You're in the bay. Once you get over to the bed,
we'll give you the story. Everything's going
to happen super fast. Welcome to the emergency
room. You know usually when we talk about a medical
diagnosis there is this this underlying expectation
of precision. Right, like it's engineering or
something. Exactly. Like you break your arm,
you go to the ER, the x -ray shows that jagged
white line right across the radius, and the doctor
just points at the screen and says, well, there
it is, broken. Yeah, it's binary. I mean, it's
completely objective. There's really no debate
about what you're looking at. Broken or not broken,
it's clean. And you know, it's comforting in
a way. We like things to be visible. We like
our pathophysiology to be neatly categorized,
boxed up, and labeled. But then you step into
the world of obstetric nursing. Oh, boy, do you
ever. Right. And specifically, you step into
the way a pregnancy interacts with the human
body's endocrine system. And suddenly, that metaphorical
x -ray machine is just, well, it's completely
broken. We're looking at a diagnostic landscape
that is honestly incredibly murky. It really
is. Because, I mean, how do you spot the abnormal
when the normal baseline is absolute chaos? Well,
it's normal third trimester pregnancy fatigue.
versus, say, a dangerous, creeping thyroid crash,
or what's normal, expected morning sickness,
versus life -threatening dehydration that could
literally put a mother into cardiac arrest. It's
the absolute definition of diagnostic muddy waters,
and that is exactly why this specific physiological
intersection is so heavily tested on nursing
board exams, specifically the NCLEX. They love
this stuff. They really do. The exam raters know
that the line between a healthy pregnancy and
a metabolic disaster is razor thin. Well, welcome
everyone to this deep dive. Now, we have a very
specific mission today for you listening right
now. We know exactly why you're here. You are
an aspiring nurse staring down the barrel of
those exams. Exactly. You're facing your OB nursing
exams, your rigorous clinical rotations, and
ultimately you are preparing to conquer the NCLEX.
So today we are officially acting as your elite
OB nursing educators. We are your personal exam
coaches and your clinical mentors. That's right.
And as your mentors, we know exactly what you're
going through. I mean, you're completely inundated
with information. So much information. You've
got these massive thousand page textbooks. You
have endless PowerPoint slide decks. You've got
hundreds of normal and abnormal lab values just
staring back at you, blurring together. It is
beyond overwhelming. So we're going to change
the strategy. Instead of drowning you in a dry
textbook reading or just walking down a syllabus
like a table of contents, we are going to sift
through your specific source materials on complications
of pregnancy, specifically endocrine disorders.
And we are going to aggressively apply the Pareto
principle. The 80 -20 rule. Exactly. As an exam
coach, I can tell you that trying to memorize
every single sentence in your textbook is a recipe
for severe burnout. It's impossible. Right. We
are going to extract the 20 % of high -yield
facts. the recognizable clinical patterns, and
those critical safety concepts that are going
to give you 80 % of the value on your exams.
We're pulling forward the most testable, most
repeated, and most safety critical content. Okay,
let's unpack this because before we even get
into the specific conditions, I want to talk
about the baseline. Setting the stage for all
these disorders requires us to get over the first
major hurdle for nursing students, which is understanding
how pregnancy inherently alters the maternal
metabolism in the first place. I want to speak
directly to you, the future nurse listening to
this right now. Put down your highlighter for
a second. Just listen. Yeah, just listen. To
think like a safe, competent future nurse, you
have to move beyond just rote memorizing random
lab values. The NCLEX doesn't just want to know
if you can memorize a number. It wants to know
if you understand what that number means for
your patients sitting on the exam table. And
understand that. We have to look pregnancy for
what it really is. I mean, it isn't just a growing
belly. Biologically speaking, pregnancy is essentially
a nine month stress test on the mother's organs.
That is the perfect way to frame it. It's a state
of accelerated starvation and massive hormonal
upheaval. The entire physiological system is
hijacked and redesigned to funnel nutrients,
oxygen, and resources to a growing fetus. And
the endocrine system is driving all of it. Right.
The glands producing the hormones, that's the
chemical engine driving the entire process. And
when that engine misfires, or when the maternal
body just can't keep up with the stress test,
we see the severe complications we're about to
discuss. So let's start with the heaviest hitter
in your materials. This is undoubtedly one of
the most tested topics in all of maternal newborn
nursing. You'll absolutely see this on your exams.
We're talking about diabetes and pregnancy. Yes.
And when we talk about diabetes and pregnancy,
we have to establish the high -yield core right
out of the gate. You have to differentiate between
the types because the path of physiology dictates
your nursing care. Right. So let's start with
pregestational type 1 diabetes mellitus. So this
is an autoimmune disorder. The mother's pancreas
has been under attack by her own immune system,
leading to the complete destruction of the beta
cells. And just to clarify for everyone, the
beta cells are the specific cells in the pancreas
that manufacture and secrete insulin. So in type
1, insulin production is completely absent. Right.
That patient comes into the pregnancy already
requiring external injectable insulin just to
survive. And then we have pregestational type
2 diabetes. Which is entirely different at a
cellular level. It's driven by insulin resistance,
heavily influenced by genetics, diet, and lifestyle
factors. The mother's pancreas is still making
insulin, sometimes even more than normal, but
her body's cells are basically ignoring the signal.
Like the locks on the cellular doors are jammed.
Exactly. The locks are jammed so the insulin
cannot open them to let the glucose inside. And
then we have the third category, which is entirely
unique to the obstetric population, gestational
diabetes mellitus or GDM. This develops during
pregnancy, usually showing up in the second or
third trimester. And your sources note that this
affects five to nine percent of all pregnancies.
Think about that practically. If you were working
on a labor and delivery floor with 20 beds, statistically,
one or two of those patients has GDM at any given
time. That is a massive chunk of your future
patient population. It's huge. And to understand
GDM, we have to ask the fundamental question.
Why does pregnancy cause diabetes in a previously
healthy woman? To answer that, you have to understand
the hormonal shifts of the second and third trimesters.
