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Welcome to the Deep Dive.
Today, we're getting into something pretty common but potentially serious.
Gastric hyperacidity, basically too much stomach acid.
Yeah, it's a big deal.
We're talking conditions like GRD, gastroesophageal reflux disease, and peptic ulcer disease, PGD.
And it's really widespread.
Our sources say something like one in six Canadians get heartburn or acid reflux every week.
That's right.
And if that balance between acid and the stomach's defenses gets thrown off for too long, well, you can end up with damage like erosive esophagitis or even precancerous changes, Barrett's esophagus, for instance.
So our mission today is to really break down the drugs used to control this acid.
We'll look at the major classes, how they work, and importantly the clinical flags healthcare pros, especially nurses, need to watch out for.
Okay, but first you understand the target, right?
We're zooming in on the stomach's gastric glands.
Three key cell types live there.
Okay.
You've got the chief cells.
They make pepsinogen, which becomes pepsin, the enzyme that digests protein.
Then the mucous cells.
They produce that thick mucous layer, super important for protecting the stomach lining from the acid itself.
And the third one, that's the main player for our drugs.
Exactly.
The parietal cells.
These are the acid factories, screening hydrochloric acid, HTL.
And what's interesting is how they get switched on.
Right.
There are like three triggers, three signals that tell them to produce acid.
Precisely.
The cell surface has receptors for acetylcholine, heistamine, and gastrin.
Any of these binding basically turns up the acid production dial.
But they all funnel down to one final mechanism.
They do.
All those signals converge on what's called the proton pump.
The proton pump.
Okay.
Yep.
It's technically the hydrogen potassium ATPase pump.
Think of it as the main gatekeeper.
It actively pushes hydrogen ions out into the stomach.
Where they meet up with chloride to make HTL.
You got it.
So if you can block that pump, you shut down acid production, no matter which of those first three signals started it.
Makes sense.
But before we jump into the blockers, there's another culprit we need to mention, especially for ulcers.
It's not just about acid, is it?
No, absolutely not.
We have to talk about H.
pylori.
It's this spiral shaped bacterium, and it's responsible for a huge percentage of ulcers, maybe 70 % of gastroquens, and up to 90 % of duodenal ulcers.
Wow.
So treating it isn't just symptom management, you need to wipe it out.
And that means combination therapy, usually triple or quadruple therapy.
Which includes what?
Always includes a strong acid suppressor, typically a PPI will get to those plus two or sometimes three antibiotics like amoxicillin or chlorothromycin.
Okay, that sets the scene perfectly.
Let's get into the drugs, starting with the oldest group,
the antacids.
These are the ones people grab for quick relief.
Exactly.
They're basic compounds.
Their main job is simple chemistry.
They neutralize the acid that's already in the stomach, bumping up the pH.
So they don't stop the acid from being made.
Nope, just deal with what's there.
They do have a secondary benefit though.
They can stimulate the stomach's own defenses,
mucus, bicarbonate production, even a small pH increase, say from 1 .3 to 1 .6, cuts acidity significantly.
But the big thing here for clinicians seems to be the side effects, and they vary depending on which metal salt is used, especially bowel issues.
That's the classic trade -off.
Aluminum salts, they tend to cause constipation.
They can also bind phosphate, which you need to watch.
Okay.
Magnesium salts, famous for causing diarrhea.
So you often see products combining aluminum and magnesium trying to balance those effects out.
Right, makes sense.
What about calcium carbonate, like Tums?
Calcium carbonate works, but it can cause constipation too, and kidney stones in some people.
And there's this thing called rebound hyperacidity.
When you stop it, the stomach might actually produce more acid for a bit.
And sodium bicarbonate, baking soda, generally not recommended.
It's got a high sodium load, which is bad news for patients with high blood pressure or heart failure.
Plus there's a risk of systemic alkalosis if you take too much.
And a really critical point for kidney patients.
Absolutely critical.
Avoid magnesium antacids and kidney failure.
The kidneys can't clear the magnesium, and it can build up to toxic levels.
Aluminum or sodium -based ones might be safer, but again, watch that sodium.
