Full transcript
0:00So, in my anatomy and physiology
0:01classes, [music] we're going into the
0:03unit 2 test covering skin, bones, and
0:05joints. And a lot of the times,
0:07professors give these weird [music]
0:08questions on their exams. So, we're
0:11going to go through 10 really detailed
0:13questions, go through the answers of
0:15them, and these are questions that I
0:16myself have given to students. [music]
0:18So, this will definitely help you as you
0:20are studying for this exam. Hey
0:22everybody, Organized Biology here, where
0:23we make [music] difficult biology
0:25concepts simple. And today I have
0:27written down 10 wonderful questions
0:29about this unit. So the first one we're
0:32going to go into the skin. Describe the
0:35role of keratinocytes and melanocytes in
0:38protecting the body from UV radiation.
0:41So we've got two words here that are big
0:44and long. So let's point those out.
0:45We've got keratin oytes and we also have
0:49melanocytes. Okay. Now, if you've taken
0:52any of my videos before or classes
0:55before, you know that site always means
0:57cell. So, we're looking at the cellular
0:59level of organization. Now, obviously,
1:01if you look at this guy, these are cells
1:03that produce the protein keratin. And
1:06that's going to be a very protective
1:07protein that protects your skin against
1:09abrasion and friction. And the
1:12melanocytes refers to melanin cells.
1:15Okay? So, this is a protein melanin. And
1:18this is going to protect us from UV
1:22radiation. UV radiation. The way we do
1:25that is because this protein almost acts
1:28as like a a sunscreen of sorts where it
1:31will prevent the UV ration radiation
1:33from getting into deeper levels of our
1:35body. So how do we with both of these
1:38cells protect from UV radiation? Well,
1:40let's see what that looks like on the
1:42basil layer of your epidermis. So with
1:45your skin, always remember you got three
1:47layers. You got an outermost layer,
1:49you've got a middle layer, and then
1:52you're going to have, if some teachers
1:54teach it as the subcutaneous
1:56layer or the hypodermis. A lot of the
1:58people uh that I know don't teach this
2:00as a part of the skin. So, these two
2:03layers of skin you've probably heard of.
2:04This is the dermis. And on the top, make
2:07sense. We have the epidermis. Okay?
2:10Epidermis literally translates to upon
2:14the skin. Derm means skin. Now, in the
2:17epidermis, we're going to look
2:18specifically at the bottom layer. This
2:21is called the basil layer of the skin.
2:25They may spell it B- A S A L or add the
2:28extra E. Kind of sounds like basal. It
2:30sounds like some sort of cool Indian
2:33food, right? Or I'm thinking of like
2:35masala. Anyway, that basil layer, if you
2:38zoom in on it, we will see several
2:41different cells. So, here I'm zooming in
2:43on that basil layer. What do we see?
2:45Well, we see these really cool tree
2:48branch looking cells and these are
2:50called our melanocytes. So, I'm going to
2:52draw one of these melanocytes here and
2:56next to them will be the basil cells.
2:58So, right here for example, I'll draw
3:00them in a different color maybe like a
3:01brown. We will have basil cells. Okay.
3:05What you need to know about these two
3:07cell types once again these are your
3:08basil cells and then these are your
3:11melanocytes. What you need to know about
3:14these are they are highly mitoic. So
3:17that means they like to divide a lot,
3:19grow and divide a lot, which makes sense
3:21because they're going to be regenerating
3:23the epidermis constantly with that
3:26stratified squamus epithelial tissue.
3:28Now the basil cells will do just that
3:31and differentiate into cells that we
3:33call keratinocytes. So we'll have
3:36keratinocytes all over the place lining
3:40your epidermis. Now these keratinocytes
3:43are very important in protecting you
3:45from all the external environment right
3:47because the epidermis comes into contact
3:49with the outside world right now in
3:52order to protect from UV radiation which
3:55is coming in right here's your UV
3:57radiation from the sun
4:01I'll put UV rad be a good band name take
4:04notes so there's UV radiation coming in
4:07if we were to not have melanin this UV
4:10radiation could go all the way through
4:12into the dermis into the subcutaneous
4:13and the muscles and cause all sort of
4:15havoc because we know UV radiation can
4:18cause mutations in DNA. It basically
4:21makes the backbone of the DNA kind of
4:23sticky uh in certain bases of the DNA
4:26and it causes some issues which could
4:28lead to cancer. So that's why we say UV
4:30radiation could potentially increase
4:32your risk for cancers. Now in the
4:34melanocytes however we said that they
4:36produce that melanin protein and that's
4:38going to protect us from the radiation.
4:41Well the way they do that is they
4:42package it into these little vesicles
4:44that we call melanosomes. So I'm going
4:47to say these are called melanosomes.
