Chapter 36: Men’s Health Drugs – Androgens & Treatments

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Welcome to the Deep Dive.

Today we're really focusing in cutting through the noise to tackle a crucial area, men's health drugs.

That's right.

This deep dive is specifically for you, the student listener, honing in on chapter 36 from Lilly's.

We want to give you those high yield concepts.

Exactly.

We're aiming to distill this down.

Think three core clinical goals,

how we boost the system, say with hormone replacement,

how we sometimes need to safely block hormones for common conditions, and critically, how to avoid some really dangerous drug interactions.

That framing makes a lot of sense.

These drugs touch on fundamental physiology.

They really do.

Androgens, prostate growth, even blood flow dynamics.

Our goal here isn't just memorizing names, it's understanding how they work.

The mechanisms.

Yes, the mechanisms of action and maybe even more importantly, the safety aspects, those critical margins that define safe practice for healthcare providers.

Before we jump into the actual medications, let's kneel down the basics, the terminology.

We should start with androgens, right?

Absolutely.

Androgens, that's the main class of male sex hormones.

And the key player, the one everyone knows, is testosterone.

Okay.

Now, when we talk about what testosterone actually does in the body, we often break it down into two main types of activity.

There's androgenic activity and anabolic activity.

So androgenic.

Yeah.

That's what most people think of, right?

Development of male characteristics,

puberty stuff, like hair patterns, deeper voice.

Exactly that.

But the anabolic side is just as important, especially when we think about therapeutic uses and misuse potential too.

Anabolic means building up.

Precisely.

Building body tissues, think bone density, muscle mass.

And to do that, the body needs to retain key electrolytes, nitrogen, phosphorus, potassium, sodium.

Interesting.

And there's one more effect of testosterone, often overlooked but clinically relevant, the erythropoietic effect.

What does it mean?

It stimulates the production of red blood cells.

That's why you'll see hemoglobin levels monitored in patients on testosterone therapy.

Got it.

Okay.

Let's unpack this more.

Starting with the drugs that boost the system, the ones used for replacement,

exogenous testosterone.

Right.

So exogenous testosterone, its main job is hormone replacement therapy.

This is for conditions like primary or secondary hypogonadism, where the body isn't producing enough on its own.

Okay.

And we also see it used vitally in masculinizing hormone therapy for transgender individuals transitioning female to male.

The goal there is virilization, achieving those desired androgenic effects we talked about, like voice deepening, stopping menses, increasing muscle.

But there's a big hurdle here, isn't there?

Yeah.

Pharmacokinetics, just taking a testosterone pill doesn't work so well.

That's the classic problem.

Standard oral testosterone gets hammered by the liver almost immediately.

That first pass effect basically destroys most of the dose before it can get into circulation.

So ineffective.

Pretty much.

So we had to get creative, find ways to bypass the liver, one way was developing synthetic derivatives.

Testosterone combined with esters like cypionate or enanthate, often formulated in oil.

This slows down absorption and makes it last longer.

Ah, so injections.

Exactly.

Injections can last maybe two to four months.

And there are other ways too, right?

Not just injections.

Definitely.

We now have non -oral methods that are quite common.

Transdermal patches, you might know androderm.

Right.

And gels, like androidea.

There's even intranasal product called Natesto.

Okay, so patches and gels.

That brings up application safety, which is huge for nursing.

Absolutely critical.

This is core patient teaching.

You must emphasize applying these patches and gels to specific areas back, abdomen, upper arms, thighs, never the scrotal skin.

Why not the scrotal?

Higher absorption rate there leads to unpredictable levels.

But the biggest risk is transfer.

Transfer.

Transfer to others.

After applying, the skin needs to be covered and rigorous hand washing is essential.

You don't want that hormone transferring to partners, children, or pregnant individuals.

It's a serious risk.

That makes perfect sense.

And, you know, talking about applying therapeutic testosterone safely,

it kind of leads us to the flip side, doesn't it?

The misuse potential.

Anabolic steroids.

