Chapter 10: Analgesic Drugs

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Welcome back to The Deep Dive.

Today, we're undertaking a really important deep dive into something universal pain.

It's one of the biggest reasons people seek medical care, honestly.

Absolutely.

And the suffering it causes.

Yeah.

It's just immense.

It impacts everything.

So our mission today, it's pretty straightforward, but absolutely critical.

We want to give you a clear, solid guide to managing pain with medications.

And we're going beyond just how the drugs work.

We're really focusing on those crucial safety measures, the things that make the difference between effective relief and, well, potential disaster.

Exactly.

We have to start with the definition, right?

Yeah.

Because it really shapes everything else.

It does.

Formally, pain is defined as an unpleasant sensory and emotional experience linked to actual or potential tissue damage.

But the practical rule, the one you hear all the time in nursing, pain is whatever the patient says it is, period.

It exists when they say it does.

Highly individual.

So true.

But the underlying physiology does give us a couple of key concepts to anchor ourselves.

Right.

Like the pain threshold.

Yeah.

The pain threshold.

That's the level of stimulus needed before you actually feel a sensation as pain.

And what's interesting is, for most people, that threshold is pretty similar.

It's more about the wiring.

But what's not similar is pain tolerance.

That's where you see huge variation.

Oh, absolutely.

Pain tolerance is how much pain someone can actually endure without it disrupting their life, their function.

And that's influenced by everything.

Culture, past experiences,

anxiety, even anger.

All those psychological factors can really lower tolerance, can't they?

Significantly.

OK, so to treat pain effectively, we need to classify it.

Let's start with duration.

Good place to start.

You've got acute pain.

Sudden onset usually serves as a warning, like, hey, something's wrong here.

Like after surgery or an injury.

Exactly.

And it typically subsides when you treat the cause or it heals, usually lasts less than six weeks.

Then there's the other side of the coin.

Chronic pain.

Right.

Persistent or it keeps coming back.

Lasts longer than, say, three to six months.

And this is often much tougher to treat.

Why is that?

Does the body change?

Yeah, in a way, the nervous system itself can undergo changes, becoming hypersensitive.

It's like it learns to be in pain.

This can also lead to needing higher doses of drugs over time tolerance.

OK, duration is one way.

What about the source where the pain is coming from?

That's crucial, too.

You've got somatic pain, think muscles, ligaments, joints, bones,

that kind of pain.

Like a sprained ankle or arthritis?

Precisely.

And this type often responds pretty well to non -opioids,

maybe NSAIDs, those nonsteroidal anti -inflammatory drugs.

But then there's visceral pain.

That sounds deeper.

It is.

It originates from your internal organs, smooth muscles.

Think appendicitis or pancreatitis.

It's often described as deep, aching cramping.

And that usually needs stronger stuff, opioids.

Generally, yes.

Visceral pain signals are often more diffuse, less localized, and they tend to require the central pain blocking action of opioids.

NSAIDs might help a bit, but often aren't enough on their own.

OK, what else?

I know there's pain related to nerve damage.

Right.

Neuropathic pain.

This is a big one.

It results from damage to the nerve fibers themselves.

Diabetes, shingles, spinal cord injury, those can cause it.

And this is tricky to treat, right?

It doesn't always respond well to standard painkillers.

Exactly.

This is where those adjuvant drugs become so important.

Things like certain antidepressants or anticonvulsants.

They target the specific mechanisms of nerve pain in ways opioids often can't.

And one more, phantom pain.

Yeah, phantom pain.

Pain felt in a part of the body that's been removed surgically or traumatically.

It's a very real sensation, even though the limb isn't there.

It originates in the brain and spinal cord.

Wow.

OK, so understanding these types is key.

Now, how does the pain signal actually get, well, signaled?

The gait theory.

The gait theory of pain transmission.

It's a great model.

Imagine a gait in the dorsal horn of your spinal cord.

It's like a checkpoint for pain signals heading to the brain.

So when you get injured.

Pain impulses travel along nerve fibers, not septors.

There are different types.

Small C fibers carry dull, aching pain signals.

When they arrive at the spinal cord, they tend to open that gait.

