This content provides a foundational overview of the neurobiology and pharmacotherapy essential for psychiatric nursing, explaining how mental disorders are physiological and how psychotropic medications work by targeting brain chemistry and function.
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Welcome to the deep dive. We're here to
give you that essential knowledge fast.
And today, uh, we're tackling a big one,
the neurobiology and phicotherapy you
absolutely need for psychiatric nursing
foundations. We're sticking strictly to
our source material here.
>> Right. So, if you need a solid, quick
grasp on why psychiatric meds work and
how they work, well, we're going to
break down brain structure, those
chemical imbalances, and really the
mechanisms of the major drug classes.
>> Okay, let's start by framing this. It's
complex, right? Mental disorders are
fundamentally physiological. We're
talking physical changes in the brain.
And these come from a mix of things,
genetics, maybe trauma, substance use,
even neurodedevelopmental factors. So
psychotropic medications, the term
actually means to turn the mind. They
aim to bring things back into balance by
targeting these uh physical changes.
>> Yeah. And what's really interesting, I
think, is that we've had these drugs for
Yeah. what over 50 years.
>> But for some of them, we still don't
know the exact mechanism. Not fully.
>> That's true. And those early ideas like,
you know, schizophrenia is just too much
dopamine or depression is just low
serotonin. The single bullet theories.
>> Exactly. We now know it's way more
complicated. It's like a huge
interconnected chemical orchestra in
there. Oversimplifying doesn't really help.
help.
>> All right, let's start with the brain's
most basic job. Maintaining homeostasis.
Think of it as the body's uh continuous
surveillance system. It's always
monitoring inside and out, making sure
everything stays stable and responds
appropriately. And that constant
monitoring, that's why our emotions and
our physical body are just completely
linked, isn't it? >> Absolutely.
>> Absolutely.
>> Like when anxiety hits, the brain kicks
the sympathetic nervous system into
gear. That's your fight or flight. And
that's why you actually feel your heart
pounding. You breathe faster, maybe get
those uh sweaty palms. It's a direct
physical thing,
>> right? And that connection emotion to
physical response. It runs straight
through our main stress regulator.
That's the hypothalamic pituitary
adrenal axis. You'll hear it called the
HPA axis. It's literally a chain
reaction. Hypothalamus releases CR that
tells the pituitary to release
adreninocorticotropen and that tells the
adrenal glands, okay, pump out cortisol,
the stress hormone.
>> And when that access gets disturbed,
it's a real sign of illness. The
material points out that people with
major depressive disorder often have
elevated cortisol, which unfortunately
also suppresses their immune system.
>> Yeah, that's a key point. And
conversely, it notes that patients with
severe PTSD symptoms, they often show
lower levels of circulating cortisol.
It's quite distinct.
>> Interesting difference.
>> We also have to think about the brain's
role in our basic drives.
>> You know, sex, hunger, thirst,
>> and also setting our internal clock.
This clock runs on circadian rhythms,
those 24-hour cycles in our physiology.
And the source mentions evidence that
the way these rhythms regulate
neurotransmitters like norepinephrine
and serotonin seem to be altered in mood
disorders. So the timing mechanism
itself might be off.
>> Okay. So if the brain structure is the
hardware, let's quickly map out the key
parts before we get into the wiring.
You've got the brain stem first. That's
the really primitive core, right?
Controls basic survival, heart rate, breathing.
breathing.
>> Crucial. And importantly, it contains
those ascending pathways, the messolyic
and messortical that send signals upward.
upward.
>> Signals going where? up to the lyic
system. This is really the hub for
emotional status and psychological function.
function.
>> And it heavily uses dopamine,
norepinephrine and serotonin.
That mealyic pathway in particular is
highlighted for its role in
psychological reward.
>> Ah so that links into substance use disorders.
disorders.
>> Yeah. Then tucked away underneath and
behind is the cerebellum.
>> Right. Our coordination center
>> manages voluntary movement balance. And
that's why some psych meds, especially
older antiscychotics, can cause those
movement side effects like tremors or
stiffness because they affect the cerebellum.
cerebellum.
>> That's a big part of it. Yes. It
disrupts that fine motor regulation.
>> Got it. And then the big one, the
cerebrum, the cortex.
>> Yes. The wrinkly bits on top. That's
where all the conscious mental activity
happens. Memory, language, our our sense
of who we are. And remember, it has
specialized loes. Frontal for thought
and movement, temporal for sound and
emotion processing, occipital for
vision, and parietal for managing sensation.
sensation.
