Chapter 54: Pharmacologic Management Summaries in Women's Health

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What do, um, seizure medications, blood pressure pills, and, like, digestion meds all have in common?

Well, they're probably not things you'd immediately associate with women's health.

Exactly.

But if you're working in this field, they're actually your secret off -label weapons for treating, well, everything from severe chronic pelvic pain to, you know, low milk supply in nursing mothers.

So, welcome to the deep dive.

We are so glad you're here with us.

Yeah, and I know a lot of you listening are advanced practice nursing students, and you're, you know, staring down the final stretch before clinicals.

You're probably looking at chapter 54 of your text,

the pharmacologic management summaries, and just feeling your blood pressure spike.

Oh, I mean, it is a massive impenetrable wall of drug classes and dosages.

It's completely overwhelming.

It really is.

It feels less like clinical medicine and more like trying to memorize a phone book.

Yeah, and we all want medicine to be straightforward, right?

Like, patient has X, so you give them Y.

But clinical pharmacology in a living, breathing human is just rarely that simple.

Right.

It's so much more dynamic.

Exactly.

You aren't just memorizing milligrams.

You are expected to understand the underlying mechanisms,

you know, the cascade of physiological effects and how these drugs actually behave in the real world.

And that is exactly our mission today.

You can basically consider this your ultimate custom tailored study guide.

We are going to translate that really dense clinical text into a logical, patient -centered workflow.

Because clinical practice isn't just about reading the side of a prescription box.

No, not at all.

It's about knowing the why and the how, you know, like why you prescribe a specific class, how it alters the body's chemistry, the side effects you actually need to warn your patients about, and the clinical pearls that will quite literally save you in the exam room.

So we're going to connect the dots for you today.

The patient's history dictates the physical exam, right?

And then the physical exam supports your clinical interpretation.

Which then leads directly to these targeted management steps.

So let's just unpack this right from the top, starting with the bread and butter of outpatient care localized pelvic complaints.

Ripping places.

Right.

So a patient comes in, they're complaining of abnormal discharge and discomfort.

Your wet mount and your exam trigger a diagnosis, let's say, somewhere in the realm of vaginitis.

Okay.

So we're primarily looking at bacterial vaginosis, trichomonas, vulvovaginal candidiasis, which is, you know, your standard yeast infection,

and DIV.

Right.

DIV, which stands for Disquimative Inflammatory Vaginitis.

Yes.

And DIV is a really great example of why you have to be so precise.

I mean, it's an inflammatory condition, right?

It's not infectious.

Oh, right.

So the treatment pathway is entirely different from the others.

Exactly.

But looking at the common infections, the regimens are incredibly specific because of the organisms involved.

So for bacterial vaginosis and trichomonas, you're bringing in the heavy hitting antimicrobials.

Specifically metronidazole, right?

You got it.

But for candidiasis, since that's a fungus, you need to shift the azoles, like muconazole, or there's a newer fungicidal drug mentioned in the text called ibrexafunger.

Oh, yeah.

Ibrexafunger is fascinating.

It's a first in class triterpenoid.

It actually blocks the yeast from building its protective cell wall.

It's really targeted.

It is.

It's sort of like tending a garden.

You know, you can't just throw bra -spectrum weed killer at everything.

You need the narrow -spectrum antifungal to target the yeast cell wall, but you need the metronidazole to disrupt the DNA of the bacteria causing BV.

That mechanism -based thinking is spot on.

And speaking of metronidazole, your text highlights a massive clinical pearl that tends to just shock students.

Oh, the alcohol rule.

Yes.

For decades, the absolute golden rule of prescribing metronidazole was no alcohol.

I mean, we were taught it would cause a severe disulfiram -like reaction, like intense nausea, vomiting, flushing.

Yeah, that blows my mind because that no alcohol rule is practically medical folklore at this point.

I feel like it's ingrained in our brains from day one of pharmacology.

It really is.

But according to the updated guidelines in the text, refraining from alcohol use while taking metronidazole is actually considered unnecessary now.

The evidence just doesn't support the severity of that interaction.

Oh, wow.

Okay, but you still have to warn them about other stuff, right?

Oh, absolutely.

You must warn them about the actual side effects.

It causes a distinct metallic taste in the mouth and it can cause urine discoloration.

