Chapter 31: Antimalarial, Anthelmintic & Peptide Drugs

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Welcome back to the Deep Dive.

I have to be honest with you.

When I first looked at the syllabus for today, or well, the chapter list,

I had a moment of hesitation.

Oh, yeah.

We are looking at chapter 31 of pharmacology,

a patient -centered nursing process approach.

And the title of this chapter is, Anti -Mullerials, Anthelmintics, and Peptides.

It is quite a mouthful, isn't it?

It is.

And my initial thought was, okay, this feels niche, I mean malaria,

worms.

It feels like we're prepping for a tropical expedition on the Amazon River, not, you know, a standard shift at a suburban hospital in the Midwest.

I get that.

I think a lot of students have that same reaction.

But then I started reading the notes you prepared and I dug into the text and I realized I was completely wrong.

This isn't just about tropical medicine.

Not at all.

This is about patient safety in a completely globalized world.

That is exactly right.

And that is the trap a lot of students and even experienced nurses can fall into.

How so?

They see anti -mullerials and they think, well, I don't live in the jungle, so I can skim this.

Right?

Not my problem.

But the reality is, your patients travel.

They go on mission trips, they go on honeymoons, they visit family abroad.

And they bring things back with them.

They bring things back.

And if you don't know what you are looking for, you miss it.

And if you miss it, the consequences can be, that can be devastating.

Precisely.

And then you throw in the peptides, which are these heavy heating antibiotics we use when everything else fails.

The last resort drugs.

Last resort.

Suddenly this chapter feels a lot more urgent.

It's not just about bugs and It's about handling the toughest, most resistant infections we face.

So here is our mission for today.

We are going to treat this like the ultimate survival guide.

I like that.

We are going to move through the text in the exact order of the chapter.

No skipping, no jumping around.

Good.

Stick to the source.

We're going to break down the mechanisms, the side effects, and most importantly, the nursing implications.

We want to get to that level of insight where the information sticks in your brain.

So you don't have to just memorize flashcards by rote.

Exactly.

I love that approach.

Let's strip away the fluff and get to the mechanism of why we do what we do.

Perfect.

Let's get into it.

So let's start where the text starts.

Context.

The book opens with a bit of a history lesson noting that malaria was actually eliminated from the United States in the early 1950s.

Which sounds like a victory lap.

It sounds like we can close the book and say, we won, it's over.

Right.

But then it immediately drops the hammer.

It says, despite that elimination, we still see about 2 ,000 to 2 ,500 cases of malaria diagnosed each year.

Right here in the US.

Right here.

That is a significant number.

I mean, that is 2 ,000 opportunities for a misdiagnosis if a provider isn't paying attention.

And the text makes it clear those cases are almost exclusively imported.

It's people traveling to endemic areas and coming back.

And looking at the global picture, the numbers are just, they're heartbreaking.

The source material cites an estimated 247 million cases worldwide.

It's staggering.

And the death toll.

Yes.

619 ,000 people.

Wow.

And it's mostly children in the sub -Saharan African region.

It is a massive global health crisis.

So even if you're practicing in Ohio or Nebraska,

you are part of that global surveillance network.

You're the first line of defense.

You're the one recognizing when someone brings this crisis home.

So to fight the enemy, we have to know the enemy.

Let's get into section one.

The disease process of malaria.

It's not a virus and it's not a bacteria.

No, it's a protozoan parasite.

The genus is Plasmodium and it has a very specific partner in crime.

The Anopheles mosquito.

That's the one.

The vector.

I always found this life cycle fascinating in a terrifying sort of way.

It's not as simple as mosquito bites you, you get sick.

No, it's a two -phase invasion.

Okay, break that down for us.

Right.

It is a stealth attack followed by an all -out assault.

The first phase is the tissue phase.

The tissue phase.

The mosquito bites you, injecting the parasite.

Those parasites don't go into the blood right away.

They head straight for the liver.

They invade the body tissue.

And the text says this phase is asymptomatic.

That is the stealth part.

You have no idea you're infected.

You feel fine.

The parasites are just multiplying quietly in your tissues.

Okay, that's creepy.

And then comes phase two.

The erythrocytic phase.

Erythrocytic, referring to erythrocyte.

