Chapter 51: The Child With an Endocrine or Metabolic Alteration

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Welcome back to The Deep Dive.

Today, we are opening up the hood to look at an engine system

body that is notoriously complex, often invisible, and frankly a little terrifying when it goes wrong in a child.

We're talking about the endocrine system.

The silent conductor of the orchestra.

That is the perfect metaphor, right?

You don't see the conductor waving the baton, but if the tempo is off or, you know, brass section is playing too loud, the whole symphony just falls apart.

And today, we are specifically looking at this through the which is titled the child with an endocrine or metabolic alteration.

And I'm glad to use the word terrifying because in pediatrics, the stakes with the endocrine system are incredibly high.

It's not just about discomfort.

It's about the fundamental blueprint of the child's life.

How so?

Because in adults, we often think of endocrine issues like, say, hypothyroidism or type 2 diabetes as chronic management.

Annoying, sure, but usually manageable

In adults, it is largely management.

In children, it's about construction.

This system controls growth, metabolism,

sexual differentiation, and arguably most importantly, brain development.

So if a nurse misses a beat here, a misdiagnosis on a newborn screen, a skip dose of cortisol during a fever,

we aren't just talking about a bad day.

We're talking about permanent intellectual disability,

stunted physical growth, or immediate life -threatening shock.

So our mission today is clear.

We need to translate these complex chemical pathways, which, let's be honest, can be incredibly dry in a textbook, into practical, life -saving nursing care.

We're going to look at the why behind the symptoms, the specific safety alerts that are flagged in the text, and the massive education burden that falls on the family.

And we need to move beyond just memorization.

It's not enough to know that a baby with congenital adrenal hyperplasia needs medication.

You need to know why a simple stomach virus could kill them if you don't adjust those meds.

That's where the real nursing judgment comes in.

Let's start at the control center, then.

The physiology.

When I look at the diagram in the source material, it looks like a scattered network.

You have the pituitary in the brain, the thyroid in the neck, adrenals sitting on top of the kidneys.

It feels disconnected.

It does look scattered, but think of it as a wireless communication network.

It works in tandem with the nervous system.

The autonomic nervous system sends a signal to the hypothalamus, which then talks to the pituitary, the master gland, and the pituitary sends chemical emails or hormones out to the target glands to tell them what to do.

And the central rule governing this whole network is negative feedback.

Yes.

This is the one concept you have to grasp to understand the pathology.

The thermostat analogy is the classic one here.

It's classic because it works.

If you set your thermostat to 70 degrees and the room heats up to 72, the heater shuts off.

The rise in temperature signals the system to stop producing heat.

Exactly.

In the body, if thyroid hormone levels rise, the pituitary should stop shouting at the thyroid to make more.

It should go silent.

And disorders happen when that loop breaks.

Either the thermostat is broken, so the pituitary keeps shouting even when levels are high.

Or the heater is broken and it won't turn on, no matter how much the thermostat demands it.

Okay, that makes sense.

But here's the critical context for our listeners today, and this is specific to pediatrics.

The source material highlights that the endocrine system is the least developed system at birth.

That surprised me.

I assumed because it's so vital for survival, it would be ready to go immediately.

Far from it.

Hormonal control is often incomplete until a child is 12 to 18 months old.

That is a long time to be under construction.

What is the clinical implication of that for a bedside nurse?

What does that mean for us?

It means infants are chemically fragile.

They have a really hard time balancing fluids, electrolytes, amino acids, and glucose.

A stomach bug that makes an adult feel gross for a day can send an infant into a full -blown metabolic crisis because their endocrine system just doesn't have the maturity to compensate yet.

The reserve capacity is basically zero.

Exactly.

Zero.

So when we suspect something is wrong, how do we prove it?

The text makes a point that random blood draws, you know, just sticking a kid at two in the afternoon, are often useless.

Right.

You can't just take a snapshot because hormones aren't released in a steady stream like a faucet.

They pulse.

They follow circadian rhythms.

Growth hormone, for example, surges at night while the child sleeps.

So if you draw blood in the middle of the day, you might find low levels even in a totally healthy kid.

You would, and you'd be chasing a ghost.

So we have to use stimulation testing.

Correct.

Think of it as a stress test for the gland.

If we suspect a gland is underperforming, we give a trigger like insulin or arginine to see if the gland can respond.