Which is super important.

You have to educate the patient on that so they don't panic when their urine suddenly turns a dark reddish brown.

Exactly.

Patient education is everything.

Cause and effect.

So let's shift slightly to sexually transmitted infections.

If your exam and testing reveal chlamydia, gonorrhea, or syphilis, the pharmacological rules get, well, very strict.

Very strict.

For chlamydia, the standard highly effective regimen is doxycycline.

But doxycycline has a pretty notorious mechanism when it comes to fetal development, doesn't it?

It does, yeah.

Doxycycline chelates or binds to calcium ions.

So the critical safety precaution here is that it is strictly contraindicated during the second and third trimesters of pregnancy.

Wait, because it binds to the fetus' calcium?

Precisely.

If a pregnant patient takes it, the drug binds to the calcium of the developing fetus and that leads to permanent tooth discoloration and impaired bone growth.

Oh, wow.

So if your patient is pregnant, you must pivot away from doxycycline and use azithromycin instead.

Exactly.

You always have to consider the patient's state.

Okay.

What about gonorrhea?

That one is tricky because of the rising antibiotic resistance.

So we're relying really heavily on ceftriaxone now, but I remember there's a major physiological caveat based on the patient's body mass.

You hit the nail on the head.

For uncomplicated gonorrhea, the recommendation is ceftriaxone 500 milligrams given intramuscularly.

But pharmacokinetics change with body size, right?

The volume of distribution is larger in a heavier patient.

Right.

So if the person weighs 150 kilograms or more, the standard dose just won't reach therapeutic levels in the tissue.

You have to double it to one gram of ceftriaxone.

Which is such a vital detail to catch during intake.

I mean, you can't just auto -prescribe.

What about syphilis?

We're still using penicillin, right?

Yes.

For primary, secondary, and early latent syphilis, you treat with benzathine penicillin G.

But this introduces one of the most interesting systemic reactions in all of medicine, the Jerrish -Herxheimer reaction.

I always have to like sound that one out in my head.

Jerrish -Herxheimer.

Explain the mechanism there for us.

So when you hit syphilis with penicillin, the spirachet bacteria die off rapidly en masse.

And as they burst open, they release huge amounts of endotoxins and lipoproteins straight into the patient's bloodstream.

Oh, so the immune system just freaks out.

Basically, yeah.

The patient's immune system detects this massive dump of debris and just goes into overdrive.

So within the first 24 hours of treatment, the patient might develop a sudden fever, headache, and severe myalgia, which is muscle pain.

So it looks and feels exactly like a severe drug allergy, but it's actually just proof that the drug is working.

Precisely.

And that is why patient education is completely non -negotiable here.

You have to warn the patient about this ahead of time.

Right.

Because if you don't, they will assume they're allergic to penicillin, they might seek emergency care unnecessarily, and they'll likely refuse future treatments.

Which would be disastrous for syphilis management.

Absolutely.

Okay, let's move from these acute localized bugs to larger maternal and metabolic physiological states,

like a common postpartum scenario.

You're taking a history and a new mother is distressed about low milk supply.

This happens all the time.

Yeah.

And she's read online about galactagogues and medications that supposedly boost milk production, and she's specifically asking for a prescription.

This is a classic expectation versus reality moment in practice.

I mean, the text is very clear that current research on the effectiveness of pharmacologic galactagogues is inconclusive at best.

And the drugs they usually ask for aren't even approved for this, right?

Right.

The drugs often requested,

like domperidone or metoclopramide, which we know as reglin, are not endorsed for this use.

And there's a very good reason for that.

Because reglin is a dopamine antagonist, right?

It blocks dopamine receptors to speed up gastric emptying and stop nausea.

Yes.

But dopamine in the brain also regulates our movement.

Right.

So because it crosses the blood brain barrier and blocks dopamine in the basal ganglia, reglin carries a black box warning in the US for tardive dyskinesia.

Exactly.

And tardive dyskinesia is a severe,

often irreversible movement disorder.

It's characterized by these repetitive involuntary muscle movements, usually in the face and jaw.

So the risk benefit analysis of, you know, risking permanent neurological damage just to potentially increase milk supply is heavily skewed against prescribing it.

Heavily skewed.

It's just not worth the risk.

That makes complete sense.