Red blood cells, exactly.

The parasites burst out of the tissue and invade the red blood cells.

They consume the hemoglobin, they multiply inside the cell.

And then what?

And then they rupture the cell to find new victims,

to go infect more red blood cells.

And that rupture, that is what causes the symptoms.

Exactly.

When those blood cells burst, they release all these toxins.

And that triggers the classic malaria presentation.

Extreme chills, high fever, and sweating.

So it's cyclical.

It is.

It aligns with the life cycle of the parasite bursting out of the cells over and over again.

That explains the flu -like description, but it sounds so much more violent.

The text notes the intubation period is 10 to 35 days.

That's a long time.

It is.

You could be back from your vacation for a whole month before you get sick.

Which is why the travel history question is so, so vital.

Right.

If you just ask, have you traveled recently?

And they say, no, you might stop there.

But they're thinking of last week, not last month.

Exactly.

You need to ask, have you traveled out of the country in the last two months?

Be specific.

That's a great distinction.

Now, the text mentions there are about 50 species of plasmodium, but only five really bother humans.

We have P.

malaria,

P.

oval, P.

vivax, and P.

falciparum.

And P.

nullacy gets a mention in some of the charts.

But really, the big two you need to be able to distinguish are P.

vivax and P.

falciparum.

OK.

So what is the breakdown there?

What's the difference?

Well, P.

vivax is the most prevalent.

If you see a malaria case, statistically,

it is likely to be vivax.

It's hardy.

It's everywhere.

OK.

But P.

falciparum, that is the killer.

That is the most severe form.

Why is it worse?

What does it do differently?

So fasciparum malaria actually changes the surface of the infected red blood cells.

That makes them sticky.

Sticky?

Yeah.

So they clump together and can block the small blood vessels in your vital organs, the brain, the kidneys.

Oh, wow.

That's how you get cerebral malaria.

It is a true medical emergency.

So if I see P.

falciparum on a lab report, I am moving a lot faster.

You're moving a lot faster.

Absolutely.

Now, because this is such a complex foe, the text outlines three strategies for eradication.

It isn't just treat the sick.

Right.

It's a three -pronged attack.

We have prophylaxis, which is prevention.

Before you even get sick.

Treatment for the acute attack.

When the symptoms are active.

When the symptoms are active.

And that prevention of relapse is really interesting because some of these parasites,

specifically P.

vivax and P.

oval, can go dormant in the liver.

They can just hibernate.

For months, even years.

And then wake up later and cause a relapse.

So you need drugs that specifically target that dormant litter phase to truly cure the patient.

But we have a problem, a big one.

The parasites are fighting back.

Grogue resistance.

It is the defining struggle of modern malaria treatment.

And the text specifically highlights chloroquine.

Oh, yeah.

For decades, chloroquine was the magic bullet.

It was cheap.

It was effective.

It was relatively safe.

But now.

But now, resistance is widespread.

The text actually says that before a provider prescribes chloroquine, they have to check if the specific strain in that region is susceptible.

You have to check the maps, the CDC data.

It's almost assumed to be resistant in many parts of the world now.

So if it is resistant, what do we do?

Then you have to bring in the heavy artillery combination therapies or even adding antibiotics like tetracyclines or chloroquinalones to the mix.

Let's dive into chloroquine, though, because it is still the prototype drug for this section.

It is.

And the text makes it clear.

If you understand chloroquine, you understand the baseline for all the anti -malarials.

Correct.

It is a 4 -ametoclinoline antiprotozole.

It's the classic.

Let's look at the pharmacokinetics because I saw a number in the text that made me do a double take.

The half -life.

I know exactly what you're looking at.

The elimination half -life is listed as 108 to 291 hours.

It's staggering.

291 hours.

That is, that's like 12 days.

For the half -life.

Just for the half -life.

Which means the drug is effectively in your system for weeks, potentially months, after the last dose.

Why so long?

It's because it binds so avidly to tissues.

It doesn't just float around in the blood.

It settles into the organs.

Which organs are we talking about?

The liver, the spleen, the kidneys, the lungs, and the eyes.

Okay.

Put a pin in the eyes because I have a feeling we're going to come back to that as a major safety issue.

We definitely are.

But first, how does it actually kill the parasite?

