Chapter 24: Hematologic & Immunologic Dysfunction in Children

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Welcome back to The Deep Dive.

We are tackling something today that feels incredibly basic, yet it's arguably the most complex system in the human body.

We are talking about the fluid of life, blood.

It really is.

I mean, it's the body's superhighway.

It's moving oxygen, nutrients, waste,

and the entire immune system.

But here's the catch.

When you're an adult, if your blood is a little off, maybe you just feel tired.

But when you're a child and that system malfunctions,

the consequences are catastrophic.

Oh, absolutely.

It affects growth, brain development, bone structure, literally everything.

That's so right.

And for the nurse, hematology is often the first place where these systemic clues really show up.

You aren't just looking at a lab report.

You're looking at a snapshot of the child's entire physiological state.

So to navigate this, we are doing a comprehensive breakdown of chapter 24 from Wang's Essentials of Pediatric Nursing, the 11th edition.

The chapter is titled The Child with Hematologic or Immunologic Dysfunction.

And it is a heavy chapter.

It's

really unpack it into something you can actually use at the bedside.

Exactly.

We want to move beyond just memorizing lab ranges and really get to the why behind the nursing interventions.

We've got a lot of ground to cover.

We're going to start with the detective work assessment and the CBC.

Then we'll get into the red blood cell disorder.

All the anemias.

Yeah.

Specifically, the anemia is like iron deficiency, sickle cell, thalassemia, and a plastic anemia.

Then we'll shift over to the clotting side of things, hemophilia, ITP, and DIC.

Right.

And finally, we will touch on the immunologic side with HIV and AIDS in the pediatric population.

A full slate.

It is.

So let's start the assessment.

When a child has a blood disorder, they don't usually walk in wearing a sign.

It's subtle.

So subtle.

You mentioned in the notes that the nurse is often the one to catch it before the doctor even sees the labs.

Absolutely.

I mean, think about what blood does.

It delivers energy.

So if that delivery system is failing,

what do you see?

You see a child who has just run out of gas.

Okay.

Parents will say things like, he used to play for hours.

Now he sits down after 10 minutes.

Or she naps three times a day now.

Lethargy is the big one.

But I mean, lots of kids are tired.

How do you distinguish blood tired from school tired or just, you know, toddler tired?

That's the key question.

You look at the skin.

Palor is key paleness.

Not just in the face, but really check the mucous membranes.

So like inside the mouth.

Yeah.

Or pull down the lower eyelid.

Was it pink or is it white?

And then you look for the leakage signs.

Patechiae.

Those are the tiny pinpoint red spots, right?

Yes.

That's blood literally leaking from capillaries under the skin.

Or purpura, which are the larger sort of purple bruises.

Got it.

And if a parent tells you, I can't stop his nose bleed or his gums bleed every time we brush, those are massive red flags for hemostasis issue.

Okay.

So you have this clinical picture.

Now you get the lab print out.

The complete blood count or CBC cable 24 .1 in the text.

For a lot of students, this is just, it's a wall of numbers.

It can be so overwhelming, but try to visualize the bone marrow as a factory.

The CBC is the shipping manifest.

It tells you exactly what is leaving the warehouse.

I like that analogy.

Let's break down the inventory.

First up, red blood cells, RBCs, hemoglobin, and hematocrit.

These are your oxygen trucks.

That's all they are.

If these numbers are low, the body is suffocating at a cellular level.

Simple enough.

But, and this is so critical, you cannot use adult numbers for kids.

Yeah.

A newborn has a much, much higher hemoglobin level than a two month old.

Because they still have fetal hemoglobin circulating.

Exactly.

And then it naturally drops.

Yeah.

So if you judge a toddler by newborn standards, you'll think they're terribly anemic.

Yeah.

If you judge a newborn by toddler standards, you might completely miss polycythemia.

You have to use age appropriate norms.

That's a huge takeaway.

Then we have the white blood cells, the WBCs, the defense force.

Yeah.

But the total number doesn't tell us much, does it?

No, not really.

A high white count just says, hey, there's a fight happening.

It doesn't tell you who the enemy is.

For that, you need the differential.

The diff.

Yep, the diff.

This breaks it down into the specific battalions.

Let's run through them.

Neutrophils.

Those are your infantry.

They're the first responders.

They fight bacteria.

