Chapter 32: Pain Management in Patients With Cancer

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You know, I was reading this statistic in our source material today and it completely stopped me in my tracks.

90%.

Yeah.

That number is wild.

Right.

Like 90 % of cancer pain can be completely relieved with just, you know, simple standard interventions.

It is a number that should be incredibly encouraging, honestly, but in reality, it ends up being deeply frustrating.

I guess it just doesn't happen.

Exactly.

Because despite having the pharmacological tools readily available,

that pain goes unrelieved in practice far, far too often.

And reading through the text,

the root of that failure seems to come down to a mix of like inadequate training and unfounded fears about addiction and just this healthcare model that gets so laser focused on treating the underlying disease, you know, the cancer itself.

Right.

The disease process.

Yeah.

And it somehow forgets to treat the profound suffering happening right in front of the provider.

And I mean, that disconnect is the entire reason we are tackling this topic today.

Absolutely.

Welcome to the deep dive.

Whether you are prepping for a massive pharmacology exam, getting ready for clinicals, or, you know, just trying to be the best possible advocate for your patients, our mission today is to summarize Chapter 32 from Leany's Pharmacology for Nursing Care, 12th edition.

Which is a fantastic resource.

It really is.

And we are focusing exclusively on the management of cancer pain today.

And we want to make a structural promise to you right out of the gate.

We are following the exact order of the textbook chapter.

No skipping around.

None.

We are taking all that dense pharmacology, the charts, the clinical decision making tools,

and well, translating them into plain, memorable logic.

Because when you understand the why behind a drug's mechanism of action, it changes everything.

It really does.

Safe medication administration stops being about rote memorization and, you know, it becomes second nature.

Okay, let's unpack this.

Before anyone can administer a drug, they need to know what they are actually treating.

I mean, what is pain, structurally speaking, and how does the body process it?

So the text draws a hard line between two major forms of pain.

And you really have to know the difference because the drugs you choose will completely depend on it.

Right.

First, there is nociceptive pain.

This is the pain you feel when tissues are actively being injured.

Like a tumor pressing into a muscle or a bone.

Exactly.

If it's bone, joint, or muscle, the text classifies that as somatic nociceptive pain.

Patients usually describe somatic pain as sharp and highly localized.

Meaning they can point exactly to where it hurts.

Right, exactly.

Now, the other type of nociceptive pain is visceral.

This happens when the injury is to an internal organ.

Like the liver or the small intestine, right?

You got it.

And visceral pain is trickier.

It's more diffuse, achy, sometimes even crampy.

You can't always put a single finger on the source.

But the good news with both somatic and visceral nociceptive pain is that they respond the most beautifully to standard pain medications like opioids and NSRs.

Yeah, they are very responsive to standard therapy.

But then the other category is neuropathic pain.

And this is an entirely different beast.

Total nightmare to treat sometimes.

It really is.

Because this isn't damage to the tissues.

This is injury to the peripheral nerves themselves.

So like the wiring is frayed.

Frayed or actively misfiring.

And that can be due to tumor infiltration or even the toxicity of chemotherapy itself.

Oh wow.

The chemo can cause it.

Yeah.

And patients use very specific words to describe neuropathic pain.

They call it burning, shooting,

jabbing.

Or they might even say the area feels strangely cold, you know, or dead.

And standard pain meds don't really work for this, do they?

They do a remarkably poor job.

I mean, you could pump a patient full of morphine and they might still feel that shooting nerve pain.

That sounds miserable.

It is.

You need an entirely different pharmacological tool belt for neuropathic pain, which we will pull out a little later.

Okay.

But first, to understand how any of these analgesics work, we need a mental model for how the nervous system handles this sensation.

Yes.

Let's build that model.

Because pain isn't just a simple alarm bell ringing in the periphery that the brain passively listens to.

It's actually a two -way street.

It's very dynamic.

Right.

The brain can send its own fire trucks down the descending nerve pathways to basically muffle the alarm.

That's a great analogy.

The body produces its own endogenous opioids like encephalins and beta endorphins.

So we have our own internal painkiller.

Exactly.

The sensation of pain a patient actually feels is the net result of activity in those two opposing pathways.

You have the pain signals traveling up.

And the brain's own opioids suppressing them on the way down.

You've got it.

And the opioid drugs we administer, you know, like morphine or fentanyl, they are essentially just pharmacological mimics.

