In this This Is Why with Dr. Busti pharmacology review, we break down the newest entrant to the antacid category—the potassium-competitive acid blocker (P-CAB), vonoprazan. You’ll see how P-CABs differ from H₂ blockers and PPIs, why their rapid onset, >24-hour acid suppression, and basal acid control make them a valuable option when PPIs fall short, and where they fit for GERD, erosive esophagitis, and H. pylori.
We connect mechanism to practice: relevant anatomy, parietal-cell signaling, PK/PD (onset, duration, metabolism), drug interactions (including pH-dependent meds and CYP pathways), adverse effects (mirroring PPI risks), monitoring, and concise patient counseling (including the chromogranin A caveat).

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Disclaimer: This content is for educational purposes only and is not intended to provide medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have heard in this content.

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Chapter Table of Contents

00:00 – Welcome & Why This Matters
02:35 – Potassium-Competitive Acid Blocker Overview
05:10 – Vonoprazan: The Only Agent in Class
07:20 – Comparing Antacid Classes (H₂RAs, PPIs, P-CABs)
11:25 – Anatomy Behind GERD & Ulcer Disease
15:40 – Parietal Cell Review: How Acid Is Made
19:05 – Mechanism: P-CAB vs PPI vs H₂ Blocker
23:30 – When Simple Antacids Fall Short
25:15 – Pharmacokinetics & Dynamics of Vonoprazan
29:20 – Safety Profile & Common Adverse Effects
34:05 – Drug Interactions & Lab Considerations
38:40 – Monitoring & Follow-Up Parameters
42:10 – Patient Counseling Essentials
44:30 – Practical Clinical Pearls
47:00 – Final Summary & Key Takeaways

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