>> Okay, let's zoom right in now down to
the cellular level. The brain's got
what, something like a 100 billion neurons
neurons
>> roughly. Yeah, a staggering number. And
they carry electrical impulses. It's
basically about moving positive ions.
Sodium rushes in, potassium flows out.
That creates the action potential of the signal.
signal.
>> But that electrical signal can't just
jump the gap between neurons, right?
>> No. Exactly. When the impulse gets to
the end of one neuron, it triggers the
release of neurotransmitters. These are
the chemical messengers. They float
across the gap, the syninnabs, and then
they bind to a receptor on the next
cell, the receiving neuron. And that
interaction, the neurotransmitter
hitting its specific receptor. That's
basically the target for almost every
single psychotropic drug we use.
>> Okay. So, the message gets delivered.
What happens then? How does the brain
clean up?
>> Good question. Yeah, there are two two
main ways. First, some neurotransmitters
get destroyed right there in the synax
by an enzyme like uh choline eststerase
breaks down acetylcholine almost immediately.
immediately. >> Okay.
>> Okay.
>> But the second way and this is really
common is re-uptake. The releasing cell
basically vacuums the neurotransmitter
back up
>> like recycling
>> sort of. It takes it back inside where
it can either be repackaged for reuse or
destroyed by enzymes inside the cell
like MAO which breaks down monomines,
norepinephrine, dopamine, serotonin
>> and that re-uptake. That's what most
modern anti-depressants mess with, isn't
it? They block that vacuuming process.
>> Precisely. They block the re-uptake pump
leaving more neurotransmitters hanging
around in the syninnapse to keep
stimulating the next cell.
>> Got it. Okay, so let's quickly connect
the main neurotransmitters to the
disorders like the table and the source
material shows
>> right the highlights. So dopamine DA
too little is linked to Parkinson's and
depression too much schizophrenia and mania
mania
>> or pinephania and EE and serotonin 5HT.
A decrease in either is connected to
depression. An increase in NE though
could be linked to mania, anxiety, even schizophrenia.
opioids, can be fatal due to respiratory depression.
depression.
>> Okay, so they provide quick relief, but
that dependence risk is serious. What's
like the number one thing a nurse should
track if someone's newly started on a
benzo to watch for potential misuse?
>> You really need to monitor how often
they're requesting it and how much. Are
they running out early? Are they
reporting escalating anxiety right when
the dose wears off? Those are definite
red flags for developing dependence or misuse.
misuse.
>> Makes sense. What about other options? Busperone,
Busperone,
>> right? Busperone is different. It's used
for generalized anxiety, but it's a
partial serotonin agonist, specifically
at the 5HT-1A receptor, not gayergic.
Key differences. >> Yeah,
>> Yeah,
>> it takes weeks to work, so it's not for
panic attacks or acute anxiety. And
importantly, it's not a controlled
substance, less risk of dependence.
>> Good distinction. All right, moving on
to anti-depressants. The big players now
are the SSRIs, selective serotonin
reuptake inhibitors like Flooxine,
Prozac. So they block that serotonin
vacuum cleaner we talked about.
>> Exactly. Leaving more serotonin
available in the syninnapse.
>> But they have well-known side effects
like sexual dysfunction, GI issues. Why
is that?
>> Because that extra serotonin doesn't
just hit the good receptors involved in
mood. It also stimulates other serotonin
receptor subtypes. Like hitting 5HT2A
and 2C receptors is linked to sexual
side effects.
>> Hitting 5HT3 and 4 often causes nausea
or diarrhea. It's about lack of perfect selectivity.
selectivity.
>> Yeah. Also, fluoxitine specifically has
a really long half-life which impacts
switching meds.
>> Okay. Then there are the SNRI's
serotonin norepinephrine reuptake
inhibitors. Then leaxine deluxine,
>> right? These block reuptake of both
serotonin and norinephrine.
>> So what's the key implication of adding
norepinephrine back into the mix?
>> Well, that norepinephrine boost can
affect blood pressure and heart rate.
It's often dose dependent. Higher doses
mean a greater risk.
>> So monitoring vital signs is important.
A potential advantage though is that
SNRIs can be quite effective for
treating neuropathic pain likely due to
that NE component.
>> Okay, let's touch on the older classes
because they teach us a lot about side
effects. TCAs, tricyclic
anti-depressants like um amatitine.
>> Yeah, these were workh horses but
they're not first line anymore. Why?