They just copy what the body is already doing.

Right.

They hijack that exact same endogenous pain suppressing system to amplify the dampening effect.

So we know the mechanics.

But how do we measure something so invisible?

Because if there is one core rule you highlight in Neon Yellow from this chapter,

it is this pain is inherently subjective.

Yes.

The gold standard for assessment, without exception, is the patient's self -report.

Whatever they say it is.

Whatever they say it is.

And the text gives us specific tools to capture that data.

If you look at figures 32 .2 and 32 .3, you see the standard pain intensity scales.

Right.

The ones everyone is familiar with.

Yeah.

For adults and older children with normal cognitive function, you just use the standard 0 to 10 numeric scale.

Zero being no pain, 10 being the absolute worst pain imaginable.

Exactly.

But clinical practice requires adaptation.

If you are assessing a young child or perhaps an older adult with advanced dementia or cognitive impairment,

asking them to assign a numerical value to their suffering is kind of useless.

Yeah.

They won't understand it.

So you pivot to the Wong Baker Faces Scale.

You show them a chart with six cartoon faces, ranging from a smiling face to a face crying with deep frown lines, and you just ask them to point to the face that matches how they feel inside.

It perfectly translates their abstract feeling into a concrete visual we can actually document.

Yes.

And documentation isn't just about grabbing a number and walking away.

A comprehensive initial assessment means, well, you have to play detective.

The chapter actually lists out all the parameters.

Like, you have to ask about the onset.

When exactly did this start?

The location.

Can you point to the exact spot?

And modulating factors.

What makes it better?

What makes it worse?

Like, does it hurt more when you lie flat?

Does an ice pack help?

And all of those details point the provider toward the right medication class.

But assessing pain is fraught with pitfalls.

Oh, absolutely.

It's outlined in Table 32 .1 regarding barriers to assessment.

Nurses have to be acutely aware of why patients might actively underreport or even overreport their pain.

Let's start with underreporting, because to me that feels completely counterintuitive.

I mean, if someone is in absolute agony, why wouldn't they tell you?

Well, the chapter lists several reasons.

A patient might want to appear stoic for their family, for one.

Oh, try to be brave.

Yeah.

Or they might harbor a massive, completely unfounded fear of opioid addiction.

Or, and this is perhaps the most heartbreaking reason, they associate increased pain with disease progression.

Wait, meaning what?

They fear that admitting the pain is worse means admitting their cancer is spreading, so they stay silent in denial.

Wow.

That is awful.

But on the flip side, some patients might overreport their pain, right?

Yes, they do.

And it's not because they are malicious.

It's because they are terrified.

The health care system is going to deny them adequate medication, so they inflate the number just to ensure they get something to take the edge off.

And this dynamic is exactly why relying on behavioral cues is a terrible substitute for self -reporting.

I've seen this trip up so many providers.

Like, if a patient tells you their pain is an eight, but they are sitting up, smiling and talking to their family.

Their pain is an eight.

Yes.

Their pain is an eight.

You do not document it, too, just because they don't look like they are suffering.

Good coping skills do not equal the absence of pain.

So true.

So we have our number, and we know we need to act.

How do we choose the right pharmacological weapon?

We look at the ladder.

Right.

The textbook relies on a framework created by the World Health Organization, shown in Figure 32 .4, as the WHO Analgesic Ladder.

The stepwise approach.

It's elegant in its simplicity, really.

Step one.

For mild to moderate pain, you use non -apioids.

Step two.

You step up to moderate opioids.

Step three.

You bring out the strong opioids.

And crucially, adjuvant medications, that supporting cast we mentioned earlier, can be used at any step of the ladder.

So let's look closely at that first one.

Step one.

The non -apioids.

This class is dominated by NSAIDs, like ibuprofen and aspirin and acetaminophen.

Okay.

They're common stuff.

Right.

Now, they both relieve mild to moderate pain, but their mechanisms of action are fundamentally different, which creates massive clinical implications.

Let's break down the NSEIs first.

Ibuprofen, niperoxine, aspirin, I mean, we all have them in our medicine cabinets.

But how are they actually stopping the pain?

So they work by inhibiting an enzyme called cyclooxygenase, or KEOX for short.

Now there are two forms of this enzyme, EOX1 and KEOX2.

Okay, the good guy and the bad guy.

Exactly.

