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Part 2 antihistamine tutorial 2025B | PharmacoPhoto | YouTubeToText
YouTube Transcript: Part 2 antihistamine tutorial 2025B
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Summary
Core Theme
This content explains the role of histamine in the body's immune and inflammatory responses, detailing how it causes symptoms like vasodilation, increased permeability, itching, and bronchoconstriction, and introduces the development and indications of antihistamines, particularly the distinction between first and second-generation drugs.
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Yeah. So now what we're going to do is
talk about histamine and antihistamines
that stay out in the periphery. So this
part right here, we're we're going to
talk about histamine just to give you a
really good picture of what histamine
is. Okay. Now, the actual questions that
I'm going to be asking
with respect to this tutorial question
will not actually ask you about
histamine, where it acts and things like
that. So please just remember that
despite the fact that you really need to
understand what histamine is, where it
acts and you know understand a little
bit about the background of histamine
before you understand what
antihistamines are good for. It's not
something that I'll probably be that I
will be asking you in this instance for
in the tutorial question.
So what is histamine? Histamine is um
some is a vazoactive substance. What do
you what do we mean by vasoactive? I
mean, basically all it really means is
that it acts on the vascule and does
something and we'll explain, you know,
what it actually does in just a little
bit, but it's a basoactive uh substance
that is involved in the local immune
response, but it's also involved in the
systemic immune response as well. So
it's not only involved in for instance
allergic rhinitis up in the nasal
passages as you have hay fever. It's
involved in uh the first process of a
asthma. So the very first kind of
constriction of the air airways is a
histamine response. It's involved all
the way through the body. It's also a
systemic type of reaction when a person
has aniflectic shock. So, as a person
takes a peanut and they are allergic to
peanuts and they inadvertently actually
take a peanut and and and just have a a
bit of a peanut, they end up with having
to do an EpiPen and uh that's a that's
that's because of the massive release of
histamine and it it binds to the
histamine one receptors on the blood
vessels, the nerves and also the
bronchi. So let's take that just a
little bit closer look at that one. So
exactly what does it do? So once again,
you're not going to understand this
fully until you put it into the context
until I put it into the context of where
it happens and how it happens and so
forth. But just in general what it do
does on the blood vessels, the uh what
we call peripheral blood vessels, the
things that are not in the central area,
not in the brain and the spinal cord. So
it's on those peripheral blood vessels.
So it increases the permeability and
dilates the blood vessels. Another thing
that it does is it binds to the nerves
and despite the fact that we don't have
any itch receptors, we've got pain
receptors and the way that histamine um
histamine one binds to the nerves, it
actually causes an itchy sensation. When
it's in excess, it does start causing
pain. uh and then and then also it binds
to the receptors on the bronchi and it
constricts the bronchi. So why does it
do all that? And that's what we're going
to do right now is just take a look at
the immune response. Now this right here
is a representation of a mast cell mast.
A mass cell is in the especially in the
nasal passages. It's in the bronchi and
especially over there. There's other
mass cells throughout the body, but uh
that's the main portions of the body
that has the mass cell. Macrophagages
will do a similar thing. Some of the
macroofagages will do a similar thing
and those would be in the tissues, the
local tissues out in the skin and so
forth. And then we have basoils which
will do a similar thing as well. They
have bags of granules just like the mass
cell does and those are involved. Those
are the the blood cells which are going
to be floating around it acting kind of
almost exactly the same way as the uh as
the mass cell is. But what happens with
the mass cell and let's take an instance
where you know this mass cell is in the
sinuses. Okay. And it's just hunting
out. It's really part of the immune
system and what its job is is to make
sure that though none of the allergens
that it's made for will actually get
into, you know, we're going to have to
get it out. If it if if it detects that
antigen, if it detects that that protein
or whatever whatever you're allergic to,
it needs to its job is to get it out in
some way. Okay? So what it does is uh it
the the allergen is going to bind to
these mass cells in this Y-shaped
protein called an imunoglobin E and that
activates the mass cell and then as the
mass cell is activated it's going to
release these bags of granules which
it's been making all through its life
and into the interstitial space. So just
thinking about where the interstitial
space just so that you can picture it
the interstitial space is really not a
space there isn't any space there in the
interstitial space there might be some
glyoproteins and fluid but this picture
actually has one cell one cell one cell
one so it has cells all over and then
there's also some of those cells would
be the mass cells but it's going to be
releasing those granules into the
interstitial spaces which this this kind
of area between these the various cells
the the local cells and then what's
going to happen is that histamine is
going to go over the capillaries for
instance and then bind to the
capillaries and there's a certain
receptor on that capillary and it's
going to do the actions that we're
talking about and we'll be talking about
it doing. Okay, so back to this picture
over here. it's released out its
granules and those bags of granules are
preformed mediators of inflammation.
