Chapter 16: Cholinergic Agonists & Antagonists

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Welcome back to the Deep Dive.

We have a massive stack of notes today, and frankly, this one is close to my heart.

We are tailoring this session specifically for the learners out there.

You know, the nursing students burning the midnight oil, the pharmacology buffs, and anyone just trying to make sense of the absolute labyrinth that is the human nervous system.

It is a labyrinth indeed, but there is a map, and that is what we are here to provide.

It's a pleasure to be back.

Exactly.

Our mission today is laser -focused.

We are doing a comprehensive page -by -page walkthrough of chapter 16,

cholinergic agonists and antagonists.

We're pulling this directly from the text pharmacology, a patient -centered nursing process approach, 12th edition.

And just to be absolutely clear on our scope today, we aren't wandering off into theoretical neuroscience or speculative treatments.

We are sticking strictly to the text provided.

We're going to guide you through the chapter, and the exact order is presented.

So all the physiology, the drug classes.

All of it.

The physiology, the classes, the specific prototypes like botanical and atropine, and this is the part that actually matters for the job, the nursing process application.

So if you're listening to this, you want the core material to master this chapter.

No fluff.

Now, to hook us in,

we need to talk about the cholinergic system.

This is the parasympathetic nervous system.

The PNS,

the famous arrest and digest system.

Right.

And what blows my mind, and I think this is the coolest part of pharmacology, is that we have chemicals that can reach into the system and either mimic it, essentially hitting the gas puddle on digestion and rest, or totally block it, slamming on the brake.

That analogy of the gas and the brake is perfect.

If you can hold on to that concept, that we are manipulating the bodies, let's call them housekeeping functions, by either pushing them forward or stopping them cold, the rest of the chapter falls into place.

Okay, fantastic.

Let's lay out the road map so everyone knows where we're driving.

We're starting with the framework, the neurotransmitters and

foundational science.

Then we dive into the agonists, the boosters, with a focus on a drug called bethenicol.

Then we flip the coin to the antagonists, the blockers, with the heavyweight champion atropine.

And we'll wrap up with the specialized stuff, you know, the drugs tailored for things like Parkinson's and motion sickness and bladder control.

A logical flow.

We have to build the foundation before we can build the house.

Absolutely.

Let's do it.

Part one, the parasympathetic framework.

The text starts by explicitly calling the parasympathetic nervous system the cholinergic system.

Why the name change?

Or is it?

Is it even a change?

It's not so much a name change as it is a chemical definition.

It's more precise.

The system is named cholinergic because of the specific neurotransmitter used at the very end of the line.

The neuron travels to the organ and to deliver its message to the muscle or gland, it releases acetylcholine.

Acetylcholine.

We see that abbreviated as ACSHA all the time.

Correct.

ACH is the currency of this system.

When your brain wants your heart to slow down or your stomach to start digesting your lunch,

the message is delivered in an envelope made of acetylcholine.

It innervates muscle and organs.

Okay, so if ACH is the letter, we need an aisle box.

The text details two specific types of cholinergic receptors at the organ cells that receive this message.

Yes, and this is where students often get tripped up, so let's slow down here.

The text has a great diagram showing this.

The two receptors are nicotinic and muscarinic.

They sound like ingredients in a strange cocktail.

I remember they're named after the alkaloids that stimulate them, right?

Precisely.

Nicotinic receptors are stimulated by, well, the alkaloid nicotine.

Muscarinic receptors are stimulated by the alkaloid muscarine, which comes from a mushroom.

But in the human body, physiologically, they both respond to our natural acetylcholine.

Okay, but the text makes a critical distinction on location, though.

It does, and this is key for understanding which drugs do what.

Nicotinic receptors are mostly affecting the skeletal muscles.

Skeletal muscles, so like the muscles in your arms and legs.

Exactly, the neuromuscular junctions.

When you decide to lift your arm, that's a nicotinic interaction eventually.

It's voluntary muscle control.

Whereas muscarinic receptors are affecting smooth muscle and slowing the heart rate.

That is the key divide.

We're talking about the involuntary stuff.

The gut, the bladder, the pupils, the heart.

And for the drugs we are discussing in this chapter, the ones used for organ function, bladder control, heart rate, we are playing primarily in the muscarinic sandbox.

So we're usually trying to leave the skeletal muscles alone.

In most cases, yes.

