Claude Skills by dromlakhani

--- name: enda-patient-education-stress-dosing-self-admin description: Educates patients with primary adrenal insufficiency on adjusting glucocorticoid doses during stressful events such as fever, illness requiring bed rest, vomiting, or surgery, and on emergency self-administration of parenteral glucocorticoids to prevent adrenal crisis. Trigger phrases include 'fever >38°C', 'illness requiring antibiotics', 'persistent vomiting', 'pre-procedure fasting', 'surgical stress dosing education ac...

Recommends fludrocortisone 100 µg daily for children with primary adrenal insufficiency and confirmed aldosterone deficiency; for infants under 12 months, adds sodium chloride supplementation. Triggered by PAI with aldosterone deficiency, evidenced by salt craving, hyponatremia, hyperkalemia, or elevated renin with low aldosterone.

Recommends initiating hydrocortisone replacement at a total starting dose of 8 mg/m2 body surface area per day, given in three or four divided doses, for children with confirmed primary adrenal insufficiency (PAI). Use when starting glucocorticoid therapy in pediatric PAI patients, adjusting the dose according to individual clinical response, growth, and need for stress coverage.

Suggests using prednisolone 3–5 mg/d orally once or twice daily as a glucocorticoid alternative in primary adrenal insufficiency. Consider this option when evaluating glucocorticoid therapy, particularly in patients with reduced medication compliance.

In pregnant women with primary adrenal insufficiency (PAI), the guideline suggests using hydrocortisone over cortisone acetate, prednisolone, or prednisone for glucocorticoid replacement. It recommends against dexamethasone due to its lack of placental inactivation, which can expose the fetus to excess glucocorticoid exposure.

Suggests using morning cortisol ≤140 nmol/L (5 µg/dL) in combination with ACTH as a preliminary test suggestive of primary adrenal insufficiency when a corticotropin stimulation test is not feasible. Use when patients present with indicative symptoms such as hypotension, hyponatremia, hyperkalemia, or fatigue and corticotropin stimulation testing cannot be performed.

Suggests reducing the fludrocortisone dose in patients who develop new-onset hypertension while on fludrocortisone replacement for primary adrenal insufficiency. Consider dose reduction when hypertension arises alongside signs of mineralocorticoid excess such as edema, weight gain, or hypokalemia.

This skill recommends simultaneous measurement of plasma renin and aldosterone in patients with primary adrenal insufficiency (PAI) to determine the presence of mineralocorticoid deficiency. It is triggered when assessing for mineralocorticoid deficiency in PAI, such as in patients with unexplained hyponatremia, hyperkalemia, or salt craving despite glucocorticoid replacement.

The Endocrine Society recommends a standard-dose corticotropin (ACTH) stimulation test to confirm primary adrenal insufficiency when clinical suspicion arises from symptoms such as hypotension, hyponatremia, hyperkalemia, or unexplained fatigue. Dosing is weight/age based: 250 µg for adults and children ≥2 years, 15 µg/kg for infants, and 125 µg for children <2 years.

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Recommends hydrocortisone stress dosing during the active phase of labor for pregnant patients with primary adrenal insufficiency, using a regimen similar to major surgical stress. Trigger phrases: "active phase of labor", "cervix dilation ≥4 cm", "contractions every 5 minutes", "PAI patient in labor".

Recommends diagnostic testing to exclude primary adrenal insufficiency (PAI) in acutely ill patients presenting with otherwise unexplained volume depletion, hypotension, hyponatremia, hyperkalemia, fever, abdominal pain, hyperpigmentation, or hypoglycemia (especially in children). Use when clinical suspicion arises from these suggestive signs or symptoms suggestive of PAI.

Determines when to avoid aldosterone suppression testing in hypertensive patients with a positive PA screen who have normokalemia and suppressed aldosterone below assay‑specific cutoffs (<11 ng/dL immunoassay or <8 ng/dL LC‑MS/MS), indicating low likelihood of primary aldosteronism. Use when a clinician asks whether to skip confirmatory suppression testing based on low pretest probability.