Letting the pain signal through to the brain.

Ouch.

Right.

But they're also larger A fibers.

These carry non painful sensations like touch, pressure, vibration.

Think about rubbing a bumped elbow.

Yeah, it does seem to help sometimes.

That's because those A fiber signals travel faster.

They reach the gait first and tend to close it, blocking or reducing the number of pain signals from the C fibers that get through.

So non painful input can literally block painful input at the spinal cord level.

Basically, yes.

And here's where it gets really cool.

Can I get to pharmacology?

Your body makes its own natural painkillers, endogenous neurotransmitters.

Like endorphins.

Exactly.

Endorphins and enkephalins.

These chemicals bind to opioid receptors in the body and brain, and they also act to close that spinal cord gait.

Ah, so they function like, well, like opioid drugs.

Precisely.

Opioid medications essentially hijack this natural pain relief system, binding to those same receptors and amplifying that gate closing effect.

OK, let's dive into the opioids themselves, the big guns in pain management.

We talk about receptors, right?

Mu, kappa, delta.

We do.

And the Mu receptor is really the most important one for analgesia.

When an opioid binds strongly to Mu, you get powerful pain relief.

But there's always a but.

There is.

Mu activation also causes euphoria, which contributes to misused potential.

And critically, it causes respiratory depression.

That's the big danger.

So most of the common opioids like morphine, fentanyl, they're strong activators.

Yes, they're called agonists.

They bind to the receptor and produce the full strong response.

But then there are others like agonists, antagonists or partial agonists.

They sound different.

They are.

They bind to the receptor, often Mu, but they only activate it partially weekly, or they might block other opioid receptors like kappa.

They have that analgesic sealing effect.

What exactly does that mean?

Why does the pain relief top out?

It means that once you reach a certain dose, giving more of the drug doesn't produce more pain relief.

All the available receptors that it can activate weekly are already occupied.

So more drug doesn't equal more effect beyond that point.

Right.

The upside is potentially a lower risk of misuse and maybe less respiratory depression compared to full agonists.

The downside, they're usually not strong enough for severe pain like bad cancer pain.

And they can even cause withdrawal if given to someone dependent on a full agonist.

OK, now for something absolutely critical, non -negotiable knowledge.

Equal analgesia, understanding drug potencies.

This is life or death.

Seriously.

Misunderstanding relative potencies is a major source of medication errors and overdoses.

Give us the crucial example.

Hydromorphone, deloaded.

Right.

Hydromorphone deloaded is approximately seven times more potent than morphine.

You need that number burned into your brain seven times.

So one milligram of IV hydromorphone gives roughly the same pain relief as as about seven milligrams of IV morphine.

Assuming they have equal potency, giving seven milligrams of hydromorphone, where you meant seven milligrams of morphine.

That's a massive overdose.

That's terrifyingly easy to get wrong if you're not vigilant.

Extremely.

Always double check equal analgesic charts and facility protocols.

OK, let's look at some specific high alert opioids.

Fentanyl.

We hear a lot about this one.

Very potent synthetic opioid.

For context, 0 .1 milligrams IV Fentanyl is roughly equivalent to 10 milligrams IV morphine.

So even more potent than hydromorphone, milligram for milligram.

And the transdermal patch,

diragesic.

Specific warnings there.

Huge warnings.

First, it's only for chronic pain management in patients already opioid tolerant.

Someone who hasn't been taking opioids regularly could easily overdose.

And it takes a while to work, right?

Yes.

Onset is slow.

12 to 24 hours to reach steady levels.

And critically,

no heat, no heating pads, electric blankets, saunas, even prolonged hot baths directly over the patch.

Why no heat?

Heat increases blood flow to the skin, which dramatically accelerates the absorption of fentanyl from the patch.

It can cause a rapid, potentially fatal spike in drug levels.

And disposal is key, too.

Absolutely.

Used patches still contain a lot of drug.

They need to be folded sticky side in and disposed of properly, often by flushing down the toilet per FDA guidelines to prevent accidental exposure to kids or pets.

OK.

What about Meparidine Demerol?

I feel like we don't see it used as much anymore.

And for good reason.