So if neutrophils are high, you should immediately think bacterial infection.

Okay.

Eosinophils.

That's the specialized unit.

They handle allergies and parasites.

So if a child has, say, a worm infection or a severe allergic reaction, you're going to see those eosinophils spike.

And limocytes?

The intelligence agency.

They handle viruses and they make antibodies.

High limbs usually point to a viral process.

No, there is a phrase in the text that comes up constantly in nursing school, but people often misunderstand it.

Shift to the left.

It sounds like a political movement, but it's definitely not.

It is definitely not political.

It's actually historical.

Back in the day, before we had digital counters, lab techs used these manual counters to tally white blood cells.

Right.

And they would write the counts on a grid.

The mature neutrophils, the segs were written on the right side.

The immature neutrophils, the bands, were written on the left.

So a shift to the left literally meant your pencil was moving to the left side of the paper more often.

Exactly.

It means there are more immature cells, more bands appearing in the blood.

Okay.

So why does that happen?

Why would the body send out immature cells?

It's pure desperation.

A match to the bone marrow factory is under attack by a massive bacterial infection.

It sends out all its mature soldiers, the segmented neutrophils, but the bacteria are still winning.

So the marrow just screams, send everyone, and starts deploying the recruits who haven't even finished their training yet.

Those are the bands.

Those are the bands.

So when you see a shift to the left, it tells you the infection is severe.

The body's struggling to keep up.

It is a major, major warning sign for sepsis.

That visual of the recruits being thrown into battle really helps.

Okay.

Let's move on to the red cell disorders.

Anemia.

The most common hematologic disorder of infancy and childhood.

But it's so important to remember anemia is not a disease.

It's a symptom.

Right.

It's like a fever.

It tells you something is wrong, but it doesn't tell you what.

It's defined as a reduction in RBC mass or hemoglobin concentration.

And we know that means less oxygen to the tissues.

But I want to dig into the hemodynamics.

The text talks about viscosity.

Yeah.

This is where a little physics comes into play.

Red blood cells give blood its viscosity.

If you have severe anemia, you just have fewer cells.

The blood becomes, well, watery.

We call that hemodilution.

Okay.

So the blood is thinner.

Now, to me, that sounds like it would be easier to pump, you know, like pumping water versus pumping syrup.

Why does this stress the heart?

It's so intuitive to think that, but it actually works the opposite way.

Because the blood is thinner, there is less resistance in the peripheral vessels.

So the

return volume, the preload, it increases.

Drastically.

This causes volume overload and a lot of turbulence inside the heart chambers.

That turbulence is actually what creates the systolic murmur you often hear in any kids.

Wow.

It's the sound of that watery blood just swooshing around way too fast.

And if the heart has to handle that increased volume constantly.

It gets tired.

The workload just skyrockets.

And then if you add an infection or some emotional stress on top of that, the heart just can't keep up.

And you can go into cardiac failure.

That's why they're a cardiac risk.

That's exactly why.

That makes the rest intervention makes so much more sense.

It's not just let them sleep.

It's really don't overwork the pump.

Precisely.

And long -term, if the cells are chronically starved of oxygen, everything slows down.

You see growth retardation, delayed sexual maturation.

The body just puts growing up on hold because it's trying to survive.

Let's zoom in on the specific types then.

The big one, iron deficiency anemia.

Oh yeah.

The most common nutritional disorder in children worldwide.

We do see it less now because of things like fortified cereals and WIC programs, but it is still so prevalent.

Who are the usual suspects here?

The at -risk groups.

It's all about growth, births and intake.

So preterm infants are at a huge risk because they miss that third trimester in the womb, which is when the fetus normally stores up iron from mom.

They're born with an empty tank.

And then toddlers.

I feel like that's the classic age.

Coddlers are the classic demographic, specifically the milk baby.

This term is fascinating.

When I think of a sick child, I think skinny, frail, but milk babies are often chubby.

And then that's the paradox.

They look well fed.

Parents think, look at those chubby cheeks.

He's so healthy.

But that weight is often from excessive caloric intake from cow's milk.

They're drinking, you know, 30, 40, even 50 ounces of milk a day.

But milk is good for you, right?

Calcium.

It's fantastic for calcium.

It is terrible for iron.

Cow's milk contains almost no iron.