Unless we are treating a specific neuromuscular disease, which we will touch on, but the main show here for general medicine is the muscarinic receptor.

Got it.

Before we get into the drugs themselves, there is this concept of the seesaw effect.

The book has a table on this.

We have the sympathetic system and the parasympathetic system.

The yin and yang of the autonomic nervous system.

You can't understand one without the other.

The text lays it out.

Adrenergic drugs, which are also called sympathomimetics, mimic the sympathetic system.

They are the fight or flight.

So heart rate goes up, pupils dilate, you're ready to run from a bear.

Exactly.

Adrenaline is the classic example.

On the other side, cholinergic drugs or

parasympathomimetics are the rest and digest.

They decrease the heart rate, constrict the pupils, and get the digestion moving.

Okay, that's straightforward.

But then the text throws in a nuance that always requires a double take from me.

I had to read it a couple of times.

The double negative.

Yeah.

The text says, a drug that mimics the sympathetic nervous system and a drug that blocks the parasympathetic nervous system can cause similar responses.

Let's unpack that because it is vital for clinical reasoning.

Imagine a car.

If you want to go faster, let's say increase the heart rate.

You can do two things.

You can step on the gas.

That is a sympathomimetic.

An adrenergic drug.

Okay, hitting the gas, adrenaline.

I'm with you.

Or you can cut the brake lines.

The parasympathetic system is the brake.

It's constantly applying a little bit of pressure to keep the heart from racing.

If you use a parasympathetic blocker, an anticholinergic drug, you're cutting the brake.

The result is the same.

The car goes faster.

Exactly.

The heart rate goes up.

That is a fantastic way to visualize it.

So, a sympathetic stimulant and a parasympathetic blocker both lead to an increased heart rate.

Correct.

And conversely, if you want to slow the car down, you can do two things.

You can block the sympathetic system with something like a beta blocker.

Taking your foot off the gas.

Exactly.

Or you can stimulate the parasympathetic system with a cholinergic agonist.

Slamming on brakes.

You get the same result.

A decrease in heart rate.

You are either taking your foot off the gas or you are actively braking.

That is the aha moment right there.

You can get to the same destination by taking two completely different physiological routes.

That's critical to understand.

It is.

And that brings us directly to our first major class of drugs.

The ones that slam on the brakes or rather the ones that activate the rest

Part two.

Cholinergic agonists.

Also known as parasympathomimetics.

I love that word.

It just sounds like what it does.

It mimics the parasympathetic system.

It does.

These drugs bind to receptors until the body.

It's time to rest.

And it's time to digest.

They mimic the action of our own acetylcholine.

The text mentions selectivity here.

We touched on this with the receptors.

The muscarinic versus nicotinic.

Yes.

Many cholinergic agonists are non -selective.

They'll hit both the nicotinic and the muscarinic receptors.

But clinically, that's messy.

It's not ideal.

Why is it messy?

Well, if you give a drug to help someone pee, which is a muscarinic effect on the bladder, you don't necessarily want their skeletal muscles twitching or cramping, which would be a nicotinic effect.

So we prefer selective agonists that target the muscarinic receptors specifically.

It's more targeted therapy.

Makes sense.

Let's look at the physiological effects.

The textbook has some great tables and figures on this.

If I take a drug that stimulates the system, what is physically happening to my body?

Think rest and digest, but cranked up to 11.

Everything gets wetter and more active.

Okay.

Let's go organ by organ.

The bladder and GI tract.

Stimulation.

Increased tone.

The smooth muscle of the GI tract churns, peristalsis increases.

You get more bowel sounds, more movement.

The bladder muscle, the detrusor muscle contracts to squeeze out urine.

The eyes.

Constriction.

The medical term is meiosis.

The pupils get pinpoint small.

This has an important side effect of helping to lower intraocular pressure, which we'll get to later when we talk about glaucoma.

Okay.

And the heart and lungs.

For the heart, you get decreased heart rate and decreased blood pressure due to vasodilation.

For the lungs, it's a bit of a double -bammy.

It acts to constrict the bronchioles and at the same time, increase bronchial secretions.

So tighter pipes and more fluid in them.

I can see why that would be a problem for someone with asthma.

A huge problem.

It's a major contraindication.

And secretions in general.

Saliva.

Sweat.

Up across the board.

Increased salivation, increased sweating, increased tears.