The placenta is not just a sac. It's an incredibly
active, powerful endocrine organ, and it produces
a specific hormone called human placental lactogen,
or HPL. Ah, HPL. The biological villain of our
story. I saw HPL all over the source text. But
let's dig into the why. What exactly is HPL doing
at a cellular level? Well, from the mother's
perspective, it might seem like a villain, but
from the baby's perspective, HPL is the ultimate
hero. The entire evolutionary purpose of HPL,
along with a surge in other pregnancy hormones
like maternal cortisol and progesterone, is to
intentionally create a state of increased insulin
resistance in the mother. Okay, wait. Stop right
there. Why on earth would the mother's body intentionally
make her resistant to her own insulin? That sounds
like biological self -sabotage. I know, it sounds
like it, right? Until you look at the mechanics
of fetal feeding. insulin's job is to push glucose
out of the bloodstream and into the mother cells
for energy. But if the mother cells become resistant
to that insulin, they can't absorb the glucose.
So more and more glucose just stays floating
around in the maternal bloodstream. And where
does all that maternal blood eventually flow?
Straight to the placenta. Exactly. By making
the mother slightly insulin resistant, HPL ensures
there is a continuous, incredibly rich supply
of glucose readily available to cross the placental
barrier and feed the rapidly growing fetus. That
is wild. It's a brilliant evolutionary survival
mechanism. The baby is basically ensuring its
own food supply. The baby is essentially hijacking
the mom's... food delivery truck by blocking
her own cells from unloading the cargo. That
is a phenomenal analogy, yes. The baby locks
the mother's loading dock, so the truck has to
keep driving straight to the placenta. Wow. Now,
in a completely healthy normal pregnancy, the
mother's pancreas recognizes this resistance.
It senses that the blood sugar is staying high.
So it compensates. How does it do that? We see
a biological process called beta -cell hypertrophy.
The insulin -producing cells in the mother's
pancreas literally grow larger and work overtime
to pump out massive amounts of insulin to overcome
the HPL resistance. So her body just turns up
the volume on insulin production to match the
resistance. Precisely. But here's where the pathology
kicks in. In some clients, this compensatory
mechanism fails. They experience beta cell dysfunction.
The pancreas just gets overwhelmed. Exactly.
It simply cannot produce enough insulin to match
the massive overwhelming resistance caused by
the rising HPL. The maternal blood sugar spikes
and stays high. And that exact moment of failure
is when gestational diabetes develops. Let's
connect that back to the timeline because this
is a massive aha moment for test taking. If HPL
is the primary driver of this resistance and
the placenta doesn't get large enough to pump
out massive amounts of HPL until the later stages
of pregnancy, well... that completely explains
why gestational diabetes usually isn't diagnosed
in the first trimester. Exactly. The platenta
just isn't big enough yet to cause the problem.
You've absolutely nailed it. That is clinical
reasoning right there. If you understand the
mechanism of HPL, you naturally understand the
timeline of GDM. You do not even have to memorize
it. It just makes logical sense. Okay, so let's
talk about the clinical presentation. Who is
most likely to experience this pancreatic failure?
Nursing exams love risk factor questions and
we need to know who to watch closely. Definitely.
The sources list several key risk factors you
absolutely must have in your mental toolkit.
A maternal BMI greater than 25 or greater than
30 for specific demographic populations and polycystic
ovary syndrome or PCOS. Let's pause on PCOS because
I want you to understand the why. Why does a
syndrome involving ovarian cysts lead to diabetes
in pregnancy? Right. What's the connection? It's
because PCOS is fundamentally an endocrine and
metabolic disorder characterized by profound
baseline insulin resistance. Women with PCOS
are already starting the pregnancy with insulin
resistance. Oh, I see. Yeah. So when you add
HPL on top of that, their pancreas fails much
faster. That's a great connection to make. Other
risk factor include a prior history of GDM in
a previous pregnancy, a strong family history
of type 2 diabetes, or a previous A1c sitting
in that pre -diabetic range of 5 .7 to 6 .4 percent.
And here is a highly tested one, a previous large
for gestational age infant. or LGA. The cutoff
they give in the literature is an infant weighing
over 4 .08 kilograms, which translates to about
nine pounds. OK, so if a patient tells you, oh,
yeah, my last baby was 10 pounds, your internal
alarm bells should be ringing for gestational
diabetes. Oh, absolutely. Now, let's talk about
why it matters clinically. As your exam coach,
I can tell you that diabetes and pregnancy is
a goldmine for NCLEX writers because it fundamentally
impacts both maternal safety and fetal safety.
It hits every priority nursing area. airway,
breathing, circulation, and fetal distress. Let's
look at the maternal impacts first. The sources
highlight an increased risk for preeclampsia,
which is a severe, life -threatening blood pressure
crisis. And there's a risk for polyhydramnios.
Let's explain that one. Poly meaning many or
much, and hydramnios referring to the amniotic
fluid. Why does diabetes cause excessive amniotic
fluid? Think about the mechanism of high blood
sugar. What happens to a diabetic adult when
their blood sugar is 300? They experience polyuria.
They urinate constantly because the kidneys are
trying to flush out the excess glucose. The exact
same thing happens to the fetus. The fetus is
swallowing amniotic fluid, processing the sugar
-rich blood from the mother, experiencing fetal
hyperglycemia, and therefore, fetal polyuria.
Oh, wow. Yeah, the baby is peeing excessively
into the amniotic sac. That excess fetal urine
is what causes the polyhydrominoes. That is wild.
The excess fluid is literally the baby's sugary
urine. That is a vivid, unforgettable way to
understand that complication. It sticks with
you. It really does. The sources also mention
an increased risk for maternal urogenital infections.
And again, the mechanism makes sense. Sugar in
the urine is basically an all -you -can -eat
buffet for yeast and bacteria. Exactly. And we
cannot ignore the long -term post -pregnancy
implications. A client who develops GDM has a
60 % recurrence risk in future pregnancies. That's
high. And even more terrifying, they have a massive
risk of developing overt permanent type 2 diabetes
mellitus within 5 to 10 years postpartum. We
are talking about a permanent life altering chronic
illness stemming from this pregnancy. I want
to slow down here for a second because the psychosocial
impact is explicitly pointed out in your materials
and it's something nurses deal with every single
day at the bedside. Imagine being a pregnant
mother. You're already exhausted and suddenly
you're handed this diagnosis, the anxiety of
potentially harming your baby, the depression.
the profound feelings of guilt or shame, feeling
like you caused this by eating the wrong things,
even though we know it's driven by HPL. It's
so unfair. Plus the sheer financial and temporal
strain. You suddenly have extra maternal fetal
medicine appointments, endless daily finger pricks,
dietary restrictions, and antenatal testing.
It's an incredibly heavy burden. It's a phenomenal
point. Empathy is a core nursing competency.
