally >=2 cm or observe.

What are the major types of thyroid cancer and their key associations?

Papillary (most common, lymphatic spread, good prognosis); follicular (hematogenous spread); medullary (C-cells, calcitonin, MEN2/RET); anaplastic (aggressive, elderly, poor prognosis).

What tumor marker is used for medullary thyroid carcinoma and what genetic syndrome must be excluded?

Calcitonin (and CEA); screen for RET proto-oncogene mutation / MEN2 (also rule out coexisting pheochromocytoma before thyroid surgery).

How is a 'low TSH with normal free T4 and T3' pattern interpreted, and what is subclinical hyperthyroidism?

Subclinical hyperthyroidism; treat if TSH <0.1 with risk factors (age >65, osteoporosis, atrial fibrillation, cardiac disease); risks include AF and bone loss.

What thyroid function pattern characterizes central (secondary) hypothyroidism?

Low free T4 with a low or inappropriately normal TSH (pituitary/hypothalamic disease); cannot rely on TSH to titrate-follow free T4.

What is euthyroid sick syndrome (nonthyroidal illness) and its classic lab pattern?

Low T3 (decreased peripheral T4-to-T3 conversion, high reverse T3) with normal/low TSH and T4 during acute illness; generally avoid testing and treating during acute illness.

What is the most common cause of primary adrenal insufficiency (Addison disease) and its lab hallmark?

Autoimmune adrenalitis; low cortisol with HIGH ACTH, plus hyponatremia, hyperkalemia, and hyperpigmentation (from elevated ACTH/POMC). Diagnose with cosyntropin (ACTH) stimulation test.

How does secondary adrenal insufficiency differ from primary in electrolytes and pigmentation?

Secondary (pituitary/ACTH deficiency) has LOW ACTH, no hyperpigmentation, and aldosterone is preserved (renin-angiotensin intact) so no hyperkalemia; hyponatremia can still occur.

What are the steps in diagnosing Cushing syndrome (screening then confirmation of source)?

Screen with 1-mg overnight dexamethasone suppression, late-night salivary cortisol, or 24-hr urinary free cortisol (2 abnormal tests). Then measure ACTH: low = adrenal; normal/high = ACTH-dependent (pituitary vs ectopic), use high-dose dexamethasone, CRH, and inferior petrosal sinus sampling.

How do high-dose dexamethasone results help localize ACTH-dependent Cushing syndrome?

Cushing disease (pituitary) usually suppresses cortisol >50% with high-dose dexamethasone and responds to CRH; ectopic ACTH typically does NOT suppress and does not respond to CRH.

What is the biochemical screening and confirmation approach for pheochromocytoma?

Screen with plasma free metanephrines or 24-hr urine fractionated metanephrines; confirm/localize with CT/MRI of adrenals (and MIBG or DOTATATE if needed).

What is the required preoperative blockade sequence for pheochromocytoma resection?

Alpha-blockade FIRST (e.g., phenoxybenzamine/doxazosin) for 7-14 days with volume/salt loading, THEN add beta-blockade if needed; never beta-block first (unopposed alpha causes hypertensive crisis).

What screening test and confirmatory step are used for primary aldosteronism?

Screen with plasma aldosterone-to-renin ratio (high aldosterone, suppressed renin); confirm with saline/oral salt loading (failure to suppress aldosterone); adrenal vein sampling distinguishes unilateral adenoma from bilateral hyperplasia.

What clinical clues suggest primary aldosteronism?

Resistant hypertension, spontaneous or diuretic-induced hypokalemia, metabolic alkalosis, and an adrenal incidentaloma; consider in all resistant/early-onset hypertension.

What hormone deficiencies are typically lost first vs last in progressive hypopituitarism?

Classic sequence of loss: GH and gonadotropins (LH/FSH) first, then TSH and ACTH, with prolactin and ADH affected last; 'Go Look For The Adenoma Please' (GH, LH/FSH, TSH, ACTH, PRL).

What is pituitary apoplexy and its management priority?

Acute hemorrhage/infarction of a pituitary adenoma causing sudden headache, visual loss, ophthalmoplegia; priority is immediate stress-dose glucocorticoids (for acute ACTH deficiency) and urgent neurosurgical/endocrine evaluation.

How are pituitary adenomas classified by size and what visual finding accompanies large ones?

Microadenoma <10 mm, macroadenoma >=10 mm; macroadenomas can compress the optic chiasm causing bitemporal hemianopsia.

What is the workup of a pituitary incidentaloma/macroadenoma to assess hypersecretion and hypofunction?

Check prolactin, IGF-1, morning cortisol/ACTH (or 1-mg dexamethasone), TSH/free T4, LH/FSH and testosterone/estradiol, and visual fields if it abuts the chiasm; macroadenoma needs full pituitary hormone panel.

What is the first-line treatment for a prolactinoma (even large ones)?

Dopamine agonists (cabergoline preferred over bromocriptine); they shrink tumors and normalize prolactin-surgery reserved for resistance/intolerance or apoplexy.

