The Lab / Core medicine / Lesson 16
One kind of cell in your stomach lining pumps out acid strong enough to break down a meal, but only when it is called. Build that cell one piece at a time, then watch four kinds of acid-reducing drugs turn it down, each at a different step.
Educational, not for clinical use
Build the idea
The stomach is a stretchy, muscular bag that churns swallowed food. Its inner layer, the lining, is dotted with tiny openings called gastric pits (gastric means “of the stomach”). Each pit leads down into gastric glands, deeper tubes that make the stomach’s juices.
Build the idea
The glands of the stomach’s domed top and main body hold large parietal cells. One face of each looks into the hollow inside of the stomach. The opposite face looks onto the blood side, where tiny blood vessels bring supplies and messages.
Build the idea
A parietal cell makes acid. A liquid is acidic when it holds many hydrogen ions: tiny electrically charged bits of hydrogen. The more hydrogen ions in the stomach, the more acidic it is. The gauge tracks how acidic the stomach is.
Build the idea
In the stomach-facing surface sit proton pumps: tiny machines that push hydrogen ions (also called protons) out into the stomach and pull potassium, another charged mineral, back in, one for one. They burn energy to push against a steep uphill difference.
Build the idea
Chloride, the charged form of chlorine found in table salt, follows through a channel, a pore in the cell surface. Hydrogen ions and chloride together make hydrochloric acid, the stomach’s acid. A second gauge tracks how much acid the cell makes.
Build the idea
Acid unravels the proteins in food and switches on pepsin, an enzyme (a protein that speeds up a chemical change) that cuts proteins into pieces. The acid also kills most germs swallowed with food.
Build the idea
Between meals most pumps rest inside the cell, packed in tiny bubbles called vesicles. When the cell is called to work, the vesicles merge with the stomach-facing surface and their pumps start. When the call stops, the pumps are pulled back in.
Build the idea
A neighbouring cell releases histamine, a messenger. It docks on a receptor, a protein on the cell surface shaped to fit one messenger: the H2 receptor (histamine type-two receptor). Docked histamine sends an on signal, and stored pumps rise to the surface.
Build the idea
Gastrin, a hormone (a messenger carried in the blood) from the lower stomach, and acetylcholine, released by nerves when you see, smell or eat food (Lesson 6), dock on their own receptors. Histamine also strengthens their push.
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Surface cells coat the lining in mucus, a thick slippery gel, laced with bicarbonate, a base: a substance that soaks up hydrogen ions and so cancels acid. Where this shield fails, acid eats a sore into the lining: an ulcer.
Build the idea
The lining also makes prostaglandins, local messengers that tell the parietal cell to ease off and the surface cells to make more mucus and bicarbonate. Pain relievers such as aspirin lower prostaglandins, which is one reason they can cause ulcers.
Build the idea
Messengers call pumps to the surface, the pumps make hydrochloric acid, prostaglandins brake the cell and the shield guards the lining. Two measures sum it up: how much acid the cell makes, and how acidic the stomach is. Drugs can lower either one.
What changes it
Proton pump inhibitors, such as omeprazole, lock working pumps shut for good. The messengers still call, but locked pumps cannot push hydrogen ions, so acid made and stomach acidity fall until the cell builds new pumps.
What changes it
H2 receptor blockers, such as famotidine, sit in histamine’s receptor without switching it on. Histamine’s push is lost, and so is its boost to gastrin and acetylcholine, so fewer pumps rise: less acid is made and the stomach is less acidic.
What changes it
Antacids, such as calcium carbonate, are bases you swallow. They cancel acid already in the stomach, so it turns less acidic quickly, but only for a while: the cell, its messengers and its pumps carry on making acid as before.
What changes it
Prostaglandin analogues, such as misoprostol, are lab-made copies of the lining’s prostaglandins. They press harder on the parietal cell’s brake and thicken the mucus and bicarbonate shield: somewhat less acid is made, and the lining is better guarded.
Start with Next, or use the arrow keys. Pictures are illustrative, not measurements.
Loading reference values…
Normal teaching baseline.
The blue line on each bar, and the large number beside it, show where an illustrative teaching model sits: not a patient measurement and not a sourced value. The shaded bands are the reference ranges quoted under each row. Selecting a drug or condition shows the expected direction of each value, compared with a normal body, and applies that state to the model. Where no direction is cited, no arrow is shown and the model holds that value where it was.
Proton pump inhibitors, H2 receptor blockers and prostaglandin analogues are animated in the Lesson and in Explore freely, but they are not listed as states here: no open reference with a checked excerpt for them was available to this page, and every state on this tab must quote its source.
The acid-base links between the stomach and the blood are taught in Lesson 11: Acid–Base Balance.
An illustrative teaching model of one settled parietal cell. Turn each messenger up or down, add drugs (they combine), and watch the pumps, the acid made and the acid left in the stomach. Dashed marks are the normal cell; solid marks are your settings.
Everything is worked out relative to the normal cell and settles at once; there is no time course. The on signal is the push of the three messengers, with histamine counted twice over: it pushes on its own (four tenths of the total) and multiplies the push of gastrin and acetylcholine (three tenths each), so losing histamine also weakens the other two. Prostaglandins divide the on signal: the more prostaglandin, the stronger the brake. In the normal cell four in ten pumps are at the surface; the share rises in proportion to the on signal until every pump is up.
Acid made is the number of working surface pumps compared with normal. A proton pump inhibitor locks a share of the surface pumps; an H2 receptor blocker plugs a share of histamine’s receptors; a prostaglandin analogue adds to the lining’s own prostaglandin, which also thickens the mucus and bicarbonate shield. An antacid touches none of this: it neutralises a share of the acid already in the stomach, so acid made stays the same while the acid left in the stomach falls. How acidic the stomach is follows the acid left on a ten-fold (logarithmic) scale, as the pH scale does. The sizes of every effect are illustrative; only their directions are meant to teach.
Left out: food’s own buffering, the timing of meals, somatostatin and other brakes, pepsin and intrinsic factor, how drugs are absorbed and cleared, and every real-world difference between people. Nothing here is a prediction for a real person, and nothing here is a treatment plan.