The mechanism is really clever.

So the malaria parasite lives inside the red blood cell and it's eating hemoglobin.

Okay.

But digesting hemoglobin releases this stuff called hemin, which is actually toxic to the parasite.

So it's making its own poison.

It is.

But normally the parasite has an enzyme that turns that toxic heme into a harmless crystal called hemezoin.

So it has a built -in waste management system.

Exactly.

And chloroquine jams that system.

It concentrates in the parasite's acid vesicles and it stops that enzyme from working.

And so the toxic heme builds up.

Builds up and essentially parasite grounds in its own toxic waste.

That is a brutal way to go.

I love it.

It is effective.

Or it was until the evolved ways around it.

So we use it for treatment and prophylaxis.

But because it hangs around in the body for so long and binds to tissues, the side effect profile is pretty distinct.

It is.

You have the standard GI stuff, anorexia, nausea, vomiting, diarrhea.

That is common with almost all antibiotics and antiparasitics.

But chloroquine has some unique ones.

The text mentions photosensitivity.

Right.

Patients get sunburned very easily.

And hair discoloration.

Yes, that too.

But the contraindications are where we need to really focus for patient safety.

Okay.

The text lists two absolute contraindications.

Hypersensitivity, which is obvious.

And ocular disease.

There it is.

The eyes.

This is crucial because chloroquine binds to melanin

and the retina of the eye is rich in melanin.

The drug concentrates there.

Over time, it can cause retinal toxicity.

So if a patient already has retinal issues or visual field changes, giving them chloroquine is like pouring gasoline on a fire.

Exactly.

It can cause corneal opacity and macular degeneration.

And is that reversible?

That's the terrifying part.

It can be irreversible.

Even if you stop the drug, if the damage is done, it is done.

That is a huge nursing implication.

We are literally protecting the patient's sight.

It's a massive responsibility.

There are other severe reactions too, right?

The text mentions the heart and the bone marrow.

Yes,

it can hit the heart.

You'll see ECG changes, hypotension, and there's a risk of cardiovascular collapse.

And the bone marrow.

A granulocytosis, a plastic anemia.

So basically, it can stop your heart or stop your body from making blood cells.

In rare, severe cases, yes.

It is a powerful drug that demands respect.

Before we move off the prototype, there is a patient safety alert in the text that is just screaming for attention.

It's a do not confuse warning.

This is a classic, a classic board exam trap, but more importantly, a real world medication error that kills people.

Do not confuse quinine with quinidine.

One letter difference.

They sound almost identical when you say them out loud.

But they are very different drugs.

Very different.

Quinine is the anti -malarial.

Quinidine is primarily an antidisrhythmic.

It's a heart medication used to control abnormal rhythms.

So if you give a malaria patient a therapeutic dose of quinidine, thinking it's quinine.

You could stop their heart.

The text is very, very clear.

Confusing these can be fatal.

Also, the text mentions quinine itself has a black box warning.

It does.

For severe muscular cramps, it's potent stuff.

Okay, that is a deep dive on chloroquine.

But because of resistance, we have other tools in the shed.

Table 31 .1 lists several other anti -malarials.

Right.

The alternatives.

I want to run through these because inch one seems to have a specific gotcha that nurses need to know.

A unique personality, let's say.

Let's start with mefloquine.

Mefloquine.

This is often used for prophylaxis for travelers,

but it has a notorious reputation.

Why is that?

The FDA added a black box warning for neurological side effects.

Okay, like what?

The text lists dizziness, loss of balance, ringing in the ears.

And it specifically notes that these vestibular issues can be permanent.

Permanent.

Imagine taking a pill for a two -week vacation and ending up with permanent tinnitus or balance issues for the rest of your life.

Wow.

But the psychiatric effects are what I hear about most with that one.

Yes.

Severe anxiety, paranoia, hallucinations, depression,

suicidal thoughts.

The text calls these out specifically.

And it can happen even after you stop taking it.

That's the other scary part.

These symptoms can persist for months after you stop taking the drug.

So if I'm doing an intake history and a patient tells me they have a history of depression or anxiety.

You need to flag that immediately.

The text lists anxiety, depression, psychosis, schizophrenia as absolute contraindication.

So you just don't give it.

