This skill outlines the emergency management of suspected adrenal crisis, recommending immediate parenteral hydrocortisone (100 mg adult, 50 mg/m² pediatric) plus fluid resuscitation, then 200 mg/24 h (50–100 mg/m²/24 h pediatric) hydrocortisone. Trigger when patient presents with hypotension, hyponatremia, hyperkalemia, or unexplained shock suggestive of adrenal insufficiency.
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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).
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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”.
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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).
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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".
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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 ratio >4:1', and 'ratio 3:1 suggestive of bilateral disease'.
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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.
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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.
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Diagnose monogenic and syndromic obesity in children and adolescents using a structured step-by-step algorithm. Use this skill whenever a clinician suspects a genetic cause of obesity, asks about leptin deficiency, MC4R mutation, POMC deficiency, PCSK1 deficiency, leptin receptor deficiency, Bardet-Biedl syndrome, Prader-Willi syndrome, Alström syndrome, or any case of early-onset severe obesity with hyperphagia. Also trigger for questions about targeted pharmacotherapy including setmelanotide or metreleptin, or when to order a genomic obesity panel. Cross-references the NHS Genomic Test Finder skill to surface the relevant R-code once a diagnosis is reached.
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Screen a child with obesity for red flags suggesting monogenic, syndromic, or secondary endocrine causes — distinguishing atypical from typical exogenous obesity. Trigger when a clinician asks whether obesity could be genetic or hormonal, suspects Prader-Willi syndrome, Cushing disease, hypothyroidism, ROHHAD, Bardet-Biedl syndrome, leptin deficiency, or craniopharyngioma, or when a child has early-onset severe obesity, short stature with obesity, hyperphagia, hypotonia, dysmorphic features, or developmental delay with weight gain.
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Select the right treatment tier for a child with obesity — behavioural, pharmacologic, or surgical — using the CMAJ 2025 pediatric obesity guideline. Trigger when a clinician asks what to do for a child with obesity, which intervention to start, whether to escalate treatment, or when to consider medication or surgery for pediatric obesity.
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Select the right pharmacologic agent for a child aged 12+ with obesity using the CMAJ 2025 guideline — choosing between GLP-1 receptor agonists, metformin, or orlistat with monitoring guidance. Trigger when a clinician asks which medication to use for pediatric obesity, whether to start semaglutide or metformin in a child, or how to manage obesity pharmacologically in adolescents.
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Decide whether a kidney from a brain-dead deceased donor (DBD) with diabetes mellitus and/or hypertension is suitable for transplantation, using the ISOT 2025 Delphi consensus and Table 4 eligibility checklist. Trigger when a clinician asks "can I use a kidney from a diabetic deceased donor", "is this DBD with HTN/DM acceptable", "ECD donor with diabetes — accept or decline", "DBD eligibility for hypertensive donor", or shares a deceased donor with diabetes or hypertension and needs an accept/borderline/decline decision.
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Complete bedside prescribing reference for Mirago (mirabegron, beta-3 adrenoceptor agonist) for overactive bladder — covering contraindications, safety screening, drug interactions, dose selection in special populations, titration, and administration. Use when a clinician asks how to start mirabegron, what dose to use in renal or hepatic impairment, is mirabegron safe in this patient, mirabegron drug interactions, or Mirago for OAB.
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Screen a child aged 13+ with obesity for eligibility for bariatric surgery (laparoscopic sleeve gastrectomy or Roux-en-Y gastric bypass) using the CMAJ 2025 guideline. Trigger when a clinician asks whether a child qualifies for weight loss surgery, bariatric surgery in adolescents, sleeve gastrectomy in a teenager, or when to refer for surgical management of pediatric obesity.
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Bedside prescribing reference for Bemdec (bempedoic acid / NEXLETOL) — indication check, dose, statin co-prescribing safety caps, monitoring plan, warnings for hyperuricemia and tendon rupture, and special population guidance. Use when a clinician asks "can I start bempedoic acid", "Bemdec indication", "is bempedoic acid safe with my statin", "patient on Nexletol has joint pain or high uric acid", "bempedoic acid in CKD or liver disease or pregnancy", or any prescribing or monitoring question about bempedoic acid.