Everything gets lubricated.

I remember a mnemonic for this from school.

Something like SLDDGE.

Yes.

SLDDGE is a great one.

Salivation, lacrimation, which is tearing urination, defecation, GI distress, and emesis, or vomiting.

It's a very descriptive, if slightly gross, way to remember the effects of overstimulation.

Wet and moving.

That's the agonist mantra.

Now the text divides these agonists into two categories, and this is an important distinction.

Direct acting and indirect acting.

This distinction is crucial because it changes how we use them and what they affect.

Direct acting cholinergic agonists act.

Well, directly.

As the name implies.

Exactly.

They look like acetylcholine, they act like acetylcholine, and they bind right to the receptors to activate the tissue response.

They are convincing imposters.

Okay, so they are the imposters breaking into the house and turning on all the lights.

What about the indirect acting ones?

These are sneakier.

They don't touch the receptor at all.

They target the enzyme colonesterase.

Colonesterase.

That's the cleanup crew, right?

The enzyme that breaks down acetylcholine.

It's the off switch.

Under normal conditions, acetylcholine is released, it does its job on the receptor, and is instantly destroyed by colonesterase, or acetylcholinesterase.

AC.

It keeps the signal short and crisp.

Indirect acting drugs tie up that enzyme.

They inhibit the cleaner.

So the acetylcholine that your body naturally produces just hangs around.

It doesn't get cleaned up.

It accumulates.

It survives for much longer in the synapse.

It just keeps hitting the receptor over and over again because nothing is there to stop it.

Okay, I think I've got an analogy for this.

Direct acting is like hiring a replacement worker to do the job.

Indirect acting is like firing the supervisor so the original workers can just keep working overtime without anyone telling them to stop.

That is actually a brilliant analogy.

Yes.

You stop the breakdown, you extend the effect of the body's own neurotransmitter.

Okay, this makes sense.

Let's zoom in on the direct acting ones first.

Part three.

Direct acting cholinergic agonists.

As we mentioned, these are primarily selective to muscarinic receptors.

So we're targeting the smooth muscle of the GI tract,

the genitourinary tract, glands, and the heart.

And we have a prototype drug here.

This is the big one students need to imprint on their brains.

Methanical chloride.

Methanical is the classic cholinergic agonist.

Its primary use, the one you'll see on exams and in the clinic, is the treatment of urinary retention and neurogenic bladder.

Urinary retention.

So the patient can't pee.

Maybe they are post -op from surgery.

That's a very common scenario.

Anesthesia often puts the bladder to sleep, so to speak.

It becomes a tonic.

Or maybe a patient has a neurogenic issue from a spinal cord injury where the nerves aren't firing correctly.

Methanical stimulates the muscarinic receptors in the detrusor muscle of the bladder.

The detrusor muscle.

Can you explain that?

That's the large muscle that forms the wall of the urinary bladder.

Methanical makes it contract.

It gives it a good squeeze.

At the same time, it helps relax the trigone and sphincter muscles at the exit.

So it squeezes the bag and opens the valve at the same time.

Perfect summary.

Squeeze the bag, open the valve.

The result.

Urination.

Let's talk pharmacokinetics.

How does this drug move through the body?

The chart in the book is interesting.

It is.

The text notes it is poorly absorbed in the GI tract.

This is important.

It means you need a higher oral dose to get the desired effect compared to, say, a subcutaneous injection.

Protein binding and half -life are listed as unknown.

Right.

It's an older drug, so some of that data isn't as robust as with newer medications, but we know it works and we know it's likely excreted in the urine.

And the timing.

This is really important for the nerves planning their shift.

What's the onset and duration?

For an oral dose, the onset is about 30 to 90 minutes.

Peak effect is around 60 to 90 minutes.

The duration is roughly one hour, maybe a bit longer.

So if you give a pill, you don't expect a result in two minutes, but you also don't wait four hours to check either.

Exactly.

You need to be ready with the bedpan or the commode within that 30 to 90 minute window.

You have to anticipate the patient's need to void.

Now, contraindications.

This is a huge safety point.

When should we absolutely not give Bethanacal?

This requires critical thinking about the mechanism.

We know it squeezes the gut and the bladder, so it is absolutely contraindicated if there is a known or suspected intestinal or urinary tract obstruction.

Because if there's a blockage, like a kidney stone or a tumor or a stricture, and you try to force fluid against it?