You do not give Mesoquine to a patient with a significant psychiatric history.

It is not worth the risk.

Moving on to Primekine.

This is the one used for preventing relapse, right?

It kills the liver forms.

Correct.

It kills those dormant forms, the hypnozoites.

But it has a genetic trap.

The genetic trap.

It can cause acute hemolytic anemia, which is the massive destruction of red blood cells.

In patients who have a specific genetic deficiency.

That's the G6PD deficiency.

Glucose 6 -phosphate dehydrogenase.

That is the one.

So what's the connection?

G6PD is an enzyme that helps protect red blood cells from oxidative stress.

Primekine causes a lot of oxidative stress.

If you don't have the enzyme to handle it, your red blood cells just pop.

They lyse.

And how would that present in a patient?

What would I see?

The text says it presents as methamaglobinemia.

Which means?

The patient turns blue.

Cynosis of the lips, the fingernails, the skin.

And they'll have dark reddish -brown urine because of all the blood breakdown products.

So practically speaking, before starting Primekine, checking G6PD status is mandatory.

It absolutely should be standard of care.

You have to screen for it.

What about hydroxychloroquine?

We've heard that name a lot in the news over the last few years.

But in this context, it's an anti -malarial and an anti -pharmatic.

It is very similar to chloroquine.

The risks are parallel.

So the eyes again.

The big one again is the eyes.

Irreversible retinal damage is a contraindication.

It can also cause cardiomyopathy damage to the heart muscle and suicidal ideation.

It really seems like eyes and mood is a recurring theme with this whole class of drugs.

It really is.

It's a pattern you have to watch for.

And finally, the combination therapies.

We see atovacone probuanil, which is commonly known as melarone.

That's a daily pill for trophallaxis.

It's very popular because it generally has fewer side effects than melphloquin.

But you have to use caution if the patient has renal impairment.

The kidneys clear it.

Got it.

And artemithorlomifentrine.

That is strictly for treating acute uncomplicated malaria.

It's not for prevention.

It is a very specific regimen.

Six doses over three days.

It's fast acting.

Okay, so we have the arsenal.

Now let's put on our scrubs and get to the bedside.

Section four, the nursing process for anti -malarials.

This is where we translate the chemistry into actual patient care.

Assessment.

Recognize cues.

We already nailed the first and most important one.

Travel history.

It cannot be overstated.

Have you traveled out of the country?

But also when?

Remember that long incubation period.

And we need to assess their sensory baseline before we start these drugs.

If these drugs can cause blindness and deafness, we need to know what the patient can see and hear before we give the first dose.

So a Snellen chart for vision, maybe some audiometry.

Exactly.

You have to document visual acuity.

Document any existing hearing loss or tinnitus.

If they come back in two weeks complaining of blurry vision, you need to know if that is new or if it was there before.

And biologically, we're monitoring the kidneys and the liver.

Always.

The liver metabolizes the drugs.

The kidneys excrete them.

If either one of those is failing, the drug can build up to toxic levels.

So I'm looking at their labs.

Monitor liver enzymes, AST, ALT, and monitor urine output.

The tech sets a benchmark.

Output should be greater than 600mL today.

Moving to take action, our interventions, what am I looking for?

We're looking for signs of toxicity.

Yellowing skin or eyes jaundice.

That tells us the liver is struggling.

Skeletal muscle weakness.

And we are watching that ECG.

Especially if they're on quinine or have any electrolyte issues.

Right.

You're watching for a widening QRS complex, QT prolongation.

The heart rhythm tells a very important story.

Now, patient teaching.

This is where I feel like nurses have the biggest impact on prevention.

Prophylaxis is not intuitive.

No, it is not.

Patients think, I'm leaving on Saturday, I'll take a pill on Friday.

And that's wrong.

Completely wrong.

For chloroquine, the tech says you start one to two weeks before you enter the endemic area.

Why so early?

You need to build up a steady state concentration in the blood.

You want the drug to be waiting for the parasite, not chasing after it once it's already in your system.

And you continue it during the trip.

Every week, on the same day.

And crucially, for four weeks after you leave.

That is the hard part for patients to understand.

Your home, your tan, you have your souvenirs, you feel fine.

Why keep taking the pills?

And the answer is.