We poke the bear to see if it roars.

That's a good way to put it.

And if it doesn't roar, we know there's a deficiency.

And conversely, if we think a gland is overactive, we try to suppress it.

If we tell it to shut up and it keeps talking, we know we have a hyperfunction issue.

Okay.

There's one more diagnostic tool we have to mention before we get into specific diseases, and that's bone age.

Yes, the x -ray, usually of the hand and wrist.

And what are we looking for there?

We're comparing the skeletal maturity to the child's chronological age.

This is crucial for growth disorders.

If a 10 -year -old boy has the bones of a 7 -year -old, that actually gives us hope.

Hope.

Why?

It means his growth plates, the epiphyseal plates, are still open.

He has growth potential left in the tank.

But if that same 10 -year -old has the bones of a 15 -year -old.

Then his growth plates are closing or already closed.

His time to grow is running out, and he might end up being a short adult.

It totally changes our treatment window.

It helps us decide if aggressive intervention is even worth it.

Okay.

Let's get into the specific disorders.

We're going to organize this by the gland or system involved, starting with a metabolic condition that I feel like every nursing student memorizes for the test, but maybe doesn't fully grasp the daily reality of PAH deficiency or PKU.

Phenylketonuria.

This is an autosomal recessive genetic error.

Meaning both parents are carriers.

Exactly.

They don't have the disease, but the child inherits two bad genes.

The result is that the body is missing a specific liver enzyme called phenylalanine hydroxylase.

Okay.

So let's unpack the mechanism.

What does that enzyme actually do?

Its job is to break down phenylalanine, which is an essential amino acid found in pretty much all protein.

Without that enzyme, phenylalanine can't be processed.

It just builds up in the blood.

And here is the scary part.

High levels of phenylalanine are toxic to the central nervous system.

Specifically, it attacks the myelinization process.

Myelin is the insulation on our nerves.

It allows signals to move fast.

Most of that myelinization happens in the first decade of life.

So if you have untreated PKU, the phenylalanine effectively strips the insulation off the wiring.

So you're looking at progressive permanent intellectual impairment, seizures, and bizarre behavior patterns.

Yeah.

It's devastating.

What makes this so tricky is that at birth, these babies look totally normal.

They do.

They've been protected by the mother system and utero because her liver was doing all the work.

But usually by around three months, if untreated, you start seeing digestive problems, vomiting, maybe severe eczema.

But the hallmark sign, the one you'll see on board exams and in the textbook, is the smell.

The source describes it as musty or mousy.

Yes, a musty odor in the urine and sweat.

That's the excreted acid.

You might also see hypertonia stiff muscles.

And interestingly, because phenylalanine affects melanin production, these kids often have significantly lighter skin, blonde hair, and blue eyes compared to their siblings or parents.

This is why newborn screening is absolutely non -negotiable.

The Guthrie test.

It's mandatory in all 50 states, but nurses need to be aware of the timing.

You cannot do it immediately after birth.

Because the baby hasn't eaten yet.

Exactly.

The baby has to have ingested protein, breast milk, or formula for at least 24 to 48 hours for the metabolite to show up in the blood.

If you do the heel stick too soon, you get a false negative.

And a false negative here is a tragedy.

It is.

You miss the window to prevent brain damage.

Let's say it comes back positive.

What does life look like for that family?

It changes everything.

The treatment is dietary and it is strict.

They need a low phenylalanine diet.

That means no meat, no dairy, no eggs, no cheese, no nuts.

That eliminates almost all standard sources of protein.

It does.

They rely on a special medical formula to get their protein without the phenylalanine.

As they grow, they can have vegetables, fruits, and some starches, but normal food, a hamburger, a slice of pizza, is essentially poison to their brain.

And we have to mention the artificial sweetener issue, aspartame.

Right.

Aspartame is basically pure phenylalanine.

So diet sodas, sugar -free gum, those are strictly off limits.

Parents have to become obsessive label readers.

Is this something they can grow out of?

I remember hearing years ago that maybe once the brain is developed, adults could relax the diet.

That used to be the thinking.

We thought, okay, the brain is built, you're safe.

But the source material is very clear.

That advice has changed.

We now know that high levels in adults cause cognitive decline, poor executive function, and psychiatric issues.