Recommends performing a dexamethasone suppression test to evaluate for autonomous cortisol secretion in patients with primary aldosteronism and adrenal adenoma. Triggered when a clinician considers whether to perform a dexamethasone suppression test in a patient with PA and adrenal adenoma.

Determines whether adrenal venous sampling (AVS) is needed in addition to CT for lateralizing primary aldosteronism before surgery. Trigger phrases include "patient with primary aldosteronism considering surgery", "unilateral adrenal adenoma on CT", "surgical candidate", and "age <35 with hypokalemia and >1‑cm adenoma".

Recommends spironolactone as first-line mineralocorticoid receptor antagonist for initial medical therapy of primary aldosteronism due to low cost and widespread availability. Use when a clinician queries which MRA to start for a patient with PA requiring medical therapy.

Recommends using mineralocorticoid receptor antagonists rather than epithelial sodium-channel inhibitors for medical treatment of primary aldosteronism. Use when a clinician asks whether to use an MRA or ENaC inhibitor for medical treatment of PA.

In patients with primary aldosteronism receiving mineralocorticoid receptor antagonist therapy, the guideline recommends titrating the MRA dose upward to raise renin when blood pressure remains uncontrolled and renin is suppressed. Consider this step when hypertension is not at goal despite MRA therapy and plasma renin activity (or direct renin concentration) is low.

Recommends correcting serum potassium to the laboratory reference range and repeating aldosterone-to-renin ratio (ARR) screening when the initial screen is negative in a hypertensive patient with hypokalemia. Use when a clinician encounters a negative PA screen in a hypertensive patient with hypokalemia and wonders whether to repeat testing after potassium repletion.

Recommends withdrawing interfering medications and repeating aldosterone-to-renin ratio screening when initial screen is negative but clinical suspicion remains due to hypokalemia or medication interference. Trigger phrases include "initial screen negative", "hypokalemia", "resistant hypertension", and use of MRAs, ACE inhibitors, ARBs, beta-blockers, clonidine, or alpha-methyldopa.

Determines whether to screen a patient with hypertension for primary aldosteronism based solely on the presence of hypertension. Use when a clinician asks whether to screen a hypertensive patient for PA, triggered by phrases such as "should we screen for aldosteronism" or "evaluate for secondary hypertension".

Selects the aldosterone-to-renin ratio (ARR) method over hypokalemia for screening hypertensive patients for primary aldosteronism. Use when a clinician asks what test to use for screening hypertensive patients with resistant hypertension or unexplained hypokalemia for PA.

Determines when adrenal venous sampling may be skipped in primary aldosteronism. Applies to patients <35 years with spontaneous hypokalemia, marked aldosterone excess, and unilateral adrenal lesions suggestive of cortical adenoma on CT.

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Determines whether to perform adrenal venous sampling (AVS) to lateralize aldosterone excess in patients with confirmed primary aldosteronism (PA) who are being evaluated for surgical treatment. Indicated when surgery is feasible and desired by the patient, or when subtype workup is planned for a surgical candidate, especially in those younger than 35 years with spontaneous hypokalemia, marked aldosterone excess, and unilateral adrenal lesions on CT.

Determines whether to add a mineralocorticoid receptor antagonist (e.g., spironolactone or eplerenone) to glucocorticoid therapy in glucocorticoid-remediable aldosteronism when blood pressure fails to normalize with glucocorticoid alone. Triggered by persistent hypertension or inadequate BP control despite optimized glucocorticoid dosing in GRA patients.

Calculates the lowest effective glucocorticoid dose (dexamethasone or prednisone) to normalize blood pressure and serum potassium in glucocorticoid-remediable aldosteronism (GRA/FH-I) by titrating to biochemical and clinical targets. Indicated when initiating medical treatment for confirmed GRA, triggered by findings such as early-onset hypertension, family history of stroke before age 40, spontaneous hypokalemia, or suppressed plasma renin activity with elevated aldosterone.