And because the kid is full of milk all the time, they refuse to eat solid foods like meat or green veggies that actually have the iron they need.

So they are calorically overfed, but nutritionally starving.

And it gets worse.

In young infants, the protein in cow's milk can be really tough to digest.

It causes inflammation in the gut lining.

Oh no.

And this leads to microscopic bleeding.

So not only are they not eating iron, they're actively losing blood and iron in their stool.

That is a vicious, vicious cycle.

So the fix is diet and supplements.

Exactly.

We start with iron -fortified cereals and limiting milk.

But usually we need oral iron supplements.

Ferrous sulfate.

And this is where nursing education is absolutely make or break.

You can't just hand the parents a bottle and say, good luck.

No, because iron is chemically very finicky.

It needs an acidic environment to be absorbed properly.

If you give it on a full stomach, or worse, with milk, it just won't work.

So why not milk specifically?

Calcium binds with iron.

They basically clump together and pass right through the gut without ever being absorbed.

So you have to teach parents, do not give this with the bottle of milk.

Give it with orange juice.

I hear that a lot.

Yes, perfect.

Vitamin C helps with absorption.

So give it between meals when the stomach acid is high and a little citrus is a great idea.

Okay, what about the side effects?

I've heard horror stories about the diapers.

Oh, yeah, it turns the stool a torii, dark green or black color.

It looks just like a GI bleed.

You must warn the parents about this.

If you don't, they will call you in a complete panic thinking their child is dying.

Or conversely, if they come back for a checkup and say, oh, his poop looks totally normal, nice and brown.

Ding, ding, ding.

Then you know they aren't giving the medication.

It's a built -in compliance test.

It's actually a gift.

That's a good way to look at it.

One other practical tip from the text, teeth staining.

Liquid iron stains, teeth black.

It's not permanent, but it looks awful and it really freaks parents out.

So you teach them to use a syringe or a dropper and place the medication behind the teeth way back in the cheek pouch.

And then brush right after.

And brush immediately afterwards.

Yeah.

Okay,

let's shift gears to sickle cell anemia or SCA.

This is a beast of a topic.

It is.

This is not a nutritional fix.

This is genetic.

It's a hemoglobinopathy, which means normal hemoglobin, HGBA, is replaced by abnormal hemoglobin S or HGBS.

And it's autosomal recessive, meaning both parents have to be carriers to pass it on.

Correct.

Let's talk about the shape.

Why does the shape of the red blood cell matter so much?

Okay, so normal red blood cells are like little donuts.

They're round, they're squishy, they're flexible.

They can squeeze through the tiniest capillaries single file.

Right.

Sickle cells, when they're triggered, turn into these rigid crescent shapes, like a boomerang or a sickle blade.

What triggers that change?

What makes them sickle?

Stress.

Any kind of stress.

Low oxygen tension, dehydration, fever, acidosis.

When that happens, the hemoglobin polymerizes.

It forms these long, stiff rods inside the cell, forcing it into that shape.

And a rigid cell can't squeeze through a tiny capillary.

No, it gets stuck.

And then another one gets stuck behind it and another.

It's a traffic jam at the cellular level.

That is the vaso -occlusive crisis, the VOC.

The blood flow just stops.

And where blood flow stops, pain starts.

Ischemia.

The tissue is starving for oxygen, and the pain is excruciating.

Patients describe it as being hammered on the bones or having glass shards flowing through their veins.

This brings us to a critical nursing priority, pain management.

The text specifically highlights the next generation NCLEX focus on this.

There is a lot of provider bias here.

A huge amount of bias.

Because these kids have chronic pain, they learn to cope in ways that can be misleading.

A 10 -year -old in a full -blown sickle cell crisis might be quietly playing a video game or scrolling on their phone.

But their pain scale is an 8 out of 10.

Exactly.

They don't always grimace and scream like a child with a fresh broken arm.

And unfortunately, some nurses interpret that as drug seeking.

Which is dangerous and completely unethical.

The text is very clear.

Do not under -medicate.

We use opioids, morphine, Dilaudid, and we use them on a schedule.

PCA pumps are great.

Not PRN.

Never PRN.

If you're chasing the vein, you've already lost.

You have to stay ahead of it.

There's also a specific warning about Meparidine or Demerol.

Yeah, do not use it.

Demerol breaks down into a metabolite called Normaparidine, which is a CNS stimulant.