4:51Okay. Now the problem with this is that
4:54the melanocytes are every about 1 to 10
4:57cells. So really, we've got one melanocy
4:59here and then if we keep going across
5:01the epidermis, there might be one way
5:03the heck over here. The problem with
5:06that is now what if the UV radiation
5:09kind of came in between? So what if it
5:10was like going this way? Well, there's
5:12no melanocy in between, right? So we
5:15need some way to spread the melanosomes
5:19with the melanin pigment inside
5:21throughout the whole epidermis. And
5:24that's exactly what we do. The way this
5:26happens is as we produce those melanin
5:29pigments proteins inside the
5:31melanosomes, the keratinocytes
5:34will quite literally nibble off some of
5:37the melanin. So this cell right here
5:40will fagitize ever so slightly some
5:43melanin and this one will as well and
5:45will continue to transfer all of that
5:47melanin to all of our keratinocytes
5:51which is really fascinating. So all of a
5:53sudden as these keratinocytes eat quite
5:55literally the melanosomes they will fill
5:58with melanin as well. And as we continue
6:01to do that and the melanocytes continue
6:03to branch off and off and off and off we
6:06almost form this full thing of treel
6:08like shade the melanin protein all
6:11throughout the epidermis. Okay? So just
6:14think of it like that. This is like a
6:16branch tree the melanocy branching off
6:18to the sides into upward. Same thing
6:21with the guys way over here. They'll be
6:22branching up and upward and all the
6:24keratinocytes will nibble off melanin
6:26giving you protection all the way
6:28throughout your epidermis. So that is
6:30how both cell types are vitally
6:33important in protecting from that UV
6:34radiation. Okay. Next up, a burn
6:37destroys both the epidermis and the
6:39dermis. Classify the burn and explain
6:42why it may be life-threatening. Oo,
6:44that's dangerous, right? So, I'm going
6:45to use that skin model again. We get the
6:47epidermis and the dermis. And we have
6:49some sort of burn that's going to damage
6:52all the way through both of these. So
6:54we'll say this is the burn, right? All
6:56right. It's very, very nasty. Now,
7:00what classification is this? Well, we
7:02classify burns based on depth. So if
7:05this would have been a firstderee burn,
7:07which it's not, it would have only burnt
7:09through the epidermis. So we consider
7:12that the first degree burn. However, if
7:14we go deeper into the dermis, we call it
7:17a second degree burn. And if we get down
7:20into the hypodermis, we'll call it a
7:22third degree burn. If it gets into the
7:24muscle tissue, the bones, that's going
7:26to be a fourth degree burn. So,
7:28obviously, in this case, we went through
7:29the dermis. We're going to have this be
7:30a secondderee burn. Now, that doesn't
7:33seem too bad, right? It's just kind of
7:35cutting a very, very small bit of your
7:37skin. But why is this life-threatening?
7:39Well, we know in the dermis this is a
7:42tissue type called dense irregular
7:47connective tissue. Dense irregular
7:49connective tissue. Now, with that, we
7:51know that there's a lot of different
7:52cell types in here. There's going to be
7:54like um sweat glands in here. So, the
7:56cuboidal cells, there's going to be
7:57fibiberblasts all over the place. So,
7:59these cells require a pretty darn good
8:03blood supply. So, in the dermis, we've
8:05got a very good blood supply. basically
8:08feeding all the cells inside of the skin
8:11as well as the basil cells of the
8:12epidermis. Okay. Now the problem with
8:15that burn is that now we have exposed
8:17the bloodstream to the outside
8:20environment. We don't like that. We
8:22don't like our blood to be in contact
8:24with the outside environment. Now why
8:26could this be life-threatening? Well,
8:28one is we could have a massive risk for
8:31dehydration
8:32especially if it is a widespread burn.
8:36That's because the more blood and
8:38intracellular fluid you're exposing to
8:41the outside environment, the more that
8:43water will evaporate and you'll you'll
8:45lose fluid out of your body really
8:47quickly because we know one of the
8:48functions of the skin is insulation. And
8:52one of the main ways we have insulation
8:55in our bodies through our skin is
8:57because of that epidermal layer. If we
8:59didn't have that, all of our fluid would
9:00just evaporate out. Now, the second main
9:03concern is going to be infection.
9:06Obviously, if you ever have a burn
9:08patient, one of the first things you're
9:10going to get as a burn patient is going
9:12to be a wide spectrum of antibiotics.
9:15Antibiotics fight bacteria because on
9:17your skin, man, there are millions of
9:19little microbes that are just sitting on
9:21the epidermis and they could hop a joy
9:23ride into your bloodstream. If they get
9:25into your bloodstream, that could cause
9:27a widespread infection called sepsis,
9:30where you basically have an infection
9:31that's spreading throughout many parts
9:32of your body. Or you could just get a
9:34localized infection in that area, and it
9:36could build up, cause a lot of just
9:38damage, inflammation, and potentially
9:41necrosis, death to that tissue. You
9:43could have lymphatic issues. All sorts
9:45of things could occur if that burn
9:48damages into the dermis. So that is why
9:50it's life-threatening specifically for
9:52dehydration and infection as well as
9:54other complications. This is a fun one.
9:56So a patient presents with yellowish
9:58skin. Which organ system might be
10:01malfunctioning and why would this change
10:04our skin color? Okay, so first off we
10:07know that I just talked about the
10:09epidermis and dermis. Now if we look at
10:11the epidermis, it's very very thin.
10:14Okay, so here's your epidermis. Very
10:16very thin. And then the dermal layer is
10:18the thickest layer of the skin and
10:20obviously it has that blood supply. So
10:22I'm going to write epidermis and then
10:24we've got that blood supply. Now we know
10:27the blood supply is relatively close to
10:29the surface of the skin. So we know
10:32blood components as well as the diameter
10:35of the blood vessels can influence our
10:37skin color. As an example, when you are
10:40exercising, what happens is your blood
10:43vessels in your skin, if you're getting
10:45too warm, will actually vasoddilate.
10:47They'll open up and that vasoddilation
10:50will lead to looking red, right? Because
10:53the blood is closer to the surface of
10:55the skin. But let's say you're going for
10:57a walk outside in like the frigid tundra
10:59of Russia. And what will happen is your
11:01blood vessels will actually vasoc
11:03constrict trying to keep your blood a
11:06little closer to the inside environment
11:08of your body which is warmer. That vasoc
11:10constriction will make you appear pale.
11:13Okay. So both the blood components and
11:16the actual size of the blood vessels can
11:18influence your skin color. Now yellowish
11:21skin. Now I only have the color orange.
11:23So we're going to use orange. But why
11:25would our skin appear yellow? Well, it's
11:28because there's going to be a pigment in
11:31your bloodstream that will actually be a
11:34yellow pigment. We call this Billy
11:38Rubin. Billy Rubin is the cause of
11:42yellowish skin. Now, Billy Rubin
11:45shouldn't really be in your blood in
11:47high amounts. Why is that? Well, we know
11:49you have an organ. So, here is the organ
11:52system part called the liver.
