Chapter 60: Immunological Medications

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Welcome to the Deep Dive.

Today we're jumping into a really vital area in healthcare,

immunological medication.

That's right.

These are the drugs that, you know, help manage quite a range of things.

Yeah, everything from like persistent viruses to organ transplants, even just common bacterial infections.

It's a it's a complex area for sure.

It is.

But understanding the basics is so important.

And we've got a great guide today, a chapter from a key nursing review book, really solid stuff.

Exactly.

Think of this as your fast track.

We're pulling out the must know info so you don't have to wade through everything yourself.

That's the plan.

So the mission here is really for you, the listener, to get a clear, concise handle on these meds, how they work, what they're for, and critically, the nursing points to keep in mind.

Saving you steady time, essentially.

Right.

We'll be covering meds for HIV AIDS, immunosuppressants, and then antibiotics.

Ready to dive in?

Let's do it.

Starting with HIV and AIDS.

Okay, so HIV, human immunodeficiency virus.

It goes after the immune system.

Right.

Weakens it.

And AIDS, acquired immunodeficiency syndrome.

That's the the later stage of the immune system is really badly damaged.

And currently, no cure, unfortunately.

No cure, but the goal of the medications is huge.

It's about slowing down or even reversing that loss of immune function.

Which keeps people healthier, longer.

Exactly.

Preserving health, prolonging life.

And the main strategy is heart, highly active antiretroviral therapy.

Usually a mix of different drugs working together.

Okay, so let's break down those drug classes first.

NRTIs.

Nucleoside nucleotide reverse transcriptase inhibitors.

That's a mouthful.

It is.

NRTIs is much easier.

So how they work.

HIV needs to copy its genetic code, its RNA, into DNA.

Using an enzyme, right.

Reverse transcriptase.

Exactly.

That new viral DNA then gets woven into the host cell's DNA.

NRTIs basically mess up that copying process.

Oh, so?

They act like faulty building blocks.

The enzyme tries to use them to build the DNA chain, but the NRPI stops the chain from growing.

No new viral DNA, no replication.

Got it.

Faulty parts stop the assembly line.

Okay, quite a few drugs in this class.

Let's hit some key ones and their side effects.

Abecavir.

Abecavir.

Well, common stuff like nausea.

But the big one, the critical thing, is a potential hypersensitivity reaction.

Not just a mild rash.

No, no.

It can be serious.

Think fever, nausea, vomiting, diarrhea, feeling awful, maybe a sore throat, cough, shortness of breath, and a rash.

It's a whole cluster of symptoms we watch for very carefully.

Okay, really important.

And when it's combined,

abacavir with lamivudine.

Well, you get the potential side effects of both, of course.

But significantly, this combo, and some others we'll see, carries a risk of lactic acidosis.

That dangerous acid buildup.

Yes.

And severe hepatomegaly, a seriously enlarged liver.

These are major complications needing immediate attention.

Okay.

Next, didanosine.

Didanosine.

Main concerns are nausea, diarrhea, and peripheral neuropathy.

Nerve damage, right.

Tingling, pain in hands and feet.

That's the one.

Also potential liver damage, hepatotoxicity, and pancreatitis.

Inflammation of the pancreas, which could be really severe.

Intricitabine.

More common things here.

Headache, diarrhea, nausea, rash.

An interesting one is hyperpigmentation.

Some skin darkening, maybe on palms or soles.

Oh, okay.

And like others, it carries that potential risk for lactic acidosis and severe hepatomegaly.

And the combo.

Intricitabine plus tenofovir.

Yep.

Same pattern.

You combine the individual risks plus that overarching risk of lactic acidosis and severe hepatomegaly.

You see this theme with several NRTI combinations.

Right.

What about lamivudine by itself?

Generally milder side effects.

More like nausea, maybe some nasal congestion.

And lamivudine combined with zetovudine.

This one can cause anemia, low red blood cells, and neutropenia, which is low neutrophils.

A type of white blood cell important for fighting infection.

Ah, so affecting blood counts.

Yes.

And again, that potential for lactic acidosis with hepatomegaly pops up to recurring concern with these combinations.

And there's even a three -drug combo.

Lamivudine, zetovudine, and abacavir.

Right.

And as you guess, it pulls the risks.