It can actually cause seizures.

Wow.

And children with sickle cell are already at a higher risk for strokes and other CNS issues.

You do not want to do anything that lowers that seizure threshold.

Okay, let's talk about the other types of crises.

Sequestration.

This one sounds terrifying because it happens so fast.

It is a true medical emergency.

The spleen is basically a filter for old blood cells.

In sequestration, the spleen stops filtering and starts acting like a sponge.

It just soaks up a massive amount of the circulating blood volume.

So the blood is still in the body, but it's trapped inside the spleen.

Correct.

Which means it's not in the heart or the brain or the lungs.

The child goes into hypovolemic shock.

You'll see a sudden, steep drop in blood pressure, tachycardia, and a huge hard palpable spleen in the abdomen.

And then there's acute chest syndrome or ACS.

This one often looks like pneumonia fever, chest pain, cough, shortness of breath.

But what's really happening is sickling in the lung vasculature.

It's the leading cause of death in patients with SCA.

A leading cause of death.

Yes.

So if a sickle cell patient comes in with any chest pain or a fever, you treat it very, very aggressively.

Okay, so the treatment pillars.

We know pain management is number one.

What about hydration and oxygen?

Hydration is the unsung hero.

Remember the viscosity, the thick blood?

We need to dilute it.

More fluid helps unstuck those log jams.

So we push fluids, either oral or IV.

And oxygen.

It seems like if the problem is sickle cells don't carry oxygen well, we should just blast them with O2.

That's a really common misconception.

Oxygen only helps if the patient is actually hypoxic.

If their O2 saturation is normal, adding more oxygen doesn't reverse the sickling that's already happened.

Oh, interesting.

And in fact,

prolonged unnecessary oxygen therapy can actually depress the bone marrow because the body sensors think, oh, we have plenty of oxygen.

I guess we can stop making new red blood cells.

So you treat the hypoxia, but you don't just use oxygen as a placebo.

Exactly.

One last comfort measure.

Heat, not cold.

Heat vasodilates.

It opens the vessels up.

Cold vasoconstricts, it clamps them down.

Never, ever put an ice pack on a sickle cell crisis.

You're just helping the blockage.

That's a fantastic point.

OK, moving to beta thalassemia, also called Cooley anemia.

How is this different from sickle cell?

It's a great contrast.

Think of it this way.

Sickle cell is a quality problem.

The factory is making the wrong kind of hemoglobin.

Thalassemia is a quantity problem.

The factory can't make enough hemoglobin.

Specifically, the beta chain of the hemoglobin molecule is either defective or completely missing.

So the red blood cells that do get made are weak and unstable.

Exactly.

And they die off really quickly.

The result is a profound, severe anemia.

But the body tries to compensate in a really dramatic way.

The bone marrow detects the anemia and it goes into overdrive.

It expands.

It physically expands.

Yes.

The marrow cavity inside the bones actually gets wired to house more blood producing tissue.

This changes the shape of the bones, particularly in the face.

You see something called frontal bossing, a really prominent forehead, and an enlarged maxilla.

The child develops these very distinctive facial features because their bones are working so incredibly hard.

So the management is transfusions, but that comes with its own price.

Transfusions keep them alive, absolutely.

But every single bag of blood is loaded with iron.

And the body has no natural way to get rid of excess iron.

So over time, that iron builds up in the liver, the heart, the spleen, it becomes toxic.

This is hemocytosis.

Iron overload, exactly.

So we have to treat the treatment.

We use telation therapy drugs like diffroxamine.

These drugs basically act like magnets that bind to the heavy metal, the iron, and allow the body to excrete it in the urine.

It feels like such a delicate balancing act, keeping the hemoglobin up without causing iron toxicity.

It is a constant balance.

The only potential cure is a hematopoietic stem cell transplant, or HSCT.

But you need a matched donor, which is usually a sibling, and not everyone has that.

Next up in the anemias, a plastic anemia.

And the name says it all.

Aplasia just means lack of formation.

The bone marrow factory just shuts down.

It goes on strike.

So it's not just the red cells this time?

No, it's everything.

It's pancetopenia.

You have anemia from low RBCs, leukopenia from low WBCs, and drombocytopenia from low platelets.

All three cell lines are depressed.

How do we diagnose this definitively?

