Pepsin depends on an acidic environment for protein digestion. Therefore, it is most effective at a pH of approximately 1.5 to 2. Low pH allows pepsinogen to cleave itself and form active pepsin. When it reaches the duodenum, though, it assumes an inactive form as the pH rises above 6. Nonetheless, protein digestion continues to take place throughout the small intestines via the effects of pancreatic enzymes: trypsin, chymotrypsin, elastase, and carboxypeptidase. As such, pepsin is not essential for life, and protein digestion can still take place in the absence of pepsin. It is worth mentioning that pepsin remains structurally stable until at least a pH of 8. Therefore, it can always be reactivated as long as pH remains below 8. This characteristic proves relevant in the pathophysiology of laryngopharyngeal reflux, as discussed later in the article.[1]
Pepsin plays a role in the pathophysiology of laryngopharyngeal reflux (LPR), a disease that originates from the digestive tract and significantly impacts the upper airway structures. Consider LPR in the differential diagnosis of a patient presenting with hoarseness, mild dysphagia, chronic cough, and non-productive throat clearing.
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Gastroesophageal reflux disease (GERD) is similar to LPR in that both disorders occur due to the reflux of the acidic contents from the stomach. However, two critical differences exist between GERD and LPR. The first is an anatomical difference as patients with GERD have weak LES while patients with LPR have weak LES and UES. The second is that pepsin plays a critical role in the pathophysiology of LPR while playing a minimal or unknown role in GERD.[10]
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Met-Cbl is a cofactor for methionine synthase enzyme. In this reaction, the methyl group of methyltetrahydrofolate transferred to homocysteine to form methionine and tetrahydrofolate. Methionine converted to s-adenosyl methionine (SAM), a methyl donor for phospholipid biosynthesis especially that of the myelin sheath. Tetrahydrofolate is the free form of folate essential for purines synthesis. Dysfunction of this reaction leads to the following:
Cbl is bound to the dietary proteins, upon food preparation and because of the heat effect, Cbl is liberated partially from food. When exposed to light, all forms of free Cbl undergo conversion to be OH-Cbl. Another source of Cbl is that bound to HC available within the bile and delivered to the GI tract via the enterohepatic circulation.
By entering the small intestine, Cbl remains bound to HC even at the relatively neutral environment of the digest. HC is sensitive to pancreatic proteases trypsin and chymotrypsin, which will degrade HC moiety. Subsequently, intrinsic factor will exclusively bind the free Cbl. Intrinsic factor binds only active Cbl received from diet and bile, ensuring that inactive analogs get excreted.
This text comprehensively reviews the current state of the art in Laryngopharyngeal Reflux (LPR) together with a comprehensive explanation and description of the known gastroesophageal reflux (GERD) literature. With chapters written by experts from around the world, this text aims to deliver what is current in reflux recognition, diagnosis, reflux related complications, and the various treatment modalities. This is the first textbook to combine the most up to date knowledge of both LPR and GERD meant for both specialties and the general medicine population. Completely unique to the reflux literature is a section detailing the substantial benefits of a mostly plant based, Mediterranean style diet in the treatment of reflux disease. Encouraging patients to read and learn about diet and health is likely the most important step in improving their disease. The text provides direction to the caregiver on how to transition to a mostly plant-based diet. Review of myths, effects of diet in the setting of other disease states, and dietary consequences are explained. Guidelines on how to transition diet, dining out while maintaining a plant-based diet, and how to wean off medication, such as PPI, are also provided.
processing.... Drugs & Diseases > Gastroenterology Postoperative Ileus Updated: Nov 01, 2021 Author: Burt Cagir, MD, FACS; Chief Editor: Vinay K Kapoor, MBBS, MS, FRCSEd, FICS, FAMS more...
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Opioid Antagonist, Selective Show All Questions & Answers Media Gallery Tables References Overview Background Ileus occurs from hypomotility of the gastrointestinal tract in the absence of mechanical bowel obstruction. When a similar condition occurs in the stomach (eg, in diabetes or after pancreatoduodenectomy), it is called gastroparesis or delayed gastric emptying (DGE). Although the exact pathogenesis of ileus remains multifactorial and complex, the clinical picture appears to be transiently impaired propulsion of intestinal contents. The complex interaction between autonomic and central nervous system function, as well as local and regional substances, may alter the intestinal equilibrium, resulting in disorganized electrical activity and paralysis of intestinal segments. This lack of coordinated propulsive action leads to the accumulation of gas and fluids within the bowel.
Dr. Chhetri is also an international authority on swallowing disorders, having published the seminal book "Dysphagia Evaluation and Management in Otolaryngology" and given many invited lectures around the world on swallowing disorders related to neurogenic and obstructive causes, as well as radiation therapy for head and neck cancer. He is also certified in Transoral Robotic Surgery (TORS) for head and neck cancer.
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