Sticking with systemic metabolic health, let's look at obesity management.

The text outlines a stepwise approach.

And you really have to understand the mechanisms of action here because they vary wildly.

They really do.

For instance, Fentermine acts directly on the central nervous system to suppress appetite.

But it is classified as category X for pregnancy.

We should definitely define category X clearly for everyone.

It means studies have demonstrated fetal abnormalities and the risks absolutely outweigh any possible benefit.

So Fentermine is strictly contraindicated in pregnancy.

Yes.

Meaning you have to ensure negative pregnancy tests monthly while the patient is actually on it.

Wow.

Okay.

Then you have an entirely different mechanism with a drug like Orlistat.

Instead of the brain, it works in the gut.

Right.

It's a gastric and pancreatic lipase inhibitor.

Meaning it literally stops the enzymes that break down fat in the diet.

So the fat just goes unobsorbed.

Which leads directly to the side effects you must counsel the patient on.

Because if the fat isn't absorbed into the body, it remains in the GI tract.

Oh, that sounds rough.

It is.

This leads to staturia, which is fatty, oily bowel movements, severe flatulence, and urgency.

It completely alters how the body processes food.

So the patient has to alter their diet to minimize those GI effects.

Okay.

But what about the injectables everyone is seeing on the news right now?

You know, the GLP -1 analogs like Wigovia or Saxenda.

Right.

So GLP -1s mimic the hormone glucagon -like peptide -1 to regulate blood sugar and slow gastric emptying.

But this is where your thorough family history intake becomes a total lifesaver.

Because of the thyroid risk.

Exactly.

GLP -1 receptors are also found on the C cells of the thyroid gland.

Because of this, there is an absolute contraindication you cannot prescribe these if the patient has a personal or family history of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2.

Because the drug could potentially stimulate those specific cancer cells.

Exactly.

So family history isn't just a box to check on an intake form.

It literally dictates the entire safety profile of the prescription.

100%.

Let's keep following that endocrine thread into hormone management and gender -affirming care.

The core principle here is that the monitoring is just as critical as the prescription itself.

It's all about cause and effect at the hematological level.

Let's take spironolactone for example.

We use it frequently as part of the feminizing regimen because of its antiandrogen effects.

But fundamentally, spironolactone is a potassium -sparing diuretic.

It blocks aldosterone in the kidneys.

So while it's helping with gender affirmation, it's also causing the body to hold onto potassium and excrete sodium and water.

Which means you absolutely must monitor their serum potassium levels to avoid hyperkalemia.

Which, I mean, that can cause fatal heart arrhythmias.

And you have to monitor their blood pressure because of the diuretic effect.

Yes, you do that with every single dose increase.

Now conversely, if you are prescribing testosterone for masculinizing therapy, you are stimulating the bone marrow.

Because testosterone drives erythropoiesis, right?

The production of red blood cells.

So you monitor the patient's hematocrit level with every single dose alteration.

You have to ensure their blood isn't becoming too thick.

Which, you know, could lead to a stroke or a blood clot.

Makes total sense.

All right, moving to another aspect of sexual and circulatory health erectile dysfunction.

The pharmacological mainstays here are the PDE5 inhibitors.

So sildenafil, tadalafil, avanafil.

Right, they all work by blocking the degradation of CGMP.

Which ultimately relaxes the smooth muscle in the blood vessels.

Allowing for blood flow.

I always think of the different options like train tickets.

Like, avanafil is the express train.

It has the fastest onset.

You can take it 15 minutes before activity.

But tadalafil is the weekend pass.

Because it lasts up to 36 hours.

I love that analogy.

That's great.

But regardless of the timing,

the safety precautions are identical because of that vasodilation mechanism.

Right, the absolute contraindication for PDE5 inhibitors is concurrent use with nitrates.

Which are, you know, often taken for chest pain.

Yes.

If you combine them, you get this profound synergistic systemic vasodilation.

The blood pressure just bottoms out entirely.

Which can be fatal.

And you also have to educate them on priapism.

Right, an erection lasting more than four hours.

Which is a medical emergency because the trapped blood becomes deoxygenated and can cause permanent tissue damage.

Exactly.

It's so important they know when to seek help.

Okay.

Let's shift our focus to the skeleton.