You have to do a bone marrow aspiration.

In a healthy child, the marrow is this rich red color.

It's full of blood -forming cells.

In a plastic anemia, the marrow is yellow.

Yellow?

Why yellow?

It's fat.

The blood -producing cells have been replaced by fatty tissue.

The factory is essentially empty.

So what's the treatment?

How do you reboot the system?

Well,

we usually assume it's an immune attack, the body's own immune system attacking the marrow.

So we use immunosuppressive therapy, or IST.

The main drugs are ATG, antithemocyte, globulin, and cyclosporine.

There's a specific nursing note on ATG in the text?

There is.

It's a horse or rabbit -derived protein, so it can cause major allergic reactions.

You have to give it through a central line.

And you are watching that kid like a hawk for any sign of anaphylaxis.

It's a high alert medication.

OK, let's cross over to the bleeding disorders.

Defects in hemostasis, starting with hemophilia.

Royal disease, right.

Hemophilia A is a deficiency in a specific protein called factor VIII.

And it's X -linked recessive, so it almost exclusively affects boys.

When you're explaining this to a patient's family, how do you describe the clotting cascade?

I like to use the analogy of a row of dominoes falling.

You need every single domino to hit the next one in the chain to get to the end.

Factor VIII is one of those crucial dominoes in the middle.

If it's missing,

the chain reaction just stops.

You can form an initial platelet plug, but you can't seal it with a strong fibrin clot.

So they don't bleed faster, they bleed longer.

Exactly.

And they bleed into spaces they really shouldn't.

The hallmark of hemophilia is hemarthrosis bleeding into the joints, especially the knees, elbows, and ankles.

What does that look like when it's happening?

At first, the child might just feel a tingling or a stiffness.

Then the joint swells up, gets hot to the touch, and becomes incredibly painful as blood fills that joint capsule.

And blood is corrosive to cartilage, isn't it?

It's very destructive.

The iron in the blood destroys the joint lining over time.

So repeated bleeds into the same joint lead to chronic pain, arthritis, and frozen cripple joints.

That's why preventing bleeds is the absolute priority.

And management is replacing the missing domino.

Replacing the missing factor.

Factor VIII infusions.

Many kids now do this prophylactically, getting a dose every few days at home to keep their factor levels up so they can play and live a more normal life.

If an injury does happen, we use rice.

Yes, rest, ice, compression, and elevation.

And notice the key difference here.

For sickle cell, NO ice.

For hemophilia, yes, yes.

Ice constricts the blood vessels and helps stop the bleeding at the source.

That is a crucial distinction for any exam.

What about lifestyle?

Do we have to bubble wrap these boys?

We used to think so.

But now we actually want them to be active to strengthen the muscles around the joints, which helps protect them.

But you have to pick smart sports.

You pick smart sports.

Swimming, excellent.

Golf,

great.

American football or rugby, absolutely not.

Aspirin.

Never, not ever.

Aspirin inhibits platelet function.

These kids already have a factor problem.

If you knock out their platelets too, they have basically zero defense against bleeding.

Use acetaminophen, Tylenol for pain.

Okay, next up, ITP immune thrombocytopenia.

This one can be confusing because the kid usually looks totally fine.

It's such a classic presentation.

A toddler had a little viral cold two weeks ago.

They got over it.

Now suddenly they're just covered in bruises and patekky.

But they aren't acting sick at all.

Nope, they're running around the exam room, happy as can be.

But you get their labs back and their platelet count is terrifying.

Normal is 150 ,000 to 400 ,000.

These kids might be under 20 ,000.

So what's happening?

It's an autoimmune mix -up.

The immune system made antibodies to fight off that cold virus.

But now it's confused and those antibodies are mistakenly tagging platelets as the enemy.

The spleen sees the tag platelets and destroys them.

So what's the treatment?

Usually nothing.

It's a self -limiting disorder in most kids.

It just goes away on its own.

We just support them and keep them safe.

But that's only if the bleeding isn't severe.

Right, if the platelets are critically low or there's active bleeding, we might use IVIG or steroids to try and calm the immune system down.

But the keeping them safe part is the hard part for parents.

It really is.

You have a toddler who feels perfectly fine but is essentially a china doll.

If they hit their head, they could have an intracranial hemorrhage.