Differentiates aldosterone-producing adenoma from idiopathic adrenal hyperplasia based on 18-hydroxycorticosterone levels, with APA patients generally having levels >100 ng/dL at 8:00 a.m. and IAH patients usually having levels <100 ng/dL. Use when reviewing 18-OHB test results to help subtype PA; triggers include 18-OHB >100 ng/dL (suggesting APA) or <100 ng/dL (suggesting IAH).

Helps distinguish unilateral from bilateral adrenal disease based on 18-oxocortisol levels, which are typically higher in aldosterone-producing adenoma than idiopathic adrenal hyperplasia. Use when evaluating 18-oxocortisol results during PA workup to guide subtype classification after a positive ARR.

Determines unilateral vs bilateral aldosterone excess based on cortisol-corrected aldosterone ratios from adrenal venous sampling, with ratio >4:1 indicating unilateral excess, ratio 3:1 suggestive of bilateral hypersecretion, and interpretation dependent on cosyntropin stimulation protocol used during sampling. Use when analyzing AVS results to guide surgical vs medical treatment decisions; triggers include 'AVS lateralization ratio', 'cosyntropin-stimulated AVS', 'aldosterone-to-cortisol ra...

Evaluates likelihood of primary aldosteronism by measuring plasma aldosterone suppression after oral captopril; normal suppression ≥30% makes PA unlikely, while lack of suppression with persistently suppressed plasma renin activity suggests PA. Use when assessing captopril challenge test (CCT) results for PA diagnosis in patients with positive aldosterone-to-renin ratio.

Determines if primary aldosteronism is confirmed based on upright plasma aldosterone ≤6 ng/dL (170 nmol/L) on day 4 at 10 AM of fludrocortisone suppression test, provided plasma renin activity ≥1 ng/mL/h and plasma cortisol concentration lower than the 7 AM value to exclude ACTH confounding. Use when reviewing FST results to diagnose PA; triggers include "FST", "upright aldosterone ≤6 ng/dL", "PRA ≥1 ng/mL/h", and "cortisol drop".

This skill interprets the oral sodium loading test for primary aldosteronism by evaluating 24‑hour urinary aldosterone excretion after a high‑sodium diet. Use when reviewing results of an "oral sodium loading test" for PA diagnosis; trigger phrases include "urinary aldosterone excretion ≤10 g/24 h" (PA unlikely) or "≥12 g/24 h (Mayo) / ≥14 g/24 h (Cleveland)" (PA highly likely).

Interprets the postural stimulation test to detect angiotensin II‑unresponsive aldosterone‑producing adenoma (APA) or familial hyperaldosteronism type I (FH‑I) when aldosterone fails to rise with upright posture. Triggered by clinical cues such as “postural stimulation test shows no aldosterone increase”, “suspected APA with non‑responsive aldosterone”, or “evaluating FH‑I in young patients with early‑onset hypertension and hypokalemia”.

Interprets the saline infusion test (SIT) to assess the probability of primary aldosteronism when a patient has a positive aldosterone-to-renin ratio (ARR) and requires confirmatory testing. Triggers include evaluating post‑infusion plasma aldosterone concentration (PAC) after a positive ARR, hypertension work‑up, or when deciding whether to proceed to adrenal venous sampling (AVS).

Selects spironolactone as first-line mineralocorticoid receptor antagonist for bilateral primary aldosteronism, with eplerenone as an alternative when spironolactone–related adverse effects are problematic. Trigger phrases include 'confirmed bilateral PA on AVS', 'idiopathic adrenal hyperplasia', 'bilateral adrenal hyperplasia', 'glucocorticoid-remediable aldosteronism', and 'initiating medical therapy for bilateral adrenal disease'.