Side effects and lethality and overdose.
>> Yeah, lethality due to heart problems.
>> Yes, specifically cardiac conduction
disturbances and overdose could be
fatal. And their side effects really
illustrate receptor blockade issues
>> like a shotgun approach
>> kind of. They block NE and serotonin
reuptake, which is what you want. But
they also hit other receptors
unintentionally. They block histamine H1
receptors, muscerinic M1 colonergic
receptors and alpha 1 adinuric receptors.
receptors.
>> And each of those blockades causes
predictable problems.
>> Exactly. H1 block that leads to sedation
and weight gain. M1 block that gives you
anticolinergic effects. dry mouth,
blurred vision, constipation, urinary
retention, alpha 1 block that causes
orthostatic hypotension, feeling dizzy
when you stand up. It's a direct link,
>> which is why newer agents are preferred
if possible. What about MAOIs? Monoamine
oxidase inhibitors like phenoline.
>> These are even older and more complex.
They work by inhibiting the MAO enzyme
inside the neuron, preventing it from
breaking down norepinephrine, serotonin,
and dopamine. But they come with major
cautions. You need a wash out period,
usually about 2 weeks before switching
from an MAOI to another antidopressant
like an SSRI or vice versa to avoid
dangerous interactions like serotonin syndrome
syndrome
>> and the diet restrictions.
>> Oh yeah, the big one. Patients must
avoid foods high in tyramine. Things
like aged cheeses, cured meats, red
wine, soy sauce.
>> Why? What happens
>> if they eat tyramine while on an MAI? It
can trigger a hypertensive crisis, a
sudden dangerous spike in blood pressure
that can lead to stroke or even death.
Requires absolute dietary adherence.
>> Wow, that's intense. It really shows how
far we've come. Any novel treatments mentioned?
mentioned?
>> Yes. The source briefly touches on
esetamine, which is related to ketamine.
It's an NMDA antagonist used for
treatment resistant depression, but it's
given under supervision due to risks
like dissociation and also Brexanol, the
first drug specifically approved for
postpartum depression. It interacts with
GABA receptors and requires a continuous
60-hour 5e infusion in a healthcare setting.
setting.
>> Okay, next up, mood stabilizers.
>> Lithium is the classic, the gold
standard for bipolar disorder. Its
mechanism isn't perfectly understood,
but it seems to affect electrical
conductivity in neurons, maybe
substituting for sodium or potassium
ions in some processes.
>> And the critical nursing point for lithium,
lithium,
>> it has a very narrow therapeutic index.
The dose that works is incredibly close
to the dose that causes toxicity.
>> So regular blood tests are non-negotiable.
non-negotiable.
>> Absolutely essential. Monitoring lithium
levels is paramount to ensure safety and efficacy.
efficacy.
>> What else is used for mood stabilization?
stabilization?
>> Anticulants are widely used now. Drugs
like valpro, depicote, carbomasopene,
tegretl, lamontrogen, ldal. They seem to
work by stabilizing neuronal membranes
making them less excitable.
>> Cautions with these.
>> Yes. Velprote needs liver function
tests, LFTs, and complete blood count,
CBC's monitored. And it carries a high
risk of birth defects. So, it's
generally avoided in pregnancy. Larry
requires a very slow gradual dose
increased titration to minimize the risk
of Stevens Johnson syndrome.
>> And didn't you mention carbomaszipene
earlier with the genetic risk?
>> Yes, that's the HLAB1502
risk. Plus, there's a key interaction.
Valpro can dramatically increase
lamadrogene levels. So if a patient is
on both the lamrogene dose usually needs
to be cut significantly.
>> Good to know. Okay. Antiscychotics big
category. FGA versus SGAA.
>> Right. First generation antiscychotics,
FGAAS, also called typicals. Think
heliperidol. They primarily work by
blocking dopamine D2 receptors. They're
generally effective for the positive
symptoms of schizophrenia,
hallucinations, delusions.
>> But their big drawback is side effects
related to blocking dopamine elsewhere.
>> Exactly. Blocking dopamine in the
nigroital pathway causes extra pyramidal symptoms.
symptoms. >> EPS
>> EPS
>> things like acute donia, muscle spasms,
achesthesia, restlessness, parkinsonism,
tremor, rigidity.
>> And the really worrying one, tardive disynesia.
disynesia.
>> Yes, tardy diskynesia TD. Those
involuntary often writhing movements
especially of the face and tongue. It
can be permanent even after stopping the drug.
drug.