It is a lifelong commitment.

And I imagine for women with PKU who want to get pregnant, the stakes are even higher.

It's critical.

If a mother has high phenylalanine levels during pregnancy, it crosses the placenta.

Even if the baby doesn't have PKU genetically,

the mother's blood can damage the fetus, causing microcephaly and heart defects.

So tight control is essential before conception.

Wow.

Okay, let's pivot to the adrenal glands.

This section of the text has a massive safety alert stamped on it.

We're talking about congenital adrenal hyperplasia, or CAH.

CAH is a fascinating but dangerous manufacturing error.

Think of the adrenal gland as a factory.

Its job is to produce cortisol and aldosterone.

But in CAH, usually due to a lack of the enzyme 21 -hydroxylase, the assembly line is broken.

It can't finish the product.

So the pituitary sees there's no cortisol, the thermostat kicks in.

Right.

The pituitary screams, make more cortisol.

It pumps out ACTH.

The adrenal gland tries harder.

It grows larger.

That's the hyperplasia part.

But it still can't make cortisol because the machinery is broken.

But it has to make something with all that raw material.

Exactly.

So it shunts all that effort into the only pathway that still works.

Androgens.

Male sex hormones.

So you have a factory trying to make stress hormones and it's accidentally flooding the child's body with testosterone.

That is the mechanism.

And the clinical presentation depends entirely on the sex of the child.

In newborn females, this excess androgen exposure in the womb leads to ambiguous genitalia at birth.

You might see an enlarged clitoris that resembles a penis or fuse labia.

That must be incredibly distressing for parents.

Is it a boy or a girl?

It is a psychosocial crisis for the family.

They need immediate support.

But physically, the baby girl is usually identified quickly because of that visible sign.

The danger is actually higher for male infants.

Because they don't look different.

Right.

A baby boy with extra testosterone just looks like a baby boy.

No one suspects anything.

So they go home.

And that is where the danger lies because they aren't just making too much testosterone.

They are failing to make cortisol and aldosterone.

This brings us to the safety alert.

The salt wasting crisis.

About 70 % of CAH cases are salt listers.

They lack aldosterone.

Aldosterone is the hormone that tells the kidneys to hold on to solvent water.

Without it, they pee out all their sodium.

So they get dehydrated incredibly fast.

Incredibly fast.

Within a week or two of birth, the baby starts vomiting, losing weight, and becoming lethargic.

If you draw labs, you see hypoentremia, dangerously low sodium, and hyperkalemia, dangerously high potassium.

This is a metabolic emergency.

Absolutely.

They can go into hypotensive shock and cardiac arrest.

So if a male infant comes in with those symptoms, vomiting, dehydration, shock, we shouldn't just assume it's a bad stomach bug.

We need to check electrolytes.

Absolutely.

Stabilization is the priority fluids and electrolytes to fix the sodium and potassium.

But long term, these kids need to replace what they're missing.

They need lifelong cortisol replacement, usually hydrocortisone, and a mineral accordicord called fluorineph to replace the aldosterone.

Now this leads to one of the most important education points in the entire chapter, the sick day rules.

This is life -saving information.

In a healthy person, if you break a bone or get a high fever, your adrenal glands naturally pump out 5 or 10 times the normal amount of cortisol to help your body cope with the stress.

But a child with CAH can't do that.

Their factory is broken.

Exactly.

So the parents have to be the adrenal gland.

If the child has a fever, the parents must double or even triple the dose of hydrocortisone.

If the child is vomiting and can't keep pills down, the parents have to give an emergency injection of hydrocortisone.

That's a huge responsibility.

You're asking parents to make medical decisions at 2 in the morning.

It is.

If they don't increase the dose, the child can slip into an adrenal crisis within hours.

Nurches have to practice this with parents, literally verify that they know how to draw up and give the shot before discharge.

It is not something you want them to figure out in a panic.

Let's move up the body to the neck.

The thyroid.

We have a few different conditions here, but let's start with the newborn period again.

Congenital hypothyroidism.

Again, we have to ask, why does this matter?

In the first two years of life, thyroid hormone, T4, is essentially brain food.

It is critical for the rapid growth of the central nervous system.

If a baby is born without a working thyroid and we miss it, the result is permanent intellectual disability.

What does that baby look like?

Because the text says the signs can be subtle.