You risk rupture.

It's plumbing 101.

You don't turn on the pump against a closed valve.

You could cause serious damage.

Okay, that makes perfect sense.

What else?

It is contraindicated in active asthma.

We said it before, but it's worth repeating.

Cholinergic agonists constrict bronchioles and increase secretions.

If someone is already struggling to breathe, you are tightening their airway and filling it with fluid.

It can trigger a severe asthma attack.

That sounds disastrous.

It is.

It's also contraindicated in bradycardia, because it slows the heart even further, and hypotension, as it can lower blood pressure.

And also, peptic ulcer disease.

Why peptic ulcer?

What's the connection there?

Cholinergic stimulation increases gastric acid secretion.

If you have an active ulcer, that's like pouring acid on an open wound.

It can worsen the ulcer, cause pain, and even lead to bleeding.

Let's run through the side effects and adverse reactions.

I'm guessing these are just the rest and digest symptoms taken too far?

Precisely.

The side effects are predictable extensions of the drug's action.

We see the wet symptoms.

Nausea, vomiting, diarrhea, that's the increased GI motility.

Hypersalivation, which is drooling.

Diaphoresis, excessive sweating.

Lacrimation, tearing.

And of course, urinary urgency.

And the cardiovascular and respiratory effects.

The book lists tachycardia as an adverse reaction, which might seem counterintuitive since we said it slows the heart.

Right, that's confusing.

It's what we call reflex tachycardia.

If the drug causes vasodilation and the blood pressure drops too low too fast, the body's own compensatory mechanisms might panic and speed up the heart to try and maintain perfusion.

But generally, the direct effect you watch for is bradycardia and hypotension.

And the really bad life -threatening issues.

Bronchospasm, wheezing, and seizures at very high doses.

Interactions are also listed in the drug profile.

Yes.

It has a decreased effect if taken with antidiarrhythmics like percanomide.

And obviously, atropine counteracts botanical.

Atropine is the antidote for an overdose.

The text mentions a couple of other direct acting agents briefly.

Metaclopramide.

Right.

Metaclopramide is used for gastroparesis.

That's a condition where the stomach empties too slowly.

You see it a lot in patients with diabetes.

It's often used for nausea and GERD as well.

It enhances gastric motility and get things moving downstream so acid doesn't splash back up.

And the other one is palocarpine.

Palocarpine is interesting.

It's primarily used in ophthalmology as eye drops.

It constricts the pupils.

And when the pupil constricts, it physically pulls on the iris, which opens up the trabecular meshwork and the Schlem canal.

That's the drain pipe for the eye, right?

That's the drain pipe.

Opening it helps drain the aqueous humor, the fluid inside the eye.

So it is used to treat glaucoma by lowering that pressure.

There's also an oral form of palocarpine used specifically to treat severe dry mouth or xerostomia by forcing the salivary glands to work.

Okay.

Let's shift gears now.

Moving on to part four.

Indirect acting cholinergic agonists.

These are the enzyme inhibitors.

The cholinesterase inhibitors.

Remember our analogy.

These are the drugs that fire the clean -up crew.

By inhibiting the breakdown of we allow the body's own astray to accumulate.

A key difference here, which is noted in the text, is that because astrea is accumulating everywhere, not just at the muscarinic sites, we get significant skeletal muscle stimulation too.

Ah, so this is where the nicotinic receptors come back into play in a big way.

Exactly.

This makes them useful for a whole different set of conditions.

The text divides these into two main types, reversible and irreversible.

Let's start with reversible.

What are they used for?

The primary use, the classic indication, is myasthenia gravis.

Myasthenia gravis.

I know that means grave muscle weakness.

It's an autoimmune disorder, right?

It is.

In myasthenia gravis, the body's immune system mistakenly attacks and destroys its own nicotinic receptors at the neuromuscular junction.

So, there aren't enough receptors for the ACST to bind to.

The signal from the nerve doesn't get to the muscle properly.

And the result is profound weakness.

Profound weakness.

By giving a reversible cholinesterase inhibitor, we prevent AC breakdown.

We flood the zone.

We keep more ACH available for a longer time to hit whatever few functional receptors are left.

This increases muscle strength.

The text lists a few examples.

Neostigmine, pyridostigmine.

Right.

They have different durations of action.

Neostigmine is short -acting.