>> So monitoring is key. The Ames scale,
>> the abnormal involuntary movement scale.
Ames, regular Ames testing is a
fundamental nursing responsibility for
anyone on an FGA to detect TD early.
FGAs also block dopamine in the tubo
infendipular pathway which can lead to
hyperp prolactmia, increase prolactin
levels causing things like breast
enlargement or lactation even in men and
menstrual irregularities in women.
>> Okay. So then came the second generation
antiscychotics SGAAs or atypicals like
respperadone, alanzipene, cloloopene.
How are they different?
>> They block dopamine D2 receptors too,
but generally less tightly than FGAs.
And crucially, they also block serotonin
5HT2A receptors. This dual action is
thought to be why they often cause less
EPS than FGAs and why they seem better
at treating the negative symptoms of
schizophrenia like apathy, lack of
motivation as well as the positive ones.
>> But they have their own major issue.
Yes. The big caution with many SGAAs is
the significantly increased risk for
metabolic syndrome,
>> meaning weight gain.
>> The significant weight gain. Yes. Plus
increased blood sugar potentially
leading to type 2 diabetes and adverse
changes in cholesterol levels. It's a
major health concern requiring regular
monitoring of weight, BMI, glucose, and lipids.
lipids.
>> And clotine is singled out. Cloopene is
often considered the most effective
antiscychotic, especially for treatment
resistant schizophrenia, but it has the
highest risk for metabolic side effects
and carries a risk for a granular
cytosis, a dangerous drop in white blood
cells, neutropenia,
>> which means
>> strict monitoring. Patients on cloopine
need regular absolute neutrfil count,
ANC blood tests, initially weekly to
catch this early. It's a very rigorous
process. Just a quick mention for the
last couple categories for ADHD. The
main treatments are psychos stimulants
like methylenadate andamines. They work
by blocking the re-uptake of
norepinephrine and dopamine. They are
controlled substances due to potential
for misuse. Comic side effects include
insomnia, decreased appetite, potential
for increased heart rate and blood
pressure and maybe some growth
suppression in kids.
>> And finally, Alzheimer's disease. What
are the targets there?
>> Two main neurotransmitter systems.
First, acetylcholine. We see a loss of
conurgic neurons in Alzheimer's.
>> So we use colonsterase inhibitors like
dunzole aerosep.
>> Exactly. They inhibit the enzyme that
breaks down acetylcholine thereby
increasing the amount available. This
primarily helps with memory and
cognitive symptoms.
>> And the other target
>> glutamate. Remember we said excess
glutamate can be neurotoxic. In
Alzheimer's there might be excessive
stimulation of NMDA receptors by
glutamate. So meantine nmenda is used.
It's an NMDA receptor antagonist. It
sort of shields the receptors from this
over stimulation, hopefully slowing down neurodeeneration.
neurodeeneration.
Hashtag outro. Okay, that was a really
comprehensive run through of a
foundational chapter. If we had to boil
it down, what are the absolute key
takeaways? I'd say three things. First,
and maybe most important,
>> mental disorders are physiological. They
involve real measurable changes in brain
structure and function. They are not
character flaws.
>> Absolutely critical point. Second.
Second, almost all psychotropic drugs
work by influencing neurotransmitters.
Primarily, they manipulate one or more
of the big five. Dopamine,
norepinephrine, serotonin, GABA, or
acetylcholine, usually by affecting
release, re-uptake, or receptor binding.
>> And third,
>> third, side effects are often
predictable. If you know which other
receptors a drug might accidentally
block, like H1 for histamine, and one
for muscerinic, alpha 1 for adronurgic,
you can anticipate common side effects
like sedation, dry mouth, or dizziness.
Right. Understanding the offtarget
effects turns wrote memorization into
actual clinical reasoning. That's
powerful. So we've talked a lot about
how drugs work, how genetics influence
metabolism, and even specific genetic
risks like HLA B1502 with carbomasopene.
It makes you wonder, doesn't it? Here's
something to think about. How different
would psychiatric care look in the
future if, say, genetic testing became
standard practice before anyone started
any psychotropic medication? Could we
shift from managing symptoms after they
appear towards a more personalized,
maybe even preventative biological
approach based on individual genetic
profiles? Just something to mle over.
Thank you so much for joining us on this
deep dive into Psych Nursing
Foundations, the neurobiology and
pharmacotherapy. We hope this helps
solidify that core knowledge. We'll see
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