They are often described as good babies.

They're very quiet.

They sleep all the time.

But that lethargy is a red flag.

Physically, you might see a horse cry, constipation, a really large tongue that sticks out, and cold mottled skin.

Quiet and cold.

That's a good mnemonic.

And hypotonic.

They feel floppy.

The treatment is straightforward.

Replace the hormone with levothyroxine.

But the text has a very specific nursing tip about administration here.

This is a classic gotcha.

There is no standard liquid form of levothyroxine in the U .S.

So parents have to crush the tablet.

But, and this is key, you cannot mix it with soy formula or iron supplements.

Soy and iron bind to the medication in the gut and prevent absorption.

If a baby is on soy formula, they aren't getting their meds and their brain isn't getting the T4 it needs.

The nurse has to review the infant's diet carefully.

Now what about when thyroid issues crop up later in childhood?

We have Hashimoto's engraved disease.

Think of these as opposites.

Hashimoto's is acquired hypothyroidism.

It's an autoimmune attack where the immune system destroys the thyroid tissue.

Everything slows down.

So the child is tired, constipated, has dry skin.

And they gain weight.

But the major red flag, the one that differentiates it from just simple obesity, is a deceleration in growth.

Oh, that's interesting.

Yeah, if a kid is gaining weight rapidly but has stopped growing taller, you need to check the thyroid immediately.

Simple obesity usually makes kids grow taller faster.

Hypothyroidism stops height in its tracks.

That is a great clinical pearl.

Now flip the coin.

Graves' disease.

Hey.

Hypothyroidism.

Everything speeds up.

The metabolic rate is through the roof.

These kids are losing weight even though they're eating constantly.

They're jittery.

They have tremors.

They can't handle heat.

You might see exophthalmos, those protruding eyes.

And behaviorally.

Often these kids get flagged for ADHD or behavioral problems in school first.

They can't sit still.

They have poor attention spans.

They're irritable.

It's not bad behavior.

It's a thyroid overdosing on its own supply.

Treatment for Graves seems a bit more aggressive.

It is.

We use anti -thyroid meds like methamazole to block hormone production.

But often that's not enough.

The definitive treatment is often to destroy the gland with radioactive iodine or remove it surgically.

Which, ironically, leaves them with hypothyroidism.

Right.

We trade a dangerous, unpredictable disease for a manageable one.

They'll need T4 pills for life, but that is so much safer than a hyperactive thyroid.

And the safety alert here is the thyroid storm.

Yes.

If a child with Graves gets an infection or abruptly stops their meds, they can go into a crisis.

High fever, extreme tachycardia, confusion, agitation.

It is rare, but it is life -threatening and requires ICU care.

Okay, let's shift gears to the brain again.

The posterior pituitary.

This is all about water balance.

The tug of war between holding water and letting it go.

This is the story of ADH antidiuretic hormone, also known as vasopressin.

I always tell students to look at the name.

Antidiuretic.

It prevents diuresis.

It stops you from peeing.

It holds water in the body.

So on one side of the spectrum, we have diabetes insipidus or DI.

High and dry.

That's the memory hook.

In DI, you don't have enough ADH.

The kidneys cannot concentrate urine.

So the child pees massive amounts of dilute, clear water.

We're not talking about just going to the bathroom a lot.

We're talking about volumes that are hard to believe.

Massive polyuria.

A potty -trained child will start wetting the bed.

And polydipsia, insatiable thirst.

They will drink water from a toilet bowl or a puddle if they have to.

They are desperate.

And the high in high and dry refers to sodium.

Right.

Because they are peeing out pure water, their blood becomes concentrated.

They develop hypernetremia, high sodium.

The source mentions a water deprivation test.

That sounds intense.

It is dangerous and must be done in a hospital.

You basically stop them from drinking and see if they stop peeing.

In a normal person, urine output would drop and become concentrated.

In a child with DI, they keep peeing dilute urine even as they become dehydrated.

It proves the kidneys aren't getting the signal to stop.

The treatment is to replace the hormone.

DDAVP synthetic ADH.

Correct.

Usually a nasal spray or a pill.

It works like magic.

But then you have to watch for the opposite problem, water retention.

Which brings us to SIADH, syndrome of inappropriate ADH.

Low and wet.

Exactly.

Too much ADH.

