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

24 sample cards from the Endocrinology, Diabetes & Metabolism 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 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).

2. 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.

3. 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.

4. 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).

5. 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.

6. 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.

7. 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.

8. 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.

9. 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.

10. 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.

11. 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.

12. 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.

13. 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.

14. 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.

15. 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).

16. 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.

17. 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.

18. 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.

19. 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.

20. 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).

21. 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.

22. 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.

23. 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).

24. 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.

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