It's almost an immediate response. It it
it's most kind of evident when you you
actually see an asthmatic individual
when they have their initial response
of, you know, that the bronco
constriction and and that kind of like,
you know, and then the cough. That thing
right there, that exact moment, that's
the histamine response and that's how
quick that it actually acts because its
job is to get whatever it is that's
irritating it, it needs to get that out.
So, uh, so one of the things that it's
going to be doing to to get that out is
dilating the blood vessels and
increasing the permeability. If you take
a look at this picture, dilating the
blood vessels, you know, because what we
have is blood vessels that have loose
junctions. And that's perfect because we
can dilate the blood vessels and
increase the permeability. But why is
that good? You know, like why is it good
in an immune response? If you think
about uh you know as you're looking at a
if as you're going down in a really busy
highway and it's just one lane it's and
it's been frustrating you then all of a
sudden it's it's a three-lane uh highway
and it's opened up and all of the cars
start going nice and smoothly but then
it goes back down to a one lane uh back
further up and and it's a busy weekend
holiday weekend and you've got all of
these cars just jammed up trying to get
back into that one lane. Well, that's
the same kind of thing that's going to
be happening with the vasoddilation
and increased permeability. So, what is
happening is you have all of these cells
and proteins that you might need for the
inflammatory response. you have enough
kind of uh permeability of the the blood
vessels to allow the the uh cells
whatever you need you know like the
lymphosytes or the macroofagages or
whatever you need you're going to
actually get it over to that area in
rescue to to rescue that us from that uh
allergen from that uh invading uh
protein or whatever it happens to be. So
hopefully you have a picture of what
that's happening. And if you apply it to
for instance your sinuses, if you apply
it to your sinuses, which are fairly
closed up and and that kind of thing,
what's happening is vaso dilation,
increased permeability, that's going to
let fluid out, isn't it? Well, as it
lets the fluid out, it's going to act
that fluid itself is going to start
acting on the sinuses on on the mucus
secretreting cells. And as the mucus
secretreting cells start releasing the
mucus then your nose starts running like
anything. So that's what's happening.
And the similar thing happens in for
instance a common cold. It's just for a
different reason. You know for a common
cold it's the viral particles that are
not really you're not really allergic to
it but the viral particles are kind of
doing the same thing and uh it's
prompting that immune response. Why is
that itch itch though? You know why does
histamine actually act on the nerves?