Pyridostigmine bromide, which is very common, is moderate acting.

There's also ambinonium, which is long -acting.

And then there's edrophonium.

What's special about edrophonium?

It's very, very short -acting.

Its effects only last for a few minutes.

Because of this, it's used for diagnostic purposes.

It's called the tensilon test.

You give a patient with suspected myasthenia a dose of edrophonium, and if they suddenly regain their muscle strength for five minutes, like their droopy eyelids lift up, you have your diagnosis.

That's fascinating.

And there's one more reversible one mentioned in the context of being an antidote.

Phisostigmine.

This is important.

It is used as an antidote for atropine toxicity or any anticholinergic overdose.

So if you overdose on the blocker, atropine, you give this reversible inhibitor to boost asase levels back up and overcome that blockade of the receptor site.

Side effects for these reversible inhibitors, are they the same wet and moving effects?

Very similar to the direct agonists, but with more potential for muscle cramps or twitching effects.

So you see hypotension, bradycardia, sweating, hypersalivation, and GI distress.

And the same contraindications apply.

Asthma, diabetes, cardiovascular disease.

You have to be cautious.

Now, the irreversible inhibitors.

These sound intense.

They are potent and dangerous.

The drug binds to the cholinesterase enzyme permanently or for a very, very long time.

The body literally has to synthesize brand new cholinesterase enzymes to overcome the effect.

A process that can take days or even weeks.

What are they used for clinically if they're so potent?

Clinically, their use is very limited.

The main one mentioned is for glaucoma in a long acting eye drop form.

The long lasting constriction of the pupil keeps that drainage canal open around the clock.

But because they are so potent, toxicity is a huge risk.

I know that certain pesticides, organophosphates fall into this category.

They do.

And so do nerve gases like sarin.

If someone gets poisoned with an organophosphate, their body is flooded with acetylcholine.

Every cholinergic system goes into overdrive.

They can't breathe.

Their heart stops.

They seizure.

It's a critical medical emergency.

The text identifies the antidote specifically for this.

It's not physostigmine.

No, it is not.

The antidote is prilodoxin chloride or 2PM.

Prilodoxin?

Yes.

It's a cholinesterase reactivator.

It acts like a chemical crowbar.

It breaks that permanent bond between the poison and the enzyme, allowing the enzyme to start working again and break down the excess acetylcholine.

It has to be given very quickly after exposure to be effective.

Okay, we've covered the drugs.

Now let's talk about what the nurse actually does.

Part 5.

Nursing process for cholinergic agonists.

Let's look at their recognized cues or assessment phase first.

As always, baseline vital signs are step one.

You absolutely need to know their heart rate and blood pressure before you give the drug.

These drugs will lower them further.

So if a patient's heart rate is already 55, you hold the drug and you call the provider.

And urine output.

Essential.

The text says to assess that urine output is greater than 1 ,500 mL per day for an adult.

We need to know the kidneys are working and that there isn't an underlying retention issue that could be an obstruction before we start trying to manipulate the bladder.

And history, of course.

You have to get a good history.

You're screening for those contraindications we discussed.

Peptic ulcer, urinary obstruction, asthma.

If the patient has any of these in their chart, giving a cholinergic agonist could be negligent.

Okay.

Moving to take action or interventions, what are the key nursing actions?

First, monitor for orthostatic hypotension.

These drugs dilate blood vessels.

If the patient stands up too fast, gravity wins, blood pools in their legs leaves their head, and they can get dizzy or faint.

So you teach them to rise slowly.

What about timing with meals?

The book is specific about this.

Yes, this is a specific point in the text.

Give the drug one hour before or two hours after meals.

Why is that?

To minimize nausea and vomiting.

If the stomach is full and you stimulate it to contract violently, that food is coming right back up.

Giving it on an empty stomach reduces that risk.

Although the text does note that if significant gastric pain occurs, you might give it with meals, but the standard rule is empty stomach.

The text mentions that we need to monitor liver and pancreatic enzymes,

amylase, lipase, AST, and bilirubin.

These levels can increase in a patient taking cholinergic agonists, which might imply some stress on the liver and pancreas.

And breath sounds.

That seems critical given the asthma contraindication.

Absolutely.

You must auscultate the lungs before and after giving the drug.

You listen for RELS or LONCHI.

Remember, these drugs increase bronchial secretions.