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Decide when to order coronary artery calcium (CAC) scoring in a primary-prevention patient and interpret the result per the 2026 ACC/AHA multisociety dyslipidaemia guideline. Covers the Class 1 indication (men ≥40 / women ≥45, borderline / intermediate PREVENT-ASCVD risk, uncertainty about LLT), CAC score interpretation (0, 1–99, 100–299, ≥300, ≥1000), how CAC modifies LDL and non-HDL goals, when to repeat CAC, and pitfalls (incidental CAC on non-cardiac CT, radiation, cost). Use when a clinician asks should I order a CAC score, CAC indications, what does CAC 150 mean, treatment goals with CAC score, repeat CAC frequency, CAC in a smoker, CAC vs CCTA, is CAC useful in intermediate risk. Grounded in the 2026 ACC/AHA multisociety dyslipidaemia guideline.
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Work a primary-prevention patient through the 2026 ACC/AHA multisociety dyslipidaemia guideline CPR framework — Calculate (10-year and 30-year PREVENT-ASCVD), Classify (low / borderline / intermediate / high), Personalize (demographic, clinical, biomarker, and reproductive risk enhancers), and Reclassify (coronary artery calcium scoring where appropriate). Use when a clinician asks how to assess ASCVD risk for primary prevention, who needs a statin, borderline risk patient what to do, intermediate risk should I start a statin, risk enhancers to look for, premature family history of ASCVD how does it change risk, pregnancy-related risk factors, PCOS and cardiovascular risk. Grounded in the 2026 ACC/AHA multisociety dyslipidaemia guideline.
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Set absolute LDL-C, non-HDL-C, and ApoB treatment goals, PLUS percent LDL-C reduction, for a primary-prevention patient on lipid-lowering therapy per the re-introduced treatment goals in the 2026 ACC/AHA multisociety dyslipidaemia guideline. Covers goals by PREVENT-ASCVD category (low / borderline / intermediate / high), by CAC score, in severe hypercholesterolaemia / FH, in diabetes with multiple ASCVD risk factors, and the ApoB targets once LDL-C and non-HDL-C goals are met. Use when a clinician asks what LDL goal to aim for, LDL target for intermediate risk, non-HDL goal, ApoB target, dual goals on statin, patient at goal or not, how low should LDL go, statin not enough what next. Grounded in the 2026 ACC/AHA multisociety dyslipidaemia guideline.
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Order and interpret lipoprotein(a) [Lp(a)] measurement at least once in a lifetime, apply the risk-enhancer threshold (≥125 nmol/L or ≥50 mg/dL), and run cascade screening of first-degree relatives for premature ASCVD, familial hypercholesterolaemia, or elevated Lp(a) per the 2026 ACC/AHA multisociety dyslipidaemia guideline. Covers the Class 1 lifetime measurement, how elevated Lp(a) affects LLT initiation and intensification, the cascade screening indications, the interaction of Lp(a) with ASCVD risk estimation, and current therapeutic limitations. Use when a clinician asks when to check Lp(a), how often to repeat Lp(a), elevated Lp(a) what next, treatment for high Lp(a), should I screen my patient's family, Lp(a) and statins, cascade screening indications. Grounded in the 2026 ACC/AHA multisociety dyslipidaemia guideline.
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Performs corticotropin stimulation test to diagnose adrenal insufficiency when morning cortisol is indeterminate (3-15 µg/dL). Triggers include morning cortisol 3-15 µg/dL requiring further AI testing.
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Administers immediate parenteral injection of 50–100 mg hydrocortisone for suspected adrenal crisis secondary to adrenal insufficiency. Triggers include hypotension, hypoglycemia, or acute illness in a patient with known adrenal insufficiency.
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Clinicians educate adrenal insufficiency patients taking nondexamethasone glucocorticoids who initiate enzyme-inducing antiepileptic drugs about early signs of adrenal insufficiency. Trigger when an AI patient on nondexamethasone GC starts an enzyme-inducing AED such as phenytoin, carbamazepine, or oxcarbazepine.
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In central hypothyroidism patients receiving levothyroxine who initiate enzyme‑inducing antiepileptic drugs, the guideline recommends checking free T4 at least 6 weeks after AED start and increasing the levothyroxine dose if free T4 falls below the target range. Triggers include: central hypothyroidism patient on levothyroxine starting antiepileptic drug such as phenytoin, carbamazepine, or oxcarbazepine.
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