11:55And one of the goals of the liver is to
11:57recycle and like basically take out bad
12:00stuff um and put it into the intestines
12:03and then keep some good stuff in the
12:04body. Now what do I mean by that? Well,
12:07let's start from square one. We have
12:10cells in our body called red blood
12:12cells. They we have so many of these. In
12:14fact, we create and destroy about 6
12:17million every second. That's crazy. Why
12:20is that? Because red blood cells get
12:21broken down really easily. They're like
12:23a Chevy car. Sorry to all of you who
12:24drive Chevys, but over like the period
12:27of 60 to 90 days that they're alive,
12:29they might just get banged up a little
12:30bit. Now, when we do that, we need to
12:32break down this red blood cell. And we
12:34do that with a macroofage that will So,
12:38a macroofage is basically a big white
12:39blood cell. So, imagine this big white
12:41blood cell coming in and it's going to
12:42eat this thing right now. We eat that
12:45red blood cell and we will actually
12:47break it up into several different
12:49components. One of the byproducts of
12:52this whole process is something called
12:55Billy Rubin. So I'm going to draw this
12:57like this and this is that Billy Rubin.
13:00Okay, so we're basically converting the
13:01components of the red blood cell. If you
13:03really want to know about it, you can
13:04watch my video on red blood cell
13:05recycling. But this Billy Rubin is then
13:07tossed into the bloodstream. Okay, now
13:10the problem with Billy Rubin is that it
13:12needs to be um uh basically dissolved in
13:16the fluid of the blood. Billy Rubin is
13:19very uh hydrophobic
13:21which means it does not dissolve in the
13:23blood well. So what we do with it once
13:25we toss it into the bloodstream here is
13:28we have to carry it with a carrier
13:30protein. I promise I'll answer the
13:31question here in a second. So here's a
13:33little carrier protein. This carrier
13:35protein is called albamin and it
13:36basically helps
13:38that billy rubin dissolve in the blood.
13:41Well where does this eventually go? We
13:43can't have too much of this in the
13:44bloodstream. Well, obviously you see me
13:47drawing this going to the liver. At the
13:49liver, the liver will conjugate this
13:52billy rubin. Okay, basically means it
13:54makes it hydrophilic. So, it'll take an
13:56enzyme, okay, and take that Billy Rubin
13:59and basically coat it. It combines it
14:01with something called glucaronic acid.
14:03And then it'll toss this conjugated
14:06Billy Rubin conjugated
14:09Billy Rubin
14:11into, interestingly enough, the
14:13intestines. So here's our intestines
14:16through the gallbladder, interestingly.
14:18So you'll have a little gallbladder
14:19here. It'll spew it out into the
14:22intestines. Now eventually it'll turn
14:23into the large intestine and it will go
14:25out of your body. So here's the
14:27intestines eventually. And we toss that
14:30out of the body. Um and that actually is
14:32what give your gives your poop the brown
14:34tint to it. You don't care about that.
14:35Okay. So why do I have to mention all
14:37this in terms of skin color? Well, think
14:39about it. If we need to take this to the
14:42liver to eventually process it out in
14:44our feces, what would happen if the
14:46liver began to fail? Let's say you're an
14:50alcoholic. You're drinking too much
14:52alcohol and you damage the liver. It
14:54becomes it has cerosis in it. So,
14:55inflammation inside the liver. Well, now
14:58what will happen is we will continually
15:00be producing Billy Rubin, Billy Rubin,
15:01Billy Rubin. And what will eventually
15:03happen is the liver will slow down its
15:07processing. Okay? Okay, it's just like
15:09an assembly line. If one person slows
15:11down the assembly line, things start to
15:12back up. So now we will start seeing
15:15more and more Billy Rubin in the
15:18bloodstream because we still got to
15:20recycle our red blood cells constantly,
15:22but the liver can't keep up with that
15:24production and the Billy Rubin will back
15:27up into the blood. It will appear as a
15:30yellowish skin color. So, interestingly,
15:32if you see an adult with uh basically uh
15:36yellow skin, that is something called
15:38jaundice and it is an indicator that
15:41their livers are failing. You also may
15:43see this in babies because they're
15:45starting to learn basically how to
15:47process this stuff out uh in their own
15:49bodies. It's usually normal. You can put
15:51them under a blue light, interestingly.
15:53Um and it'll help basically clear those
15:55different pigments out. But again, this
15:57is called jaundice. gives your skin
15:59yellow color and it is life-threatening
16:01if it's an adult because their liver is
16:03failing. Very good. All right. So, now
16:05we're into the skeletal system. Compare
16:07compact bone and spongy bone in terms of
16:09structure, blood supply, and mechanical
16:12function. Okay. So, with this, we're
16:14looking at any bone of the body. Now,
16:17with any bone, this is the femur
16:19specifically. So, we're going to be just
16:21using the leg, the main leg bone of the
16:23body. And in the femur, the bone is
16:25going to be different depending on where
16:27we're talking about. So, generally along
16:29the outside of any bone of the body, we
16:33will have something called compact bone.
16:35So, I'm going to kind of draw an outline
16:36here all the way through the femur. And
16:39on the outermost part of the femur,
16:41we're going to have compact bone. Okay.
16:44The name is exactly what it sounds like.
16:46It is very dense and compact and
16:48mineralized. There's really no openings
16:51to all of that compact bone section. But
16:53then on the inside part, the interior
16:56side, so the deep part of the bone, we
16:58will have little things that look almost
17:01spongylike. Okay? And this is obviously
17:04going to be called spongy bone. So I'm
17:06just going to draw a bunch of lines and
17:08dots here all the way throughout the
17:10inside of the bone. And this is going to
17:12be our spongy bone. Now, that does not
17:15mean that it feels spongy. All of this
17:17is the same bone material. It's
17:19mineralized. It's called hydroxyapatite.