The abacavir hypersensitivity, the zetovudine, lamivudine anemia, and neutropenia, and that general NRTI combo risk of lactic acidosis and hepatomegaly.

Stavidine is another NRTI.

Stavidine shares some risks with didanosine, actually.

Yeah.

Nervous neural neuropathy and pancreatitis are key concerns here, too.

Shows how drugs in the same class can sometimes overlap and side effects.

Good point.

And lastly, for NRTIs, tenofovir alone and zetovudine alone.

Tenofovir, more commonly nausea and vomiting.

Zetovudine can cause nausea, vomiting, but also anemia, leukopenia, that's a general drop in white blood cells, muscle weakness, fatigue, headache.

So a lot of variation even within one class.

Definitely.

Same target enzyme, but different potential effects to watch for in each patient.

Critical monitoring needed.

Absolutely.

Okay, let's shift gears.

Next class, NNRTIs, non -nucleoside reverse transcriptase inhibitors.

How are these different from NRTIs?

Okay, so they both target reverse transcriptase, that key enzyme, but they do it differently.

NRTIs are like those faulty building blocks, right?

NNRTIs instead bind directly to the enzyme itself, but at a different spot than where building blocks attach.

This changes the enzyme shape, so it just can't work properly.

Ah, like jamming the mechanism instead of giving it bad parts.

Exactly.

A good way to put it.

And that difference can matter for things like drug resistance patterns.

Okay.

So key NNRTIs and their side effects.

Let's see.

Bilaverdin can cause rash, changes in liver function tests, and pruritus that's intense itching.

Itching, okay.

Effaverins.

Effaverins is often linked with CNS effects, central nervous system.

It can be milder things like dizziness, trouble concentrating,

or more significant stuff like really vivid or abnormal dreams, even confusion, or rarely, encephalopathy.

Wow, those CNS effects sound like they could really impact daily life.

They definitely can.

Something patients need to be aware of.

Then there's estravarine.

What about that one?

Etravarine can cause rash, GI upset, headache, but importantly also hypertension, high blood pressure, and peripheral neuropathy, that nerve damage we talked about.

Okay, hypertension and neuropathy.

And the last NNRTI listed is nevirapine.

Nevirapine also carries a risk of rash, but it can be more serious.

We worry about Steven's Johnson syndrome, a severe skin reaction.

Oh, right.

SJS.

Very serious.

Very.

And also hepatitis liver inflammation and elevated liver enzymes, which signal potential liver injury.

So again, different profiles, even though they're all NNRTIs.

It really drives home that you need to know the specifics for each drug.

Okay, moving on.

Protease inhibitors, PIs, what part of the HIV life cycle do these guys target?

Okay, so after HIV makes those initial long protein chains, they aren't functional yet.

They need to be cut into smaller specific pieces to build new infectious virus particles.

Like needing final assembly.

Precisely.

And the enzyme that does the cutting is called protease.

Protease inhibitors block that enzyme.

So no cutting, no mature virus.

Exactly.

It stops the virus from being properly assembled and becoming infectious, hinders its spread.

Clever.

Okay.

PIs and their side effects, adizanavir.

Adizanavir can cause nausea, headache, infection risk, vomiting, diarrhea, drowsiness, insomnia, fever,

also some metabolic stuff,

hyperglycemia, so high blood sugar, and hyperlipidemia, high blood fats.

Metabolic changes, okay.

Yes.

And it can also increase bleeding risk in people with hemophilia.

You see some overlap with other classes, but these metabolic issues are pretty common with PIs.

Phosempranavir.

That one can cause nausea, vomiting, headache,

altered taste, and sometimes a weird tingling or numbness around the mouth called puerial peristhesia.

Tingling around the mouth, interesting.

Yeah.

Also rashes and maybe increased liver function tests.

So potential liver effects too.

What about indinovir?

Indinovir can cause nausea, diarrhea, and hyperbilirubinemia, high bilirubin, which can cause jaundice, yellowing of skin and eyes.

Ah, jaundice.

And it can also cause nephritis, kidney inflammation, and kidney stones.

So staying well hydrated is usually pretty important with this one.

Good tip.

We also have a combo,

lopinavirotonavir.

Right.

This combo can cause nausea, diarrhea, altered taste, and a similar tingling,

but maybe more on the whole circumference of the mouth's circumoral peristhesia.

