Chapter 36: Targeted Cancer Therapy Medications

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Welcome back to The Deep Dive.

Today we are on a very specific mission.

If you're a nursing student, maybe a pharmacology student, or honestly just anyone trying to get their head around the incredibly complex world of modern oncology, you're in the right place.

You definitely are.

We are tackling chapter 36 from pharmacology,

a patient -centered nursing process approach, 12th edition.

That's right.

And specifically, we are diving into targeted therapies to treat cancer.

But I think, you know, before we even open the book, we kind of had to acknowledge the elephant in the room.

Which is?

Just this sheer intimidation factor of it all.

Oh, absolutely.

When students hear oncology, pharmacology, they panic.

I mean, they just think of a thousand different drug names, terrifying side effects, really complex biology, and just a ton of memorization.

It feels overwhelming.

It really does.

I think for so many students, cancer treatment used to just mean one thing, chemotherapy, you know, the heavy hitters, hair loss, the nausea, the fatigue.

But this chapter, I mean, this chapter makes it so clear that we've stepped into a completely new era.

Absolutely, a new era.

And to borrow a military analogy,

because, let's face it, cancer treatment is basically biological warfare.

It really is.

We're moving from the era of carpet bombing to the era of the sniper.

And that is the fundamental shift we're talking about today.

I love that analogy, carpet bombing versus the sniper.

Let's unpack that right at the start, because that really frames everything else we're going to get into.

So traditional chemo is what the text calls

cytotoxic.

Correct.

Cytotoxic, cyto meaning cell, toxic meaning, well, poisonous.

Traditional chemotherapy is indiscriminate.

It targets any cell that divides rapidly.

Now, cancer cells, they divide rapidly, so it kills them.

But so do a lot of other things.

What else in your body divides rapidly?

Hair follicles.

Exactly.

First thing people think of.

And the lining of your gut.

Right.

And your bone marrow cells.

So traditional chemo, yes, it kills the cancer, but it also wipes out your hair.

It tears up your stomach lining, which is where the ulcers and the nausea come from, and it just depletes your immune system.

It's messy.

It's carpet bombing.

It takes out all the innocent bystanders along with the enemy.

Which totally explains all those classic side effects we associate with chemo.

But targeted therapy,

the whole point of chapter 36 is different.

It's fundamentally different.

The text describes it as being specific, deliberate, and cytostatic.

Cytostatic.

Okay, let's define that.

So that means it stops the growth rather than just blasting everything in sight.

Exactly.

Instead of just killing the cell outright, it blocks the growth and spread of cancer by interfering with very specific molecules that are involved in that tumor's growth.

It's the cornerstone of what we now call precision medicine.

Ah, precision medicine.

We're just treating lung cancer as one big thing anymore.

We're looking at a person's specific genes and proteins to decide how to treat their specific lung cancer.

So instead of just throwing everything at the wall and seeing what sticks, we're actually finding the specific biological switch that's stuck in the on position.

And we're flipping it off.

We're flipping it off.

Precisely.

And the text outlines three main approaches for how we find those targets.

It's actually pretty fascinating how they identify where to aim that sniper rifle.

Okay, walk us through those three approaches.

So first we can compare individual proteins.

We look at the cancer cells versus normal cells.

So for example, in some breast cancers, there's a protein called

ERB2.

You've probably heard of it as HER2.

It's expressed at super high levels on the cancer cells but not really on the normal cells.

So if you can target that specific protein, you can shut down the cancer without hurting the healthy cells that don't really have it.

Exactly.

The second approach is identifying mutant proteins.

So for instance, in melanoma, there's often a mutated gene called

BRAF.

It's like a broken accelerator pedal in a car.

It's just floored telling the cell to go, go, go.

So we can develop a drug to specifically block that broken pedal.

We can target that specific broken pedal.

And the third approach.

What's the third?

Looking for abnormal chromosomes.

This is massive in leukemia.

You're going to hear us talk a lot today about the Philadelphia chromosome.

The Philadelphia chromosome?

It sounds like something out of a spy novel.

It does, doesn't it?

But it's actually where two genes fuse together to make a brand new protein that just shouldn't exist.

So if we can target that fusion protein, you can stop the leukemia and it's tracked.

You can stop the leukemia.

Okay.

