Junhyung Park

Junhyung Park

A Passionate Student. Always Striving to Become a Person of Value.

Episode with Gastritis

5 minute read

Introduction

This post contains information concerning gastritis, or inflammation of the stomach lining, and medications usually prescribed to treat gastritis, as well as their chemical structures and physiological mechanism of action.

Motivation

On January 28, 2025, I was in a lot of pain again due to chronic gastritis. I suppose my stomach didn’t take my dinner well or perhaps I was too stressed from what had happened the day before.

At any rate, starting around 9 PM, the pain was so unbearable that I couldn’t study at all. Actually, rather than feeling like my stomach was burning, it felt as if someone had punched me hard in the stomach, leaving a deep bruise on my stomach lining. It was as if someone struck my upper abdomen with a baseball bat.

Around 9:30 PM, I took two gastritis-relief tablets before going to bed. But six hours later, at 3:10 AM, I woke up again because of the pain. This time, I took two famotidine-containing pills before going back to sleep. Fortunately, when I woke up the next day, my stomach felt better.

The next day, I had an upper endoscopy at the internal medicine clinic, and the doctor told me that I had severe gastritis. Fortunately, the Helicobacter pylori test came back negative, and even more fortunately, the results of the endoscopy showed no signs of a stomach ulcer. However, the doctor did mention that my gastritis was quite severe for my age and recommended better stress management. He also emphasized the importance of maintaining a regular, healthy, and proper eating habit.

In retrospect, I feel strongly that these kinds of events should be recorded. If I were in pain, I should record information such as, what the pain felt like, how long its duration was, and why I think I was in pain. By doing so, I can think about what I need to do to avoid the same pain later on. Plus, if I look up why I was in pain and understand exactly how taking certain kinds of medicine alleviates the symptoms, some of the frustrating questions I previously had may be answered. Most importantly, the notes I keep will become a valuable reference later on.

Returning to the main topic, after briefly looking up the causes of stomach pain and acute gastritis, as well as the medications I took, I found that: The main ingredients of the pills I took were dicyclomine hydrochloride (link) and papaverine hydrochloride(link), as well as famotidine.

Dicyclomine hydrochloride helps relieve abdominal pain through a dual-action mechanism as an antispasmodic and anticholinergic agent (link). In other words, it blocks acetylcholine, a neurotransmitter responsible for muscle contractions, from acting on specific receptor sites (link).

A Brief Analysis

Question 1

But how are muscle contractions and stomach pain related? How does an anticholinergic drug, which blocks acetylcholine (a neurotransmitter responsible for muscle contraction), help relieve stomach pain?

First, when the smooth muscles of the gastrointestinal tract contract involuntarily, it can cause spasms and pain (link). Anticholinergic antispasmodic drugs help by preventing acetylcholine from binding to nerve cell receptors, which in turn relaxes the smooth muscles of the digestive tract. In other words, these drugs work by blocking acetylcholine activity in both the central and peripheral nervous systems (link). This blocking action suppresses involuntary muscle movements in various organs, including the stomach and intestines, thereby reducing pain and spasms.

Question 2

What exactly is acetylcholine, and does preventing it from binding to nerve cell receptors cause muscle relaxation?

Acetylcholine (ACh) is an organic compound that functions as a neurotransmitter in both the central and peripheral nervous systems (link). It is synthesized from choline and acetyl-CoA and is stored in synaptic vesicles at the nerve cell terminals until it is released (link).

Once released, acetylcholine travels across the synaptic cleft and binds to two types of receptors:

  • Nicotinic acetylcholine receptors (nAChR)
  • Muscarinic acetylcholine receptors (mAChR)

Since acetylcholine binding to receptors triggers muscle contraction, preventing it from binding to nerve cell receptors results in muscle relaxation.

Question 3

How does acetylcholine binding to receptors cause muscle contraction?

1. Release of Acetylcholine (ACh)

First, motor neurons at the neuromuscular junction release acetylcholine (ACh). (Motor neurons are nerve cells that transmit commands from the central nervous system to muscles or glands. (link))

2. Binding to Receptors

The released ACh then binds to nicotinic acetylcholine receptors (nAChR) on the muscle fiber membrane (sarcolemma) (link).

3. Opening of Ion Channels

This binding opens ion channels, allowing sodium ions (Na⁺) to enter the muscle cell (link).

4. Depolarization and Action Potential

The influx of sodium ions depolarizes the muscle fiber, triggering an action potential.

5. Muscle Contraction

This action potential leads to a series of intracellular events that result in muscle contraction.

Question 4

Anticholinergic drugs prevent acetylcholine from binding to nerve cell receptors. How does this process work?

Anticholinergic drugs work by competitively inhibiting acetylcholine (ACh) from binding to muscarinic and nicotinic receptors (link).

1. Competitive Inhibition

Anticholinergic drugs compete with ACh for binding sites on receptors (link).

2. Receptor Blockade

If an anticholinergic drug binds to the receptor first, ACh cannot attach and activate the receptor.

3. Signal Disruption

By blocking ACh binding, anticholinergic drugs interrupt the transmission of nerve signals that would normally be triggered by ACh (link).

As a result, smooth muscle contractions in various organs, including the digestive tract, are reduced, leading to muscle relaxation and relief from spasms.

References

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