17:22That's actually the main part of the
17:24bone. Okay. And that hydroxyapatite is
17:27going to be made of some calcium and
17:29phosphorus that is actually mineralized,
17:32crystallized, and it makes it very, very
17:35hard. In fact, pound-for-pound, it's
17:37denser than concrete. Now, if we think
17:40about it, however, calcium and
17:41phosphorus are not alive, right? But our
17:44bones we know are living tissue. So we
17:46have to have cells inside of them. So we
17:49need to look deeper into the spongy and
17:51compact bone to actually see the cells
17:53so that we can see how this is
17:54connective tissue. But before that let's
17:57answer the mechanical side, right?
17:59What's the mechanical function of both
18:01of these? Well, in the compact bone, you
18:03can probably predict this is going to be
18:05mainly for protection, right? So the
18:08protection is going to be very very hard
18:10bone on the outside part of the bone. So
18:12if that bone were to get hit in any way,
18:15shape or form, the compact bone would
18:17basically protect the inner parts.
18:19However, you also see the spongy bone
18:21that is a little more loose. There's
18:23some openings inside. In fact, inside
18:25the spongy bone, there's going to be
18:26something called marrow, either red or
18:30yellow marrow. So we'll have yellow
18:32marrow, preferably in or mostly in the
18:35long bones. And then we'll also had red
18:37marrow in the flat and irregular bones.
18:41So mechanically, however, what's the
18:43point of spongy bone? Why would we want
18:45it to be all loosey goosey inside of our
18:48bones? Well, this allows our bones to be
18:51lighter. Okay, so now they're going to
18:54be less dense. They're not as compact
18:55all the way through. It's going to allow
18:57basically for some space inside. So our
19:00bones can be lighter. So we don't have
19:01to like pick up our legs in order to
19:03move it. Our bones are very light. In
19:05fact, in birds, the compact bone layer
19:08is so so so thin. So the bones can be
19:11really light so that they can fly. So it
19:13makes us lighter. And the second thing,
19:14it almost serves as a scaffolding. Okay,
19:17what do I mean by that? Well,
19:18scaffolding holds things up well. And so
19:21we'll see in the in the spongy bone,
19:24there will be these long lines that are
19:26basically traveling through the
19:27diaphosis, the main shaft of the bone.
19:30And these lines are going to be called
19:32stress lines. So all of your bones will
19:35organize their uh sorry stress lines.
19:38All of your bones
19:40never speak and write at the same time.
19:42It's difficult. All of your bones will
19:43have these stress lines associated with
19:46them. So that basically means the force
19:48will be redirected down the shaft of the
19:50bone and the spongy bone will basically
19:52organize itself based on where that
19:54stress is coming from. That's called
19:56Wolf's law. Okay. Now moving on. That
19:59was the mechanical, but what about like
20:00the blood supply and what about the
20:01cells, all the stuff that's inside of
20:03it? Well, let's separate these out.
20:05We're going to draw basically a
20:06cross-section of spongy bone and we're
20:09going to do a cross-section of compact
20:11bone. So, we'll do spongy bone here and
20:14we're going to do compact bone here.
20:16Again, let's remember that bone tissue
20:19is connective tissue. And with any
20:22connective tissue, we're going to have
20:24cells and then we're going to have
20:26matrix essentially. So, gels and fibers
20:28is how I usually remember it. But in
20:30this case, our gels and fibers are going
20:33to form our hydroxyappatite.
20:35And we'll also have collagen fibers
20:38inside of them that we won't necessarily
20:40see, but think of collagen as like the
20:42steel rods of the of the bone matrix
20:45itself. Keeps it upright and strong.
20:47Hydroxy appatite is much more like that
20:48concrete, really hard and dense, so it
20:51protects us. Now, let's zoom in on
20:53spongy and compact bone. Let's do
20:56compact bone first. In compact bone,
20:58you're going to see a very big dark
21:00circle in the center and you're going to
21:02have these concentric circles around it.
21:06So, we're going to basically have all
21:07these concentric circles around that
21:10central area. It almost looks like a
21:12tree ring. And inside the compact bone,
21:14you're going to see some cells dotted
21:16throughout. Maybe like here, here, and
21:19here, and so forth. So, I'll draw a few
21:21around. Okay. So, what did we do here?
21:24How how did I get this picture? Well,
21:26it's basically like we're zooming in on
21:29part of that compact bone. So, that's
21:31what we're looking at here. So, you can
21:34see in the center, we aptly name this
21:37the central canal. Central canal. And
21:41I'm drawing it in red because there's
21:43going to be a very good blood supply
21:45running through this. Okay. Now, this
21:48part that actually runs through the
21:50entire length of the bone is called the
21:51hverian canals. And then we'll also have
21:54basically sideways perpendicular uh
21:57blood vessels that are going to be
21:58called Vulksman's canals. So horizontal
22:01will be these Vulkman's canals. I think
22:03I'm spelling this right.
22:05Canals. And then if we're running up and
22:08down, we're going to have these things
22:10called Hverian
22:13canals. And that's going to be basically
22:15our central canal that we're looking at
22:17here. Okay. Okay, so we got the blood
22:19supply, but we also see that we have
22:21these concentric rings. We call each
22:24layer of the compact bone. Remember,
22:26this is really dense tissue. Like if I
22:27were to feel this, it's really hard and
22:29strong because it's made of hydroxy,
22:30appetite, and collagen. Each ring is
22:33going to be called a concentric because
22:36we're making basically concentric
22:38circles on itself. Lamela. I almost
22:41think of lamela as layer. So concentric
22:44layering of the compact bone. Now here's
22:48the problem that I want to present. If
22:49we have the blood supply here and we
22:51have cells way out here, these are
22:54called osteocytes.
22:57Okay, how do the osteoccytes get
23:00nourished if there's basically concrete
23:02in between the cell and the central
23:04canal? Well, we know that there will
23:07actually be these very very thin I'm
23:10going to call them canals and they're
23:12called canaliculi. Okay. So, there's
23:14going to be these canals that are
23:15running almost like spokes on a wheel
23:17all the way throughout this compact
23:20bone. So, again, these little tiny
23:23canals are literally called canaliculi.
23:27Canaliculi.