So we've got the targets, but how did the drugs actually work?

The text lists five main mechanisms.

I think it's worth running through these quickly, just so you have a mental framework before we get bogged down in all the specific drug names.

Good idea.

So number one, signal transduction inhibitors.

Think of these as blocking the text messages that are telling the cell to divide.

If the cell doesn't get the grow text, it just stops.

Block the signal, stop the growth.

Simple enough.

Got it.

Number two,

changing proteins within the cancer cells to cause cell lysis, which basically means the cell just breaks apart from the inside.

Number three is one of my favorites, just conceptually,

stopping angiogenesis.

Oh, this is crucial.

Angio means blood vessel.

Genesis means creation.

So angiogenesis is the formation of new blood vessels.

A tumor is like an invading army.

It needs a massive blood supply to grow and survive.

It travels on its stomach.

It really does.

So if you can cut off the blood supply, you starve the tumor.

Brutal, but very effective.

Okay.

And number four, triggering the immune system.

We're essentially flagging the cancer cells, putting a big neon sign on them.

So your body's own immune system can finally find them and kill them.

And then number five is just being toxic only to the cancer cells and sparing the healthy ones.

The ideal scenario.

Right.

Now, before we get into the specific drugs, and wow, there are a lot of them, we need to help everyone out with the names because looking at this list, it's just a soup of mabs and nibs.

It is an alphabet soup, but there is a code.

And honestly, if you're a student getting ready for an exam, memorize this code immediately.

It'll save your life on multiple choice questions.

Okay.

Lay the code on us.

What's the secret?

First, just divide them into small molecules and large molecules.

The small molecules are usually pills you take orally.

They're small enough to get inside the cell membrane.

These almost always end in nib or MIB.

Okay.

Nib and MIB, like nibble, a small bite.

If that helps, use it.

Specifically, NIB usually stands for a tyrosine kinase inhibitor.

We'll talk a lot about those.

And MIB is a proteasome inhibitor.

Got it.

Small pills, nib and MIB.

What about the large molecules?

So these are the monoclonal antibodies.

They're huge proteins.

They're way too big to take as a pill.

Your stomach acid would digest them just like a piece of steak.

Ah, okay.

So they're always given IV.

And they end in MAB, M -A -B, for monoclonal antibody.

That's easy enough to remember.

But the text breaks down the mabs even further, doesn't it?

The letters that come before the mab actually tell you a story.

They do.

They tell you where the antibody came from.

And this really matters for patient safety.

If it ends in MOMAB, it comes from a mouse.

Right.

Murine.

MOMAB is from a mouse.

Got it.

If it's EMAB, it's chimeric, which means it's a mix of human and mouse proteins.

If it's IMABib, it's humanized, so it's mostly human.

And if it's UMAB, that's U -M -A -B, it's fully human.

Why does that matter so much?

Is that just, you know, trivia for a test?

No, not at all.

It's critical for clinical safety.

The more mouses in the drug, the higher the risk of a serious allergic reaction.

Your body recognizes mouse protein as foreign and it attacks it.

So a MOMAB is much more likely to cause a severe infusion reaction than a fully human UMAB.

Wow.

That is a golden nugget for clinical safety right there.

Okay, we have our framework.

We have our decoder ring.

Let's dive into the first class of drugs in the chapter,

the angiogenesis inhibitors.

Let's do it.

So we established these are the ones that starve the tumor by cutting off its blood supply.

Right.

And these drugs usually target something called VEGF, Vascular Endothelial Growth Factor.

That's the signal the tumor sends out to basically say, hey, I'm hungry over here, build me some blood vessels.

The first drug on the list here is Ziviflebercept.

That is a mouthful.

It is.

Ziviflebercept.

It's a really fascinating drug because of how it works.

It acts as a soluble receptor.

Explain that.

What does that mean?

Okay, so imagine the tumor is a pitcher throwing baseballs and those baseballs are the VEGF molecules.

Normally the catcher, which is the receptor on a blood vessel, catches the ball and the game starts, a blood vessel grows.

Right.

Ziviflebercept is like a fake catcher's mitt just floating in the air.

It catches the ball before it can ever reach the actual catcher.

So it just intercepts the message.

Exactly.

It binds up VEGF, A and B, preventing them from ever reaching their native receptors.