KEOX2 is the bad guy in this scenario.

It's produced at the site of tissue injury and causes inflammation and pain.

So by blocking KEOX2, NSAIDs provide relief.

That sounds great.

But there's a catch.

Right.

Because most conventional NSAIDs don't just block KEOX2.

No, they don't.

They also block KEOX1.

And KEOX1 is the good guy.

It's your physiological housekeeper.

KEOX1 protects your gastric mucosa, your stomach lining.

Right.

It maintains healthy blood flow to your kidneys.

And it promotes platelet aggregation, meaning it helps your blood clot.

So if I give a patient a conventional NSAID, I'm blocking the pain, but I'm also knocking out their housekeeper.

You're evicting the housekeeper.

That completely explains the massive adverse effects the text lists.

Without KEOX1 protecting the stomach, you get gastric ulceration.

Without it supporting the kidneys, you risk acute renal failure.

And crucially, without KEOX1 helping platelets clump together, you get bleeding, which leads us to a massive clinical safety alert for nursing students.

Oh, this is a big one.

It is.

If you have a patient undergoing chemotherapy, you have to be incredibly careful with conventional

NSAIDs.

Chemotherapy naturally suppresses bone marrow function, which leads to thrombocytopenia, which is a dangerously low platelet count.

What's fascinating here is the cascading effect of that drug choice.

If you take a chemo patient who already lacks platelets, and you give them a conventional NSAID or aspirin that stops their few remaining platelets from clumping together.

It's a disaster.

Yeah, you have just introduced a severe, potentially life -threatening bleeding risk.

So what is the safe alternative on step one?

Acetaminophen.

Acetaminophen acts centrally in the central nervous system.

So it bypasses the periphery.

Wait, it lacks those peripheral anti -inflammatory effects, but more importantly, it does not inhibit platelet aggregation.

It is safe for the thrombocytopenic patient.

But acetaminophen has its own severe baggage that you must monitor for.

It has two major interactions you need to know.

First, alcohol.

Combining acetaminophen with even moderate amounts of alcohol can cause fatal liver damage.

It's highly apetitoxic.

Yeah.

And second, warfarin and anticoagulant.

I actually need a better way to visualize that interaction, because it feels like we just fixed one bleeding risk by avoiding NSAIDs, only to create a completely different bleeding risk with acetaminophen.

Right.

So think of the liver's metabolic pathways like plumbing.

You have a specific drain that clears out drugs.

OK, I'm with you.

Warfarin normally uses that drain to leave the body at a steady rate.

But when you introduce acetaminophen, it aggressively competes for that exact same drain.

It effectively clogs the pipe.

Ah.

So the warfarin has nowhere to go.

Exactly.

It just backs up and accumulates in the bloodstream, pushing the patient's coagulation levels dangerously high.

So you have a thrombocytopenic chemo patient who now has toxic levels of a blood thinner in their system.

Pharmacology really is a balancing act of risks.

And eventually, those non -opioids are going to hit their therapeutic ceiling anyway.

They absolutely will.

You can only give so much acetaminophen or ibuprofen before the organ toxicity far outweighs any analgesic benefit.

So when a patient hits that ceiling and the pain persists or worsens, we have no choice but to scale the ladder.

Step two and step three.

We are moving into opioid territory.

Now, with pure opioids, there is no ceiling to pain relief.

Wait, really?

No ceiling at all?

Theoretically, no.

You can keep increasing the dose until the pain is completely gone, limited only by the side effects.

But you have to select the appropriate opioid.

Looking at table 32 .2, we have pure agonists like morphine and fentanyl.

And then we have agonist antagonists like buprenorphine or butarfanol.

Let's talk about the agonist antagonist because why is the textbook so strict about avoiding them in cancer patients?

So an agonist is like a master key that slides into a lock, the opioid receptor, and turns it fully, giving you maximum pain relief.

And morphine is a pure agonist.

Right.

Morphine turns the lock all the way.

An agonist antagonist is like a poorly cut key.

It slides into the lock and turns it halfway.

Okay.

So you get some relief.

You get some pain relief, but it hits a hard ceiling.

It won't turn any further no matter how much you push.

But worse, because it's jammed in the keyhole, it blocks the master key from getting in.

So if a patient is already taking morphine, they're physically dependent on it, and you give them an agonist antagonist, you instantly kick the morphine off the receptors.

