How do I install the Glp1 Pancreatobiliary Risk Monitor skill?

Run npx skillmds@latest add dromlakhani/glp1-pancreatobiliary-risk-monitor in your terminal (requires Node.js), paste this page's agent-chat prompt into Claude, Cursor, or any MCP-connected agent, or download the SKILL.md file and copy it into your agent's skills directory.

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Is Glp1 Pancreatobiliary Risk Monitor free to use?

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Who published Glp1 Pancreatobiliary Risk Monitor?

dromlakhani (@dromlakhani) published this skill. Their other Agent Skills are listed on their SkillMD profile.

Glp1 Pancreatobiliary Risk Monitor by dromlakhani

Name: Glp1 Pancreatobiliary Risk Monitor
Rating: 4.5 (4 reviews)
Author: dromlakhani

Glp1 Pancreatobiliary Risk Monitor

Assess and monitor pancreatobiliary risk (acute pancreatitis, cholelithiasis, cholecystitis, lipase/amylase elevations) in patients on GLP-1 receptor agonists. Use when a clinician asks about gallstone risk on semaglutide/liraglutide/tirzepatide, "GLP-1 and pancreatitis", lipase elevation interpretation, prophylactic ursodeoxycholic acid, or whether to start a GLP-1 in a patient with prior pancreatitis or gallbladder disease. Grounded in Gorgojo-Martínez 2023 §5.

dromlakhani Updated Sep 8, 2026 10 repo stars

File contents

GLP-1 Pancreatobiliary Risk Monitor

Purpose

Pancreatobiliary AEs with GLP-1 RA are uncommon but real — especially in obesity (higher relative risk than in T2D). This skill triages who needs extra caution, which biochemistry to interpret carefully, and what prophylaxis to consider.

Activation

Trigger when:

Patient has prior pancreatitis or gallbladder disease and is being considered for GLP-1.
Lipase or amylase is elevated on GLP-1 therapy.
Right upper quadrant pain or biliary symptoms develop on GLP-1.
Clinician asks about prophylactic ursodeoxycholic acid.

Baseline Risk Numbers

Acute pancreatitis (AP): < 1% across all GLP-1 RA trials.
Cholelithiasis: 0–< 1% in most trials; up to ~3% in some obesity cohorts.
Cholecystitis: anecdotal.
Meta-analysis signal: RR 1.37 (95% CI 1.23–1.52) for gallbladder/biliary disease overall; RR 2.29 (95% CI 1.64–3.18) in obesity trials vs RR 1.27 in T2D trials. Higher dose + longer duration → higher risk.

Mechanism (why obesity > T2D risk)

Rapid weight loss promotes biliary lithogenicity (same mechanism as post-bariatric surgery).
Direct GLP-1 effect on biliary secretion + gallbladder motility (delayed emptying).

Pre-Initiation Triage

Patient profile	Action
No prior pancreatic/biliary disease	Standard initiation; counsel on red-flag symptoms
Prior cholelithiasis	Consider ursodeoxycholic acid prophylaxis during therapy
Prior acute pancreatitis	Caution — share decision; only proceed if benefit clearly outweighs risk
Prior cholecystitis / gallbladder disease	Caution; closer monitoring
Active acute pancreatitis	DO NOT initiate

Lipase / Amylase Interpretation

Asymptomatic elevations up to 3× ULN (lipase) or 5× ULN (amylase) are common on GLP-1 RA.
These elevations are poor predictors of AP — do not stop the drug for asymptomatic elevation alone.
Levels normalise after drug withdrawal.
Stop and investigate only if accompanied by clinical features of pancreatitis (epigastric pain radiating to back, nausea/vomiting unrelated to titration, systemic features).

Volume-Depletion Pitfall

GLP-1-induced vomiting/diarrhoea → volume depletion → severe renal failure risk in vulnerable patients.
Aggressive hydration and prompt symptom management mitigate this rare but serious complication.

Patient Education for Pancreatitis Recognition

Tell patient to report immediately:

Severe upper abdominal pain (epigastric, often radiating to the back).
Pain that is constant and worsens.
Pain accompanied by nausea/vomiting that is qualitatively different from titration AEs.
Fever or jaundice.

Management If Pancreatobiliary AE Develops

Manage according to local centre protocols.
Stop the GLP-1 RA pending workup if AP is suspected.
Reintroduction after AP is generally not recommended.