Because the parasite could be in that silent incubation phase.

Or it could be hiding out in your liver.

If you stop early, you are just inviting the malaria to surface a month later.

What about the GI upset?

If the pills make them nauseous, they're not going to take them.

You have to teach them to take it with food or milk.

It makes a huge difference in tolerability.

And the big red flag for reporting.

The one thing they have to call us about immediately.

Vision.

Any change in vision.

Blurring, trouble focusing, reading difficulties.

You have to tell them.

If your vision changes, stop the drug and call us immediately.

Do not wait.

All right.

We have successfully navigated the mosquito -infested jungle.

Now we're going to get down and dirty.

Literally.

We are moving to section five.

Anthelmintics.

The worms.

Helminths.

Parasitic worms.

I have to admit, this topic makes my skin crawl a little bit.

It's a natural reaction.

But clinically, it is incredibly common around the world.

And the text notes that transmission usually occurs in areas of poor sanitation.

Infected soil is a major vector.

Or contaminated food.

And the impact on the host, the human,

is parasitic in the truest sense of the word.

It is.

The worm feeds on host tissue.

It steals nutrients.

In children, the text highlights that if left untreated, this can cause significant developmental delays, stunted growth, and cognitive issues.

Why?

Because the worm is literally eating the child's lunch from the inside.

Okay.

Let's meet the cast of characters.

The text breaks them down into four main groups.

First up, cestodes.

Cape worms.

These are the nightmares of the Victorian age.

Pork tapeworms.

Beef tapeworms.

Fish tapeworms.

The description is graphic.

They're segmented.

Yes.

And they have a head.

It's called a scolax.

And it's equipped with hooks or suckers.

Yikes.

They hook it to the intestinal wall and just hang out, absorbing nutrients.

The segments break off and pass in the stool, which is how they spread.

Next group, trematodes.

Flukes.

These are flat, loose -shaped parasites.

You have liver flukes, lung flukes, blood flukes.

They migrate to specific organs.

Then the intestinal nematodes.

These are the roundworms.

This is a really big group.

It includes ascaris lumbricoids, the giant roundworm.

But the most important one for US nurses to know.

Let me guess.

Pinworm.

Enterobius vermicularis.

The pinworm.

It is the most common helminth infection in the United States.

It runs rampant in daycares in elementary schools.

And finally, the extraintestinal nematodes.

These are the ones that invade tissue.

Trichinella spiralis is the classic example here.

It causes trichinosis.

Or that is the undercooked pork disease, right?

Exactly.

The larvae are insisted in the muscle of the pig.

You eat the muscle, the meat without cooking it enough, and the larvae wake up inside of you.

The text is very clear on prevention here.

Cook your pork.

Thoroughly to the correct internal temperature.

So how do we get rid of them?

Section 6 covers anthelmintic drug treatment.

And we have a prototype that has been in the news for,

let's say, controversial reasons lately.

Ivermectin.

Yes.

But we are sticking strictly to the text here.

What does our pharmacology book say ivermectin is for?

It says it's a broad -spectrum antiparasitic of the ivermectin class.

Its FDA -approved uses are quite specific.

Which are?

River blindness, which is onchocercesis,

Strongyloidesis, which is a type of round worm,

scabies, and head lice when it's used as a topical lotion.

And the text explicitly addresses the controversy.

It does.

It has a disclaimer in a box stating clearly, ivermectin is not an antiviral drug and is not FDA -approved for treating or preventing COVID -19.

It also warns about animal formulations.

That they're highly concentrated and can be toxic to humans.

Good to have that clarified.

So how does it kill the worms?

It targets the parasite's nervous system.

It binds with chloride ions, which increases the cell permeability.

And it basically causes paralysis and death of the parasite.

What about the pharmacokinetics?

It has a pretty long half -life, 16 to 28 hours for the oral pill.

But the topical lotion, 6 .5 days.

It sticks around to keep killing the lice or scabies mites.

Any serious adverse reactions to watch for?

It can cause lymph node swelling, lymphadenopathy, dizziness, seizures in rare cases.

And Stevens -Jawson syndrome, which is that severe blistering skin reaction, is listed as a potential risk.

Let's look at the other worm killers in table 31 .2.

Preziquantel.