The pain comes rushing back.

And you throw the patient into immediate severe withdrawal.

It is a guaranteed way to lose your patient's trust forever.

Yeah.

That sounds like a nightmare.

The text also highlights a specific pure agonist to avoid, which is meparidine, or demoral.

If you use it for more than a few days, it accumulates a toxic metabolite called normeparidine.

And that causes dysphoria, agitation,

and even seizures, right?

Exactly.

Avoid it.

So, assuming you've selected a pure agonist like morphine, we need to talk about dosing.

Because for persistent cancer pain, PRN, or as -needed dosing, is completely inappropriate.

Totally inappropriate.

You must use around -the -clock, or ATC, dosing.

The goal is to prevent the pain from recurring in the first place by maintaining a steady state of the drug in the bloodstream.

Then you provide short -acting rescue doses for breakthrough pain.

Right, those sudden transient spikes of severe pain that punch right through the baseline medication.

And one of the most effective tools for managing this is the PCA pump patient -controlled analgesia.

It's an IV pump that delivers a continuous basal rate of the opioid, but the patient holds the button.

Empowering the patient.

Yes.

When they feel breakthrough pain coming on, they press the button to deliver a small immediate bolus of medication.

I can already hear the family members panicking, though.

Like, if my mom is in pain and she's holding a button that dispenses morphine, what stops her from just mashing that button 20 times in a row and accidentally overdosing?

And that is exactly the education piece the nurse has to provide.

You explain the lockout interval.

The machine is strictly programmed.

Once the patient pushes that button and receives a bolus, the pump locks out.

It will not deliver another bolus for a set period, say 10 or 15 minutes, no matter how many times the button is pushed.

Oh, so it physically won't let them overdose.

Correct.

It guarantees the first dose has enough time to take full physiological effect before another dose can be introduced.

But even with perfectly programmed pumps,

we still have to manage the side effects.

And opioids are famous for them.

Let's talk about the big scary one first.

Respiratory depression.

It is the most feared side effect, but the text is actually very clear.

In patients who have developed tolerance,

clinically significant respiratory depression is actually incredibly rare.

That's reassuring.

It is.

When it does happen, it is usually during the initial dose titration.

The key nursing implication here is that sedation always precedes respiratory depression.

So they get sleepy first.

Always.

If your patient is becoming excessively sleepy or difficult to arouse, you delay the next dose.

If severe respiratory depression does occur, you use naloxone, an opioid antagonist, but you titrate it very carefully.

Because if you give too much, you completely reverse the analgesia and send the patient into agonizing pain.

Right, you slam them into withdrawal.

I have to throw a tough, real world clinical scenario at you because students will inevitably face this on the floor.

Let's say you have a patient who is actively at the very end of life.

Their breathing is becoming shallow and irregular, but they're clearly in severe agonizing pain.

My instinct as a newer nurse would be to hold back the strong opioid dose out of fear that I might cause that final respiratory depression and hasten their death.

What does the text say we do?

It is a profound clinical dilemma, but the textbook provides a very definitive answer.

You do not withhold the medication.

As we just established,

clinically significant respiratory depression is rare in a tolerant patient.

But more importantly, unrelieved agonizing pain can exhaust the body and hasten death all on its own.

That makes sense.

The pain itself is a trauma.

Exactly.

The textbook's stance is that when death is imminent, the absolute priority is comfort.

Providing that comfort takes precedence over the theoretical risk that the medication might bring the end slightly sooner.

Comfort is the ultimate goal.

Okay.

Moving from the heaviest side effect to the most common one, constipation.

Oh, this is a major nursing implication because unlike sedation or nausea, a patient never develops tolerance to opioid -induced constipation.

Never.

Just a constant battle.

Yes.

Therefore, prophylaxis is mandatory from day one.

You don't wait for them to be constipated.

You start them on a stimulant laxative like Senna and a stool softener like DocuSate immediately.

If it gets severe, we can even escalate to a drug like methylnoltrexone.

Methylnoltrexone.

Yes.

It specifically blocks opioid receptors in the gut without crossing the blood -brain barrier to ruin the pain relief.

That's amazing.

So we are prophylactically treating the gut to keep things moving.

Right.

We've climbed the ladder.

We're managing the heavy side effects of the opioids.

But what if we go back to that neuropathic pain we talked about at the very beginning?

