The physiology behind LPR involves the malfunction of the upper esophageal sphincter (UES) and the lower esophageal sphincter (LES), which are critical in preventing the reflux of stomach contents back into the esophagus and, in the case of LPR, up into the larynx and pharynx.
LPR has significant clinical implications, as it can lead to a range of symptoms and complications, including:
The larynx is highly sensitive to acid. While the esophagus can withstand up to 50 episodes of acid reflux per day without injury, as few as can cause severe laryngeal inflammation. The Pepsin Mechanism (The Primary Destructive Agent) Lpr Physiology Book Pdf
[Gastric Refluxate] │ ├─► Hydrochloric Acid (Lowers pH, denatures tissue proteins) ├─► Pepsin (Proteolytic enzyme; active up to pH 6.5; causes cellular injury) └─► Bile Salts & Trypsin (Duodenogastric reflux; highly destructive in alkaline/neutral pH) Hydrochloric Acid (HCl)
Controls entry from the esophagus to the stomach. The physiology behind LPR involves the malfunction of
Maintaining a strict alkaline diet (avoiding foods with a pH below 5) ensures that pepsin bound to throat tissues remains dormant.
Laryngopharyngeal Reflux (LPR) Physiology: A Deep Dive Into the "Silent Reflux" Mechanism Share public link Pepsin is a stomach enzyme
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Pepsin is a stomach enzyme responsible for breaking down dietary proteins. It requires an acidic environment to activate but remains stable at neutral pH levels (up to pH 7.4).