You are not just treating a blood glucose level,
you're treating a terrified mother. Your patient
education needs to be delivered with immense
compassion, reassuring her that the placenta's
hormones are driving this, not her occasional
craving for ice cream. So true. OK, let's pivot
to the fetal and newborn impacts, because this
is where the really critical high -stakes exam
questions live. First, congenital malformations.
The literature is specific here. This is primarily
a risk with early pregestational diabetes, specifically
type 1 or type 2, that is poorly controlled during
the very first trimester. Right. And you must
understand the timeline of fetal development
to know why. The first trimester is the period
of organogenesis. This is when the neural tube
is closing, the heart chambers are forming, and
the spine is developing. High levels of maternal
circulating glucose are teratogenic. The oxidative
stress from hyperglycemia literally disrupts
the cellular formation of the heart and the neural
tube. If the sugar is out of control in week
six, the baby's heart might not form properly.
But with gestational diabetes, which develops
later in the second or third trimester, the organs
are already fully formed. So what's the danger
there? The danger shifts entirely from organ
formation to fetal growth and birth trauma. Here
is the absolute golden rule you must memorize.
Maternal glucose crosses the placenta. Maternal
insulin does not cross the placenta. Let me repeat
that because it's so crucial. Sugar crosses.
Insulin does not. Exactly. So the fetus is being
continuously bathed in a high sugar environment.
The fetal pancreas recognizes this massive sugar
load and responds by pumping out huge amounts
of its own fetal insulin to manage it. Makes
sense. And here is the kicker. Insulin is a remarkably
powerful anabolic growth hormone. It builds tissue.
So a fetus producing massive amounts of insulin
is going to grow excessively large. This leads
to macrosomia. And a large, macrosomic baby leads
to a cascade of delivery complications. Preterm
birth. Birth trauma. and the absolute dread of
every labor and delivery nurse shoulder dystocia.
A true nightmare. This is when the baby's head
is delivered, but the baby is so disproportionately
large in the torso that the shoulders get physically
wedged behind the mother's pubic bone. The baby
is stuck. The umbilical cord is compressed. It
is a catastrophic obstetrical emergency where
you have mere minutes to dislodge the baby before
a permanent hypoxic brain injury occurs. Yes.
The text also mentions organomegaly, meaning
the baby's internal organs, particularly the
liver and heart, are physically enlarged due
to that insulin growth factor. But let's talk
about the absolute most critical, highest yield
newborn complication you will see on your exams.
The number one priority assessment for a baby
born to a diabetic mother. Postnatal hypoglycemia.
Yes. And I want to break down the cellular mechanism
here, because it feels incredibly counterintuitive
to students. The baby was just swimming in sugar
for nine months. They are huge. They are macrosomic.
Why on earth are they born with dangerously low
blood sugar? Right. Let's paint the clinical
picture. Imagine the moment of birth. For nine
months, that fetus has been receiving a massive,
continuous, flavy infusion of maternal glucose
through the umbilical cord. To handle that firehose
of sugar, the fetal pancreas has hypertrophy.
It's huge and it's churning out massive industrial
amounts of insulin. Then the baby is delivered.
The obstetrician clamps and cuts the umbilical
cord. In that exact fraction of a second, the
maternal glucose supply is completely and totally
cut off. But the baby's pancreas doesn't know
the cord was cut. That is exactly the mechanism.
It takes hours or even days for the newborn's
hypertrophied pancreas to realize the sugar supply
is gone and to down -regulate its insulin production.
So for those first few critical hours of life,
the newborn has astronomically high levels of
circulating insulin with absolutely zero maternal
glucose coming in to balance it out. So all that
excess insulin acts like millions of little Pac
-Men violently shoving whatever tiny amount of
glucose the baby has left into the cells, stripping
the bloodstream bare. Their blood sugars absolutely
plummet. And glucose is the only fuel the brain
can use. If left untreated, severe neonatal hypoglycemia
will cause seizures, coma, and permanent irreversible
brain damage. So critical. This is why, as a
newborn nursery nurse, your absolute top priority
for a macrosomic baby is checking that heel stick
blood glue case within the first hour of life
and watching for signs of hypoglycemia. Things
like jitteriness, lethargy, poor feeding, a high
-pitched wheat cry, or apnea. That is such a
clear way to visualize it. Cut the cord, cut
the sugar, but the insulin keeps pumping. Okay,
let's look at expected versus concerning findings
for the mother. How do we separate a normal pregnancy
from a diabetic one? Expected findings are your
standard, annoying pregnancy symptoms. But you
also need to have the expected lab values memorized.
For a pregnant client, a normal fasting blood
glucose is less than 95 milligrams per deciliter.
A one -hour postprandial, meaning exactly one
hour after finishing a meal, should be less than
140. A two -hour postprandial should be less
than 120. And the hemoglobin A1c should be less
than 6%. So what are the concerning cues? The
text points out that classic diabetes symptoms
might actually be entirely missed by the provider
because they perfectly mimic normal pregnancy.
Polyphagia, polydipsia, polyuria being excessively
hungry, thirsty, and peeing all the time. Slow
wound healing, dry skin, and visual disturbances.
I mean, what pregnant woman isn't hungry and
peeing all the time? Exactly. Relying on subjective
symptoms is dangerous. The clinical pearl here,
the thing you must look for in a clinical scenario,
is objective data. A massive concerning finding
is a positive discordance in fundal height. Let's
explain fundal height. This is when the nurse
uses a tape measure to measure from the mother's
pubic bone to the top of her uterus, the fundus.
After 20 weeks, the measurement in centimeters
should roughly equal the week's gestation. Right.
So if she's 28 weeks pregnant, she should measure
about 28 centimeters. But if she's 28 weeks pregnant
and measuring 34 centimeters, you have a positive
discordance. She's measuring significantly larger
than her gestational age dictates. You must immediately
suspect macrosomia and polyhydrominoes, and what
causes those? Gestational diabetes. Let's move
into priority nursing actions. If you are the
clinic nurse, what are you doing? Step one is
screening. The tech says we do a glucose tolerance
test, or GTT, prior to 24 weeks for at -risk
clients, like those with PCOS or a BMI over 30.
But the standard universal screening for every
single pregnant woman occurs between 24 and 28
weeks, and that is the one hour GTT. And you
must know the parameters of the one hour GTT
for your exams. This is a screening tool, not
a diagnostic tool. It requires absolutely no
fasting. The client comes in, drinks a highly
concentrated 50 gram sugary glucola drink, and
their blood is drawn exactly one hour later.