You are listening for any signs of fluid congestion or mucus in the lungs.

If they sound wet or wheezy, you have a problem.

Hygiene is also mentioned, which seems like a small detail but is important.

It's a comfort and skin integrity issue.

Because of the diaphoresis, the excessive sweating, the patient might be drenched.

You may need to increase the frequency of bathing and linen changes to keep them comfortable and prevent skin breakdown.

Wet skin is fragile skin.

And finally, the ultimate safety net.

What do you need to have on hand, just in case?

You must have IV atropine sulfate available.

The dose listed is 0 .6 to 1 .2 mg for an adult.

This is the direct antidote for a cholinergic overdose or cholinergic crisis.

You need to recognize the early signs of overdose.

Flushing, salivation, sweating, nausea, abdominal cramps.

If you see those, you stop the drug, notify the provider, and reach for the atropine.

Patient teaching is the final piece of the nursing process here.

What are the key takeaways for the patient?

Teach them to report dizziness or a heart rate below 60 beats per minute.

Teach them to rise slowly from a sitting or lying position to handle that orthostatic hypotension.

And oral hygiene.

If they are salivating excessively, they need to keep their mouth clean to prevent infection or breakdown of the oral mucosa.

Alright, that is a fantastic breakdown of the agonists.

Now we're going to flip the script completely.

Part 6.

Cholinergic antagonists.

The anti -cholinergics, also known as muscarinic antagonists, parasympathetics, or blocking agents.

I like antispasmodics too, which is listed in the text.

It hints at what they do.

They stop spasms in the gut or bladder.

It does.

These drugs inhibit the actions of acetylcholine.

They do this by occupying the ACE receptors.

And this is key.

They don't activate the receptor.

They just sit there.

They're competitive antagonists.

They park a bus in the parking spot, so ACE can't park its car there.

And the result of blocking that receptor?

By blocking the parasympathetic nerves, the rest and digest system, we allow the sympathetic or adrenergic system to dominate.

So we're back to that seesaw.

If we block, rest, and digest, then fight or flight takes over by default.

Exactly.

The brake pedal is lifted, so the car's natural idle speed seems faster.

Let's look at the major body responses.

The book has a great table and figure for this, just like it did for the agonists.

Heart rate increased.

It blocks the vagus nerve stimulation that normally acts as a brake on the heart.

GI tract.

Decreased motility and peristalsis.

The gut goes to sleep.

This could be a desired effect, but it often leads to constipation.

Decretion.

Try it out.

All of them.

Decreased mucus, decreased salivation, decreased perspiration.

The.

The opposite of bethanical.

It causes urinary retention.

The detrusor muscle relaxes, and the internal sphincter constricts.

It makes it harder to urinate.

The eye.

This is significant and has two components.

First, dilation of the pupils, which is called madriasis.

Second, paralysis of the ciliary muscles, known as cycloplegia.

This means the eye can't focus on close objects.

Everything up close becomes blurry.

In the CNS.

Depending on the drug and dose, you can see decreased rigidity and tremors.

This is why, as we'll see later, they are useful in treating some symptoms of Parkinsonism.

At high doses, you can see excitement, confusion, and delirium.

So if agonists are wet and moving, antagonists are dry and stopped.

Dry and stopped is a perfect summary.

Or you might hear the mnemonic, can't see, can't pee, can't spit, can't.

We can figure out the last one.

Right.

Let's meet the prototype.

Part seven.

Atropine.

Atropine sulfate.

It was first derived from the deadly nightshade or belladonna plant.

It is the classic quintessential muscarinic antagonist.

Pharmacodynamics.

How does it work, specifically?

It is a potent competitive blocker of acetylcholine at the muscarinic receptors.

Specifically, it blocks vagus stimulation to increase heart rate, and it paralyzes the iris synctor muscle to dilate the pupil.

What are the primary therapeutic uses?

When does a nurse see atropine being ordered and used?

There are several very important scenarios.

Preoperative is a big one.

It is used to decrease salivary and respiratory secretions before surgery.

Why do we care about spit during surgery?

What's the risk?

The risk is aspiration.

If a patient is under anesthesia and unconscious, they can't manage their own secretions.

If they are producing a lot of saliva, they might inhale it into their lungs, which can cause pneumonia.

Atropine dries them up before we induce anesthesia.

Ah, that makes perfect sense.

What else?