Managing bone density and osteoporosis.

The most common first line agents are bisphosphonates.

Like oral alendronate.

Yes, they bind directly to the bone to slow down the osteoclasts.

Which are the cells that break down bone.

But there is a very rigid clinical instruction for taking them.

The patient has to remain completely upright for at least 30 minutes after taking it.

And the reason why is fascinating though.

A bit scary.

Bisphosphonates are highly acidic and localized.

Absolutely.

So if the patient swallows the pill and then lies down, that pill can easily reflex back up.

And it will literally burn and ulcer directly into the esophageal lining.

The localized irritation is just intense.

So if a patient has severe renal impairment, existing esophagus problems, or simply an inability to sit up for 30 minutes, you have to avoid oral therapy entirely.

Wow.

And while we're discussing the power of these bone medications, the specialized ones have rare but severe complications.

Dinosumab, for instance, is a NKL inhibitor.

It profoundly stops bone turnover.

But because it halts the natural remodeling process, you have to watch for osteonecrosis of the jaw, right?

Yes, literally the death of the bone tissue in the jaw, which is often triggered by something as simple as dental surgery.

That is terrifying.

And then there's teraparotide.

Unlike the others that stop bone breakdown, teraparotide is a synthetic parathyroid hormone that actually builds new bone.

Right.

But because it's actively stimulating cell growth, there's an increased risk for osteosarcoma, a type of bone cancer.

So you'd never prescribe it for someone who already has an elevated risk, like a patient with Paget's disease or a history of radiation therapy to their skeleton.

Exactly.

It highlights a core truth of pharmacology.

Anytime you dramatically push a cellular pathway in one direction, you invite risks on the other side of that scale.

Such a good point.

All right.

Let's bring our focus back to the pelvis and abdomen.

When a patient presents with severe pelvic pain, you're faced with a pretty high -stakes differential diagnosis.

You really are.

I mean, it could be an acute infection, a chronic structural issue, or a mimicker in the GI or urinary tracts.

So let's say it's an acute infection like pelvic inflammatory disease.

For outpatient management of PID, you need to cover multiple potential organisms, including gonorrhea, chlamydia, and anaerobes.

So the guidelines recommend a triple threat.

Which is ceftriaxone IM plus doxycycline plus metronidazole?

Exactly.

But what if the pain is structural, like endometriosis or uterine fibroids?

You'd usually start with NSAIDs and combined oral contraceptives to control the bleeding and inflammation, right?

Right.

But sometimes that's just not enough, and you have to move to specialty medical interventions like GnRH agonists.

Oh, like luprolide.

Yes.

Luprolide is a common one.

GnRH agonists work by initially overstimulating the pituitary gland, which causes a brief flare of symptoms.

But then the receptors completely downregulate.

Oh, so the pituitary just stops sending signals to the ovaries.

Exactly, effectively shutting down estrogen production.

You create a state of pseudomenopause to starve the fibroids or the endometrial tissue of the estrogen they need to grow.

But dropping a patient of reproductive age into sudden menopause causes brutal systemic side effects, like the hot flashes, the bone density loss, the mood swings.

Which is why the text emphasizes add -back therapy.

You intentionally shut down their natural estrogen, but then you prescribe Northendrone, a specific progestin, to take daily.

So this adds just enough hormone back into the system to minimize those hypoestrogenic side effects and protect their bones, while still keeping the overall estrogen levels low enough to treat the fibroids.

You got it.

It's a delicate balance.

Medicine is wild.

You create a problem to fix a problem and then use another drug to fix the new problem.

Pretty much.

Now, what if that pelvic pain isn't gynecological at all?

Like, what if it's irritable bowel syndrome or a kidney stone?

Well, differentiating the source is key.

If it's IBS, you start conservative, reassurance, and a low FODM diet.

And FODMA stands for fermentable oligosaccharides, disaccharides, monosaccharides, and polyols.

Which is basically short -chain carbohydrates that pull water into your GI tract and get rapidly fermented by gut bacteria, causing immense gas and spasm.

Right.

So you remove those dietary sugars and add bulk -forming agents like psyllium.

If that fails, you target the exact symptom.

So you use loprimide to slow gut motility if diarrhea is the primary issue.

Yes.