So it's no contact sports, no rough housing,

soft toothbrushes only, a lot of vigilance.

Briefly on DIC -disseminated intravascular coagulation.

This is the ultimate paradox disorder.

It's the worst of both worlds.

You are clotting and bleeding at the exact same time.

It's always a secondary response to something huge, like sepsis or major trauma.

How does that even work?

The body triggers this massive, widespread clotting cascade everywhere, which uses up all the available platelets and clotting factors.

Then, because there are no factors left, the patient starts to spontaneously bleed from every IV site, their gums, their nose.

It's a nightmare scenario.

It is.

The only way to stop it is to treat the underlying cause, the sepsis or the shock, to try and break the cycle.

Before we move to immunology, let's handle a very practical one.

Epistaxis.

Nose bleeds.

Everyone thinks they know how to stop a nose bleed, and almost everyone does it wrong.

This drives me crazy.

The number one rule.

Do not tilt the head back.

Why not?

That's what my gym teacher always said to do.

Because gravity works.

If you tilt your head back, the blood runs down your throat, down the nasopharynx, the child swallows it, it irritates the stomach, and then they vomit blood.

Plus, you can aspirate it into your lungs.

Okay, so what's the correct protocol?

Sit up straight, lean forward, let it drip out if it needs to, and pinch.

But don't pinch the bridge of the nose.

That bone bone doesn't bleed.

You pinch the soft fleshy part, the alae, firmly against the septum.

And for how long?

Ten continuous minutes.

By the clock.

No peeking after two minutes to see if it stopped.

Every time you peek, you break the clot that's trying to form.

Continuous pressure.

Lean forward.

Got it.

Last section.

Immunologic deficiency.

Specifically HIV and AIDS in kids.

The landscape here has just changed miraculously in the last few decades.

Perinatal transmission from mom to baby has dropped over 90 % because of antiretroviral therapy or art during pregnancy.

That's incredible.

But when we do have a baby born to an HIV positive mother, the testing is tricky.

The standard test doesn't work.

Right.

In adults, we use tests like the ELISA and Westerblat.

These tests are looking for HIV antibodies.

But a baby born to a positive mom has her antibodies.

They cross the placenta.

So the baby will test positive for the antibodies even if they aren't actually infected.

Yes, exactly.

Those maternal antibodies can stick around for up to 18 months.

So an antibody test is totally useless.

All it tells you is that the mom has HIV.

So how do we know for sure if the baby has the virus itself?

We have to look for the virus, not the antibody.

We use a test called HIV polymerase chain reaction PCR.

It detects the proviral DNA directly.

We test the infant at birth, again at one to two months, and again at four to six months to confirm their status.

That distinction antibody test versus PCR is a huge concept and management is aggressive.

Very.

We don't wait.

We treat with combination RT and we also use prophylaxis against opportunistic infections,

specifically pneumocystis pneumonia, which can be absolutely lethal in infants with a compromised immune system.

We have covered the factory, the transport trucks, the clotting crew, and the immune system.

It's a lot to take in.

It is.

But if you step back, I think the running theme through all of this is balance.

How so?

The blood needs to be thick enough to climb but thin enough to flow.

The immune system needs to be strong enough to attack enemies, but smart enough not to attack its own marrow or its own platelets.

Everything is a fine balance.

And the nurse is the guardian of that balance.

That's a great way to put it.

Whether it's calculating the precise hydration rate for a sickle cell crisis or teaching a terrified parent how to give iron without staining their child's teeth.

The nurse is that bridge between the complex pathology and the child's actual life.

And I want to leave our listeners with one final thought to mull over.

We talked a lot about the cells and the drugs and the pathways, but think about the invisible weight these kids carry.

Imagine being 12 years old with hemophilia or sickle cell.

You look normal to everyone at school, but you can't play soccer with your friends.

You live with this looming constant fear of pain or a catastrophic bleed.

It's a hidden disability.

They face so much isolation and anxiety that their peers just don't understand.

And as nurses, we aren't just treating the hemoglobin level.

We're helping a child navigate a world that feels fundamentally dangerous to them.

We have to treat that anxiety and the psychosocial impact just as aggressively as we treat the anemia.

That is the art of nursing.

Thank you for diving deep with us into Chapter 24.

Thanks for listening.

Stay curious.

This has been the Last Minute Lecture Team.

Signing off.