Hepatitis is also a potential risk.

And rotonavir is often used as a booster, right?

Exactly.

Small doses of rotonavir can boost the levels of other PIs, making them work better.

Okay.

Nelfinavir.

Nelfinavir is mostly known for GI side effects.

Nausea, gas flatulence, and diarrhea are the main ones.

And rotonavir on its own, not just as a booster.

Yeah.

When used alone at higher doses, it can cause nausea, vomiting, diarrhea, altered taste, that sort of moral peristhesia again, hepatitis.

And notably, it can really hug up triglyceride levels, another blood fat.

High triglycerides, okay.

Sequinavir.

Sequinavir.

Nausea, diarrhea,

and one to note is photosensitivity.

Increased sun sensitivity, easier to get sunburned.

Headache is also possible.

Photosensitivity avoids strong sun.

Got it.

And the last PI here is tepronavir.

Tepronavir carries a pretty significant warning for hepato toxicity liver damage.

Okay.

Big one for the liver.

Yeah.

Also nausea, vomiting, diarrhea, headache, fatigue.

So you see the trend.

GI issues are common with PIs.

Metabolic changes like high lipids or sugar can happen.

And liver function definitely needs watching.

Crucial monitoring, for sure.

Okay.

Let's look at some other classes targeting different steps.

There's an integrase inhibitor.

Raltogravir.

What's its job?

Right.

Raltogravir.

Remember we said the virus's DNA gets integrated into the host cell's DNA.

Yeah.

It becomes part of our own blueprint.

Integrase is the enzyme that does that integration step.

Raltogravir blocks that enzyme.

So it stops the viral DNA from becoming a permanent fixture in the host cell.

Stops replication at that key point.

Neat.

And it's usually used with other drugs.

Yes.

Typically in combination therapy.

Side effects for Raltogravir.

Generally considered pretty well tolerated.

Common ones are nausea, diarrhea, fatigue,

headache, maybe some itching.

Compared to some older meds, often fewer troublesome side effects.

Next, a CCR5 antagonist.

Marvirac.

How does this one work?

Marvirac works on viral entry.

Some strains of HIV need to latch onto a specific receptor on the surface of immune cells called CCR5 to get inside.

Like needing a specific key for a lock.

Sort of, yeah.

Marvirac blocks that CCR5 receptor.

Acts like a gatekeeper, preventing those specific HIV strains from attaching and infecting the cell.

It won't work for all HIV strains though.

Interesting.

Potential side effects.

Most common.

Cough, dizziness, fever, pyrexia, rash, some abdominal pain, muscle or bone aches, upper respiratory infections.

Importantly, there are warnings about potential liver injury and maybe some cardiovascular events, so it needs careful monitoring too.

Liver and heart potential issues, okay.

And then a fusion inhibitor in Fufritide mechanism.

Fufritide also works on entry, but slightly differently.

It stops the outer envelope of the HIV virus from actually merging or fusing with the host cell membrane.

So it stops the docking and merging process.

Exactly.

Prevents the virus from getting inside that way.

And side effects, since it inhibits fusion.

Well it's an injectable medicine, so the most common side effect by far is skin irritation right at the injection site.

Makes sense.

Other possibilities include fatigue, nausea, trouble sleeping,

insomnia, and sometimes peripheral neuropathy.

Fascinating how many different points in the life cycle these drugs can attack.

Now the Pew also mentions other meds for complications, like opportunistic infections in HIV AIDS.

Yes, that's critical.

Because HIV weakens the immune system, people become vulnerable to infections from bugs that wouldn't normally cause problems in healthy individuals' opportunistic infections.

Like PCP pneumonia.

Right.

Pneumocystis gerbacei pneumonia is a classic example.

So you'll use anti -infectives like sulfamethoxazole trimethobrim, often called Bactrim or Ceptra, to prevent or treat that.

Sulfosalazine might be used for inflammation.

And antifungals too.

Absolutely.

For things like candidases, which is thrush or yeast infections, or more serious things like cryptococcal meningitis, a fungal brain infection, and antivirals for other viruses, CMV, herpes, varicella zoster, which causes shingles.

So managing these OIs, as they're called, is a huge part of HIV care.

A massive part.