Its use is really discourage, especially for long term pain or in patients with kidney problems.

Why's that?

Because it gets metabolized into a substance called Normaparadime.

This metabolite is neurotoxic.

It can build up, especially if kidney function is poor and it lowers the seizure threshold.

It can cause tremors, muscle twitches and outright seizures.

Not good for long term use.

Got it.

Avoid Demerol for chronic pain, especially with renal issues.

How about methadone?

It's used for addiction treatment, but also pain.

Yes, methadone is unique.

It has a very long half life around 25 hours or even longer.

This allows for once daily dosing and detoxification programs.

For pain, it can provide good long lasting relief.

Many advantages.

A key one is that it's eliminated primarily by the liver.

So it's generally considered safer than some other opioids for patients with kidney failure.

But it's long and variable half life also makes titration tricky and carries overdose risk, if not managed carefully.

And codeine, often found in cough syrup, but also used for pain.

Right.

Codeine itself isn't very active.

It's a pro drug.

It needs to be metabolized by the liver, specifically by the CYP2D6 enzyme into morphine to provide pain relief.

Only about 10 percent gets converted.

So its effectiveness can vary depending on a person's genetics for that enzyme.

Exactly.

Some people are poor metabolizers and get little relief.

Others might be ultra rapid metabolizers and get a much stronger effect.

Also, a common side effect is GI upset, nausea, constipation.

People often mistake this for an allergy, but usually it's just a side effect.

OK, let's talk adverse effects across the board for opioids, the big one.

The most serious, the one that kills an overdose is CNS depression leading to respiratory depression,

slowed shallow breathing.

That's the primary concern.

And beyond that, what's almost universal?

Constipation.

Opioids slow down gut motility significantly.

It doesn't get better over time, like some side effects.

Anyone on regular opioids needs a bowel regimen, increased fluids, fiber and usually soul softeners or stimulant laxatives.

Proactive management is key.

Nausea and itching are also common, right?

Yes.

Nausea often improves after a few days.

Itching or pruritus is often due to histamine release, not a true allergy.

And histamines can help.

And if the worst happens, respiratory depression overdose.

What's the reversal agent?

The loxone, Narcan, it's a pure opioid antagonist.

It bumps the opioid off the receptor sites, reversing the respiratory depression almost immediately.

But there's a catch with its duration.

Big catch.

Naloxone has a relatively short half life, maybe 60 to 90 minutes.

Many opioids, especially long acting ones like methadone or extended release formulations, last much longer.

So the Naloxone can wear off while the opioid is still active.

And the respiratory depression can return.

That's why patients need to be monitored closely after receiving Naloxone.

And repeated doses are often necessary until the opioid is cleared.

OK, let's shift gears to non opioids, the most common one out there.

Acetaminophen, Tylenol, ubiquitous.

Its main actions are blocking pain impulses peripherally, probably through inhibiting prostaglandins and lowering fever by acting on the hypothalamus in the brain.

What doesn't it do?

Critically, it does not have significant anti -inflammatory effects.

That's a key difference from NSAIDs like ibuprofen or naproxen.

And it's preferred for fever in kids.

Yes, it's the drug of choice for fever in children and adolescents, because aspirin use in that age group during viral illnesses is linked to Ray's syndrome, a serious condition causing brain and liver swelling.

What's the major safety concern with acetaminophen?

A patotoxicity liver damage.

This is directly related to the dose.

Overdose is the primary cause of acute liver failure in many Western countries.

So dosage limits are absolutely crucial here.

What are they?

For healthy adults, the generally accepted maximum daily dose is 4000 milligrams.

However, many manufacturers and health systems now recommend capping it at 3000 milligrams per day just to be safer.

And what about patients with liver issues or who drink alcohol regularly?

That limit drops significantly.

For patients with liver disease or chronic heavy alcohol use, the maximum recommended daily dose is 2000 milligrams per day, sometimes even less.

That's a huge reduction.

And it's tricky because acetaminophen is in so many combination products, cold medicines, other pain relievers.

Exactly.

Patients need to be educated to read labels carefully and track their total daily intake from all sources.

Before starting someone on regular acetaminophen, especially if they might be higher risk, you'd want to look at their liver function tests.