And the magic number here is a 140. If the result
is greater than 140 milligrams per deciliter,
the nurse must flag it. That is the threshold.
greater than 140 triggers the next step, which
is preparing the client for the definitive diagnostic
three -hour screening. I love the analogy you
used earlier. The one -hour test is just the
bouncer at the club. It just flags people who
look suspicious. The three -hour GTT is the actual
interrogator. How does the three -hour test work?
For the three -hour GPP, the rules change entirely.
The client absolutely must fast overnight. They
come into the clinic in the morning and get a
baseline fasting blood draw. Then they drink
an even heavier 100 gram glucose load. Then they
have to sit in the waiting room and their blood
is drawn at exactly one hour, two hours, and
three hours post ingestion. And to confirm a
clinical diagnosis of gestational two or more
of those four values must be out of range. Let
me list those ranges for our listeners to visualize
and memorize. Fasting greater than 95, one hour
greater than 180, two hour greater than 155,
three hour greater than 140. If two of those
hit they have official GDM. So once the doctor
makes that diagnosis, what is the nursing treatment
cascade? Treatment step one is always, always
non -pharmacological first, assuming the numbers
aren't wildly out of control. We start with nutritional
counseling and moderate exercise. The dietary
breakdown the text provides is very specific
and highly testable. 30 to 35 kilocalories per
kilogram of body weight spread evenly throughout
the day in three meals and two to three snacks
to prevent spikes and crashes. The macronutrient
split is also specific. 40 percent carbohydrates,
20 percent protein and 40 plus a massive focus
on complex, high -fiber carbohydrates, because
fiber physically slows down the digestion and
absorption of glucose in the gut, preventing
those sharp blood sugar spikes. But if diet and
exercise aren't enough to keep the fasting glucose
under 95, we move to treatment step two, which
is pharmacological intervention. And this is
where we have to look closely at the different
types of diabetes. For type two, they either
continue their pre -pregnancy regimen, switch
to an oral medication like Glebaride or Metformin,
or start insulin. The target blood glucose is
exceptionally tight, between 3 .0 and 7 .0 millimoles
per liter, or 55 to 126 milligrams per deciliter.
And here's where we hit one of the absolute biggest,
most devious exam traps regarding type 1 diabetes.
I want everyone listening to pause and focus
on this because it shows up on the NCLEX all
the time. Oh yeah, a client with pregestational
type 1 diabetes will actually need a decreased
dose insulin during the first trimester and then
they will need a massively increased dose in
the second and third trimesters. Okay, I have
to stop and play the role of the confused nursing
student here because that feels like a trick
question. Why on earth Would a type 1 diabetic
need less insulin in the first trimester? They
are pregnant, they are growing a human being,
their metabolic rate is increasing. Shouldn't
they need more of everything? It absolutely feels
like a trick, which is exactly why it is a classic
NCLEX trap. The test writers want to see if you
understand the physiology or if you are just
guessing. Think about what actually happens in
the first trimester of pregnancy. Number one,
the rapidly developing fetus is vigorously utilizing
maternal glucose for its initial cellular development,
naturally siphoning sugar out of the mother's
blood. OK, so the baby is acting like a little
glucose vacuum. Exactly. Number two, what is
the hallmark universal symptom of the first trimester?
Nausea and vomiting. Severe morning sickness.
Right. The mother is frequently nauseous. She's
eating significantly less. She has food aversions
and she's often vomiting up what little she does
manage to eat. So her overall intake of carbohydrates
drops off a cliff. Oh, I see it now. If she continues
injecting her normal pre -pregnancy dose of insulin
while simultaneously eating way fewer carbs,
Andee having the fetus vacuum up the glucose
in her blood, she's going to crash. Precisely.
She is at a massive critical risk for severe
maternal hypoglycemia. Her blood sugar will absolutely
tank. So to keep her safe, the provider must
decrease her exogenous insulin requirement early
on. That is brilliant clinical reasoning. It
isn't just a fact to memorize. It is a mechanism.
And then once she hits the second trimester,
the nausea fades, she starts eating again, and
more importantly, the placenta gets huge and
starts pumping out massive amounts of HPL. Yep.
The insulin resistance skyrockets and suddenly
her insulin needs shoot way, way up. You have
to understand the timeline of the symptoms and
the hormones to get the medication titration
right. That is how you pass the NCLE -X. Absolutely.
Moving on to intrapartum, which means during
labor and postpartum care. The text notes we
should consider inducing labor before week 40.
Often providers will induce around 39 weeks if
the client is on insulin, or even earlier if
there is suspected fetal macrosomia to prevent
that shoulder dystocia we talked about. During
labor, they need continuous CTG cardiotocography
monitoring. Why? Because the placenta of a diabetic
mother degrades faster, putting the fetus at
high risk for distress during the contractions
and postpartum. The absolute priority postpartum
is exactly what we discussed earlier, monitoring
neonatal glucose levels with heel sticks to catch
that hypoglycemic crash. We also vigorously encourage
early and frequent breastfeeding. Colostrum,
the early breast milk, provides the baby with
an immediate, easily digestible source of glucose
to stabilize their blood sugar. And for the mother,
her placenta is gone, so the HPO is gone. Her
insulin resistance should drop immediately. Yes,
her insulin needs plummet the moment the placenta
is delivered. But you must test her fasting glucose
and HKONC at her six -week postpartum visit to
see if the GDM truly resolved or if the pancreatic
damage was permanent and she is transitioning
into overt type 2 diabetes. Okay, let's lock
this entire section in with some memory anchors.
When you're sitting in your exam and a question
about dietary rules pops up, I want you to visualize
the 424 rule. 40 % carbs, 20 % protein, 40 %
fat. 424. And for the one -hour screening cutoff,
memorize the symbol phrase. 140 is the one -hour
limit to know. If that one -hour Grucula test
comes back over 140, you are picking up the phone,
calling the provider, and setting up the three
-hour diagnostic test. Let's summarize the gestational
diabetes section. We promised you the 80 -20
rule. If you only remember five things from this
massive topic for your exams, make it these five.
Number one, human placental lactogen, or HPL,
is the placental hormone that intentionally causes
insulin resistance in the second and third trimesters
to feed the baby. Number two, a one -hour GTT
greater than 140 milligrams per deciliter demands
a three -hour GTT follow -up. The one hour is
the screen, the three hour is the diagnosis.