It's the go -to drug for certain cardiac emergencies, specifically symptomatic sinus bradycardia.

If the heart is beating too slow and the patient is dizzy or their blood pressure is dropping, atropine cuts that vagal brake cable and speeds the heart rate right up.

And in ophthalmology.

For eye exams, when the doctor needs the pupil dilated, that's midriasis, to get a good look at the retina and optic nerve.

It's also used to treat inflammatory conditions like iritis by relaxing the eye muscles.

As we mentioned before, it's an antidote.

Yes, it is the primary antidote for muscarinic agonist poisoning.

If someone overdoses on botanical or is exposed to a cholinesterase like a pesticide or nerve gas,

atropine is life -saving.

It blocks the effects of that overwhelming amount of acetylcholine.

Let's talk pharmacokinetics.

It's well -absorbed and, importantly, it crosses the blood -brain barrier.

This means it can have central nervous system effects like confusion, restlessness, or drowsiness.

It has a relatively short half -life of two to four hours.

And the side effects?

This is the dry list again, I assume?

It is.

Xerostomy of very dry mouth is extremely common.

Nasal dryness, constipation from the slow gut, urinary retention, and a really important one is anidrosis.

Anidrosis.

It means a lack of sweating.

The drug blocks the sweat gland.

Vision issues.

Definitely.

Blurred vision from the cyclic Asia and photophobia,

a painful intolerance to bright light because the pupils are stuck wide open and can't constrict to block the sun.

Cardiac and CNS.

Tachycardia, obviously.

That's often a desired effect, but it go too far.

Headache, confusion, drowsiness, and at high doses delirium and hallucinations.

And any specific life -threatening reactions?

Severe dysrhythmias, laryngeal spasm, and coma are possible with toxicity.

And the text mentions the atropine flush, which is a characteristic flushing of the face and neck caused by vasodilation.

Okay, so atropine is the heavy -header, the non -selective blocker.

But the text also outlines some specialized anticholinergic groups in Part 8.

Yes, these are variations on the theme.

These are drugs that have been developed to be more selective, tailored for specific conditions where we want just one anticholinergic effect, not the whole dry and stopped package.

First up, anti -Parkinson anticholinergics.

In Parkinson's disease, there's an imbalance between dopamine and acetylcholine in the brain.

These drugs affect the CNS to block acetylcholine, which helps suppress the tremors and muscular rigidity.

The text clarifies, they are good for tremors, but have little effect on the bradykinesia, the slow movement, or weakness.

The prototype here is benztropine.

Benztropine.

It's used for Parkinsonism and also for drug -induced extrapyramidal symptoms.

That's the pseudo -Parkinsonism you sometimes see as a side effect of older antipsychotic drugs.

How does it work?

It blocks muscaritic receptors in the brain, and also has a mild effect of blocking dopamine reuptake.

It's trying to rebalance those dopamine and acetylcholine scales in the brain.

Any specific cautions mentioned for benztropine?

Alcohol and other CNS depressants will potentiate the sedation, so no drinking while on benztropine unless you want to be extremely drowsy or even pass out.

Next specialized group, motion sickness.

Here, the main drug is scopolamine.

You've probably seen this.

It's a small, round transdermal patch that's placed behind the ear.

It delivers a slow, steady dose of the drug over three days.

It's a classic for cruises, flying, or long car trips.

And antihistamines are mentioned here, too.

Why is that?

Drugs like diamond hydronate, which is dramamine, and meclizine.

Many first -generation antihistamines have significant anticholinergic properties.

That's why taking dramamine makes your mouth dry and makes you so sleepy.

It's the anticholinergic side effects.

Xerostomia, drowsiness, blurred vision.

Finally, the last specialized group,

bladder control.

This is a huge class of drugs for overactive bladder.

The prototype the text discusses is tolterodine tartrate.

How is it different from just giving a small dose of atropine?

It's more selective.

It has a greater affinity for the cholinergic receptors in the urinary bladder.

So it's designed to decrease urinary frequency, urgency, and incontinence without necessarily drying out your mouth and eyes as badly as a non -selective drug like atropine would.

And a food interaction note here that's important.

Grapefruit juice.

It may increase the drug levels of tolterodine.

You always have to watch out for the grapefruit juice in pharmacology.

It messes with the metabolism of many, many drugs.

Okay.

Part nine.

Nursing process for anticholinergics.