Opioids are terrible at fixing that burning, shooting nerve pain.

They are.

And that's where the supporting cast steps in to tackle what the opioids miss.

Table 32 .4 lays out the adjuvant analgesics.

Right.

The most critical concept to understand here, and this is a classic exam trap, by the way, is that adjuvants are used alongside opioids.

They do not replace them.

Got it.

Let's look at tricyclic antidepressants or TCA's like amitriptyline.

These are incredibly effective for neuropathic pain.

But wait, amitriptyline is an antidepressant.

Why are we giving an antidepressant to a cancer patient who is simply in physical pain?

Are we implying the pain is just making them depressed?

It's a very common misconception.

We aren't treating depression here.

TCA's actually work on the descending nerve pathways in the spinal cord to inhibit the transmission of pain signals.

Oh, so it physically blocks the pain.

But I know TCA's cause heavy sedation as a side effect.

That seems like a bad idea for a patient who might already be sleepy from opioids.

Well, it is unless you use pharmacology to your advantage.

What do you mean?

You intentionally schedule the amitriptyline dose at bedtime.

You take that adverse effect sedation and turn it into a therapeutic feature.

The patient gets nerve pain relief and a good night's sleep.

Brilliant clinical application.

OK, next we have anti -seizure medications like gabapentin and carbamazepine.

Right.

Think about the pathology of a seizure.

It is spontaneous chaotic neuronal firing.

Neuropathic pain is similar.

It is sharp darting pain from nerves firing inappropriately.

So these drugs just suppress that chaotic firing.

Exactly.

Just be aware that carbamazepine carries a risk of bone marrow suppression, so monitor those blood counts closely.

Then we have CNS stimulants like dextroamphetamine.

Why give a stimulant?

To counteract that profound opioid sedation we talked about earlier.

Yes, it wakes the patient up and can actually enhance the overall pain relief.

Finally, glucocorticoids like dexamethasone.

They don't relieve pain directly, but they are powerful anti -inflammatories.

Right.

If a tumor is compressing the spinal cord, causing massive edema and pain, dexamethasone reduces that swelling.

As a bonus, it also improves appetite and imparts a general sense of well -being.

And we can't forget the non -drug therapies.

Invasive procedures like neurolytic nerve blocks, where they actually destroy the pain transmitting neurons.

Or radiation therapy to shrink the tumor pressing on the nerve.

Or even physical interventions like heat, cold, or 10NS units.

If we connect this to the bigger picture, all of these physical and psychosocial interventions, even peer support groups, are vital, but they are complements to drug therapy.

They are not replacements.

Exactly.

Yeah.

You don't offer a patient with severe bone metastases a heating pad instead of an opioid.

You offer it in addition to the opioid.

Beautifully said.

So we have all these tools, the ladder, the adjuvants, the non -drug therapies.

But we can't apply them uniformly to every single patient, can we?

The standard rules of pharmacology shift depending on who is sitting in the bed.

Yes, they absolutely do.

Let's start with older adults, because aging changes everything about how a drug moves through the body.

It does.

Older adults generally have a heightened sensitivity to drugs.

This is primarily driven by a natural decline in organ function.

Their kidneys aren't filtering as robustly, and their liver enzymes aren't metabolizing as quickly.

So if the liver isn't breaking the drug down and the kidneys aren't excreting it, the drug just stays in the system longer and accumulates.

Right.

And because of that accumulation, the risk of adverse effects skyrockets.

But here is the critical trap nurses fall into.

They get so worried about the drug accumulating that they end up severely undertreating the There is a persistent myth that older adults somehow feel less pain, or that their nervous systems are just dulled to it.

And the text makes it very clear that is completely false.

They feel every bit of it.

So the pharmacological strategy is to start with a lower dose to account for that reduced clearance.

Yeah.

But then you titrate up carefully until the pain is actually relieved.

Yes.

Start low, go slow, but definitely go.

What about the other end of the age spectrum,

children?

The biggest hurdle with pediatric patients, especially preverbal or nonverbal children, is assessment.

It is incredibly easy to misread their cues.

Like what?

Well, a nurse might look at an infant who is sleeping soundly and document that they are comfortable.

But I remember learning that sleep can actually be a physiological coping mechanism for severe overwhelming pain.

The body just like shuts down.

Exactly.

If you assume sleep automatically equals comfort, you risk a false negative assessment and end up leaving a child in sheer agony.