Number three, Type 1 diabetics require a decrease
in their insulin dose during the first trimester
due to nausea and fetal glucose use to prevent
severe hypoglycemia. Number four, fetal macrosomia
and devastating neonatal hypoglycemia are the
highest risk complications that you must monitor
for. And number five, your immediate postpartum
priority is monitoring the newborn's heel stick
glucose. And your maternal priority is reevaluating
her glucose at six weeks postpartum. That is
high yield exam passing gold right there. Okay,
we are going to smoothly transition away from
the pancreas. We just talked about how HPL alters
maternal metabolism, and we briefly touched on
how first trimester nausea can affect blood sugar.
Now, we're going to look at that early pregnancy
nausea, but we're going to look at what happens
when it crosses the line from annoying morning
sickness into an acutely dangerous, life -threatening
metabolic crisis. Let's dive into topic number
two, hyperemesis gravidarum, or HG. Let me be
very clear. Hyperemesis gravidarum is a severe
pathological condition. It affects up to 3 %
of all pregnancies and frequently requires acute
hospitalization. It is vital that you, as a clinician,
do not dismiss this as just bad morning sickness.
Morning sickness is physiological. HG is pathological.
Let's hit the path of physiology. What exactly
causes a woman's nausea to become so extreme
that she cannot keep down a sip of water for
weeks? The sources point to massive abnormal
elevations in HCG human chorionic gonadotropin.
This is the hormone that turns a pregnancy test
positive. Yes, HCG is a primary driver of the
nausea center in the brain and the text specifically
links these massive HCG spikes to two phenomena.
Multiple gestations like twins or triplets where
you simply have more placental tissue pumping
out the hormone and more dangerously Let's take
a quick detour and explain what a molar pregnancy
is because that shows up on exams all the time
as a distractor or a related concept. A hydatidiform
mole, or molar pregnancy, is basically a genetic
error during fertilization. Instead of growing
a viable embryo, the tissue that was supposed
to become the placenta grows into an abnormal,
non -cancerous tumor inside the uterus. And if
you look at it on an ultrasound, it looks like
a cluster of grapes. Because it's placental -type
tissue growing out of control, it secretes astronomical,
dangerously high levels of HCG, far higher than
a normal pregnancy. So if a patient has a molar
pregnancy, their nausea is going to be incredibly
violent. The sources also mention an increase
in estradiol, genetic predispositions, and surprisingly,
infections with Helicobacter pylori or H. pylori.
Now, I have to ask for the mechanism here. H.
pylori is the bacteria famous for causing stomach
ulcers. Why on earth would a stomach bug cause
extreme pregnancy vomiting? It's a fascinating
physiological intersection. H. pylori alters
the gastric pH and causes baseline inflammation
of the stomach lining. When you take a stomach
that is already inflamed and infected by H. pylori,
and then you dump massive amounts of pregnancy
hormones like estrogen and HCG on top of it,
the stomach becomes hypersensitized. Oh, that
makes sense. Furthermore, there is a theory of
cross -reactivity, where the immune response
to the H. pylori infection inadvertently amplifies
the hormonal nausea triggers in the brain. If
a patient has severe intractable HG, testing
them for an underlying H. pylori infection is
a critical diagnostic step. That is why. The
risk factors to watch for are null -apparice
clients, meaning this is their first pregnancy,
so their body has never been exposed to these
hormone levels before, and clients with a previous
history of HG in a prior pregnancy. But let's
talk about why it matters clinically and why
we need to slow down and really look at the psychosocial
impact here. HG leads to severe clinical dehydration
and profound electrolyte imbalances, which we'll
discuss. But the psychosocial trauma is staggering.
Imagine this clinical vignette. You have a 24
-year -old patient who's been vomiting 15 to
20 times a day for six straight weeks. She cannot
work. She cannot care for her other children.
She literally cannot leave the bathroom floor.
The smell of her partner's soap makes her violently
ill. She's experiencing profound social isolation.
And on top of that, she goes to the ER and a
provider who doesn't understand HG tells her,
well, if pregnancy is tough, try some ginger
ale and saltines. The medical gaslighting is
immense. Horrible. These women experience deep
depression, suicidal ideation, and even legitimate
post -traumatic stress disorder from the sheer
trauma of relentless, uncontrollable vomiting.
and starvation. As a nurse, validating their
suffering, telling them, I believe you, this
is not normal, and we are going to fix this,
is just as important as the IV fluids you're
about to hang. That is so true. Empathy is a
vital sign. So as a nurse, how do we separate
the expected versus concerning? Your textbooks
give us expected normal lab values that you need
to have memorized. Potassium should be 3 .5 to
5 mGqL, sodium 136 to 145 mGdL, calcium 9 to
10 .5 mGdL. Leukof 74 to 106mgdL. Those are expected
in a healthy pregnancy. The concerning priority
findings are persistent nausea and vomiting coupled
with objective signs of clinical dehydration.
You are assessing the patient for dry mucus membranes.
Look at her mouth, lips, and eyes. Look for skin
tinting. Ask about dizziness upon standing, which
indicates orthostatic hypotension from low blood
volume. You also need to assess her urine output.
dark concentrated or strong smelling urine or
very infrequent urination means the kidneys are
panicking. They're holding on to whatever tiny
amount of fluid is left in the body to maintain
blood pressure. You'll also see a rapid heart
rate tachycardia. The heart is trying to pump
a significantly lower volume of dehydrated blood
around the body, so it has to beat faster to
maintain perfusion. And a very late, incredibly
dangerous sign is confusion or lethargy. That
indicates severe electrolyte derangement or cerebral
dehydration. This brings us to the priority nursing
actions. And there is a very specific objective
assessment tool mentioned in the text that you
need to know. The PUQE. score. PUQE, the Pregnancy
Unique Quantification of Emesis score. Right.
To use the PQE score, the nurse assesses three
specific things over the past 12 -hour window.
The duration of nausea and hours, the absolute
number of actual vomiting episodes, and the number
of dry -heaver retching episodes. Okay, let me
provide an analogy here. In neurology, we use
the Glasgow Coma Scale to assess consciousness.
We don't just say, he looks pretty out of it.