23:31There might be an extra n there or
23:32something. I'm not sure. So, canaliculi
23:34or in a single canaliculus. You may hear
23:36both of them. That's going to deliver
23:38the blood to all of these cells. Okay?
23:40So that's how we get it from basically
23:42the central canal out through the
23:43canaliculi feeding these osteoccytes.
23:45Now the osteocytes literally translates
23:47to bone cell and these are going to be
23:51our maintainers. They are basically
23:53maintaining the matrix of the bone
23:55tissue and there's not a whole lot to
23:57do. They're just going to keep things
23:59pretty well and constant. All right. Now
24:02this whole unit of compact bone we call
24:05an oion. Okay. Oion. So great blood
24:10supply in the middle got some
24:11osteoccytes doesn't change much but it's
24:13protecting us from basically external
24:15damage. Then we look at the spongy bone
24:17which is very very different. In spongy
24:20bone we are going to have the unit call
24:22a tacula tacula
24:26or tbecula. And it's as if we are
24:28zooming in just on one little section.
24:30So, this is really hard to kind of draw
24:32just with a marker, but it's as if we're
24:34zooming in on the particular spongy bone
24:38matrix that is kind of forming these
24:39little scaffolds, right? And we're
24:41looking inside of it. Okay? It's like
24:43we're looking at a scaffolding beam that
24:45is a cross-section. Kind of weird to
24:47think about. Okay. Um, so let's look at
24:49it. Well, what do we have? Well, we've
24:51got some cells on the inside. We will
24:53also have those lamela. Okay. So very
24:56similar, but in this case, we're going
24:58to have these big cells on the outside
25:00that look kind of like this. We're also
25:03going to have lining cells around the
25:05outside like this all the way
25:07throughout. I'm not going to draw all
25:09the way through, but there's going to be
25:10a lot of cells on the outside. And we'll
25:11also have some cells here in the middle
25:13of that rod as well. Now, you may notice
25:17a very big difference. Number one is we
25:20don't have that big central canal.
25:22However, we do have canaliculi. So there
25:25will be these lines running through like
25:27spokes of a tire. But the question is
25:30where is the blood coming from in this
25:31case? Well, in this case the blood
25:34supply is actually coming from outside
25:37in. Why? Because all this space outside
25:41of the tbecula itself is going to be
25:45basically marrow. We call this marrow
25:48because there's some gelatinous fluid.
25:50There's some blood all the way
25:51throughout wrapped around the
25:53scaffolding rods. Okay. So it's as if
25:55around this rod there's a bunch of blood
25:57supply just running right next to it.
25:59And this is all in different marrow.
26:01Okay. So that's how we get the blood to
26:04the cells. But we have three different
26:06types of cells here. We have on the
26:09inside we have those osteoccytes again.
26:11So these are all osteoccytes the
26:13maintainers. But we also have two other
26:15cell types. These big ones are called
26:17osteoclasts.
26:19They actually kind of look like the
26:20little Pac-Man ghosts. If you've ever
26:21played Pac-Man they kind of look like
26:23the ghosts. Now, class means to break
26:26apart.
26:27So, these are cells that are actually
26:29going to dissolve bone if we ever need
26:32to basically remodel the bone. It'll
26:34kind of dissolve it, break it down, and
26:36actually release some of the calcium
26:37into the bloodstream. Whereas, on the
26:39flip side, we also have our osteoblasts.
26:42Osteoblasts, as you could probably
26:44guess, are the bone builders. So they
26:47are going to add to the matrix of the
26:50tbecula and help build up that spongy
26:53bone tissue. So as we can see spongy
26:57bone has all three cell types. Therefore
26:59we can remodel spongy bone a lot better
27:03than we can compact bone because we only
27:05have osteocytes in the compact bone.
27:07Okay. So that's the hisytological or
27:10tissue difference between spongy and
27:12compact bone. Both of them are
27:14important. This one's more for
27:15protection. This one's more for
27:16scaffolding and can be remodeled based
27:18on those stress lines. So based on what
27:21pressure you put on your bones, the
27:23trabacula will reorient themselves to
27:25basically support you through that
27:27stress. Okay, next up, a child has a
27:30fracture across the epiphysal plate or
27:33the growth plate. Why is this more
27:34concerning than the same fracture in the
27:37diaphosis? Okay, so we need a little
27:39more bone anatomy here. When we look at
27:42any bone, I'm just going to draw it as a
27:43rectangle to make it easier. The main
27:46shaft of the bone right here is going to
27:48be called the diaphosis. Okay, that
27:51means through basically the functional
27:54unit. So, it's basically through the
27:56bone, the shaft of the bone. Okay? Now,
27:58on the ends in children, we will see
28:01these dark lines of cartilage. So, I'm
28:03going to draw these dark lines here, and
28:06these are cartilage, specifically
28:08highland cartilage. And we call these
28:10the epiphosal
28:13plates. Okay, epiphysal plates otherwise
28:17known as our growth plates.
28:20Now this is basically where bone can
28:23develop into. So say we have like
28:25osteoblasts and osteoclast down here. We
28:28can lengthen the bone by growing into
28:30that cartilage. So as we do that
28:33obviously say we were to do that um for
28:35a little while and now we're turning
28:36into an older and older child we can
28:39actually lengthen that bone and if they
28:41are still growing we'll still see that
28:44epiphysial plate because again we're
28:46growing into that cartilage. That bone
28:50development into cartilage is called
28:52endocchondrial
28:54okay into cartilage oification otherwise
28:58known as bone development or bone
29:00growth. So in order to grow essentially
29:03we need these growth plates because bone
29:06really can't develop and lengthen into
29:08bone. We have to have cartilage. Again
29:10this epiphysial plate if you have this
29:12on a test is made of hyelin cartilage.
29:16Okay. So if a child, let's do the easier
29:20fracture. If a child were to get a break
29:23in the diaposis. Let's say there's a
29:24breakage here. What would happen? Well,
29:27we have basically broken bone tissue.