This leads us to maybe the biggest headache with antacids.
They mess with other medications.
A lot.
They really do.
It's a huge interaction risk.
There are basically four ways they interfere.
Okay.
What are they?
One, they change the stomach pH, affecting how well other drugs dissolve.
Two, they can change urine pH, affecting how drugs get excreted.
Three is adsorption.
They physically stick to other drug molecule.
What's a sponge?
Sort of, yeah.
And four is chelation.
They bind with certain drugs forming clumps that can't be absorbed.
So the bottom line for patients and nurses is you must separate antacids from other oral meds.
Give them at least one, preferably two hours apart.
And failing to do that can seriously impact the other drug.
Traumatically.
The example in our sorts is quinolone antibiotics like Cipro.
Taking it with an antacid can cut its absorption by more than half.
That means treatment failure, potentially antibiotic resistance.
It's a big deal.
Okay.
Let's shift gears to drugs that actually prevent acid production.
The H2 receptor antagonists or H2 blockers.
Things like ronitidine, thymotidine.
And cimetidine, the oldest one.
These drugs work more selectively.
They competitively block the histamine type 2 or H2 receptor specifically on those parietal cells.
So they block one of the three main triggers.
Right.
And by blocking histamine, which is a major player, they make the parietal cell less responsive to the other two signals as well.
HE and gastrin, the overall effect.
Up to a 90 % reduction in acid secretion.
90 % is quite significant.
So they're used for GERD, PUD.
GERD, PUD, erosive esophagitis.
Also really important for preventing stress ulcers, especially in ICU patients.
And generally they have fewer side effects in some other classes, right?
But there's a big warning with cimetidine.
That's right.
The overall adverse effect rate is less than 3%.
But cimetidine, yeah, it's the problematic one.
It significantly inhibits the liver's CYP450 enzyme system.
Ah, the system that metabolizes tons of other drugs.
Exactly.
So cimetidine can cause levels of other drugs to shoot up dangerously.
Think warfarin, the blood thinner, or phenytoin for seizures, or leadocaine.
It can lead to toxicity.
And doesn't it have some weird hormonal side effects too?
It does, though.
Less common.
Things like erectile dysfunction and gynecomastia, breast enlargement in men.
Because of all that, the newer H2 blockers like famotidine, which don't mess with CYP450 nearly as much, are generally preferred now.
Good to know.
And there's a timing rule here too.
Yes.
If someone needs both, take the H2 blocker about one hour before the antacid for West effect.
Oh, and smoking.
It actually decreases how well H2 blockers work.
Interesting.
Okay, now for the most potent class.
The proton pump inhibitors, the PPIs,
omeprazole, lanceprazole, pantoprazole.
Everyone knows these names.
They are definitely the heavy hitters.
Much more powerful than H2 blockers.
And their mechanism is different, right?
They go straight for that final pump.
They do.
Remember the proton pump, the hydrogen potassium ATPase?
PPIs bind to it irreversibly.
They basically break the pump.
Irreversibly.
So it's completely shut down.
Pretty much.
It stops virtually all gastric acid secretion, leading to a state called
basically,
no acid.
And the effect lasts until the parietal cell can make brand new pumps.
Wow.
Total blockade.
So understandably, these are first line for the serious stuff.
Absolutely.
Gold standard for erosive esophagitis, really bad symptomatic GARD, treating PUD, especially an SAID -induced ulcers.
And like we said, essential for killing H.
pylori, along with antibiotics.
But this incredible effectiveness has led to a bit of a problem, hasn't it?
Lots of people on them long term.
And now there's this push for deprescribing.
What are the risks driving that?
Yeah, long term high dose use has definitely raised some red flags.
There are four main concerns we're seeing in the literature.
First, without stomach acid to kill bugs, there's an increased risk of gut infections, especially C.
difficile, which can be really dangerous.
Second, there's a link to osteoporosis.
We're seeing higher rates of wrist, hip, and spine fractures in long term users.
Might interfere with calcium absorption somehow.
Okay, two more.