We assign numbers to eye -opening and motor response
to get an objective score. The PUQE score is
essentially the Glasgow Coma Scale for throwing
up. That is a brilliant comparison. And it's
so important because, as we mentioned with the
medical gas lighting, relying on a 1 to 10 pain
scale for nausea is highly subjective. A patient
might say her nausea is a 10, and a dismissive
provider might think she's exaggerating. But
the PUQE score removes the subjectivity. It forces
the clinician to quantify the danger. If you,
the nurse, document that the patient has vomited
eight times in 12 hours, dry heaved six times,
and experienced continuous nausea for 10 hours.
That generates a severe PUQE score. It mandates
medical intervention. It empowers the nurse to
advocate with hard, objective data. Doctor, her
PUQE score is severe. She is hypovolemic. We
need admission orders. Exactly. It protects the
patient. So what orders are we anticipating?
You need to draw labs immediately. A CBC to look
for hemoconcentration because her blood is literally
thicker due to fluid loss. A comprehensive metabolic
panel to look at those electrolytes, specifically
potassium and sodium. and an H. pylori screening.
Let's talk about potassium, because this is a
massive NCLEX safety priority. When you vomit,
you are losing massive amounts of gastric acid,
which is rich in potassium. Right. And hypokalemia
low potassium is deadly. Potassium is the electrolyte
responsible for the repolarization of the cardiac
muscle cells. Without sufficient potassium, the
electrical action potential of the heart becomes
unstable. Severe hypokalemia from HG can cause
fatal cardiac arrhythmias. Wait, really? from
throwing up. Yes. This patient could literally
go into cardiac arrest from throwing up. That
is why checking the potassium level is an absolute
priority. Wow. OK. So for treatments, we're immediately
starting IV fluids, usually lactated ringers
or normal saline, to correct the dehydration.
In severe refractory cases where the patient
cannot tolerate anything by mouth for weeks,
they might need TPN total parenteral nutrition.
This is IV nutrition delivered through a central
line directly into the bloodstream, bypassing
the paralyzed inflamed gut entirely. Pharmacologically,
we are giving potent antimetics like undansetron
or promethazine, antihistamines which act on
the vestibular system, and high dose vitamin
B6, which has been shown to reduce pregnancy
nausea. And do not neglect the non -pharmacological
nursing care. Help the client identify and avoid
sensory triggers. Use ginger supplements, which
actually have robust clinical evidence for reducing
mild to moderate nausea. Try acupressure wristbands.
And crucially, provide that psychological support.
Now let's talk about the top exam traps for HG.
I'm going to give you a mock NCLE -X question
scenario right now. A client at eight weeks gestation
presents to the emergency department with severe
unremitting nausea, vomiting 10 times a day,
and a weight loss of eight pounds. Which of the
following provider orders should the nurse anticipate?
Option A, instruct the client to eat dry saltine
crackers before getting out of bed. Option B,
administer a one hour glucose tolerance test.
Option C, prepare the client for a pelvic ultrasound.
or option D, administer oral potassium supplements.
Oh, that's a tricky one. Let's break it down
using the distractor answer strategy. Option
A, the salting crackers. That's the ultimate
distractor. That's the treatment for normal morning
sickness. This patient has lost eight pounds
and is vomiting 10 times a day. She is way past
crackers. Option B, the GTT, is for diabetes
at 24 weeks. Completely irrelevant here. Option
D oral potassium while she's following 10 times
a day if you give her an oral pill She's gonna
throw it right back up exactly which leaves option
C Prepare the client for a pelvic ultrasound.
Why? Because you must identify the underlying
cause of the abnormally high HCG causing the
hyperemesis. You are anticipating an ultrasound
to check for twins or more dangerously, that
high -date form mole we discussed. High gag means
high HCG. You have to look inside the uterus
to see what is producing it. That's fantastic
logic. Let's get some memory anchors for this
section. For the PUQE score criteria, remember
the acronym, VHD vomiting, heaving. VHHD over
a 12 -hour window. And as the expert just said,
the ultimate hook to remember the etiology is
high HDG equals high GAG. Look for the mole.
Look for the twins. All right. Let's solidify
the five most important things to remember about
hyperremesis gravidarum for your exams. Number
one, HG is pathological, not physiological, morning
sickness. It is severe, persistent, nausea and
vomiting, leading to clinical dehydration, starvation,
and dangerous electrolyte shifts. Number two,
elevated HCG, frequently from multiple gestations
or a molar pregnancy, is a primary culprit you
must investigate via ultrasound. Number three,
you must monitor the metabolic panel and know
the normal versus abnormal ranges for potassium.
Remember, low potassium causes lethal cardiac
arrhythmias. Number four, the PUQE score standardizes
the assessment of HG severity by objectively
measuring vomiting, heaving, and nausea duration
over a 12 -hour window. And number five, priority
treatment is fluid and electrolyte replacement
via IV, potent antibiotics, and in the worst
cases, TPN to bypass the gut. Excellent. We're
moving methodically through these endocrine disasters,
and you are building a massive foundation of
clinical judgment. We're going to pivot one last
time, and we're going to use a concept we just
learned to build a bridge to our final topic.
We just talked extensively about how ECG levels
spike in early pregnancy, causing nausea. Well,
it turns out, at a molecular level, ECG has another
trick up its sleeve. It does, and it's a fascinating
quirk of human biology. At a molecular structural
level, the HCG hormone looks very, very similar
to TSH thyroid stimulating hormone. They share
a nearly identical alpha subunit. OK, so they
look like identical twins to the body's receptors.
Exactly. So as HCG levels rise rapidly in early
pregnancy to support the fetus, the mother's
thyroid gland gets confused. The HCG binds to
the thyroid's receptors, pretending to be TSH,
and tricks the thyroid into thinking it's being
ordered to work. work harder. This leads to an
increase in T4 hormone secretion and a temporary
physiological enlargement of the thyroid gland.
This physiological quark provides the perfect
organic transition to explore the metabolic engines
of pregnancy. Topic number three, thyroid disorders.
Let's start with the high yield core for hypothyroidism.
an underactive thyroid. The text says overt hypothyroidism
affects about three to five percent of pregnancies.
We already know there's a massive increased demand
on the thyroid after implantation because the
metabolic rate of the mother increases. But there
is a second highly testable factor here, estrogen.
Estrogen is surging during pregnancy. What does
it do to the thyroid? High levels of pregnancy
estrogen trigger the liver to increase the production
of something called thyroid binding globulin
or TBG. Now binding is the key word here. When
thyroid hormones, T3 and T4, are bound to these
proteins in the bloodstream, they're inactive,
they're handcuffed. They cannot enter the body's
cells to do their metabolic job. Oh, wow. So
because estrogen creates a massive army of these
binding proteins, the thyroid has to work twice
as hard to produce significantly more hormone
just to ensure enough of it remains free and
active in the blood to keep the metabolism running.