Rules & Constraints

Don't stop the drug for asymptomatic enzyme bumps — clinical correlation required.
Ursodeoxycholic acid is for selected high-risk (prior cholelithiasis), not universal.
Obesity dose > T2D dose carries higher pancreatobiliary risk — factor into shared decision.
Always include "severe abdominal pain → call now" in the patient brief.
Volume depletion is the silent killer — keep hydration central in any management plan.

Reference

Gorgojo-Martínez JJ et al. J Clin Med 2023;12:145. §5 (Uncommon AEs), Table 3.

---name: glp1-pancreatobiliary-risk-monitordescription: Assess and monitor pancreatobiliary risk (acute pancreatitis, cholelithiasis, cholecystitis, lipase/amylase elevations) in patients on GLP-1 receptor agonists. Use when a clinician asks about gallstone risk on semaglutide/liraglutide/tirzepatide, "GLP-1 and pancreatitis", lipase elevation interpretation, prophylactic ursodeoxycholic acid, or whether to start a GLP-1 in a patient with prior pancreatitis or gallbladder disease. Grounded in Gorgojo-Martínez 2023 §5.---# GLP-1 Pancreatobiliary Risk Monitor## PurposePancreatobiliary AEs with GLP-1 RA are uncommon but real — especially in obesity (higher relative risk than in T2D). This skill triages who needs extra caution, which biochemistry to interpret carefully, and what prophylaxis to consider.## ActivationTrigger when:- Patient has prior pancreatitis or gallbladder disease and is being considered for GLP-1.- Lipase or amylase is elevated on GLP-1 therapy.- Right upper quadrant pain or biliary symptoms develop on GLP-1.- Clinician asks about prophylactic ursodeoxycholic acid.## Baseline Risk Numbers- **Acute pancreatitis (AP):** < 1% across all GLP-1 RA trials.- **Cholelithiasis:** 0–< 1% in most trials; up to ~3% in some obesity cohorts.- **Cholecystitis:** anecdotal.- **Meta-analysis signal:** RR 1.37 (95% CI 1.23–1.52) for gallbladder/biliary disease overall; RR **2.29** (95% CI 1.64–3.18) in obesity trials vs RR 1.27 in T2D trials. Higher dose + longer duration → higher risk.## Mechanism (why obesity > T2D risk)- Rapid weight loss promotes biliary lithogenicity (same mechanism as post-bariatric surgery).- Direct GLP-1 effect on biliary secretion + gallbladder motility (delayed emptying).## Pre-Initiation Triage| Patient profile | Action ||---|---|| No prior pancreatic/biliary disease | Standard initiation; counsel on red-flag symptoms || Prior cholelithiasis | Consider **ursodeoxycholic acid prophylaxis** during therapy || Prior acute pancreatitis | Caution — share decision; only proceed if benefit clearly outweighs risk || Prior cholecystitis / gallbladder disease | Caution; closer monitoring || Active acute pancreatitis | DO NOT initiate |## Lipase / Amylase Interpretation- Asymptomatic elevations up to **3× ULN (lipase)** or **5× ULN (amylase)** are common on GLP-1 RA.- These elevations are **poor predictors of AP** — do not stop the drug for asymptomatic elevation alone.- Levels normalise after drug withdrawal.- **Stop and investigate** only if accompanied by clinical features of pancreatitis (epigastric pain radiating to back, nausea/vomiting unrelated to titration, systemic features).## Volume-Depletion Pitfall- GLP-1-induced vomiting/diarrhoea → volume depletion → severe renal failure risk in vulnerable patients.- Aggressive hydration and prompt symptom management mitigate this rare but serious complication.## Patient Education for Pancreatitis RecognitionTell patient to report immediately:- Severe upper abdominal pain (epigastric, often radiating to the back).- Pain that is constant and worsens.- Pain accompanied by nausea/vomiting that is qualitatively different from titration AEs.- Fever or jaundice.## Management If Pancreatobiliary AE Develops- Manage according to local centre protocols.- Stop the GLP-1 RA pending workup if AP is suspected.- Reintroduction after AP is generally not recommended.## Rules & Constraints1. **Don't stop the drug for asymptomatic enzyme bumps** — clinical correlation required.2. **Ursodeoxycholic acid is for selected high-risk** (prior cholelithiasis), not universal.3. **Obesity dose > T2D dose** carries higher pancreatobiliary risk — factor into shared decision.4. **Always include "severe abdominal pain → call now"** in the patient brief.5. **Volume depletion is the silent killer** — keep hydration central in any management plan.## ReferenceGorgojo-Martínez JJ et al. *J Clin Med* 2023;12:145. §5 (Uncommon AEs), Table 3.

Frequently asked questions