It does.

It's fascinating, really, the line between therapy and misuse.

These anabolic steroids are synthetic derivatives like oxandrolone.

And they do have real medical uses.

Oh, yes.

For example, treating muscle wasting in conditions like HIV -associated wasting syndrome.

But they are schedule four controlled substances and cannot have for a reason.

High misuse potential.

Athletes.

Primarily, yes.

Athletes seeking enhanced performance, muscle gains.

But the consequences of misuse are incredibly serious.

We're talking sterility, major cardiovascular diseases.

And you mentioned a liver issue earlier.

Yes.

Peliosis of the liver.

This is a really dangerous condition.

It involves blood -filled cavities forming in the liver.

They can rupture, cause massive hemorrhage.

It can be life -threatening.

Wow.

So even with legitimate use, liver function monitoring is key.

Absolutely.

Baseline assessment and ongoing monitoring.

The therapeutic window, as you said, is narrow.

The risks are significant.

Okay.

Let's pivot now.

We've talked about boosting the system.

Now let's talk about blocking aspects of it, specifically for a super common condition.

Benign prostatic hyperplasia.

BPH.

Right.

BPH.

Non -malignant enlargement of the prostate gland.

And when you say common, it's extremely common.

Affects something like 85 % of men by the time they're 80.

85%.

Yeah.

And the main problem it causes is urinary obstruction.

That's the primary clinical issue.

Yes.

Difficulty starting urination, weak stream frequency, urgency, waking up at night to go.

All those classic lower urinary tract symptoms.

So how do we treat this pharmacologically?

What's the main approach to actually shrink the prostate?

The major class here are the five alpha reductase inhibitors.

The two main drugs you need to know are Finasteride and Dutasteride.

Okay.

Five alpha reductase inhibitors.

How do they work?

Well, they target the fuel source for prostate growth, essentially.

They inhibit the enzyme.

Five alpha reductase.

And what does that enzyme normally do?

It converts testosterone to a much more potent androgen called dihydrotestosterone or DHT.

Yes.

And DHT is really the principal hormone that stimulates prostate growth.

So if you block its production by inhibiting that enzyme.

You reduce the stimulus and the prostate can shrink.

Exactly.

That helps ease the urinary obstruction and improve symptoms.

But, and this seems important, it's not instant, right?

You mentioned this takes time.

That's a key caveat for listeners.

Absolutely.

Unlike drugs that just relieve symptoms quickly, these are working on the underlying structure.

It takes time.

Patients won't see the full clinical effects for maybe three to six months of continuous therapy.

Three to six months.

That needs clear patient education.

Definitely.

And Finasteride, it has that important dual indication.

Right.

Not just BPH.

Also.

Male pattern hair loss.

Androgenic alopecia.

Because DHT, that same hormone, also plays a key role in hair follicle miniaturization.

So blocking DHT helps with hair loss, too.

Okay.

Now, the absolute number one critical safety point for Finasteride.

Teratogenicity.

Yes.

This cannot be overstated.

Finasteride is absolutely contraindicated in pregnant people and also in children.

And the risk isn't just from taking the pill.

No.

This is crucial for anyone handling the medication, like pharmacists, nurses, or caregivers.

Pregnant individuals must wear gloves if they have to handle broken or crushed Finasteride tablets.

Because it can be absorbed through the skin.

Yes.

Topical absorption is a real risk.

And exposure can cause serious birth defects in a developing male fetus.

It's a category X drug in terms of pregnancy risk in many places for that reason.

Wow.

Okay.

Essential safety point.

Right.

Now, just to round out BPH treatment quickly, there's another class of drugs used, right?

The alpha blockers?

Yes.

The alpha -1 -edrenergic blockers.

Drugs like Tamsalucin, they work completely differently.

Oh, so?

They don't shrink the prostate.

They work on the smooth muscle in the prostate gland and the bladder neck.

They relax that muscle.

Ah, so they help urine flow better, but don't change the prostate size itself.

Exactly.