It's used for metastatic colorectal cancer, usually combined with a chemo regimen called 5th all AOI.

Now, for all the nurses listening, what's the big safety alert here?

Because if we're stopping blood vessel formation, that sounds risky for other things, like just normal healing.

You absolutely hit the nail on the head.

The biggest risks are severe bleeding and wound healing complications.

I mean, think about it.

If your body receives a system -wide signal that says stop building blood vessels, how on earth can it heal a simple cut?

It can't.

It can't.

So if a patient is scheduled for surgery, you have to be incredibly careful.

You have to stop the drug well in advance.

Right.

The text explicitly warns about wound adhesions,

which is just a fancy medical term for a surgical incision splitting open because the tissue can't knit itself back together.

It also warns about GI perforation, literally a hole forming in the stomach or intestine.

Yikes.

So clinically,

as a nurse, what are we looking for?

Black tarry stools.

Yes, Melina.

Sudden severe abdominal pain.

Those are huge red flags for a perforation or a bleed.

Also, oddly enough, diarrhea and dehydration are really common side effects too.

But the bleeding and the wound healing issues, those are the really scary ones.

Okay.

Let's move to the prototype drug for this class.

Bevacizumab.

Bevacizumab.

It's a recombinant humanized monoclonal antibody.

So notice the name Bevacizumab.

And that looks who tells you it's humanized.

So less risk of a big allergic reaction than one of the mouse -based ones.

Correct.

It binds to VEGF directly and just neutralizes it.

It's a real workhorse drug.

It's used for colorectal, lung, kidney, ovarian, cervical cancers,

even glioblastoma in the brain.

But the side effects profile, I'm guessing, is pretty similar to ZIVA flavorcept.

Very similar.

GI perforation, wound adhesions, severe bleeding.

But Bevacizumab also carries a specific risk of something called nephrotic syndrome, which is serious kidney damage and hypertensive crisis.

So blood pressure monitoring is absolutely key.

Critical.

You can see patient's blood pressures just skyrocket.

And there's one patient safety alert.

The text highlights in big bold letters.

Do not confuse Bevacizumab with Bortizumab.

They do sound similar.

Bevacizumab, Bortizumab.

They sound very similar, but Bortizumab is a totally different class of drug that we'll get to later.

Bevacizumab is the angiogenesis inhibitor.

Bortizumab is a protetesum inhibitor.

Mixing those up could be catastrophic for a patient.

Okay, let's move to section two.

The EGFR inhibitors, epidermal growth factor receptor.

Right.

So EGFRs are receptors found on the surface of cell membranes.

In many epithelial cancers, like lung and pancreatic cancer, these receptors are just overexpressed.

They're stuck in the on position, constantly telling the cell to divide, divide, divide.

So these drugs are designed to jam that signal.

The prototype here is Elocanib.

Erolitanib.

It inhibits the tyrosine kinase enzyme that's associated with that receptor.

It basically just cuts the power cord to the receptor.

It's used very heavily in non -small cell lung cancer, or NSCLC, and also pancreatic cancer.

Now, I saw a very, very specific administration rule for Erolitanib in the text.

This seems like one of those things that will definitely be on the final exam.

Oh, absolutely.

This is classic NCLEX material right here.

Erolitanib must be taken on an empty stomach, one hour before or two hours after meals.

Why is that?

Usually we're telling people to take meds with food to protect their stomach.

It's the opposite here.

In this case, food actually increases the absorption in a way that makes the drug much more toxic.

It seriously increases the risk of side effects.

So empty stomach is the strict non -negotiable rule.

Okay, empty stomach.

What about interactions?

This is where it gets really interesting.

It does, especially for lifestyle assessment.

Smoking.

Tobacco decreases the effectiveness of Erolitanib.

Wait, really?

We tell lung cancer patients to stop smoking for obvious reasons.

I mean, it causes cancer.

But you're saying the smoking actually messes with the medication itself?

Yes.

The hydrocarbons in tobacco smoke, they induce the CYKE1A2 enzyme in the liver.

That enzyme chews up the drug.

So if your patient smokes, they are metabolizing the drug way too fast and they just aren't getting a therapeutic dose.

That is wild.

So a smoker might essentially be taking a placebo because their liver is destroying the drug so quickly.