You have to look at other physiological markers and use appropriate scales.

Furthermore, when treating neonates, you have to remember their physiology is incomplete.

Specifically, their blood -brain barrier is not fully formed.

Which means drugs cross over into their central nervous system much more readily than in an adult.

Yes.

Opioids will flood their CNS, putting them at a significantly heightened risk for profound respiratory depression.

You start them at a fraction of the standard weight -based dose and monitor their respirations obsessively.

Another critical population to consider involves patients with a history of opioid use disorder.

The text is incredibly firm here.

These patients still get cancer, they still experience severe pain, and they unequivocally deserve adequate pain relief.

Yes, they do.

The biggest pitfall here is that healthcare providers often confuse relief -seeking behavior with drug -seeking behavior.

That bias is so real.

It is.

If a patient with a history of substance use tells you they are in severe pain, the standard of care is to believe them.

And from a pharmacological standpoint, treating them is going to look different.

Because of tolerance.

Because they already have a significant baseline tolerance to opioids,

giving them a standard starting dose of morphine isn't going to do anything.

They will actually require a much higher starting dose than a naive patient just to achieve the same baseline level of comfort.

I'm really glad you brought up the word tolerance, because this touches on something that causes massive anxiety for patients and their families.

I want to step in here and make sure we completely separate three terms that get constantly mixed up.

It's so important.

Tolerance, physical dependence, and addiction.

It is a vital distinction, both for exams and for bedside nursing.

Let's start with tolerance.

Tolerance simply means the body has adapted to the presence of the drug over time.

Because of that adaptation, you now need a higher dose to achieve the exact same pain relieving effect you used to get with a lower dose.

It's just a normal physiological response.

It happens to everyone who takes these drugs long term.

The same goes for physical dependence.

Physical dependence means the body's systems have adapted to the drug to the point that they expect it to be there.

So if you were to abruptly stop the opioid, the patient would experience physical withdrawal symptoms.

Sweating, tremors, tachycardia.

But again, that is just biology.

That is a normal expected physiological response to long term opioid therapy.

It doesn't mean the person is an addict.

Right, because addiction is a completely different phenomenon.

Addiction is a psychological behavior pattern.

Yes, exactly.

It is defined as the continued compulsive use of a psychoactive substance despite the physical, psychological, or social harm it is causing.

And the textbook emphasizes a crucial point.

The behavior pattern of true addiction rarely develops in patients who are taking opioids in a structured, therapeutic setting for the management of cancer pain.

But patients don't inherently know that.

They just hear morphine and panic.

That is why patient education is arguably your most important nursing intervention.

You have to sit down and break down those fears.

You have to explain that physical dependence is not something to be terrified of, and it doesn't mean they are an addict.

You also have to explain the why behind the adjutant prescriptions.

If you hand a cancer patient a prescription for duloxetine, an antidepressant, without context, they might think you believe their pain is all in their head.

Or that you are just treating them for depression.

Right.

You have to proactively explain,

we are using this specific drug because it targets the nerve pathways causing your shooting pain.

Education builds trust, and trust enhances compliance and pain relief.

We've covered a massive amount of ground today.

We started at the cellular level with pain pathways,

scaled the WHO analgesic ladder from non -opioids up to strong, pure agonists.

Managed the heavy baggage of side effects.

Right.

Brought in the adjuvants and adapted our pharmacology for every patient from an infant to an older adult.

The core takeaway from Chapter 32 is that pain management cannot be passive.

It must be proactive, it must be highly individualized based on the patient's specific physiology, and it must be driven by compassionate ongoing assessment.

But before we let you go, I want to leave you with one final thought to mull over.

We spent a lot of time talking about how subjective pain is, and how incredibly unreliable behavioral cues can be.

Think about this scenario.

You walk into a room,

your patient looks you dead in the eye, perfectly calm, hands neatly folded in their lap, watching TV, and tells you their pain is a 10 out of 10.

A classic situation.

Right.

And you feel your hand hesitating over the medication drawer because they just don't look like a 10.

Ask yourself, are you treating the objective clinical data in front of you, or are you treating a flawed behavioral assumption?

A completely necessary question to carry into your clinical practice.

Keep pushing, keep studying, and keep advocating for your patients.

A massive thank you for sitting with the Last Minute Lecture team.

We'll catch you on the next Deep Dive.