その他のスキル

This skill recommends urgent treatment (within 24–72 hours) of hypercortisolism when life‑threatening complications of Cushing's syndrome such as infection, pulmonary thromboembolism, cardiovascular events, or acute psychosis are present. Trigger phrases include sepsis, PE, chest pain with hemodynamic instability, new‑onset psychosis, or delirium in a patient with known or suspected Cushing's.

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This skill recommends unilateral resection by an experienced adrenal surgeon for all cases of benign unilateral disease causing Cushing's syndrome. Trigger when a CS patient has a unilateral adrenal lesion confirmed benign via imaging and biochemical assessment.

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This skill suggests radiation therapy or radiosurgery for adult patients with Cushing's disease who have failed transsphenoidal surgery (TSS) or have recurrent disease after initial remission. Consider when postoperative urinary free cortisol or late-night salivary cortisol remains elevated, or when clinical recurrence is suspected.

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This skill recommends using radiation therapy for corticotroph adenomas in Cushing's disease when imaging shows invasive features or mass‑effect concerns such as cavernous sinus invasion, suprasellar extension, or knobby protrusion. Consider RT when postoperative medical therapy has normalized cortisol but tumor progression or residual invasive disease is suspected.

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This skill recommends regularly evaluating for corticotroph tumor progression using pituitary MRIs and ACTH levels in patients with known Cushing's disease who underwent bilateral adrenalectomy and in patients undergoing this procedure for presumed occult ectopic ACTH secretion. Triggers include postoperative follow‑up after bilateral adrenalectomy, rising ACTH levels, or new pituitary lesion on MRI suggestive of tumor progression.

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This skill suggests medical therapy to block aberrant hormone receptors for bilateral macronodular adrenal hyperplasia (BMAH) when surgery is not preferred or feasible. Consider this approach in patients with confirmed BMAH and evidence of aberrant hormone receptor expression (e.g., GIP, LH/hCG, serotonin) driving cortisol excess.

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Recommends initial surgical resection of the primary lesion(s) causing Cushing's syndrome when surgery is feasible and likely to significantly reduce glucocorticoid excess. Trigger phrases include overt Cushing's syndrome, ACTH-dependent CS, ectopic ACTH secretion, adrenal adenoma, bilateral macronodular adrenal hyperplasia, and persistent hypercortisolism.

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This skill recommends obtaining serum free T4 and prolactin levels within 1–2 weeks after transsphenoidal surgery (TSS) for Cushing's syndrome to screen for overt hypopituitarism. Use in postoperative Cushing's syndrome patients during the early recovery window when evaluating for new pituitary hormone deficiencies.

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This skill defines the treatment goals for patients with overt Cushing's syndrome, focusing on normalizing cortisol levels or action to eliminate symptoms and treat comorbidities. Use when a clinician asks about treatment objectives for a newly diagnosed overt Cushing's syndrome patient; triggers include "overt CS," "treatment goals for overt Cushing's," and "normalize cortisol in overt CS."

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This skill directs lifelong treatment of cardiovascular risk factors, osteoporosis, and psychiatric symptoms in all patients with Cushing's syndrome until biochemical resolution of hypercortisolism. Use when managing any CS patient for long‑term comorbidity control; triggers include persistent hypertension, dyslipidemia, low bone density, depression, anxiety, or cognitive changes in the setting of known or suspected CS.

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Suggests repeat transsphenoidal surgery for patients with persistent hypercortisolism after initial transsphenoidal surgery when imaging shows evidence of incomplete resection or a pituitary lesion. Clinical triggers include postoperative MRI revealing residual adenoma, persistent elevated UFC or late-night salivary cortisol, and visible pituitary lesion on imaging.

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Recommends steroidogenesis inhibitors as second-line treatment after transsphenoidal surgery (TSS) in Cushing's disease, as primary therapy for occult or metastatic ectopic ACTH syndrome (EAS), and as adjunctive cortisol reduction in adrenocortical carcinoma. Use when evaluating CS patients post‑TSS, with occult/metastatic EAS, or ACC; triggers include “persistent hypercortisolism after TSS,” “occult EAS,” and “adjunctive for ACC.”

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This skill provides a shared decision-making framework for selecting second-line therapies in patients with ACTH-dependent Cushing's syndrome who have persistent hypercortisolism after transsphenoidal surgery or for whom surgery is not feasible. Clinical triggers include "failed TSS", "non-curative pituitary surgery", "persistent UFC elevation post-op", and "surgery contraindicated".

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This skill recommends obtaining a postoperative pituitary MRI within 1–3 months after successful transsphenoidal surgery (TSS) to establish a new baseline for future recurrence assessment. Use when a Cushing’s syndrome patient has achieved biochemical remission post‑TSS and is entering routine follow‑up.

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This skill suggests pituitary-directed medical treatments (e.g., cabergoline, pasireotide) for patients with Cushing's disease who are not surgical candidates or have persistent disease after transsphenoidal surgery. Use when a CD patient cannot undergo surgery or has residual disease post-TSS; triggers include "not a surgical candidate", "persistent disease after TSS", "ongoing hypercortisolism despite prior surgery".

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Recommends checking and managing vitamin D according to Endocrine Society guidelines to avoid hypocalcemia in patients receiving bisphosphonates or denosumab for hypercalcemia of malignancy. Use when a clinician notes risk factors for hypocalcemia (e.g., low 25‑OH vitamin D, renal insufficiency) and asks about baseline labs before antiresorptive start.

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Computes albumin‑adjusted (corrected) serum calcium using total calcium and albumin to adjust for hypo‑ or hyperalbuminemia. Triggered when a clinician notes hypoalbuminemia and requests corrected calcium to assess true hypercalcemia of malignancy severity.

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The guideline suggests checking serum magnesium and phosphate levels and repleting if low in patients receiving antiresorptive therapy for hypercalcemia of malignancy. Clinicians should consider this when they note electrolyte abnormalities or inquire about supportive care during bisphosphonate or denosumab treatment.

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Interprets the aldosterone-to-renin ratio using active renin concentration (ARC) to screen for primary aldosteronism. Triggered when a clinician has PAC and ARC results and asks 'How do I interpret this ARR using active renin concentration?'

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Determines whether a hypertensive patient should be screened for primary aldosteronism based on clinical features associated with higher PA prevalence. Triggered when a clinician asks 'Should I screen this hypertensive patient for PA?' or observes spontaneous hypokalemia, resistant hypertension, hypertension onset before age 40, adrenal tumor, young-onset stroke, or sleep apnea syndrome.

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Advises evaluating creatinine clearance or estimated glomerular filtration rate prior to intravenous bisphosphonate administration to guide dosing and ensure safety. Triggered when a clinician is planning to give zoledronic acid or pamidronate and asks about renal safety checks.

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Recommends initiating intravenous isotonic saline hydration as initial management for hypercalcemia of malignancy (HCM) while awaiting antiresorptive therapy, with fluid rate adjusted according to cardiac function. Triggered when a clinician encounters a patient with HCM (e.g., serum calcium >12 mg/dL, symptoms of hypercalcemia) and seeks immediate measures before specific drugs are available.

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Recommends combination of calcitonin and an intravenous bisphosphonate or denosumab as initial treatment for severe hypercalcemia (serum calcium >14 mg/dL). Indicated when a clinician notes severe HCM or seeks rapid calcium lowering in symptomatic patients.

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The skill suggests adding a calcimimetic for hypercalcemia of malignancy due to parathyroid carcinoma that persists after intravenous bisphosphonate or denosumab therapy. It is triggered when a clinician notes refractory HCM despite antiresorptive therapy and considers adding a calcimimetic.

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