Third, there's growing evidence associating long term PPI use with chronic kidney disease.
And fourth, they can cause low magnesium levels or hypomagnesemia.
So a pretty significant list of potential long term issues.
It is.
And that's why there's so much focus now on making sure patients who are on them, especially long term, still actually need them.
Reassessing the need is key.
And how should people take these?
Best taken on an empty stomach, usually 30, 60 minutes before the first meal of the day, like breakfast.
That optimizes their ability to find and shut down the active pumps.
And just a quick note, Panda Prozole is the only one currently available for IV use in Canada.
All right, let's quickly touch on a few other agents that work differently.
Like suculfate.
I've heard it called the liquid bandage.
That's a great description.
It's unique because it works right at the ulcer site.
It binds to proteins in the damaged tissue, forming a protective barrier, like a patch, that shields the ulcer from acid and pepsin.
Does it get absorbed much?
Hardly at all.
It acts locally.
Important dosing point.
Yeah.
Give it one hour before meals and at bedtime.
And you need to avoid antacids for about 30 minutes before or after taking suculfate, because the antacid can interfere with its binding.
Got it.
Next up, mesoprostol.
This one's a synthetic prostaglandin.
Yes, a prostaglandin E analog.
Its main job is to help protect the stomach lining, particularly for patients taking NSAIDs long -term, which are notorious for causing ulcers.
It has a cytoprotective effect.
But it comes with a huge warning label, especially regarding pregnancy.
Absolutely critical warning.
Mesoprostol causes strong uterine contractions.
It can induce labor or cause abortion.
So it is completely contraindicated in anyone who is pregnant or might become pregnant.
Full stop.
Major safety point.
Okay.
Duly noted.
And lastly, semethicone.
This one's often in combination products.
Right.
It's an anti -flagellant.
It doesn't touch acid at all.
It just works on gas bubbles, reducing their surface tension so they break down into smaller bubbles, making them easier to get.
Will expel.
Helps with bloating.
So putting this all together for clinical practice, what's the nurse's role here?
It really comes down to careful assessment and thorough patient education, doesn't it?
Exactly.
Start with baseline checks.
You need to know the patient's liver and kidney function, especially before starting H2 blockers or PPIs.
And remember that kidney function dictates antacid choice, no magnesium if kidneys are impaired.
And checking for hidden sodium in antacids, especially for heart patients.
Yes.
Crucial for those with hypertension or heart failure.
And always be alert that these drugs, particularly in cassids, can mask symptoms of something more serious, like a GI bleed or even cancer.
If symptoms aren't resolving, investigate further.
On the implementation side, timing is everything.
PPIs before meals, omeprazole capsules swallowed whole, though some, like lancoprazole granules, can be mixed with applesauce.
Right.
Antacids need a good amount of water, about 240mL to help them dissolve and work properly, and hammer home that one -two -hour separation rule from other meds.
And for IVH2 blockers?
Infuse them slowly.
Rapid infusion can cause hypotension.
And for patients on those multi -drug H -pylori regimens, stress that they must take every single dose, especially the antibiotics exactly as prescribed, for the full duration.
Compliance is key for eradication.
Finally, monitoring.
Watch for improvement, less pain, fewer GRD symptoms.
But also watch for side effects, whether it's constipation or diarrhea from antacids, or those longer -term PPI concerns we discussed.
So to quickly recap the main players.
Antacids neutralize existing acid.
H2 blockers block histamine receptors, cutting acid by up to 90%.
And PPIs block the final pump, stopping almost all acid production.
And remember those key warnings.
Keep antacids away from other oral drugs, especially things like quinolones.
Be cautious with cimetidine due to its drug interactions.
And misoprostol is an absolute no -go in pregnancy.
And maybe a final thought for you to take away.
Particularly with PPIs, the question of long -term use requires constant vigilance.
Given the known risks,
C, diff, fractures, kidney issues, always ask, does this patient's current condition still warrant exposure to such a potent drug?
It's about continuously weighing that risk versus benefit for each individual.
Excellent point.
A warm thank you from the Last Minute Lecture Team for joining us on this deep dive.