Like ALT levels and kidney function, too, right?

BUN, creatinine.

Definitely.

ALT, alanine aminotransferase, is a key liver enzyme.

Elevated levels suggest liver stress or damage.

And checking DUN, blood urea, nitrogen and creatinine gives you a picture of kidney function, which is important for clearing many drugs, though acetaminophen is more of a liver issue.

Impaired clearance means the drug hangs around longer, increasing toxicity risk.

If an overdose happens, is there an antidote?

Yes, thankfully.

The antidote is acetylcysteine, brand name sedetidote.

It works best if given within eight to 10 hours of the overdose.

It helps prevent the formation of the toxic metabolite that damages the liver.

I hear it's not pleasant to take.

Notorious for its rotten eggs smell and taste.

It's often given IV now, which bypasses that issue.

But the oral form is memorable.

OK, moving on to some miscellaneous agents.

Tramadol, Ultram.

How does that one work?

Tramadol is interesting.

It has a dual mechanism.

It binds weakly to the mu -opioid receptor, providing some opioid -like analgesia.

But that's not the whole story.

No, its main action is actually inhibiting the reuptake of norepinephrine and serotonin, two neurotransmitters involved in pain modulation pathways.

So it works centrally in a couple of different ways.

Any specific safety flags for tramadol?

Yes, seizures.

Seizures have been reported and the risk is increased if tramadol is taken along with other drugs that also lower the seizure threshold.

Like what kinds of drugs?

Things like SSRIs, selective serotonin reuptake inhibitors used for depression and anxiety.

MAOIs, monamine oxidase inhibitors and other class of antidepressants and some antipsychotics.

Combining them needs careful consideration.

Got it.

And one more.

The Laticane Transdermal Patch, Litterderm, topical relief.

Yes, it's a topical anesthetic patch, really useful for localized neuropathic pain, like the pain that lingers after shingles post -therpetic neuralgia.

It delivers lidocaine directly to the painful area of skin.

Any usage restrictions?

The key safety point is wear time.

To avoid absorbing too much lidocaine systemically, which could potentially cause cardiac issues or CNS toxicity, the patch should be worn for no more than 12 hours within a 24 hour period.

So 12 hours on, 12 hours off.

OK, let's bring this all together in terms of nursing practice.

Assessment is paramount.

Pain is often called the fifth vital sign.

It absolutely should be assessed regularly.

We use various tools depending on the patient, the standard 0 to 10 numeric rating scale for adults who can use it.

Or the FACES scale with the different facial expressions, often for kids.

Right.

And for nonverbal patients, maybe infants or someone who is cognitively impaired or intubated, we use behavioral scales like the FLACC scale, face, legs, activity, cry, consolability.

Plus, as we mentioned, assessing liver and kidney function labs is vital before starting or managing analgesics.

When it comes to giving the medication implementation, what's a key principle for timing?

Don't wait for the pain to get severe.

It's always better to administer analgesics before the pain reaches its peak.

It takes less medication to prevent pain than to treat it once it's established.

And for pain that's expected to be persistent, like after major surgery or with cancer.

Around the clock, scheduled dosing is generally preferred over PRN or as needed dosing.

Why is that better?

Scheduled dosing maintains a more constant level of the drug in the bloodstream, a steady state.

This helps prevent those peaks and valleys where the pain breaks through significantly before the next dose is due.

It provides more consistent relief.

This brings us to the idea of multimodal approach, right?

Using different types of drugs together.

Yes, multimodal analgesia or using adjuvant therapies.

This is a cornerstone of modern pain management.

The idea is to attack pain using different mechanisms simultaneously.

So maybe an opioid plus an NSAID or plus something for nerve pain.

Combining, say, an opioid with acetaminophen or an NSAID often provides better pain relief than just increasing the opioid dose alone.

This is called a synergistic effect.

And the benefit is.

You can often achieve good pain control with lower overall opioid doses.

This helps minimize those dose dependent opioid side effects, especially respiratory depression and sedation.

It's almost essential for complex pain, particularly neuropathic pain.

There's a standard approach for cancer pain, isn't there?

The WHO ladder.