29:29Okay. What will happen first is there
29:31will be a lot of internal bleeding,
29:33which is actually a good thing. We're
29:35going to have a hematoma form here. And
29:38luckily we will have tissue called the
29:40endostium that will be wrapped around
29:43from here to here and form what's called
29:47a callus once we oify that. So that's
29:49called a callus. Okay. Now as the bone
29:52realizes, wow, we just broke that's not
29:55a good thing. It will redevelop all of
29:57its bone tissue into that area into that
30:00space with all the blood. It will
30:02actually calcify in the callus. So we'll
30:05have kind of some bumps on our bones and
30:06eventually our osteoclasts
30:08will trim those down, trim those down,
30:10trim those down until we have a
30:12relatively smooth bone. Now that's not
30:14always the case. Sometimes you can still
30:16feel a callus like if you broke your
30:17collar bone, you might be able to feel
30:18where it broke. Um but typically we will
30:20shave it back off. The problem becomes
30:23what if we have that damage in the
30:25growth plate. So now let's say we damage
30:27it right here. Okay. Well, the bone will
30:30get that signal, right? and it will
30:32begin bleeding internally. So now we've
30:35got bleeding in here. Well, the bone
30:38wants to fix itself. That's its main
30:40priority. So a lot of the times we will
30:42regenerate bone tissue here and we'll
30:45also regenerate bone tissue into this
30:48area itself.
30:50So now instead of it being hyelin
30:52cartilage, what is this tissue right
30:55here? It's actually bone tissue. Why
30:59would that be a problem? Well, now if we
31:02have bone tissue, we cannot develop bone
31:05into that. We can't lengthen this bone,
31:07right? We had to have that clear line of
31:09cartilage to grow the entire bone. So
31:12now this bone potentially will not be
31:14able to grow this direction anymore. So
31:17let's say the kid is only 8 years old
31:19and this is like their femur. Well, now
31:21their femur will not be able to develop
31:22properly. And now you might have one leg
31:25longer than the other because the other
31:27leg's growing just fine, but the broken
31:28leg does not. Okay, so a lot of the
31:31times this is a very concerning thing
31:33for doctors and they've got to do all
31:34sorts of different interventions to try
31:36to mitigate it. All right, y'all. This
31:38will be a quick one. Osteoclast activity
31:41increases dramatically in a patient.
31:43Predict how this will affect blood
31:45calcium levels and bone density. Okay,
31:48so we were talking about how the
31:49osteoclast are basically these weird
31:51looking uh ghost cells. Okay, and they
31:53literally have these little projections
31:54inside of them. Again, these are
31:56osteoclast. What do you remember about
31:58them? Well, they are the bone breakers.
32:00Okay. So, if we have bone tissue right
32:02here, so here's some bone tissue. We
32:04know the bone is made of calcium and
32:07phosphorus. Now, what could happen is if
32:10this osteoclast activity ramps up. So,
32:12now these osteoclast are super hyper for
32:14some reason. Interestingly, this happens
32:16as you age. These guys just get really
32:18excited as you age. Not sure why. Maybe
32:19they're having a party. They're like,
32:20"Woo, you're getting older." Anyway, but
32:23that's not good. Why? Because they will
32:25release these digestive enzymes. Okay.
32:28And they're actually uh it's actually
32:29acid, too. And it'll actually break off
32:32some of the bone tissue. So, I'm going
32:34to draw calcium as these tiny little
32:36dots. And we're breaking off some of
32:38that bone tissue. Now, that calcium will
32:40free itself, and it's going to dissolve
32:42as calcium 2+. That basically just means
32:45it is now dissolved in the fluid. That
32:47calcium will find its way into the
32:49bloodstream. That's right next to all
32:51those osteoclass. Remember, in the um
32:53the bone marrow, in the spongy bone.
32:55Okay. So obviously your blood calcium
32:58levels will dramatically increase. What
33:00will happen to your bone density?
33:03Well, obviously we're kind of chiseling
33:05off some of your bones. So now your
33:07bones will get potentially very holy,
33:09right? And holy bone syndrome is
33:12literally called osteoporosis,
33:15the condition of holy bones. And no,
33:18that does not mean you are a saint.
33:20However, as you get older, hopefully you
33:21are becoming more like a saint. But it
33:23literally means that you have holy
33:26bones. Basically openings inside your
33:28bones because the osteoclasts are
33:29breaking them down, releasing the
33:30calcium into the blood, raising your
33:32blood calcium dramatically. That could
33:34lead to seizures. It could lead to heart
33:35palpitations and other issues and
33:37potentially muscle contraction and
33:39spasms and other things like that
33:40because calcium is important in neural
33:42transmission as well as muscle
33:44contraction. All right, Elsa. Now we're
33:45into joints. So this is going to be a
33:47quick overview of joints. Classify the
33:49structure and functional type of the
33:51following. the intervertebral disc
33:53joint, the suture between cranial bones,
33:55and then the shoulder joint. Okay, so
33:58what they're describing here, the I I'll
34:00write them out here real quick. So, we
34:02have the intervertebral,
34:04if I can spell that. [laughter]
34:07Man, I'm struggling. Interver Oh, that's
34:10what I missed. The R vertebral
34:14disc joint.
34:16Okay, we also have the sutures between
34:19the cranial bones. the cranial bones.
34:23And then we lastly have the shoulder
34:25joint. Okay. Now, hopefully if you've
34:28gone through this class, you know that
34:30joints have three major classifications.
34:33Yes, the we're going to have the
34:35cartilagynous joints, we're going to
34:36have the fibrous joints, and then we're
34:38going to have the synenovial joints. So,
34:39let me write those down real quick in
34:41case you don't know them. They're going
34:42to be the cartilagynous joint.
34:46We'll also have the fibrous joints. And
34:49then we're also going to have the
34:50synenovial joints. Now, if your teacher
34:53is good, chances are they've spent more
34:55time on these guys than these guys. Why?