That's a great way to put it.

Exactly.

And I also see a note in here about pH.

Yes.

Erolitanib needs a certain level of acidity in the stomach to be absorbed properly.

So if a patient is popping Tums all day or taking a proton pump inhibitor like Umrazol for their heartburn, they're reducing the effectiveness of their cancer drug.

And think about how common that is.

Cancer patients often have GI upset.

So they reach for antacid.

Nurses really, really need to check that med list.

100%.

And in terms of side effects, just remember, this targets epidermal growth factor.

Epidermal means skin.

So skin reactions are huge here.

Huge.

A classic acneiform rash.

It looks like acne, but it's not actually acne.

So standard acne creams won't work.

It can be incredibly severe.

It can peel.

It can blister.

Also, ocular changes, corneal perforation is a risk.

So nurses need to be watching the patient's skin and their eyes very closely.

There's another drug in this class.

Gifitinib.

It has a really weird side effect that stuck out to me.

The eyelashes.

Yes.

Abnormal eyelash growth.

It sounds kind of cosmetic and maybe even nice, right?

But it's not.

The lashes can go really long and curly and sometimes they turn inward and scratch the eye.

So Gifitinib causes conjunctivitis in this bizarre long eyelash growth.

But otherwise it's pretty similar to Erolitanib used for lung cancer.

Lots of skin issues.

Diarrhea.

And one more in this group.

Alzheimertinib.

This is a newer one.

It's specifically for patients with a certain mutation, the T790M mutation.

So it's very, very targeted.

But the safety alert here is all about the heart.

It can cause

cardiomyopathy, which is a weakness of the heart muscle, and QT prolongation.

QT prolongation.

That's where the heart's electrical recharging cycle takes too long, isn't it?

Yes.

And it can lead to fatal arrhythmias, like torsades appoint.

So you absolutely need baseline EKGs for these patients before you start.

Okay.

Let's shift gears to section three.

Tyrosine kinase inhibitors, or TKIs.

Now, I know we just talked about drugs that inhibit tyrosine kinase in that EGFR section, but this section seems to focus on a different target entirely.

BCRABL.

Correct.

This is the holy grail of targeted therapy in many ways.

We are talking about CML chronic myelogenous leukemia.

And this is where that Philadelphia chromosome comes back into play.

Right.

So in CML, pieces of chromosome 9 and chromosome 22 swap places.

This creates that fusion gene we mentioned earlier.

That fusion gene creates a brand new enzyme called BCRABL tyrosine kinase.

This enzyme is the engine driving the leukemia.

They're constantly on, telling the white blood cells to divide.

And the prototype drug that stops this is imatinib mesylate.

Also known by its brand name, this is the drug that completely changed the world for leukemia patients.

Before this drug, the prognosis for CML was really poor.

Imatinib blocks the ETP binding site on that enzyme.

It literally shuts off the engine.

It induces apoptosis programmed cell suicide in those cancer cells.

Now, let's contrast this with erlitinib.

We just said erlitinib is a strict empty stomach drug.

What about imatinib?

Imatinib is the total opposite.

It should be taken with food and a GI irritation.

It's very, very hard on the stomach lining.

So erlitinib equals empty.

Imatinib equals meal.

Got it.

What are the big risks with imatinib?

Fluid retention.

Edema.

And I'm not just talking about swollen ankles, so that definitely happens.

We're talking potential cerebral edema, which is brain swelling, or even cardiac tamponade, which is fluid building up around the heart.

So the nurse needs to be weighing the patient daily.

That's a key intervention.

Absolutely.

The tech says to report a weight gain of more than two pounds in a single day or four pounds in a week, that's not fat.

That's fluid.

It's a major sign of overload.

And what about grapefruit juice?

No grapefruit juice.

This is a theme you'll see a lot in pharmacology, but it is critical here.

Grapefruit inhibits the enzyme to break the drug down, so the drug levels can spike to toxic levels in the blood.

Okay.

There are a couple other drugs in this TKI category.

Let's hit nilotinib next.

Melotinib is often used when the imatinib stops working, but it comes with a huge black box warning for QT prolongation.

It carries a real risk of sudden cardiac death.

Sudden cardiac death.

That definitely gets your attention.

It does.