Yes, the World Health Organization three step analgesic ladder.

It's a framework mainly for cancer pain, but applicable elsewhere.

Can you walk us through the steps briefly?

Sure.

Step one is for mild pain.

Use a non -opioid like acetaminophen or an NSAID, potentially with an adjuvant drug if needed for mild to moderate pain.

Or a step one isn't enough at a mild opioid like codeine or tramadol, sometimes called opioids for moderate pain to the non -opioid and adjuvant therapy and step three for moderate to severe pain or if step two fails, switch to a strong opioid like morphine, hydromorphone, fentanyl, continuing the non -opioid adjuvant or adjuvant if appropriate.

The key is to escalate treatment systematically based on the patient's pain level.

OK, switching gears slightly to a critical safety issue.

PCA by proxy, PCA being patient controlled analgesia.

Yes.

PCA pumps allow patients to self -administer small preset doses of opioid medication by pressing a button when they feel pain.

There are lockouts to prevent overdoses.

The danger comes when someone else presses the button for the patient.

Exactly.

That's PCA by proxy.

A well -meaning family member sees the patient sleeping or looking uncomfortable and thinks, I'll just push the button for them.

But the patient sedation level is actually the safety mechanism, right?

If they're too sleepy, they won't push the button.

Precisely.

If someone else overrides that, giving doses when the patient is already sedated, it can lead to dangerous over sedation and respiratory depression.

Tragically, deaths have occurred because of this.

So the rule is absolutely firm.

Only the patient pushes the PCA button.

Unequivocally, patient and family education on this is vital.

The Institute for Safe Medication Practices, ISMP,

has issued strong warnings against proxy use.

Finally, let's clarify two terms that often get confused.

Tolerance versus addiction.

Very important distinction.

Tolerance is a normal physiological response.

Over time, the body adapts to the drug and you might need a higher dose to achieve the same level of pain relief.

It's expected with long term opioid use.

Physical dependence often accompanies tolerance, meaning withdrawal symptoms will occur if the drug is stopped abruptly.

So tolerance and physical dependence are not the same as addiction.

Correct.

Addiction or psychological dependence, now often termed opioid use disorder, is different.

It's a chronic neurobiological disease characterized by compulsive drug seeking and used despite harm.

It involves cravings, loss of control over use, used for non -therapeutic reasons like mood alteration.

So needing higher doses for came relief over time doesn't automatically mean someone is addicted.

Not at all.

Tolerance is physiology.

Addiction is pathology.

Confusing the two often leads to patients being under legitimate pain due to unfounded fears of causing addiction.

While addiction can occur, it's far less common than tolerance in patients taking opioids appropriately for pain.

OK,

so wrapping up, we've covered a lot of ground.

Key takeaways.

Understanding acute versus chronic pain.

The specific neurotoxic danger of meparidine, making it a poor choice for long term use.

Absolutely.

Nailing down that seven times potency difference between IV hydromorphone and IV morphine.

Critical for safety.

And those strict acetaminophen limits 4000 milligravity max for healthy adults, maybe even 3000, but down to 2000 milligravity for those with liver issues or heavy alcohol use.

We've laid out the safety rules, the mechanisms, but there's an ethical layer, too, isn't there?

Especially in certain situations.

There really is.

When you're dealing with terminal conditions like advanced cancer pain, the entire goal shifts.

Patient comfort, quality of life.

Those ethically and clinically have to take priority over concerns about causing tolerance or even addiction.

That's a powerful point.

How does recognizing that physical dependence is almost inevitable with long term opioid use while true addiction is much rarer in that context?

How does that shape our responsibility?

It really forces us to consider the moral imperative.

When someone is facing profound chronic suffering, especially near the end of life, providing adequate relief becomes paramount.

Withholding effective pain control due to misplaced fears can itself be unethical.

Definitely food for thought.

Ensuring compassionate and effective pain control, balancing the risks and benefits based on the individual patient and that prognosis.

Exactly.

It's about using this knowledge wisely and humanely.

Well, thank you for joining us for this deep dive into analgesic drugs and the nursing process.

We hope this was helpful.

Thanks for listening.

We'll see you next time on The Deep Dive.