It often involves taking quite a few different medications alongside the antiretrovirals.

Right.

Okay, let's shift focus now to our next big category.

Immunosuppressants.

What's their main job in medicine?

Immunosuppressants are generally used in two main situations.

First, for organ transplant recipients.

They stop the body's immune system from seeing the new organ as foreign and attacking it, preventing rejection.

Crucial for transplant success.

Absolutely.

Second, they're used for autoimmune disorders.

That's where the immune system mistakenly attacks the body's own tissues.

Think lupus, rheumatoid arthritis,

MS, immunosuppressants calm down that misguided attack.

Okay, first class listed, calcineurin inhibitors.

How do they work?

Calcineurin inhibitors target a protein called calcineurin inside T cells.

T cells are key immune cells, driving transplant rejection and autoimmune attacks.

Calcineurin is like a messenger that tells the T cell to get activated and multiply.

These drugs block that message, suppressing T cell activity and the overall immune response.

Two main ones are cyclosporine and tacrolamus.

Let's start with cyclosporine.

Uses and key adverse effects.

Cyclosporine is used a lot to prevent rejection after various organ transplants, kidney, heart, liver.

It's usually given with a steroid like prednisone and maybe another immunosuppressant.

And the downsides?

The big ones are nephrotoxicity, kidney damage, really common, and increased risk of infections because you're suppressing the immune system.

Also hypertension, high blood pressure, and hirsutism, which is unwanted hair growth.

Kidney damage and infection risk.

Seems like a recurring theme.

What about tacrolamus?

Also, a calcineurin inhibitor, similar action.

Primarily used for liver and kidney transplant rejection prevention.

It's very effective, but yeah, it has its own list of potential issues.

Such as?

Nephrotoxicity, again,

also neurotoxicity affecting the nervous system, maybe causing headaches,

seizures,

GI issues like nausea, diarrhea,

hypertension, high potassium, hyperkalemia, high blood sugar, hyperglycemia, hirsutism again, and also gum hyperplasia, overgrowth of gum tissue.

Wow, quite a list.

Kidney issues seem prominent with both.

They definitely require close monitoring of kidney function.

Okay, next class, cytotoxic medications.

How do these suppress immunity?

Cytotoxic drugs work more broadly by interfering with cell division.

Immune cells, especially when they're actively responding, divide rapidly, so these drugs hit them hard.

But not just immune cells.

Right, that's the issue.

They can affect other rapidly dividing cells too, like in the bone marrow or the gut lining.

That's why they often have side effects like low blood counts or GI problems.

What are some specific cytotoxic immunosuppressants?

Azathioprine is one, often used with other drugs for kidney transplant rejection.

Main adverse effects are myelosuppression, meaning bone marrow suppression, leading to low neutrophils, neutropenia, and low platelets, thrombocytopenia.

So risk of infection and bleeding.

Exactly.

Then there's cyclophosphamide, used more for autoimmune diseases.

It can also cause neutropenia and a specific problem called hemorrhagic cystitis bladder inflammation with bleeding.

Drinking plenty of fluids is important with this one.

Mesotrexate is another well -known one.

Yes, used widely for autoimmune conditions like rheumatoid arthritis, psoriasis, sometimes in transplants too.

Potential long -term issues include liver fibrosis or cirrhosis, bone marrow suppression, painful mouth sores, ulcerative stomatitis, and kidney damage.

Requires lots of monitoring liver, kidney, blood counts.

And the last ones here, mycophenolimofacial and mycophenolic acid.

These are common after kidney, heart, and liver transplants to prevent rejection.

And side effects can include pretty significant diarrhea and vomiting, neutropenia, and a higher risk of serious infections, even sepsis.

And sepsis, wow.

Yeah.

And long -term use is linked to an increased risk of cancers, especially lymphomas, because of that ongoing immune suppression.

So with cytotoxics, infection risk and bone marrow effects are major concerns.

Next up, antibodies.

How are these used?

Antibody therapies are often more targeted.

They're designed to latch on to specific cells or proteins involved in rejection or autoimmune attacks, either neutralizing them or marking them for destruction.

More selective, then.

Generally, yes.

Compared to the broader action of cytotoxic drugs.

Examples from the review.

Basiliximab is used for kidney transplant rejection prevention.