Absolute contraindications are hypokalemia, so low potassium, hypomagnesemia, low magnesium, or a history of long QT syndrome.

You have to fix the patient's electrolyte before you even think about giving this drug.

And what about the administration rules for this one?

Empty stomach.

Again, no food for two hours before or one hour after taking the dose.

But there's a do -not -crush note that was really interesting.

Yes.

You can't crush the capsule, but if a patient can't swallow pills, you are allowed to open it and sprinkle the contents on one teaspoon of applesauce.

Only applesauce.

Not like yogurt or something.

Only applesauce.

The text is very specific.

Not yogurt, not ice cream.

Just applesauce.

It's a very specific chemical stability issue.

That is so specific.

Merces, write that down.

Nylotinib equals applesauce only.

Okay, let's move on to section four.

The multi -kinase inhibitors.

The MPIs.

As the name suggests, they don't just hit one kinase target, they hit multiple kinase enzymes.

It's a bit of a broader attack, maybe more like a directed shotgun than a sniper rifle, if we stick with that analogy.

We have Dacitinib here first.

Dacitinib is used for CML and also allel, which is acute lymphoblastic leukemia.

The big things to watch for are electrolyte imbalances, especially low calcium and low phosphate, and significant bleeding risks.

Also, just like Erlognib, antacids will slow down its absorption.

Then there's Sorphinib.

Sorphinib is used for liver, kidney, and thyroid cancers.

A really classic side effect here is something called Hand and Foot Syndrome.

What is that?

It sounds pretty descriptive.

It is.

It's this painful redness, swelling, and sometimes blistering on the palms of the hands and the soles of the feet.

It can be really uncomfortable for the patient, making it hard to walk or even hold things.

And the last one in this group, Sunitinib.

Sunitinib inhibits over 80 different receptors.

It's a powerhouse.

But because it hits so many targets, it has a really weird side effect profile.

It can cause skin discoloration, a distinct yellowing of the skin and the whites of the eyes.

Is that jaundice from liver damage?

It can look like it, and it can cause liver issues.

But the text distinguishes it as a specific skin discoloration or even depigmentation that's related to the drug's color and mechanism, separate from just liver toxicity.

It can also cause left ventricular dysfunction, so heart monitoring is definitely key.

Okay, section five.

We're getting into some of the real tongue twisters now.

MTR, kinase inhibitors, and proteasome inhibitors.

Let's start with MTR.

The main drug here is Timsorolimus.

And what does MTR do?

So MTR is a protein that basically regulates cell growth and survival.

If you inhibit it, you arrest the cell cycle in what's called the G1 phase.

The cell just stops dividing.

Timsorolimus is given IV.

What's the catch with this one?

Hypersensitivity reactions.

They're very, very common.

So you have to pre -medicate the patient with an antihistamine, like defenhydramine, which is Benadryl, about 30 minutes before you start the infusion.

And I see a warning about live vaccines.

Yes, the immune system is suppressed, so no live vaccines.

Also, it causes hyperglycemia.

High blood sugar.

Yes, to the point where patients might need to go on insulin or oral anti -diabetic drugs while they're on this medication.

It really messes with glucose metabolism.

Okay, now for the proteasome inhibitors.

You used a great phrase for this earlier.

Something about taking out the trash.

Right.

A proteasome is like the cell's garbage disposal.

It breaks down old or damaged proteins that the cell doesn't need anymore.

And if you block the garbage disposal.

The trash just piles up.

All these unwanted proteins accumulate to toxic levels inside the cell and the cell dies.

It's essentially cell death by trash accumulation.

The prototype drug here is bortezomib.

Bortezomib.

Used for multiple myeloma and mantle cell lymphoma.

Now, I need everyone listening to stop what they're doing and hear this safety alert.

I'm listening.

Intrathickel administration is an absolute contraindication.

Intrathickel.

That means injecting it into the spinal fluid.

Correct.

If you inject bortezomib into the spine, it is fatal.

It might be bad, but fatal.

You must never ever do that.

It is for IV or subcutaneous use only.

That is a life or death nursing detail.

How could a mistake like that even happen?

Well, sometimes other types of chemo are given intrinsically for leukemia.

So if you have multiple syringes on a tray for one patient.

You just have to be incredibly vigilant with your checks.