And it's probably we we hypothesize that
the reason is really because of of the
same reason the pain se receptors are
there. You know the pain receptors are
going to tell us that we have pain. You
know, a diabetic who has lost their
ability to feel what's happening down at
their toes has a really good chance of
losing their feet and they're, you know,
having amputations because they don't
know what's happening down there. Well,
with the histamine response, we know
that something's happening. We know to
wash it with with water. Um, possibly
the the scratching itself will take some
of the allergens away and that kind of
thing. Uh, but anyway, we get it out of
there. we're informed and we're going to
get it out. If it's uh in the sinuses,
we might be, you know, splashing
ourselves with cold water and and that
kind of thing to get it out. So it get
getting that picture just still getting
that picture of the histamine response
and why is v bronco constriction
important in immune response and that's
for the kind of reason where you know if
you're going through and having a
allergens actually go down into the
respiratory system that's not a good
thing is this is a foreign particle that
you don't like. So therefore, you're
going to try to close it off. You're and
the only way we can do it is to
constrict the bronchi. So hopefully you
get that picture of bronco constriction
and everything. You'll use that picture
of the bronco constriction more in
asthma uh because uh the things that
we're talking about in this tutorial are
not really going to use that bronco
constriction too much. So this is for
you to answer in the chat board. What
symptoms would you expect in the sinuses
if the histamine is binding to the blood
vessels and in the eyes if it's binding
to the blood vessels? Okay. So, uh yep,
runny nose,
uh watery watery eyes, streaming mucus,
uh yeah, eyes watering, itchy eyes, red
eyes, bloodshot eyes. Yeah. all of those
things in the sinuses. Those are the
kind of things that histamine is going
to be because it acts on the blood
vessels, it acts on the nerves and the
itchy kind of feeling that your eyes
just you just want to get rid of those
uh and then just try to scratch your
eyes. Okay. So, what symptoms would you
be expecting in the skin if it's binding
to for instance the blood vessels of the
skin? Now these are the classic signs of
inflammation and hives. Hives is a a
good one actually because hives is an
allergic reaction. Itchiness uh heat but
it's the four classic signs of of
inflammation. Heat, redness, swelling
and uh itchiness at first but pain in
the end. So those are the f four classic
signs of inflammation. So when you see
the fourth classic signs of
inflammation, some sort of a skin
problem, then the antihistamines are
going to be indicated for that kind of condition.
condition.
Okay, good. And using what we've just
learned, what are the indications of
anti-histamines that stay out in the
periphery? We're just still getting used
to those terms, the indications. What
are the indications that stay? and just
continue on and saying, you know, not
only what we've been talking about there
in the eyes, in the in the nasal
passages, on the skin, think about all
of that right now and then just give
give it to me in the chat board if you
would please. Indications. What is it
indicated for? What conditions would it
be good for?
Yeah, hay fever. So allergic rhinitis,
allergies, any kind of allergies of the
eyes, of the nasal passages. If the
person has uh red eyes and itchy eyes,
then they probably have a allergic
reaction and they're probably going to
benefit from the antihistamines and
bites and reactions. Yeah. in the skin
like hives that uh result in heat,
redness, swelling, and pain. Yeah, all
of those things. But the one thing that
we didn't talk about yet, and I didn't
expect you to actually put it down,
another indication of anti-histamines
is going to be when a person has
aniflectic shock. So anaphylactic shock
is a type one hypersensitivity reaction
just like hay fever is a type one
hypersensit sensitivity reaction but the
thing is the allergen is actually
getting systemic
and then we're using our basoils and
there's lots of them they're going all
through the entire body they're
releasing histamine massive amounts of
histamine and so forth. Histami
anti-histamines are not the primary
thing that you will give a client who
has an allergic reaction. They are
probably already taking around an EpiPen
and then they inject their usually their
thigh with the EpiPen and they have the
adrenaline happening in their system. As
that happens, what's going to happen is
that they're going to be rushed over to
the hospital anyway, regardless of the
fact that they kind of feel a little bit
better because the adrenaline. They'll
be assessed at the hospital and given a
very large dose of anti-histamines.
And those, just think about it, you
know, you've got a massive release of
histamine. Uh adrenaline is what's
called the physiological antagonist of
histamine. So it does exactly opposite
thing that the histamine does. It undoes
it. But then also uh what happens is
that there's going to uh be a need need
to even decrease the effect of histamine
more. So anti-histamines are going to be
given for a couple days after the uh the
the the allergic the aniflectic shock in
a lot of instances.
But the uh but but don't think that you
know just because it's indicated for it
that it can be used as a sole therapy
for that. It would be a uh an an an
additional therapy.
Okay. So now we have just about all of
the background information that you'll
need in order to understand the question
and begin to answer the multi-part
tutorial questions about the anti-histamines.
anti-histamines.
This first question will give you the
rest of the background information as we
answer the question. So, let's just get
into the question. But just to make
sure, remember that you need to place
this question in your workbook under
multi-part question A on antihistamines
and under question one. So, you actually
need to type that out into your workbook.
workbook.