Or disceclamine, which is an antispasmodic, to relax the smooth muscle of the gut if cramping abdominal pain is the chief complaint.

Okay.

And if it's a kidney stone, nephrolithiasis.

For acute treatment of a stone under 10 millimeters,

you're managing pain with analgesics, but you also want to facilitate stone passage.

So you can use Tamsilotion, an alpha blocker that relaxes the smooth muscle in the ureter to let the stone drop.

And here's a crucial procedural note from the text, instruct the patient to strain their urine.

Yes.

They need to physically catch the stone in a filter and bring it in for lab analysis.

Knowing if it's a calcium oxalate stone versus a uric acid stone dictates all their preventative care moving forward.

Makes sense.

Okay.

Let's talk about a really challenging clinical scenario.

A patient presents with localized burning vulvar pain, but your physical exam shows absolutely zero sign of infection or structural abnormality.

So we're looking at vulvodynia.

Right.

And the treatments here generally go off label because we are treating localized nerve dysfunction.

Yes.

For topical relief, 5 % lidocaine is often used, but you want to prescribe the ointment, not the cream.

Because the base ingredients in creams can actually further irritate the delicate vulvar tissue.

Exactly.

But for deeper systemic neuropathic pain, you have to look at medications originally designed for the brain.

So you prescribe anticonvulsants like gabapentin or tricyclic antidepressants like amitriptyline.

Right.

Because they calm the hyperactive pain signals firing along the nerves.

But you have to start at a very low dose and titrate up slowly, educating the patient that they might experience sedation or dry mouth as their body adjusts.

That's a huge part of the patient counseling.

That neurological crossover leads us perfectly into our next major clinical hurdle, endocrine dysfunction and menstrual irregularities.

Let's break down polycystic ovary syndrome, PCOS.

The pharmacological management isn't a one -size -fits -all, is it?

No, not at all.

It's heavily symptom targeted.

PCOS is an incredibly complex cascade.

The root is often insulin resistance, which triggers the ovaries to produce excess androgens, leading to irregular menses.

So if the primary goal is just regulating the cycle and combating the acne from those androgens, combination hormonal contraceptives are first line.

Right.

And if they just need contraception and protection against endometrial cancer, because those missed periods allow the uterine lining to build up dangerously,

a liver -nergestral IUD is fantastic.

But to target the metabolic route, the insulin resistance, Metformin is the go -to.

It decreases glucose production in the liver.

But to save the patient's GI tract, the clinical rule is start low, go slow.

Yes, you start at 500 mg with a meal and slowly titrate up to minimize the nausea and diarrhea it's so famous for.

And if their primary distress is hirsutism, excess facial and body hair from the androgens, you can use spironolactone to block those receptors.

But again, you must ensure the patient is using highly effective contraception, because blocking androgens in a male fetus would be catastrophic for its development.

So when a patient presents with abnormal uterine bleeding, or AUB, how do you triage the pharmacological options based on the tables?

You have to look at the source and the current state of the bleeding.

If the patient has heavy menstrual bleeding, but they aren't actively hemorrhaging right in front of you, tranexamic acid is a fascinating non -hormonal option.

Oh right, it's an anti -fibrinolytic.

It basically binds to plasminogen to stop the body from breaking down blood clots in the uterus.

They only take it during their menses to reduce the volume.

Exactly.

But what if they're unnavulatory and actively bleeding?

You need to halt the hemorrhage.

Then you turn to high -dose hormones, right?

Yes.

The text recommends a continuous monophasic oral contraceptive.

You have them take the active hormone pills every single day, completely skipping the placebo week to quickly stabilize and maintain the uterine lining.

But before you hand over any of these estrogen -based options, you have to rule out pregnancy and you have to assess their risk for venous thromboembolism or VTE.

Crucial step.

Estrogen increases clotting factors in the liver.

If they smoke or have a history of blood clots, you cannot safely give them estrogen.

Because safety always comes before symptom management.

Always.

We are in the home stretch now.

We are finishing the chapter's progression with quality of life and functional management.

So let's look at severe premenstrual dysphoric disorder, PMDD.

The first line pharmacological treatment for PMDD is SSRI's selective serotonin reuptake inhibitors.

But there is a crucial clinical pearl regarding the dosing schedule based on the patient's exact symptoms.

Right.