We are focusing on atropine here.

What are the key assessment cues?

First and foremost, check for glaucoma.

Specifically, narrow angle glaucoma.

This is a big red flag.

The myriasis, the pupil dilation caused by atropine, can physically block the drainage of aqueous humor and cause a sudden dangerous spike in intraocular pressure.

It can cause blindness.

What about checking for GI obstruction?

Absolutely.

If the gut is already blocked or moving very slowly, a condition called paralytic helios, giving atropine will just make it worse.

It stops the gut entirely.

The bowel just goes dead.

And urinary retention or BPH?

Same principle.

BPH or benign prostatic hypertrophy in a large prostate already makes it hard to pee.

Atropine will make it even harder, potentially causing complete urinary retention, which is a medical emergency.

Moving on to interventions for a patient on an anticholinergic.

Monitor vital signs report any significant tachycardia.

Monitor fluid intake and output very carefully.

And here's a crucial tip from the text.

Encourage the patient to void before taking the medication.

Because once they take it, that retention effect starts to set in.

Empty the bladder where you still can.

It's a simple preventative measure.

Bowel sounds.

You need to listen for them every shift.

The absence of bowel sounds could suggest a paralytic helios is developing.

You need to be proactive.

Encourage high -fiber foods, fluids, and ambulation to combat the constipation.

And safety.

Bed alarms for confused or elderly patients.

Remember atropine crosses the blood -brain barrier and can cause CNS excitement or drowsiness.

There's a classic phrase.

Mad as a hatter, blind as a bat, red as a beet, dry as a bone.

Describing anticholinergic toxicity.

The confusion part is real.

Mouth care.

It's essential for that xerostomium.

Offer frequent sips of water, hard candy, ice chips, or sugar -free gum.

It helps stimulate whatever little saliva is left and provides comfort.

Let's wrap up with patient teaching.

There are some specific environmental warnings that are really important.

This is one that patients and even new nurses can forget.

You must teach them to avoid hot environments and excessive exertion.

Why is that so critical?

Anidrosis.

The drug stop you from sweating.

Sweating is the body's primary way to cool down.

If you can't sweat, you can overheat very rapidly.

You are at a high risk for heat exhaustion and heat stroke, which can be fatal.

That is a critical life -or -death teaching point.

What about their eyes?

Teach them to wear sunglasses even indoors if the lights are bright.

Their pupils are dilated and can't constrict.

The photophobia will be painful and disorienting without sunglasses.

Driving?

Avoid it.

Tell them not to drive or operate heavy machinery until they know how the drug affects them.

The drowsiness and blurred vision make driving unsafe.

And diet.

As we said, lots of fiber and fluids to keep the gut moving and prevent that constipation.

This has been a massive deep dive.

Let's head to the outro and try to summarize this whole chapter.

If you take nothing else away from chapter 16, remember the balance of fluids and motion.

It's a tale of two extremes.

The agonists.

The agonists are wet and moving.

Think salivation, urination, diarrhea,

sweating.

Everything is flowing and the heart is slow.

And the antagonists.

The antagonists are dry and stopped.

Think dry mouth, urinary retention, constipation.

Nothing is flowing and the heart is fast.

It really is that binary.

Now before we go, I want to leave you with a thought from the clinical judgment case study in the text.

It's a great critical thinking exercise.

The 70 -year -old male scheduled for surgery.

Right.

He is 70.

He is scheduled for gallstone surgery.

He also has a slight tremor.

The provider wants to start him on benztropine for the tremor after his surgery.

But preoperatively, he is given atropine.

So he is getting atropine, which is a potent anticholinergic.

And then he's scheduled to start benztropine, which is another anticholinergic.

Exactly.

Here is the question for you to mull over.

Considering his age and that double dose of anticholinergics, how heavily must a nurse monitor for the cumulative drying and slowing effects?

Specifically, what happens to his bladder and his bowel function if we aren't paying extremely close attention?

It's a classic case of additive effects.

It can be a very dangerous cocktail, if not managed with precise observation and intervention.

Think on that.

Apply that dry and stopped rule, but now double it.

Thank you so much for joining us for this deep dive.

We hope this makes Chapter 16 a little less daunting.

Keep studying.

Keep connecting the dots between the mechanism and the patient.

And a warm thank you from the entire Last Minute Lecture team for tuning in.

We'll see you next time.