So, the relevant portion of the workbook
looks like this. and you will place the
entire question in this area right here
where I've just begun the first few
words of the question. Okay. So the
whole question goes like this. Discuss
first and second generation medications
using the drug class cited in the
tutorial. Describe any advantages of one
over the other. The first thing that we
need to understand when we talk about
first and second generation medications
is that they have to do with a thing
called the drug classes.
Now there's a lot of different ways that
we can divide our drugs. For instance,
we can divide it by therapeutic class.
An example of a therapeutic class is for
instance anti-dopressants. And another
example is heart medications.
Those are very large groups of
medications and they have many different
general mechanisms of action. But under
the therapeutic class lies a se a
separate class of medications called the
drug class.
And the definition of a drug class is a
group of medications that works by a
similar mechanism of action and often
has a similar chemical structure.
On this next slide, we see examples of
drug classes like beta blockers, ACE
inhibitors, non-steroidal
anti-inflammatory drugs, selective
serotonin reuptake inhibitors, and of
course the one that we're going to be
talking about today, which is anti-histamines.
anti-histamines.
Each of those fit the description of a
drug class in that they are a group of
medications that works by a similar
mechanism of action and often has a
similar chemical structure. As you see
here, the non-steroid anti-inflammatory
drugs are analesics, but the term
analesic is a therapeutic class and the
first and second generation medications
are not applicable to those. Same thing
with selective serotonin reuptake
inhibitors. Those are anti-depressants.
Uh the selective serotonin reuptake inh
inhibitors is a drug class. But when
you're talking about anti-depressants,
that's a therapeutic class. There's a
number of different drug classes under
the anti-depressants. Uh for instance,
there's the selective serotonin
re-uptake inhibitors, the triccyclic
anti-depressants, the selective uh
sorry, the serotonin nor adrenaline
re-uptake inhibitors, and those are all
uh drug classes under the therapeutic
class of the anti-depressants.
So hopefully you understand what a drug
class is. It's a group of medications
that works by a similar mechanism of
action and it often times also has a
similar chemical structure. Just
remember back in module one when we
talked about the drug classes we uh
because a lot of them have common
suffixes or at least common affixes. So
somewhere in the portion in a portion of
the generic name is a a snippet of the
word that is common to all medications
of that drug class. For instance, beta
blockers block the beta receptors on the
heart and they all end in the suffix o
like propranolol, tyol and others. The
beta blockers were first introduced in
the 1960s and they were great because
they decreased the heart rate and
decrease the contractility of the heart
in patients who had chronic heart
failure. the heart of the patients who
had chronic heart failure was racing and
it was going so fast that it was
actually counterproductive
and the beta blockers blocked the action
of adrenaline on the heart decreasing
the heart rate and decreasing the
contractility. So that was really
beneficial in those patients. The big
problem with the first of those
medications was that it blocked the
receptors on the lungs as well. So, it
blocked not only the beta 1 uh receptor,
which we wanted to block, but we also
blocked the beta 2 receptor. And if
you're blocking the dilating effects of
adrenaline on the lungs, it's almost
like you are constricting the lungs in
some people, especially those with lung
problems like asthma and that kind of
thing. So, people with any kind of lung
problems weren't able to take the first
of those beta blockers. They were
contraindicated for those people. What
we needed to do is block the beta 1
receptor on the heart without actually
affecting the beta 2 receptors very
much. So along came the 1970s and 1980s
and we're finding different drugs that
were much more selective for the exact
receptor that they should be acting on.
And in that effort, what we did was we
found that certain beta blockers could
actually be fairly selective for the
beta 1 receptor, not really affecting
that beta 2 receptor very much. And when
they did that, they had a lot fewer side effects.
effects.
And since they were so much better than
the initial beta blockers, they were
termed second generation beta blockers.
So those selective ones were just that
were just introduced were were named
second generation beta blockers. And it
was only at that time that the first of
those drugs were then called first
generation beta blockers. Now before
that just be you know they they were
just beta blockers. They weren't first
or second generation beta blockers. They
they they were the only ones on the
market. So they were just beta blockers.