What non-prolactinoma causes must be excluded in hyperprolactinemia, and what is the 'stalk effect'?

Exclude pregnancy, hypothyroidism, renal failure, and dopamine-antagonist drugs (antipsychotics, metoclopramide). Stalk effect: non-prolactinoma sellar masses raise prolactin modestly (usually <100-150) by interrupting dopamine inhibition.

How is acromegaly diagnosed biochemically?

Elevated IGF-1 (best screening test); confirm with failure of GH to suppress <1 ng/mL during a 75-g oral glucose tolerance test; then pituitary MRI.

What are first-line treatment and medical options for acromegaly?

Transsphenoidal surgery is first-line; medical therapy includes somatostatin analogs (octreotide/lanreotide), the GH-receptor antagonist pegvisomant, and cabergoline.

Who should be screened for osteoporosis by bone density (DXA) and what T-score defines osteoporosis?

All women >=65 and men >=70 (and younger postmenopausal women/men 50-69 with risk factors); osteoporosis = T-score <=-2.5; osteopenia = -1.0 to -2.5; severe if <=-2.5 with fragility fracture.

What are first-line pharmacologic agents for osteoporosis and a key anabolic option for very high risk?

Bisphosphonates (alendronate, risedronate, zoledronic acid) or denosumab first-line; anabolics (teriparatide, abaloparatide, romosozumab) for very high fracture risk-follow anabolics with an antiresorptive.

What rare adverse effects are associated with long-term bisphosphonate/denosumab therapy?

Osteonecrosis of the jaw and atypical femoral (subtrochanteric) fractures; denosumab discontinuation also causes rapid rebound bone loss/vertebral fractures, so transition to a bisphosphonate.

What labs distinguish primary hyperparathyroidism from familial hypocalciuric hypercalcemia (FHH)?

Both have high calcium with high/inappropriately normal PTH, but primary HPT has high urinary calcium (24-hr) while FHH has LOW urinary calcium (calcium/creatinine clearance ratio <0.01, benign CASR mutation).

What are indications for parathyroidectomy in asymptomatic primary hyperparathyroidism?

Calcium >1 mg/dL above upper normal; osteoporosis (T<=-2.5) or fragility/vertebral fracture; eGFR <60, 24-hr urine Ca >400 mg or nephrolithiasis/nephrocalcinosis; or age <50.

How do PTH levels and calcium/phosphate differ between primary hyperparathyroidism and CKD-related secondary hyperparathyroidism?

Primary: high Ca, low phosphate, high PTH. Secondary (CKD/vitamin D deficiency): low/normal Ca, high phosphate (in CKD), elevated PTH driven by low calcium/calcitriol and high phosphate.

How is male hypogonadism diagnosed and how are primary and secondary forms distinguished?

Confirm low morning total testosterone on two occasions with symptoms; primary (testicular) has HIGH LH/FSH; secondary (hypothalamic-pituitary) has low/inappropriately normal LH/FSH-then check prolactin, iron studies, and pituitary MRI.

What are common pathologic causes of gynecomastia to evaluate, beyond physiologic/pubertal causes?

Drugs (spironolactone, antiandrogens, cimetidine, marijuana), hypogonadism, hyperthyroidism, cirrhosis/liver disease, renal failure, and estrogen/hCG-secreting tumors (testicular germ cell, adrenal); check testosterone, LH, estradiol, hCG, TSH, LFTs.

What are the Rotterdam criteria for diagnosing polycystic ovary syndrome (PCOS)?

At least 2 of 3: oligo/anovulation; clinical or biochemical hyperandrogenism; polycystic ovaries on ultrasound-after excluding thyroid disease, hyperprolactinemia, and nonclassic CAH (17-OHP).

What are first-line management options for PCOS by goal (menstrual regulation, hirsutism, fertility)?

Combined oral contraceptives for cycle regulation/hirsutism (add spironolactone for hirsutism); lifestyle/weight loss and metformin for metabolic/insulin resistance; letrozole first-line for ovulation induction/fertility.

What are the ATP III criteria for metabolic syndrome (>=3 of 5)?

Waist >40 in men / >35 in women; triglycerides >=150; HDL <40 men / <50 women; BP >=130/85; fasting glucose >=100 mg/dL.

For which four high-risk groups do guidelines recommend high-intensity statin therapy (ASCVD prevention)?

Clinical ASCVD (secondary prevention); LDL >=190 mg/dL; diabetes age 40-75; and primary prevention when 10-year ASCVD risk is high (>=20%, or >=7.5% with risk enhancers after risk discussion).

What is the most common identifiable secondary cause of very high triglycerides and the main acute risk above 500-1000 mg/dL?

Uncontrolled diabetes/alcohol/obesity (and drugs/hypothyroidism); triglycerides >500 (especially >1000) markedly raise risk of acute pancreatitis-treat with fibrates, omega-3s, and glycemic/lifestyle control.