This is the drug of choice for flukes and tapeworms.

It basically makes the worm spasm and release its grip on the intestinal wall.

But there's a fascinating contraindication mentioned, ocular cysticercosis.

Right.

Which means?

It means if the tapeworm larvae have formed cysts in the eye,

you can't use this drug carelessly.

Why not?

Because killing the worm inside the eye can cause a massive inflammatory response that can destroy the patient's vision.

Wow.

So again, the eyes are a major danger zone in this chapter.

What about pyrantal?

Pyrantal pomode.

This is the go -to for pinworms and hookworms.

It's often available over the counter.

It paralyzes the worm so it just gets pooped out.

The regimen is usually a single dose, repeated in two weeks.

Why repeat it?

To break the cycle of reinfection.

The first dose kills the adult worms that are alive at that moment.

But not the eggs.

Exactly.

There might be eggs that haven't hatched yet.

So you wait two weeks for them to hatch, then you hit them with the second dose before those new worms can mature and lay new eggs.

Very smart.

And albendzolol.

That's used for more serious infections like neurocysticercosis.

That's tapeworm infection in the brain.

It's serious stuff.

The main thing to watch for is bone marrow suppression.

Let's move to the nursing process for anthelmintics.

Oh.

History is key.

But it's a different kind of history than we ask for malaria.

What are we asking?

We ask about travel, yes.

But also food intake.

Do you eat rare steak?

Do you eat raw fish?

Like sushi?

Undercooked pork?

And sanitation habits.

The text specifically mentions walking barefoot in soil.

Specifically for hookworms.

Hookworm larvae live in contaminated soil.

If you step on them with bare feet, they can bore right through the skin of your foot.

Oh, stop.

They enter your bloodstream, travel to your lungs, get coughed up, swallowed, and then they end up in your gut to live happily ever after.

That is a journey.

It is horrifyingly impressive.

But that is why do you walk barefoot outside?

It's a legitimate medical question.

For pinworms, the assessment is often based on the whole household, right?

Yes.

It is so highly transmissible.

If one kid in a daycare has it, you can assume many of them do.

If one kid in a family has it, you treat the whole family.

And the classic symptom.

Intense anal itching, especially at night.

That is when the female worm migrates out of the anus to lay her eggs on the surrounding skin.

I am so sorry to everyone listening who is eating lunch right now.

It is nature.

It's important to know.

Interventions.

Hygiene is the number one weapon here.

Hand washing.

It sounds so basic, but it stops the cycle.

You have to teach patients and parents to wash hands before eating and after every toilet use.

Because if you scratch the itch and then put your fingers in your mouth.

You reinfect yourself.

It's the fecal oral route.

We also have to collect stool specimens.

This is a specific nursing skill.

It is.

You need a clean container.

But the text is a very specific warning.

Do not let the stool touch water or urine.

Why is that?

Urine can be acidic or contain chemicals that can damage the parasites.

And toilet water.

Well, it dilutes everything and can also contain cleaners.

If you destroy the worm or the eggs before they get to the lab, the lab can't find them.

And the patient gets a false negative.

A false negative.

They don't get treated.

So keep the sample pristine.

The text also mentions monitoring nutritional status.

Because the worms are thieves.

They steal iron, iodine, vitamin A.

So you need to monitor for signs of anemia and malnutrition.

Patient teaching.

The text has a specific and memorable rule.

Showers, not baths.

This is specifically for pinworms.

If you take a bath, you're sitting in warm water.

The eggs wash off your pure enal area and they float in the bath water.

And can get everywhere.

Potentially getting into your mouth or sticking to other parts of your body.

You're sitting in a soup of reinfection.

A shower rinses it all away.

Exactly.

It rinses it down the drain.

Also linens.

Change sheets, towels, and underwear daily.

Wash them in hot water to kill any eggs.

And explain compliance.

Warn them that they might need that second dose in two weeks.

If they skip it because they feel better, the worms will just come back.

All right.

We are washing our hands thoroughly and moving to the final section.

Section 8.

Peptides.

We are leaving the world of parasites and entering the world of bacteria.

But not just any bacteria.

We are talking about the superbugs.

That's right.

The text sets the stage by discussing the CDC and the rise of drug -resistant infections.