But then when that significant change
happened then they would started to be
termed first generation beta blockers.
Okay. So hopefully that made sense. And
what I'd like you to do now, I think you
have enough information to make an
attempt at your first draft for this
question. So the question goes, discuss
first and second generation medications
using the drug class cited in the
tutorial. Describe any advantages of one
over the other. So make sure that you
discuss beta blockers in this instance.
uh we'll go on to the antihistamines in
the other four questions in this uh
multi-part tutorial question. I'll give
you a couple minutes to do a draft of
that and then when we get back I'll just
reflect on your answer. Also, I'm going
to cut out the time that I give the
students in the live tutorial. So, if
you're working on the video tutorial
series, you're going to need the need to
stop the video right now so that you can
kind of make an attempt at your own uh
Okay. So, the way that I would approach
that is to say something to the effect
of the first generation and second
generation medications have to do with
the drug class.
When a medication of a given drug class
is released to the public and it has a
major advantage over the earlier
versions of the medications of that same
drug class, it may be termed a second
generation medication of that drug
class. At that time, the first of those
medications would be termed first
generation medications. For example,
beta blockers were initially non-
selective and had adverse effects being
contraindicated in people with lung
disorders. And then later the drug
manufacturers began to make some of the
beta blockers much more selective for
just the beta 1 receptor and that
eliminated the bronco constriction. So
those became known as the second
generation beta blockers and it was at
that time that the old type of beta
blockers became known as the first
generation beta blockers.
Now something like that would be good
for a pass and if you supplemented it
for with for instance uh examples of
first and second generation beta
blockers and uh spend a little bit of
time perfecting the answer you'd score
much higher. But just remember it is
difficult to get the distinction high
high distinction. it's really uh it gets
more and more difficult because you your
answer has to be really quite spot-on in
order to get up uh in that range. And
also remember that the answer that I
give in the tutorial is my answer. It's
not your answer. This has to be in your
words. So if you're using my words,
you're going to get uh zero credit for
that. That is a breach of academic integrity.
integrity.
So just to reflect on all of that, I
need everybody to be really clear that
it's not always that a second generation
medication is more selective than the
first generation medications. And a good
example of that is right there with the
beta blockers. There's there's now a
third generation beta blocker. And it's
actually less
selective in the way that it actually
blocks some of the alpha 1 receptors.
alpha 1, you know, we're blocking beta
one receptors. The first and second
generation medications didn't actually
block the alpha one receptor.
Now, u the third generation medications
actually block some of the effects on
the alpha one receptors. And what that
does is it gives them the additional
vasoddilation. So, it's got a couple
different mechanisms now, which are
really good for people with heart
problems. So, so that's why they termed
it a third generation. So, so just be
really clear about the fact that a first
generation, second generation medication
just means that the the latter one has
some advantages over the earlier one.
And another example is the penicellins.
A first generation penicellin was the
basically made from the fungus and then
the second generation penicillans were semiynthetic
semiynthetic
and they were designed to resist
bacterial enzyatic degradation.
So it's just termed another generation
when there's a major change uh that
could be beneficial for some uh patients.
patients.
Um okay so does everybody kind of
understand that? Okay, I think what
you're ready to do now is understand the
questions that I've specifically have
about the antihistamines. And this is
the first one. Let's uh take a look at
it. Briefly discuss first and second
generation anti-histamines
that the tutorial focused on emphasizing
the reasons that the second generation
antihistamines have a better side effect
profile in comparison to the first
generation antihistamines. and what are
the indications of these second
generation anti-histamines?
So, in order to address that question,
let's take a little look at the history
of the antihistamines.
Antihistamines first came out in the 1940s.
1940s.
And they were great for things like
allergic rhinitis or hay fever. You
know, allergic rhinitis is hay fever.
Um, they they helped with symptoms of
the common cold and they helped decrease
the itchy eyes associated with
allergies. They also helped uh with
you know a number of different skin
reactions involving itchiness. But
before antihistamines you know people
would have to resort to things like
nasal rinses and corticosteroids for
their kind of decrease of the uh
symptoms of the hay fever. So now that
the antihistamines
came on the market that was really good
because you know that take care of those
allergic skin reactions. that take care
of the uh sinus reactions and and so
forth fairly effectively.