What are the other major side effects?

Peripheral neuropathy.

That numbness and tingling in the hands and feet is very common.

And cardio toxicity is also a risk.

And I see the note again.

Do not confuse bortezomib with bevacizumab.

We mentioned that earlier, but it's worth repeating.

Bortezomib is the trash compactor blocker.

Bevacizumab is the blood vessel blocker.

Do not mix them up.

And also green tea.

That's random.

It is a weird one.

Green tea contains flavonoids that actually decrease the effects of bortezomib.

Patients need to skip their matcha lattes while on this treatment.

Okay, we are in the home stretch of the drug classes.

Section six, monoclinal antibodies or the MABs.

Right.

These are the large molecules.

Always give an IV because your stomach acid would just digest them.

And their job is to flag cancer cells for the immune system.

They do three main things.

First is neutralization, just blocking signals.

Second is something called ADCC, which stands for antibody dependent cell mediated cytotoxicity.

Wow.

That's a mouthful, but it basically means calling in the immune system's cavalry, the killer cells.

And third is CDC complement dependent cytotoxicity, which activates a part of the immune system called complement to punch holes in the cell membrane.

Let's talk about l -amtuzumab first.

L -amtuzumab targets CD52.

This is an antigen that's found on B and T lymphocytes.

The huge risk here is severe lymphopenia.

It completely wipes out your white blood cells.

So the infection risk is massive.

And what about cetuximab?

Cetuximab targets EGFR.

So we're back to that epidermal growth factor again.

Remember what we said about epidermal growth?

It's always about the skin.

Exactly.

Cetuximab has a black box warning for severe dermatologic toxicity.

An acne -formed rash occurs in 90 % of patients.

90%.

That's almost a guarantee then.

It basically is.

And actually in clinical practice, getting the rash is sometimes seen as a good sign that the drug is working.

It means you've hit the target.

But it's miserable for the patient.

It also carries a high risk of severe infusion reactions.

Airway obstruction.

Hypotension.

You have to watch them like a hawk during that first infusion.

Now this next group sounds like something out of science fiction.

Radioactive monoclonal antibodies.

Ibrutumumab tuxitin and tocitumumab.

This is fascinating stuff.

They take a monoclonal antibody that's designed to find a specific cancer cell and then they strap a radioactive backpack to it.

Either utrium -90 or iodine -131.

So it delivers a dose of radiation directly to the tumor's doorstep.

Correct.

And it creates what's called a crossfire effect.

The radiation hits the target cell and also kills the cells right next to it.

It's very localized radiation therapy.

But the safety precautions must be huge here.

Oh, absolutely.

The patient effectively becomes radioactive for a period of time.

You need strict waste disposal protocols.

Their urine is radioactive.

You have to follow very strict safety rules for handling any bodily fluids.

Let's talk about the big one in this class.

Rituximab.

The prototype.

Rituximab targets the CD20 antigen on B cells.

It is the go -to for non -Hodgkin lymphoma and CLL.

It's also used for autoimmune diseases like rheumatoid arthritis.

What are the biggest dangers with this one?

Tumor lysis syndrome.

Because it kills the cancer cells so effectively and so quickly, the cells literally burst open and dump all their contents.

Potassium, uric acid, phosphorus into the blood.

This can completely overwhelm the kidneys and cause renal failure.

So hydration is absolutely key.

Hydration and also giving drugs like alloturinol to help manage the high uric acid levels.

Also, severe infusion reactions are very common.

You must pre -medicate with diffenhydramine and acetaminophen 30 minutes prior to the infusion.

And what's this about hepatitis B?

It can reactivate a dormant hepatitis B infection.

So you have to screen patients for hep B before you ever start treatment.

If you don't and they have a history of it, the virus can flare up and cause acute liver failure.

Okay, last one in this massive group.

Trastuzumab.

Most people probably know it as Herceptin.

Trastuzumab targets HER2.

This is that protein that's overexpressed in some very aggressive types of breast cancer and some gastric cancers.

And the black box warning.

Cardiomyopathy and congestive heart failure.

It can be directly toxic to the heart muscle.

So echocardiograms are mandatory, I assume.

Regular monitoring of their left ventricular ejection fraction or LVEF.

If you see their heart functions start to drop, you have to stop the drug.