The faucet is turned off.

The body hoards water.

They stop peeing.

They swell up with fluid retention.

And because they're holding all this water, their sodium levels are diluted.

They develop hyponutremia.

And the text highlights a specific sodium level to watch out for.

If sodium drops below 125, you are in the seizure zone.

The brain cells swell cerebral edema.

This is why SIADH is so dangerous.

What's the nursing priority here?

Strict fluid restriction.

And I mean strict.

You have to explain to a child who wants to drink out of habit that they can't.

You're also monitoring for neurological changes, confusion, lethargy, which are signs of that brain swelling.

Let's talk about growth again, but specifically regarding puberty.

We have precocious puberty.

Sexual development before age 8 in girls or 9 in boys.

Parents often worry about the social aspect.

A 7 -year -old girl developing breasts or getting her period.

And that's valid.

But the medical concern is actually height.

It seems counterintuitive.

Parents think, oh, she's growing fast.

She'll be tall.

But sex hormones do two things.

They trigger a growth spurt.

But then they tell the growth plates in the bones to close.

So they sprint early, but they finish the race way too soon.

Exactly.

They have a massive growth spurt at age 7, but they start growing entirely at age 10.

Without treatment, they end up being very short adults.

So we hit the pause button.

We use GnRH agonists like Lupron.

It basically tells the pituitary to stop sending the puberty signal.

It preserves their childhood and crucially keeps the growth plates open so they can reach their full potential height.

On the other end of the spectrum, we have growth hormone deficiency.

These kids are falling off the growth chart below the 5th percentile.

They often have a cherubic appearance,

angelic, young -looking faces, often with higher body fat around the middle because GH also helps build muscle.

And the treatment here is quite a burden for a family.

Daily subcutaneous injections every single night.

And it's expensive.

It requires a huge commitment from the family to keep this up for years.

And socially, these kids are often treated like babies because they look so young, which can be really hard on their self -esteem.

We have to move on to the biggest topic in this chapter.

The one that likely consumes the most nursing hours, diabetes mellitus.

Type 1 and type 2.

And we need to be crystal clear on the difference because the management is totally different.

Let's start with type 1.

This is the predominant form in children, though that is shifting.

This is autoimmune destruction of the beta cells in the pancreas.

Absolute insulin deficiency.

The pancreas just stops making it.

The body is starving in the midst of plenty.

There is glucose in the blood, but without insulin, which acts like a key, that glucose can't get into the cells, so the cells starve.

And we see the classic three P's.

Polyuria, peeing out the glucose because the kidneys can't hold it all.

Polydipsy, extreme thirst because of that fluid loss.

And polyphagia, excessive hunger because the cells are screaming for energy.

If we miss those signs, we end up in DKA, diabetic ketoacidosis.

This is a life -threatening emergency.

Because the body can't use glucose, it starts burning fat for fuel.

The waste product of burning fat is ketones.

Ketones are acidic.

So the blood essentially turns to acid.

Yes.

And the body tries to fix it.

That is why you see cousmal respirations, those deep, rapid, gasping breaths.

The child is trying to blow off CO2 to reduce the acidity.

And the smell.

Acetone.

Fruity breath.

It smells like nail polish remover or rotting fruit.

If you smell that on a child who is vomiting and confused, check their sugar immediately.

Managing type 1 is a constant balancing act.

We have basal insulin and bolus insulin.

Right.

Basal is the long acting, like Lantus or Glargine.

It has no peak.

It just hums along in the background to keep things steady.

Bolus is the rapid acting, like Lispro, given with meals to handle the food.

The text emphasizes rotation of injection sites.

Why is that so important?

I feel like kids naturally want to use the same spot that hurts the least.

They do.

Usually the thigh or tummy.

But if you keep picking the same spot, you get lipohypertrophy.

These are fatty lumps of scar tissue.

The problem isn't just cosmetic.

Insulin doesn't absorb well into that tissue.

So you give the shot, but the blood sugar doesn't come down.

Nurses have to teach checkerboard rotation to ensure consistent absorption.

Let's talk about the highs and lows.

Hypoglycemia versus hyperglycemia.

Hypoglycemia is the immediate danger.

Cold and clammy, need some candy.

The brain is running out of fuel.

They get shaky, sweaty, confused, irritable.