The benefit is immediate symptomatic relief.

Unlike the three, six -month wait for Finasteride, Tamsalucin starts working right away to improve flow.

So they might be used together or chosen based on the patient's main issue size versus obstruction symptoms.

Precisely.

Understanding that contrast, immediate symptomatic relief versus delayed structural change is key for tailoring therapy.

Okay.

And quickly on monitoring for BPH, obviously assessing urinary symptoms.

But what about PSA levels?

Right.

Prostate -specific antigen.

With effective 5 -alpha reductase inhibitor therapy, you'd expect PSA levels to decrease, which can be a marker of therapeutic response.

But there's some controversy around PSA screening in general, isn't there?

There is, yes.

It's important for students to know that routine PSA screening for prostate cancer mortality benefits is still debated.

Current guidelines, particularly for men aged 55 to 69, emphasize shared decision -making.

Meaning the patient and provider need to discuss the potential risks like false positives leading to anxiety and unnecessary biopsies versus the potential benefits of early detection.

It's not an automatic test anymore.

It's a conversation.

That's a really important clinical nuance.

Okay.

Let's shift gears one last time.

Let's talk about treating erectile dysfunction, ED, another very prevalent issue.

Highly prevalent, yes.

And often linked with other health problems, especially cardiovascular disease.

It's estimated to be about one and a half times more common in people with CDD.

Which raises a critical safety question right away, doesn't it?

How do these popular ED drugs work safely, especially in patients who might already have heart conditions?

Exactly.

That's the crucial context.

The main drug class here, the ones most people have heard of, are the phosphodiesterase inhibitors, or PDE inhibitors.

Like sildenafil.

Sildenafil, yes.

Also, Tadalafil and Vardenafil.

Those are the mean ones.

Okay.

PDE inhibitors.

What's the mechanism?

How do they actually work?

It's actually quite elegant physiologically.

They inhibit the enzyme phosphodiesterase, specifically type five in the erectile tissue.

Okay.

Inhibiting this enzyme leads to a buildup of a chemical messenger called cyclic guanosine monophosphate, or CGMP.

CGMP.

And what does that do?

CGMP is the molecule that causes smooth muscle relaxation in the corpora cabrinosa, the erectile tissues of the penis.

Relaxation allows blood to flow in, causing the erection.

So more CGMP means more relaxation, better blood flow.

Precisely.

But, and this is key, it doesn't cause an erection spontaneously.

It enhances the natural response to sexual stimulation.

That stimulation is still needed to kick things off.

Got it.

What about pharmacokinetics?

How quickly do they work?

How long do they last?

Sildenafil is generally known for a fairly rapid onset.

Usually within about an hour, it lasts maybe four to six hours.

Okay.

One important point with sildenafil though, taking it with a high -fat meal can significantly delay absorption, maybe by about an hour.

So timing matters.

Good tip.

And Tadalafil.

Tadalafil is known for its longer duration of action.

It's often marketed as lasting up to 36 hours.

36 hours.

Okay.

Now, the single most critical safety warning in this entire chapter, the absolute contraindication.

This is the one thing, if you remember nothing else, you must remember this as a practitioner.

Concurrent use of any PDE inhibitor, sildenafil, Tadalafil, any of them with nitrates, is absolutely a 100 % contraindicated.

Nitrates like nitroglycerin for chest pain.

Exactly.

Nitroglycerin, isosorbide mononitrate, isosorbide dinitrate, any organic nitrate.

Why is this combination so dangerous?

What happens?

It's a potentially fatal interaction.

Both drug classes are vasodilators.

Nitrates work by increasing nitric oxide, leading to vasodilation.

PDE inhibitors enhance the effect of nitric oxide via CGMP, put them together.

Massive vasodilation.

Profound, severe hypotension.

A drastic drop in blood pressure that often doesn't respond well to treatment and can absolutely be fatal.

So taking a thorough medication history, specifically asking about nitrate use, is step number one before prescribing these.

Non -negotiable first step.