And there's a do not confuse warning for trastuzumab and atortrastizumab entansine?

They are not interchangeable at all.

Atortrastizumab entansine is the antibody plus a chemotherapy bomb that's attached to it.

The dosing, the schedule, everything is totally different.

Mixing them up could be fatal.

Okay, we have covered a massive amount of pharmacology.

We've gone through the whole alphabet soup.

But let's bring this into the so what section.

Section seven, the nursing process.

How do we actually apply all of this?

You are the nurse on the floor.

What are you doing?

Assessment is step one.

You have to be a detective.

You need a detailed medication history.

We've mentioned CYP3A4 inducers and inhibitors a dozen times today.

Like St.

John's wort.

St.

John's wort is the enemy of so many of these targeted therapies.

It induces enzymes and clears the drugs out of the body too fast.

Grapefruit juice does the opposite.

It inhibits enzymes and causes toxicity.

You have to ask specifically about these things.

Patients think St.

John's wort is just a harmless herbal tea for their mood.

You have to educate them that it has serious interactions.

And baseline labs.

CBC, liver function, renal function, electrolytes.

You can't know if the drug is causing neutropenia or hypokalemia if you don't know where the patient started from.

Now for planning and interventions.

We talked a lot about bleeding.

So you're monitoring for black stools, coffee ground vomit.

Those are the classic signs of an upper GI bleed, which is a real risk with those angiogenesis inhibitors.

And what about skin care?

With the EGFR inhibitors, you know the skin is going to peel, blister, and rash.

So you're teaching patients to avoid the sun, use very gentle non -alcoholic cleansers, and to report any worsening rash immediately.

It's not just dry skin.

It's a drug toxicity.

What about those infusion reactions?

If you are hanging a bag of a monoclonal antibody, especially rituximab or cetuximab, you need to have the crash cart nearby.

Epinephrine, corticosteroids, everything.

Be ready for anaphylaxis.

It can happen, and it happens fast.

And pregnancy.

All of these drugs are toriogenic.

They can cause severe birth defects.

So women of childbearing age need strict, reliable contraception during treatment, and often for months after.

And breastfeeding.

Absolutely not.

The text is very clear.

Stop during treatment and for at least 60 days after the final dose.

Cation education is just so huge here.

We've mentioned all the specific food rules.

You have to review every single drug, Erlotinib, no food, imotinib, with food.

It's not one size fits all.

You can't just guess.

And weighing daily.

Report a gain of more than two pounds in a day.

That could be fluid retention, a sign of impending heart failure, or kidney failure.

And infection risk.

Avoid crowds.

Avoid sick people.

If you get a fever, you call the doctor immediately.

A fever is an emergency when your immune system is wiped out by one of these drugs.

The text ends with a case study about a patient with non -Hodgkin lymphoma who's receiving rituximab.

The patient asks why it has to be given IV and why they can't just do it at home.

And the nurse's answer combines everything we've talked about today.

First, it's a large protein molecule.

So it has to be IV because your stomach acid would just digest it like food.

And second, the risk of a severe infusion reaction anaphylaxis is just too high.

You need to be in a medical setting with resuscitation equipment ready to go.

It really emphasizes that these aren't just pills.

They are powerful, powerful biological agents.

So let's wrap this up.

We've gone from blocking blood vessels with ziviflib receptor to blocking receptors with erlitinib, shutting down the leukemia engine with imatinib, and flagging cells for destruction with rituximab.

It's an incredibly complex landscape.

And these therapies, they're precise, but that does not mean they are safe.

They carry very specific, very significant risks.

Bleeding, heart failure, skin toxicity, QT prolongation.

And I think for the student listening, the big takeaway has to be that precision medicine absolutely requires precision nursing.

That's the key right there.

You can't just hang the bag or hand over the pill and walk away.

You have to know the specific drug -food interaction, the specific lab value to watch, the specific side effect to look for.

The margin for error is small, but the potential benefit for the patient is just huge.

Well said.

That brings us to the end of our deep dive into Chapter 36.

Hopefully that whole alphabet soup of mabs and nibs makes a little more sense now.

I think it does.

Keep studying, always check those labels, and please watch out for the grapefruit juice.

Thanks for listening from the Last Minute Lecture Team.

Good luck with your exams.