If the primary issues are irritability and mood lability, intermittent dosing is often severe.

They only take the SSRI during the luteal phase, which is the two weeks between ovulation and menstruation.

But if they have severe somatic symptoms like crushing fatigue, breast tenderness, and physical discomfort, intermittent dosing just won't cut it.

They need continuous daily dosing to maintain a baseline to control those physical symptoms.

So you're tailoring the pharmacokinetics to the clinical presentation.

Next, let's talk about the bladder, urinary incontinence.

Antimiscarinics, like oxybutynin, are standard here.

They block acetylcholine receptors.

Acetylcholine is the neurotransmitter that tells the smooth muscle of the bladder to contract.

By blocking it, the bladder relaxes, increasing its capacity to hold urine.

But blocking acetylcholine systemically is a massive red flag for older adults, isn't it?

Oh, absolutely.

Antimiscarinics are strictly contraindicated in older adults with cognitive impairment or dementia.

Acetylcholine is crucial for memory and cognition in the brain.

So if you block it, the anticholinergic burden can cause severe confusion, hallucinations, and delirium.

You might fix their incontinence, but you'll severely worsen their cognitive state.

Exactly.

So the alternative for an older patient is a beta -3 adrenergic agonist, like mirabagran.

It stimulates beta -3 receptors in the bladder to relax it without crossing the blood -brain barrier and causing that anticholinergic brain fog.

But there's a trade -off there, too.

Stimulating adrenergic receptors can increase cardiovascular tone.

You have to monitor their blood pressure closely.

It can cause hypertension.

And it shouldn't be used if their BP is over 160 over 100.

Right.

You fix the bladder, but you have to make sure you aren't stressing the heart.

Right.

Finally, let's talk about female sexual health.

For postmenopausal women, vulvovaginal atrophy causes severe discomfort.

Localized vaginal estradiol therapy like creams, rings, tablets rejuvenates the tissue by improving elasticity and blood flow.

And the beautiful pharmacological principle here is that if you are only using local low -dose estradiol vaginally, it doesn't absorb systemically enough to stimulate the uterine lining.

Which is great news for the patient.

Right.

Because therefore, there is no need to add daily progesterone to protect the uterus from cancer, which simplifies their regimen immensely compared to systemic hormone replacement.

Exactly.

Now, for hypoactive sexual desire disorder, or HSDD, in premenopausal women, the mechanisms get more complex.

The FDA -approved daily oral treatment is flavanserin.

And that works on serotonin and dopamine pathways in the brain, but it causes vasodilation, so you have to strictly monitor for hypotension and syncope, especially if the drug is mixed with alcohol.

Alternatively, there is an on -demand subbutaneous injection called bremelanotide, a melanocortin receptor agonist, taken 45 minutes before anticipated activity.

And the text notes transdermal testosterone is sometimes used off -label for HSDD, but it comes with a heavy counseling requirement.

You have to warn the patient about viralizing side effects.

Yes.

Increased facial hair, scalp hair loss, a deepening of the voice, and potential liver toxicity.

It requires a very candid conversation about risk tolerance.

Wow.

Take a breath.

We just navigated the entire chapter.

We took that intimidating wall of drug classes and traced the logical path from the patient's complaint through the physiological mechanisms all the way to the precise pharmacological management.

We really did.

And, you know, if we pull back and look at the bigger picture, I want to leave you with a thought to mull over.

Notice how many highly effective treatments in women's health rely on off -label use.

Like we said at the very beginning, seizure meds for vulvar pain, digestion meds for lactation, blood pressure pills for gender affirmation.

Exactly.

It highlights a profound reality of advanced practice.

True clinical excellence isn't just a matter of matching a disease to an FDA -approved label on the side of a box.

It relies entirely on your deep, mechanistic understanding of pharmacology.

Right.

When you know how a drug works at the receptor level, you can creatively and safely harness those mechanisms to improve your patient's quality of life.

That is an incredibly empowering way to look at it.

You aren't just memorizing tables.

You are mastering the physical tools of your trade.

To our student listeners, thank you for sticking through this massive review.

You understand the physiology, you know the safety warnings, and you are fully prepared for clinicals.

From everyone here at The Deep Dive, serving as your last -minute lecture team, you're going to do great.

We'll see you next time.