Precisely. A healthy thyroid just revs up, hypertrophies
slightly, and handles the extra workload. But
a marginal thyroid or a thyroid that's under
autoimmune attack simply fails under the stress
of needing to produce so much extra hormone.
The primary causes of hypothyroidism listed in
your sources are Hashimoto's disease, which is
an autoimmune condition where antibodies destroy
the thyroid gland, congenital issues, or an iodine
deficiency. Let's explain the iodine piece because
it helps you remember the pathology. Why does
a lack of iodine in the diet cause the thyroid
to fail? If you look at the molecular structure
of thyroid hormone, it is literally built out
of iodine atoms. T3 has three iodine atoms. T4
has four. Right. If a pregnant mother does not
have enough dietary iodine, her thyroid physically
lacks the building blocks to manufacture the
hormone, no matter how hard the brain yells at
it to work. That's a great mechanistic explanation.
Now let's briefly look at hyperthyroidism. an
overactive thyroid. This is much rarer in pregnancies,
almost entirely driven by Graves' disease. In
Graves' disease, the body produces a rogue mutant
antibody called thyroid stimulating immunoglobulin.
or TSI. And just like HCG mimics TSH, this rogue
TSI antibody also mimics TSH. It locks onto the
thyroid gland and permanently turns the switch
to the on -end position, forcing the thyroid
to churn out massive toxic amounts of T4 hormone.
So on a lab report, you will see a dangerously
elevated T4 level, but interestingly, you will
see a nearly undetectable TSH level. Why is the
TSH near zero if the thyroid is overactive? because
of the negative feedback loop. The brain senses
that there is way too much T4 flooding the body,
so the pituitary gland panics and completely
shuts off its own production of TSH, desperately
trying to tell the thyroid to stop. But the thyroid
isn't listening to the brain, it's listening
to the rogue TSI antibodies. That is a classic
NCLEX lab interpretation question right there.
High T4 plus low TSH equals hyperthyroidism.
But let's step back and ask why this matters
so much in the context of pregnancy. Beyond the
mom feeling tired or jittery, why are we so worried?
Let me be very direct here as your clinical mentor.
Unmanaged thyroid issues are absolutely catastrophic
for fetal development. The fetal thyroid gland
does not begin functioning on its own until around
10 to 12 weeks of gestation. So for the entire
first trimester, the baby has no working thyroid
of its own? None. Before week 12, the fetus is
100 % reliant on the maternal thyroid hormone
crossing the placenta to survive. And what exactly
does the fetus use that maternal thyroid hormone
for? Neurological development, brain growth,
the architectural wiring of the fetal central
nervous system is entirely dependent on T4. Severe
untreated maternal hypothyroidism in the first
trimester severely and irreversibly impacts the
cognitive development of the fetus, leading to
profound intellectual disabilities. That is terrifying.
It is. It also massively increases the risk of
early pregnancy loss, preeclampsia, placental
abruption, where the placenta violently tears
away from the uterine wall postpartum hemorrhage,
and preterm labor. The mother's thyroid is literally
building the baby's brain. What about the risks
of hyperthyroidism? Hyperthyroidism carries its
own severe risks, notably maternal heart failure.
The hypermetabolic state forces the heart to
beat so fast and so hard that it eventually fails.
There's also the risk of thyroid storm, which
is a life -threatening acute hypermetabolic crisis
involving fever, extreme tachycardia, and altered
mental status. For the fetus, the massive influx
of maternal TSI antibodies can actually cross
the placenta and cause fetal hyperthyroidism,
leading to fetal tachycardia, poor growth, and
fetal goiter. This is why your sources emphasize
the absolute need for serial ultrasound. on growth
indicators for hyperthyroid clients. OK, let's
talk expected versus concerning presentations.
The expected lab values provided in your source
are critical to memorize for your exams. The
normal reference range for TSH is 0 .35 to 4
.9 MIUL. The normal reference range for T4 is
0 .6 to 1 .8 MZDL. Now, the text mentions subclinical
cases where the labs might be slightly off, but
the patient feels fine. We are worried about
overt cases. Let's do another clinical vignette.
A 32 -year -old pregnant client at 28 weeks comes
into the clinic. She complains of profound fatigue.
She has severe constipation. She has gained 15
pounds in the last month. She feels cold all
the time. And she has peripheral edema swollen
ankles. OK, stop right there. I have to push
back as a student again. Fatigue. weight gain,
constipation, swollen ankles. Isn't that literally
just a normal Tuesday for a woman in her third
trimester of pregnancy? How in the world is a
triage nurse supposed to look at a pregnant woman
who says, I'm tired, my feet are swollen, and
I can't poop and think, oh yeah, she has Hashimoto's
disease. You have just identified the ultimate
most devious NCLEX trap for thyroid disorders
in pregnancy. You are exactly right. The symptoms
of overt hypothyroidism perfectly seamlessly
mimic a normal, albeit uncomfortable, pregnancy.
This is why it is so easily missed by providers.
So how do we catch it? What's the golden ticket?
The key clinical differentiator, the objective
data point you must look for in an exam question
to distinguish a hypothyroid crash from a normal
pregnancy, is the vital signs, specifically the
heart rate. Yes. Normal pregnancy causes a slight
increase in maternal resting heart rate due to
the massive increase in blood volume. The heart
is pumping more fluid, so it beats a little faster.
If you have a pregnant client presenting with
fatigue, edema, weight gain, and a resting heart
rate of 52 beats per minute, alarm bells should
be ringing loudly. Bradycardia points directly
to a systemic metabolic slowdown, which means
you need to check those TSH and T4 lab values
immediately. That's a phenomenal distinction
to make. Look at the vital signs. What about
overt hyperthyroidism? How does that present?
Hyperthyroidism is the exact opposite. It's an
engine redlining. The concerning signs are flushing,
Perfuse sweating, even in a cool room. Severe
anxiety or panic attacks. Erasing heart or severe
tachycardia. Fine hand tremors. Changing bowel
habits. Often frequent diarrhea because the gut
motility is hyperactive. And a total inability
to sleep. All right, let's move to priority nursing
actions in pharmacology. If the patient is hypothyroid,
we must administer a synthetic thyroid replacement
hormone, primarily levothyroxine. And there is
a massive patient education point here. that
nursing instructors absolutely love to test.