Establishes age- and gender-specific blood pressure goals for pediatric patients with primary aldosteronism (PA) using published normative data to assess treatment adequacy and avoid over-treatment. Use when managing hypertension in children with PA to evaluate if BP is adequately controlled; triggers include pediatric PA hypertension, BP not normalized with glucocorticoid therapy, and need for age‑specific BP targets.

Determines age- and body weight-appropriate glucocorticoid dosage for pediatric patients with primary aldosteronism, particularly glucocorticoid-remediable aldosteronism (GRA), to avoid over-treatment. Use when prescribing glucocorticoids to children with confirmed or suspected PA; triggers include pediatric PA, GRA, or need to dose glucocorticoid based on age and weight.

This skill determines whether confirmatory testing can be omitted after a positive aldosterone-to-renin ratio (ARR) in patients with suspected primary aldosteronism. It is applied when a patient exhibits spontaneous hypokalemia, undetectable renin, and a plasma aldosterone concentration ≥20 ng/dL (550 pmol/L).

Determines when to pursue genetic testing for glucocorticoid-remediable aldosteronism (FH-I/GRA) in patients with confirmed primary aldosteronism (PA). Indicated when PA onset is before age 20 or there is a family history of PA or stroke before age 40.

Determines when to test for germline KCNJ5 mutations indicating familial hyperaldosteronism type III in very young patients with primary aldosteronism. Triggered by severe early-onset hypertension with hypokalemia in infants or young children (<20 years) with confirmed PA.

Determines whether to recommend unilateral laparoscopic adrenalectomy or medical therapy with a mineralocorticoid receptor antagonist for patients with confirmed unilateral PA (aldosterone-producing adenoma or unilateral adrenal hyperplasia). Triggered when discussing treatment options after confirming unilateral PA in a hypertensive patient with hypokalemia or resistant hypertension.

Recommends ACTH stimulation during AVS to improve success rate of bilateral selective catheterization, acknowledging unclear impact on diagnostic accuracy for laterality. Triggers include when setting up AVS and asking 'Should I administer ACTH?' or considering procedural optimization.

Identifies patients with normokalemia and no adrenal tumors on CT who likely have bilateral PA and may proceed directly to medical therapy without AVS. Triggers include when a clinician notes normokalemia and clean adrenal CT and asks 'Is AVS necessary if I suspect bilateral disease?'

Identifies young patients with classic primary aldosteronism features who may proceed directly to unilateral adrenalectomy without adrenal venous sampling based on high probability of unilateral disease. Triggered when a clinician sees a patient <35 years with hypokalemia, unilateral adrenal tumor on CT, and high plasma aldosterone concentration and asks whether AVS can be bypassed.

Determines successful catheterization in adrenal venous sampling by applying selectivity index cut‑offs with and without ACTH stimulation. Triggered during AVS when measuring cortisol levels and asking “Is the catheter properly positioned?” or when reviewing results for technical adequacy.

Determines when adrenal venous sampling (AVS) is indicated for functional subtyping of primary aldosteronism (PA) when surgical treatment is feasible and desired by the patient. Triggered when a clinician confirms PA diagnosis and asks 'Do I need AVS for subtyping?' or evaluates surgical candidacy.

This skill provides criteria to distinguish unilateral from bilateral primary aldosteronism using adrenal venous sampling results, including lateralization index, contralateral ratio, and clinical factors. It is triggered after AVS when clinicians analyze results and ask 'Is this unilateral or bilateral PA?' or need to guide treatment decisions.

Provides a checklist of five evidence-based measures to enhance the technical success of adrenal venous sampling procedures. Triggers include when preparing for AVS and asking 'How can I maximize success rate?' or troubleshooting failed attempts.

Identifies patients with a positive aldosterone-to-renin ratio screening who may proceed directly to subtype testing without confirmatory testing based on specific clinical criteria. Triggers include spontaneous hypokalemia, baseline plasma aldosterone concentration >100 pg/mL (CLEIA), renin suppression, or a clinician questioning the need for a confirmatory test after a positive screen.