You need 15 grams of fast carbs juice, candy, glucose tabs immediately.

And hyperglycemia.

High and dry, thirsty, tired, peeing a lot.

It's a slow onset, but leads to DKA if ignored.

The source material has a really interesting section on sick day management for diabetes.

It seems counterintuitive.

If a kid is sick and throwing up and not eating, a parent might think, Well, I shouldn't give insulin because he's not eating.

And that is the dangerous trap.

That logic makes sense, but it is wrong.

When a child is sick, stress hormones cortisol again flood the system.

These hormones naturally raise blood sugar.

So even if the kid isn't eating a bite of food, their sugar might be skyrocketing just from the infection.

So the rule is?

You never stop insulin completely.

You check blood sugar and ketones every three hours.

You might need to adjust the dose, but if you stop it, they will go into DKA.

Now, types of diabetes used to be called adult onset.

We can't say that anymore.

Tragically, no.

We are seeing an epidemic in children due to obesity and lifestyle factors.

This is insulin resistance.

The pancreas is working, often working over time, but the cells aren't listening to the signal.

Is there a physical sign we should look for?

Acanthosis nigricans.

It's a velvet -like dark pigmentation, usually on the back of the neck or in the armpits.

Parents often try to scrub it off thinking it's dirt.

It is not dirt.

It's a physical marker of high insulin levels.

If you see that, screen for type 2.

And for type 2, the first line is lifestyle change.

But there is one oral med approved for kids.

Metformin.

It helps reduce glucose production by the liver and sensitizes the cells to insulin.

But without diet and exercise changes, the medication can only do so much.

Before we wrap up the diabetes section, I want to touch on the developmental challenges.

Because managing diabetes in a 3 -year -old is wildly different than in a 15 -year -old.

Oh, completely.

Take toddlers.

They are picky eaters.

You can't give the insulin before the meal if you aren't sure they're going to eat it.

You might have to give it right after, based on what they actually swallowed.

And preschoolers engage in magical thinking.

Right.

They might think the shot is a punishment for being bad.

You have to separate the ouch from the behavior.

And then the adolescence.

The danger zone.

The perfect storm.

You have puberty hormones making blood sugar erratic.

You have a brain that is wired for risk -taking and peer acceptance.

They don't want to be different.

They don't want to leave class to check their sugar.

They don't want to pull out a pump at a party.

Rebellion is natural, but here it is lethal.

Exactly.

Rebellious skip doses are a huge cause of DKA in teenagers.

The nurse has to be part negotiator, part medical professional.

You have to help them transition to independence without abandoning them to their own poor impulse control.

We have covered a massive amount of ground today.

From the mousy smell of PKU to the salt wasting of CAH, the thyroid storms, and the daily grind of diabetes.

It is a lot.

But if you pull back, the theme is homeostasis.

The endocrine system is constantly trying to keep things balanced.

In pediatrics, our job is to step in when that balance is lost and help the child and the family find a new normal.

What stands out to me is the role of the family.

In almost all these conditions, PKU, diabetes, CAH, the parents are the ones doing the heavy lifting 24 -7.

They are the primary care providers.

We see the kid for 15 minutes.

They see them for the other 23 hours and 45 minutes.

That's why education is the single most important intervention we do.

I want to leave our listeners with one final thought to chew on.

The text mentions the honeymoon phase in type 1 diabetes.

Ah, yes.

This is a cruel physiological trick.

Explain that, because it sounds positive.

Shortly after diagnosis and starting insulin, the pancreas seems to wake up a little.

The remaining beta cells sputter out a last burst of effort.

Blood sugars normalize.

Needs for insulin drop drastically.

So parents think the doctors were wrong.

He's cured.

We can stop the shots.

Exactly.

They hold on to that hope.

But the nurse has to be the one to gently anchor them in truth.

To explain that this is temporary.

It will last a few weeks, maybe months, but those cells will fail.

It feels like managing hope is just as hard as managing the disease.

It is.

If you let them believe the cure is real, the crash when the diabetes comes back is devastating.

Preparing them for the end of the honeymoon is an act of compassion.

A sober reminder of the emotional weight these families carry.

That is it for this deep dive into Chapter 51.

Thanks for listening and go be that conductor for your patients.

Stay curious.

This is the Last Minute Lecture Team signing off.

Thank you.