MRSA, VRE, CRE.

These are the bacteria that laugh at penicillin.

They are multidrug -resistant.

And when a patient has one of these, we are running out of options.

That is where peptides come in.

The text defines them as broad -spectrum antimicrobial peptides, or AMPs, derived from Bacillus septilis.

They're the heavy artillery,

the last line of defense.

They work by targeting the bacterial cell membrane.

They weaken it, puncture it, and the bacteria basically bleeds out and dies.

But like any heavy weapon, there is collateral damage.

Significant collateral damage.

These drugs are toxic.

We only use them when we absolutely have to.

Let's look at Callistimdat, or Callistin.

It targets aerobic gram -negative bacteria like Pseudomonas and Klebsiella.

These are the nasty bugs that cause things like ventilator -associated pneumonias and sepsis in critically ill patients.

But the side effects.

The text highlights two major ones.

Neurotoxicity and nephrotoxicity.

Nerves and kidneys.

Let's break those down.

Neurotoxicity, what does that look like?

Tingling in the extremities, slurred speech, paresthesia, which is that numbness or pins and needles feeling,

dizziness.

And nephrotoxicity.

Kidney damage.

It can shut the kidneys right down.

You have to monitor BUN and creatinine religiously when a patient is on this.

So it's a trade -off.

It is.

Sometimes we are in a position where we are saving the patient's life from the infection, but we're damaging their kidneys in the process.

It's a very delicate balance.

The text also mentions a risk with the inhalation route.

Yes.

Colistin can be nebulized and given directly into the lungs for a bad pneumonia.

But it can cause bronchoconstriction and acute respiratory distress syndrome or ARDS.

So you could fix the pneumonia because ARDS.

Again, high risk, high reward.

Then we have polymixins.

The text mentions polymixin B and polymixin E.

Which is colistin.

They're in the same family.

The administration is tricky.

The text says an IM injection causes intense pain.

So we avoid that if we can.

We usually give it IV.

We give it IV, but it must be a slow infusion.

If you push it too fast, you spike the serum levels, and you hit the kidneys and nerves too hard, too fast.

The text notes that the neurotoxicity and nephrotoxicity are usually reversible when the drug is stopped.

Which is the good news.

But you have to be monitoring closely so you can catch it early.

Section 9 covers a couple of other agents.

Basitracin.

We all know this one.

It is in the over -the -counter ointment we put on cuts and scrapes.

It inhibits cell wall synthesis.

But the text makes an interesting point about its absorption.

It is not absorbed by the GI tract.

If you were to swallow it, it would just pass right through you.

So that's why it's mostly topical or ophthalmic for the eye?

Exactly.

Is it ever given by injection?

The text says IM is not recommended because it causes renal failure and ototoxicity hearing damage.

So stick to the ointment.

Now we arrive at the final boss of this chapter.

A drug that every nurse will give a thousand times.

Metronidazole.

Brand name Fledgel.

This is the prototype for this section.

It's a nitroimidazole.

A workhorse drug.

It seems to do everything.

The text says it's an antibiotic and an antiprotezole.

It is incredibly versatile.

It's used for H.

pylori, which causes stomach ulcers.

It's used for trichomonas vaginalis, an STI, bacterial vaginosis, rosacea, and all sorts of anaerobic bacterial infections like in the gut or an abscess.

How does it work?

It actually disrupts the DNA structure of the organism, which inhibits its protein synthesis.

Yeah.

It basically unzips their DNA so they can't replicate.

Now there is one interaction with metronidazole that is legendary.

It is bolded in my mind, it's bolded in the text, and it should be bolded in every patient's discharge instruction.

Alcohol.

What happens if you drink alcohol while taking metronidazole?

You trigger what's called a disulfiram type reaction.

Break that down.

What does the patient actually feel?

It is not just a bad hangover.

It is immediate severe illness.

Flushing of the face, a throbbing headache that feels like your head is splitting open.

Tachycardia,

racing heart palpitations, difficulty breathing, severe nausea, and projectile vomiting.

Patients often think they're having a heart attack or dying.

Why does that happen?

It prevents the normal breakdown of alcohol metabolite so you get a buildup of this toxic substance called acetaldehyde.

It's essentially pleasing to you.

Correct.