34:58These are highly movable and they're the
34:59most common in your body. These are less
35:02common. But let's just step back. What
35:04the heck is a joint? It's just basically
35:06a space between two bones. Okay? So,
35:11where two bones come together, what's in
35:14between the space? Well, you could
35:15probably guess in the space between
35:17fibrous joints. So, when we have two
35:20bones coming together forming a fibrous
35:21joint, the only thing we're going to
35:23find is going to be ligaments. Ligaments
35:26are those dense regular connective
35:28tissue really connecting things very
35:29well. So, in a suture as an example,
35:32let's say we have a bone here and then
35:34we'll have a bone right next to it.
35:36Okay? So, these are especially your
35:38cranial bones like maybe your frontal
35:40bone connected to the parietal bone. We
35:42will have sutures connecting them. This
35:44is going to be a sutral
35:47joint. Why do we call it a sutral joint?
35:49Well, if we zoom in on this sutral
35:51joint, what we will see is the two bones
35:54coming together. But the way they are
35:57coming together is through literally a
36:00suture of a ligament that will look like
36:02this. Okay? So, you know, like a suture
36:05is almost like um when you're stitching
36:07somebody back together and you have
36:08those loops and you're tying it back up.
36:10Well, these are called sutural. this
36:12going to be S ligaments.
36:15And these sutral ligaments are super
36:17super strong. Ligaments can withstand a
36:19lot of force and they're basically
36:21cementing these two bones together with
36:23this sutral ligament. Okay. Now, there's
36:25other fibrous joints I won't get into,
36:26but it's the key there is we only have
36:29ligaments between the two joints. Okay.
36:31Now, in the cartilagynous joints, we can
36:34decide which cartilage um is between the
36:36joints. So, we can have fibroartilage.
36:40Okay. We can also have hyelin cartilage
36:44and we can also have elastic cartilage.
36:47So there's three different types. The
36:49highland one would be like the space
36:51between your your sternum and your rib
36:53bones. There's that highin cartilage.
36:55That'd be a cartilagynous joint. The
36:57elastic cartilage would primarily be
36:58found um in the epiglatus and there's
37:00really no attachment. So we don't talk
37:02about that as much. So we don't really
37:04talk about that as a joint but it's just
37:05elastic cartilage. But then the
37:07fibroartilage joints. That's what we're
37:09talking about here with the
37:10intervertebral disjoint. Fibroartilage I
37:13want you to think of as like a
37:14temporedic mattress where we've got
37:17basically these two vertebrae. I'm not
37:18going to draw them perfectly. Here are
37:20your two vertebrae stacked on top of
37:22each other and you know that you are a
37:25bipedal human, right? You have two feet
37:27and you walk upright. So therefore,
37:29every time you jump or walk, there's
37:31pressure compressing those discs or the
37:33the vertebrae together. So let's just
37:35say this is like cervical four and
37:37cervical five vertebrae compressing
37:40together. Well, you would really like to
37:42have some padding between them and you
37:44do. This padding is the intervertebral
37:48disc. So intervertebral disc and it is
37:51made of that fibro cartilage. So
37:54therefore it's like this temporedic
37:56mattress between the two vertebrae. Now
37:59I do need to mention this. There's
38:01fibroartilage yes padding it. But there
38:04also could be some ligaments. So for
38:06example, there are some wings of the
38:08vertebrae. There will be some ligaments
38:10connecting the two wings of the
38:11vertebrae. So really in between the
38:13joint, we're really just focusing on the
38:15fibroartilage, but there could be
38:17ligaments associated with tying those
38:19bones together. What's the difference
38:20between that and this fibrous joint? The
38:23only thing found between it is the
38:25ligament. That's why we call it just
38:26fibrous. This one could be cartilagynous
38:28because we've got cartilage between it,
38:29but there could be ligaments associated
38:31with it as well. Now with the synenovial
38:34joint, the shoulder joint, I'm not going
38:35to draw the shoulder joint because I am
38:36not talented, but with any shoulder
38:39joint in any senovial joint, you will
38:41have a bone coming in and you'll have
38:44another bone right below it. Okay? And
38:47usually the articular process of it, so
38:50the spot that's actually touching or
38:51close to touching the next bone has kind
38:54of grooves that match it. Okay? So think
38:56like ball and socket joint. You got the
38:58acetabulum of your hip. It's like a
38:59socket and then you get the ball of the
39:01femur sitting inside it. So it fits
39:03perfectly inside. Now in between this
39:06space we have several things. The first
39:08thing we will usually see and we will
39:11always see with the synenovial joint is
39:12something called the fibrous capsule. So
39:15this is going to be a fibrous capsule
39:16encapsulating the whole entire synovial
39:19joint. Fibrous capsule and that's going
39:22to keep everything that's inside of it
39:24inside of it and strong and tight. Then
39:28you're going to have the actual
39:29synenovial membrane itself lining the
39:33inside of this whole cavity. Okay? So
39:35I'm going to say this is the synenovial
39:37membrane.
39:39Now with the synovial membrane, this is
39:41a type of cirrus fluid. Cirrus just
39:43basically means we're lubricating spaces
39:46between the body. Now the synenovial
39:48membrane will produce fluid inside of
39:50this capsule and that is going to be
39:52called synenovial fluid. I want you to
39:55think of this as your joints is WD40,
39:58the greaser between the bones that
40:01allows the bones to glide just
40:03seamlessly across in basically a
40:05frictionless environment. So as you're
40:06like contracting, relaxing your bicep,
40:08same thing with this synenovial joint of
40:10your elbow, it's just gliding perfectly.
40:12There's no friction between it. Okay.
40:14Now, that being said, the synenovial
40:16joint contains synenovial fluid. But
40:19you'll likely see like in your knee, you
40:21will often see some ligaments. So we'll
40:23talk about the ACL and the PCL later on.
40:26We'll talk about maybe the LCL and maybe
40:28the MCL, right? You've got these
40:30ligaments connecting the bones together.