And assessing cardiac history in general.

Okay.

Beyond that critical interaction,

what are other side effects or adverse events to watch for?

Common ones are things like headache, facial flushing, dyspepsia, or indigestion.

Usually relatively mild.

But Yes.

The main urgent one is priapism.

An abnormally prolonged direction, typically defined as lasting longer than four hours, and it's often painful.

This is a medical emergency.

It requires immediate intervention to prevent permanent damage to the erectile tissue.

Four hours is the cutoff.

Seek help immediately.

Absolutely.

And another potential, though rarer, serious effect is unexplained vision loss.

Patients should be counseled on that as well.

Are there any other types of ED drugs besides the PDE inhibitors?

There is another option, less common, called alprostadil.

It's a prostaglandin.

How is that given?

It's administered locally, not orally, either by direct injection into the corpora cavernosa or as a tiny urethral suppository.

Okay.

So let's quickly tie this all together with the nursing process.

Assessment priorities.

Okay.

Summarizing assessments.

For testosterone therapy, definitely assess liver function beforehand.

Remember that peliosis risk and get a baseline weight because fluid retention can occur.

Right.

For BPH drugs?

Assess urinary patterns thoroughly.

Frequency, urgency, flow, nocturia.

Monitor those PSA levels, expecting a decrease with finasteride or dutasteride if it's working.

And for the ED drugs, the PDE inhibitors.

Assessment is almost entirely focused on cardiovascular status, and above all, that medication history.

Ruling out nitrates is paramount.

Check blood pressure, too.

Okay.

And key implementation and patient teaching points.

For finasteride, protect tablets from light and heat.

Never crush them, especially if someone pregnant might handle them.

Remind patients about the delayed onset.

For testosterone.

Council patients on masculinizing therapy that changes are gradual over months to years.

And crucially, reinforce that testosterone therapy is not contraception.

Reliable birth control is still needed if pregnancy is possible.

And for ED

Reinforce seeking immediate help for priapism erection longer than four hours.

And timing matters take sildenafil about an hour before anticipated activity, keeping the potential food interaction in mind.

And the nitrate warning again and again.

Absolutely.

Okay.

So let's bring it all back.

What does this mean for the student listener?

The core knowledge needed from this chapter?

Well, I think we've hit the three main pillars.

First, testosterone, understanding its replacement role, its anabolic effects, the delivery challenges, and the dangers of anabolic steroid misuse, including liver risks.

Okay.

Pillar one.

Second, finasteride and the five alpha reductase inhibitors.

Knowing they block DHT production to treat BPH and alopecia.

Remembering that delayed onset and critically the teratogenic risk, the absolute contraindication in pregnancy.

Filler two, blocking DHT.

And third, the ED drugs, the PDE inhibitors.

Understanding their mechanism via CGMP, their kinetics, common side effects, the emergency of priapism, and that life or death absolute contraindication with nitrates.

That's a really powerful summary.

Boosting with testosterone, blocking with finasteride and the critical safety with ED drugs and nitrates.

We covered the hormone dynamics, BPH management, and that vital interaction warning.

Exactly.

And maybe, maybe a final provocative thought for you, the listener, to chew on.

Okay.

Think about how pharmacokinetics plays out in real life.

We talked about how a high -fat meal delays sildenafil absorption.

Now, layer onto that, what happens to drug clearance as a patient ages?

Or if they develop kidney or liver issues.

Ah, so clearance decreases.

Right.

Meaning the same dose could lead to higher plasma concentrations, potentially for longer.

That increases the risk of side effects, maybe even toxicity, from a drug that seemed fine earlier.

So it's not just about the drug, but the whole patient context over time.

Precisely.

Thinking about that interplay drug properties,

patient factors like age and organ function interactions, even diet.

That comprehensive view is what really makes you a safe and effective practitioner.

That is fantastic food for thought.

A great place to wrap up.

Thank you so much for joining us for this deep dive into men's health drugs.

And a warm thank you from the last minute lecture team.