The nurse must teach the client to avoid taking
their prenatal vitamins within four hours of
taking their levothyroxine. Let's explain the
why so you don't have to blindly memorize it.
Why separate them? Because prenatal vitamins
are packed with heavy minerals, specifically
iron and calcium. If a patient swallows an iron
pill and a levothyroxine pill at the same time,
the iron and calcium physically and chemically
bind to the levothyroxine molecule inside the
stomach. It turns it into an insoluble complex
that the intestines cannot absorb. So it just
passes right through their digestive tract. Exactly.
If they take them together, it's as if they didn't
take their thyroid medication at all. Their T4
levels will stay dangerously low, putting the
fetal brain at risk. You must aggressively educate
the patient. Take the liofluroxine first thing
in the morning with a glass of water on a completely
empty stomach, wait an hour to eat, and do not
take your prenatal vitamin until lunch or dinner.
What about pharmacological actions for hyperthyroidism?
We administer anti -thyroid medications, but
the timing is highly tested. The text gives us
two specific drugs, propylthiuracil, or PTU,
and methamazole. PTU is given until the 16th
week of pregnancy. Methamazole is given after
the 16th week. The reason for this complex medication
switch is a balancing act between teratogenicity
for the baby and liver toxicity for the mother.
Methamazole works better overall and has fewer
side effects for the mother, but it is associated
with specific severe birth defects like a plage
acutus where the baby is born missing skin on
their scalp if given during the critical first
trimester organogenesis window. So methamazole
is dangerous early on. Right. PTU on the other
hand does not cross the placenta as easily and
is much safer for the fetus early on. However,
PTU carries a very high risk of causing sudden
severe maternal liver toxicity. So we make a
clinical compromise. We use PTU for the first
16 weeks when the baby is forming and is most
vulnerable to defects. Once the organs are fully
formed, we immediately switch the mother to methamazole
for the remainder of the pregnancy to protect
her liver from the PTU. The goal is always to
use the absolute lowest possible dose of either
medication to maintain the maternal T4 in the
high normal range. ensuring we don't accidentally
push the mother into hypothyroidism and starve
the fetal brain. Let's hit the memory ankles
for this section. To remember the medication
timing for hypothyroidism, use the acronym PTU.
Pre -16 treatment, usually. PTU, pre -16 treatment,
usually. And for the levothyroxine separation,
remember this rhyme. Four hours for four. Wait
four hours between levothyroxine, which is T4,
and your prenatal vitamins. And fundamentally,
if you get confused on an exam, just remember
what the metabolic engines do. Hypo equals a
slow metabolism bradycardia, cold intolerance,
constipation, weight gain. Hyper equals a fast
metabolism tachycardia, hand tremors, diarrhea,
weight loss. Okay, if you only remember five
things about thyroid disorders from this deep
dive, lock these in your brain. Number one. Maternal
hypothyroidism severely threatens fetal neurological
brain development in the first trimester because
the baby relies entirely on the mom's T4. Number
two, the physical symptoms of overt hypothyroidism
seamlessly mimic normal pregnancy, but the key
objective clinical differentiator is bradycardia.
Number three, you absolutely must educate the
patient to separate levosyroxine and prenatal
vitamins by at least four hours to prevent physical
absorption blocking by iron and calcium. Number
four, for hyperthyroidism, use PTU until week
16 to protect the baby, then switch to methamazole
to protect the mom's liver. And number five,
normal TSH during pregnancy is 0 .35 to 4 .9
MIUL. Excellent summary. We have covered a massive,
massive amount of highly testable ground today.
We really have. We stepped back from the dry
textbook, we sifted through your sources, and
we pulled out the absolute most critical high
yield facts for your exams. We talked about how
the placenta acts as a rogue endocrine organ,
bumping out human placental lactogen to drive
insulin resistance and gestational diabetes,
ultimately putting the newborn at massive risk
for severe postnatal hypoglycemia once the cord
is cut. We explored how surging HCG levels, especially
from molar or multiple pregnancies, drive the
severe dehydration, hypokalemia, and psychosocial
trauma of hyperemesis gravidarum and how to objectively
quantify that danger using the PUQE score to
advocate for your patient. And finally, we discussed
how thyroid hormones act as the master metabolic
engine, dictating fetal neurological development
and the critical importance of medication timing
and spacing to ensure that hormone gets absorbed.
You have absolutely mastered the 80 -20 breakdown
of endocrine disorders in pregnancy. As you head
into your clinical rotations and eventually sit
for your NCLEX, I want to offer a final piece
of strategy as your exam coach. Nursing exams
are not trying to trick you for the sake of being
mean, they're trying to ensure you are safe.
When you read a complex, paragraph -long question,
always cut through the noise and prioritize maternal
airway, circulation, and fetal distress. Ask
yourself, what will kill this patient the fastest?
That's the golden rule. Right. And always, always
look for the abnormal finding hiding inside the
expected complaints of pregnancy. Look for the
bradycardia hiding behind the normal fatigue.
Look for the extreme dehydration and weight loss
hiding behind the morning sickness. That is phenomenal
advice. Trust your clinical judgment. You know,
before we wrap up looking at all these live values
and specifically the mechanisms of gestational
diabetes, it got me thinking about something
bigger. Something beyond just the nine months
of pregnancy. It's a fascinating rabbit hole.
We know from the text that gestational diabetes
gives a mother a 60 % recurrence risk and a massively
elevated risk of developing permanent type 2
diabetes within a decade. But I want you to think
about the fetal environment. Right. The baby
inside that high sugar environment. Exactly.
If that newborn was bathed in a high glucose,
high insulin environment for nine critical formative
months of cellular development, how does that
epigenetic programming alter their own metabolic
baseline. How does it affect the architecture
of their pancreas 30, 40, or 50 years down the
line? Wow, that's heavy. It is. When you are
a nurse managing a pregnant client's blood sugar
today, teaching her the 424 diet, you aren't
just nursing two patients. You might very well
be witnessing and positively influencing the
metabolic blueprint for the next generation.
Your nursing interventions today literally echo
into the future. What a powerful, profound way
to look at the impact of OB nursing. You are
literally shaping the future of human health.
To the aspiring nurse listening to this, you've
got this, you have the knowledge, you understand
the why behind the pathophysiology, you have
the clinical reasoning, and you have this exam
in the bag. Thanks for diving deep with us.