The problem with the first of those
antihistamines was that they crossed
into the brain and as they crossed into
the brain there's receptors. Histamine
is in the periphery is in the outside of
the brain is a vazoactive substance but
in the brain there's histamine is a neurotransmitter.
neurotransmitter.
So, as the anti-histamine broke into the
bloodb brain barrier, it started binding
to all of these histamine receptors and
stopped the histamine from binding onto
its own receptor. And of course, that's
going to give you a lot of problems. You
know, histamine is responsible for the
sleep wake cycle. It made people tired.
It it it did a lot of things which we'll
cover a little bit later, but for now,
you just understand that that is one of
the problems. It broke into the bloodb
brain barrier. And then the other thing
that it did, it was very non selective.
In other words, what it did is not only
bind to the histamine one receptor, but
it also bound to the acetylcholine
receptor, the muscerinic receptors. So
the parasympathetic nervous system was
affected. Uh there's a decrease in the
actions of the parasympathetic nervous
system. then it went over into the brain
and blocked the acetylcholine receptors
in the brain as well leading to more uh
side effects, neurologic side effects.
So hopefully you get that picture of
those first generation antihistamines
were great for certain things but uh had
their problems. Eventually what happened
is that the drug companies found out how
to make those antihistamines a bit
better because they made them more
selective and also made them more
difficult to cross into the bloodb brain
barrier and lauratine is an example of
one of those types of anti-histamines.
Loratine is indicated in allergic
rhyitis. So that's hay fever. Uh the
nasal and eye symptoms associated with
the common cold.
It's indicated in skin reactions
involving heat, redness, swelling, and
itchy or or painful uh sensations like
hives. And it's indicated in, you know,
for instance, itchy eyes associated with allergies.
allergies.
But interestingly, if you actually just
look that up in a simple search like a a
Google search or um a a Wikipedia search
or something like that, what you find is
that if you look up the side effects and
contraindications of dyenhydramine or
especially the side effects of
daphenhydramine versus lauredine, you
may find a really similar side effect
profile, but that the problem is that
that doesn't tell the whole story
because the side effects of laoredine
are much less frequent and much less
severe than in first generation
medications like dyenhydramine.
So yeah, um I think that you probably
have a good idea of that. Probably good
enough to try this one on your own. and
briefly discuss first and second
generation antihistamines that the
tutorial focused on emphasizing the
reasons that the second generation
antihistamines have a better side effect
profile in comparison to the first
generation antihistamines and then what
are the indications of second generation
anti-histamines and once again I'll give
you a couple minutes to start developing
your answer now and then I'll come in
and the way that I would discuss This
one is to say something like in the
1940s dyen hydramine was one of the
first antihistamines that came out and
while it was very beneficial for mild to
moderate allergic conditions it was
associated with a number of side effects
due to the non- selective nature of the
drug binding to and blocking the
acetylcholine receptor and also because
of the ease of crossing into the bloodb
brain barrier. And later in the 1980s,
it's more selective medications like
loredine came out and they had the added
advantage of not only being more
selective but also not crossing into the
bloodb brain barrier as much and
therefore uh they were not associated
with the severity of side effects seen
with the first generation anti-histamines.
anti-histamines.
Lauratine is indicated in allergic
rhinitis. It's in indicated for the
sneezing, runny nose, watery eyes
associated with allergic rhinitis. It's
indicated for hives and other skin
reactions involving heat, redness,
swelling, and itchy sensations.
Yep. So, something like that is what I
would expect for a pass. And once again,
it'll be pretty easy to get a pass. Uh
but as you get into the distinction and
high distinction level, that's going to
be a bit more difficult. Quite a bit
more difficult. And uh what you'll need
to do is supplement your answer with
maybe some additional uh indications. So
you do a little bit of research in
these. We don't need references, but uh
we it will be um good to use the kind of
references that you've been using with
your case studies.
Okay. So unless you have any uh
questions on that, what we'll be doing
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