The key, though maybe rare, risk is a severe acute hypersensitivity reaction, potentially anaphylaxis.

Life -threatening allergy.

Then there's lymphocyte immune globulin and antithymocyte globulin, or ATG.

These are mixtures of antibodies targeting T cells.

Used for preventing and treating rejection in various transplants.

Kidney, heart, liver, bone marrow.

Side effects for those.

Can cause fever, chills, low white blood cell count, leukopenia, skin reactions.

Also possible are anaphylactoid reactions, which are similar to anaphylaxis.

And finally, under immunosuppressants, another category with serolimus.

How does this one fit in?

Serolimus, sometimes called rapmomycin, is used for kidney transplant rejection.

It works differently than calcineurin inhibitors.

It mainly stops T cells from multiplying after they get activated, rather than blocking activation itself.

And its adverse effects.

Increased infection risk, naturally.

Also raised cholesterol and triglycerides, hyperlipidemia, potential kidney injury.

Other things can include rash, acne, anemia, low platelets, joint pain, diarrhea, and low potassium, hypokalemia.

Okay, so looking back across all these immunosuppressants, calcineurin inhibitors, cytotoxics, antibodies, serolimus, it really sounds like monitoring for infection is absolutely paramount for nurses.

Without a doubt.

These drugs deliberately lower the body's defenses.

So nurses need to be incredibly vigilant for any sign of infection, even subtle ones.

Fever, cough, sore throat, burning with urination, anything.

And patient education too, right?

Tell them what to look for.

Huge.

Patients need to know to report any potential signs of infection immediately.

Okay.

HIV meds, immunosuppressants, done.

That brings us to our last big category.

Antibiotics.

We know they fight bacteria.

Can you give us the overview of the classes covered here?

Sure.

Antibiotics work by stopping bacteria from growing, either killing them outright that's bactericidal, or preventing them from multiplying bacteriostatic, letting the immune system finish the job.

Lots of different ways they do that.

Yeah.

The main classes listed in our resource are aminoglycosides, cephalosporins, floriculones, macrolides, lincosamides, monobactams, penicillins, including the penicillinase resistant ones,

sulfonamides, tetracyclines, antimicrobacterials for things like TB, and also antifungals are mentioned though they target fungi, not bacteria.

Right.

And there's a table summarizing key adverse effects.

Let's hit the highlights for each class.

Eminem glycosides.

Big ones here.

Ototoxicity and nephrotoxicity.

Damage to ears, hearing loss, balance issues, and damage to kidneys.

Critical to monitor hearing and kidney function.

Cephalosporins.

Very common class.

Can cause GI upset, nausea, vomiting, diarrhea.

A serious concern is pseudomembranous colitis, that's severe colon inflammation often from C.

diff.

C.

diff.

Right.

And nephrotoxicity is also possible, especially with older ones.

Fluoroquinolones,

like Cipro or Lavaquin.

Key things.

CNS affects headache, dizziness, insomnia, GI effects too, and photosensitivity increase sunburn risk.

Plus, newer warnings about tendon issues, even rupture, and possible heart rhythm changes.

Pendant rupture, wow, macrolides, erythromycin, azithromycin.

Often cause GI upset, nausea, vomiting, diarrhea.

And like cephalosporins, they can potentially lead to C.

diff.

colitis.

Lincosamides, clindamycin is the main one.

Yes, GI effects are common, and clindamycin has a relatively higher risk of causing C.

diff.

colitis compared to some others.

Also,

possible bone marrow depression, low blood counts.

Monobactams, like Astrionem, sometimes used for penicillin allergies.

Generally tolerated a bit better than some other related antibiotics, but still can cause GI effects, potential liver toxicity, hepatotoxicity, and allergic reactions.

Tendocillins, huge group, obviously crucial, key adverse effects.

GI effects, including mouth issues like sore tongue.

Super infections can happen, new infections popping up during treatment.

But the absolute critical one is hypersensitivity.

Allergy.

Yes, from mild rash all the way to life -threatening anaphylaxis.

Always, always ask about penicillin allergy before giving it.

Essential check, sulfonamides,

like Bactrim.

Sulfonamides have a fairly wide range of potential side effects.