And the teaching has to be strict.

No alcohol, not a glass of wine, not a beer with dinner, nothing.

And check hidden sources, right?

Yes.

Cough syrup that contains alcohol, some mouthwashes.

And for how long do they need to avoid it?

During the entire course of treatment, and this is the key part that people forget, for at least 48 hours after the last dose.

Because the drug is still in their system.

Exactly.

You have to give it time to clear out completely.

What about other side effects?

The very common but harmless one is a metallic taste in the mouth.

Patients hate it, but it's not dangerous.

Sugar -free candy can help with that.

And their urine color.

It can turn the urine a reddish -brown color.

It looks alarming, like there's blood in it.

It's not.

It's not.

The text says it's harmless.

Yeah.

But you have to warn the patient so they don't panic when they see it.

And the serious adverse reactions.

Seizures are rare, but possible.

Stevens -Johnson syndrome again.

And super infection.

Meaning?

It kills the bad bacteria, but it also kills a lot of good bacteria in your gut and mouth.

So you can get a candidate overgrowth.

That means a yeast infection or oral thrush.

Let's wrap up the nursing process for peptides in Section 10.

Assessment is all about the kidneys.

You're watching renal function, BUN, and creatinine and urinary output.

If urine output drops while a patient is on colistin, you are in the trouble zone.

In allergies.

Especially to polymixins.

Intervenches.

Monitor for that super infection.

Look at the patient's mouth.

Do you see white patches?

That's thrush.

And neurostatus.

Yes.

Ask them.

Are your fingers or toes tingling?

Do you feel dizzy or off balance?

Patient teaching.

Report decreased urination immediately.

That is a critical sign that the kidneys are taking a hit.

Read all the instructions.

And again, for metronidazole, no alcohol.

Seriously,

no exceptions.

Section 11 wraps up with a clinical judgment case study.

Let's walk through it because it really ties everything together.

Okay.

We have a 40 -year -old missionary.

He returns to the U .S.

from a malaria endemic area.

He presents with a fever and a headache.

He gets diagnosed with acute malaria.

He was prescribed a chloroquine for prophylaxis.

But then he returns to the clinic a week later and he's much worse.

Why?

The text says he admits that he was only taking the pills every other day or skipping doses and then he just stopped entirely because they made him sick.

Non -adherence due to GI upset.

A classic problem.

So the breakdown was in the teaching.

The nurse failed to teach him how to manage the side effects.

Exactly.

The analysis in the book is that the nurse needed to teach him to take the medication with food to handle the nausea.

And explain the why.

And crucially, explain the danger of stopping the prophylaxis early.

Because he stopped, the parasite wasn't killed, it rebounded, and now he is sicker than he was before.

It highlights that just prescribing the right drug isn't enough.

The patient has to actually take it.

And they won't take it if it makes them miserable unless they understand why it is so necessary and how to mitigate that misery.

The text ends with some review questions.

Let's do a rapid -fire recap.

Let's do it.

Meflikine requires what kind of specific monitoring?

Liver function tests, LFTs, and definitely mental health monitoring for those psychiatric side effects.

Colostimethate is used for what kind of bacteria?

Gram -negative bacteria like Pseudomonas.

The really tough ones.

And the big contraindications for metronidazole.

Early pregnancy, so the first trimester, and of course alcohol use.

We have covered a massive amount of ground today.

We really have.

From mosquitoes to superbugs.

If you had to sum it all up for our listeners, a key takeaway for each section.

For anti -malarials, remember this is global health.

Watch the eyes, watch the liver, and always, always respect the travel history.

For anthelmintics.

It is all about hygiene.

Identifying the specific worm you're fighting and breaking that cycle of reinfection.

And for peptides.

These are power tools.

Use them when you have to, but watch the kidneys and the nerves like a hawk.

And remember, behind every one of these drugs is a patient who has been somewhere or eaten something or is fighting something terrifying.

Your job is to be the detective.

That is the essence of nursing right there.

Thank you so much for guiding us through the treacherous terrain of chapter 31.

It was a pleasure.

Anytime.

And to our listener, thanks for sticking with us through the jungle and the microscope.

Keep studying, check those labels, and please wash your hands.

We will see you on the next deep dive.

Goodbye everyone.