GI issues, liver toxicity, kidney toxicity, bone marrow depression, skin reactions including photosensitivity and serious rashes, and even CNS effects like headache or dizziness.

Tetracyclines, doxycycline, tetracycline.

Known for GI upset, liver toxicity.

Uniquely, they can cause permanent tooth staining and affect bone development in young children.

So generally avoided in kids under eight and pregnant women.

Photosensitivity and super infections are also concerns.

Tooth staining, important one.

Antimicrobacterials.

For TB, leprosy.

Drugs like isoniazid, refampin, can cause GI effects, nerve inflammation, neuritis, often peripheral neuropathy, CNS effects.

Refampin famously turns body fluids like urine and tears a harmless red -orange color.

Red -orange fluids, good to know.

And finally, the antifungals mentioned.

Right, targeting fungi can cause GI effects, liver toxicity,

hearing loss, peripheral neuritis, different targets, different drugs than antibiotics.

Okay, that's a whirlwind tour of potential badness.

What are the general nursing considerations that apply across the board when giving antibiotics?

Several really important ones.

Number one, allergies.

Always check for allergies before giving any dose.

Monitor labs, kidney function, liver function, blood counts before and during therapy as needed.

Watch the patient closely for any adverse effects and report them promptly.

Like that diarrhea we mentioned.

Exactly.

Ensure correct administration, right route, right time, with or without food as indicated.

Give clear instructions to the patient.

Monitor intake and output.

Encourage fluids unless there's a reason not to.

Hydration, okay.

Implement safety precautions if there are potential CNS effects like dizziness.

And crucially,

emphasize completing the entire course.

Even if they feel better, don't stop early, don't save leftovers.

This is vital for preventing antibiotic resistance.

Finish the full course.

So important.

Okay, the resource had a critical thinking scenario.

Patient on ceftriaxone, a cephalosporin, gets severe diarrhea.

What's the key nursing action?

Severe diarrhea with ceftriaxone immediately raises a red flag for C.

diff colitis, pseudomembranous colitis.

Right, we just talked about that risk.

So the priority action is immediate notification.

Tell the RN, tell the healthcare provider right away they'll likely stop the ceftriaxone, order tests for C.

diff toxin and start appropriate treatment if it's positive.

And maybe isolation.

Yes, contact precautions would likely be needed to prevent spreading C.

diff.

Acting fast is key.

Makes total sense.

Now the chapter wraps up with practice questions.

We sort of hit the concepts behind them as we went.

They reinforce knowing specific side effects and monitoring.

Yeah, things like nirvaripines, rash and liver issues, checking a CBC for zetovudine due to anemia risk, watching amylase for didanosine because of pancreatitis.

Checking blood pressure with cyclosporine, hearing with amikacin, creatinine with foscarnate.

Exactly.

Risk of infection with pentamidine, especially if leukopenic, avoiding sun with sequinevir, liver monitoring and avoiding alcohol sun with ketoconazole, watching gate for neuropathy with stavidine.

It connects the drug to the specific nursing action or patient teaching.

Good reinforcement.

And the chapter also mentions things like pyramid to success and client needs.

What's the point there?

It's about putting the pharmacology into the bigger nursing picture.

Remembering client rights, safety, promoting health, dealing with psychosocial aspects, physiological integrity.

It's not just about giving meds.

It's about holistic care.

Right.

The whole patient.

Well, I think that brings us to the end of our deep dive into this chapter on immunological medications.

We've covered a lot of ground.

We really have.

From HIV AIDS drugs through immunosuppressants for transplants and autoimmune disease to the wide world of antibiotics and antifungals.

We looked at how they work, why they're used and those critical nursing points.

Hopefully you, the listener, have a much clearer picture now.

Yeah, a solid foundation.

It really highlights how complex but vital manipulating the immune system and fighting infections can be.

We hope you're feeling more confident about these crucial medication classes and what they mean for patient care.

You know, looking at all this, especially the newer immunological therapies, it does make you think.

How is the nurse's role in managing these complex meds going to keep evolving?

That's a great question.

With therapies getting more targeted, more complex,

what kind of continuous learning will be most important for nurses to stay sharp in this area?

Definitely something to chew on as medicine keeps advancing.

Indeed.

And with that thought, we'll conclude this comprehensive deep dive.

We've covered the key information from this chapter on immunological medications.