40:32So it's not fibrous because it's got
40:34synenovial fluid included inside of the
40:37joint. Furthermore, you'll also see some
40:39articular cartilage on the tips of the
40:41bone. So on the tips of these bones,
40:43you'll likely see this highin articular
40:45cartilage.
40:47Okay? That basically just protects the
40:49bone. It's like a little cap on the
40:50bone. So in a senovial joint, I want you
40:52to remember the reason it's synenovial
40:54is got synenovial fluid, but it also has
40:57cartilage inside of it. It's also got
40:58ligaments associated with it most of the
41:00time, right? So although it contains
41:03these other two components, it is
41:04synenovial because it has that
41:05synenovial fluid. Awesome. All right,
41:08here's a very common occurrence. Sadly,
41:10a football player tears their ACL. What
41:13movement likely caused the damage? Okay.
41:16So, with ACL injuries, we need to
41:18understand it's in the knee, but what
41:20happens? What does it look like? So,
41:22we're going to draw that knee joint
41:23here. And it's not going to be perfect.
41:24Okay. So, just do your best with me. So,
41:26here's your knee joint. Okay. Here's
41:29that tibia.
41:30And we'll also have the femur up here.
41:32So, I'm going to write femur. We'll
41:34write tibia. And then on the lateral
41:37side, we're going to have our fibula
41:39kind of branched off here. Okay. So,
41:42here's your fibula. Now, the fibula
41:44always well tells lies because it
41:46doesn't take any weight, so it is a fib.
41:48But it also tells you to the truth about
41:50what knee we're looking at. If we're
41:52looking at this person anteriorly, we
41:55know this is actually their right knee.
41:58Whoops, right knee. I can't spell knee.
42:01Oh man, that's funny. Okay, this has
42:03been a common occurrence in this video.
42:04So, you're looking at the right knee
42:05because the fibula is always on the
42:06lateral side. Okay, so here's your
42:08lateral side. Here's your medial side.
42:10So let's mark that L and M. That's going
42:13to become important because there are
42:15several ligaments associated with this
42:18um synovial joint. So first off, we've
42:21got our ACL. ACL is going to attach from
42:24the back of the femur. So I'm going to
42:26do a dotted line to the front of the
42:29tibia. So back of the femur to the front
42:31of the tibia. And then the PCL is going
42:33to be behind it. And it's going to
42:35basically do the equal and opposite.
42:37Okay? So it's going to come in here and
42:39attach about to the top of the tibia.
42:41Whereas we also have our lateral
42:44collateral ligament and our medial
42:47collateral ligament. So let's label all
42:48these. This is your LC here. This is
42:52your MCL here. What does that stand for?
42:56Lateral collateral meaning around the
43:00outside ligament. This is going to be
43:02our medial collateral ligament because
43:05it's on the medial side on the outside.
43:07But then we mentioned the ACL here and
43:11then the PCL
43:14here.
43:15Okay. Why those names? Well, anterior
43:18and posterior. So this one's in front,
43:20that one's in back. That C stands for
43:24cruciate. Okay, cruciate means cross.
43:28Just like crucifix in uh in the Bible is
43:30basically a cross. Jesus died for our
43:33sins on the cross, right? And so that's
43:34where um that's why we need him, right?
43:38[laughter] Pun intended. Okay, so we got
43:40the ACL and PCL. Now, in this case, the
43:42football player, right, tore their ACL.
43:45Now, I want you to remember that
43:47ligaments don't like to stretch.
43:49Ligaments do not like to stretch. They
43:54are very very strong in one direction
43:57but if they stretch they have risk of
43:59just popping okay they can't take a lot
44:01of force. So what's going to happen is
44:03that ACL just think of it extending. If
44:06it were to get forced that direction and
44:08that direction we will likely have some
44:11rupture. So, usually what happens is,
44:14think about this, if we have some sort
44:16of uh blunt force to the towards the
44:21medial side of the knee from the lateral
44:23side, that force, if you think about it,
44:26is going to force the knee inward. What
44:29will that do? Well, this lateral side
44:31and this medial side will pull apart,
44:33right? It'll pull apart and that will
44:35potentially cause it to tear. So anytime
44:38we have a lateral force going in on the
44:40knee, that is one mechanism of how we
44:43can damage it. At the same time, we can
44:45also have an anterior action hitting
44:47this way, pushing that tibia backwards
44:49and the femur backwards, and that can
44:51also pop it because remember we're
44:53connecting front uh back to front. And
44:55so if we pull those apart, essentially,
44:57if you get hit in the femur, especially
44:59you get hit in the femur, pushes it
45:01back, it'll also pop it apart. Now, the
45:04more common one isn't the lateral force
45:06and isn't the force to the femur, but
45:08it's actually an internal
45:12rotation
45:14of the knee. I can't draw this very
45:17well, but what that looks like is as if
45:19you are running in a straight line to
45:21the right. So, I'm talking about my
45:22right knee, right? Running to the right,
45:23run to the right, and then you stop and
45:25you pivot inward. If you were to do
45:27that, let me kind of show with my phone
45:29real quick. So you're planting right
45:31with your right knee and you're going to
45:33turn inward. So you're trying to push
45:35out. Yes. What does the knee do? Well,
45:37it internally rotates. And again, that's
45:40going to put stress on that ACL. Again,
45:42that ACL is like this. And now it's
45:44pulling apart and it could potentially
45:47pop just like that. All right, just two
45:49more. Y'all are doing great. And if this
45:51has been helpful, please consider liking
45:52this video, subscribing to the channel,
45:54uh ordering some stuff from our shop,
45:56and that type of thing. and be happy uh
45:58to continue making videos like this for
45:59you guys to be successful. So here we
46:01got explain why osteoporosis is more
46:04common in post-menopausal women and
46:06describe one physiological mechanism
46:09behind this. Okay, this will be a pretty
46:10short one. So if you are post menopause,
46:14so post menopause
46:17that is basically when the ovaries stop
46:19producing estrogen. Okay, so you're
46:22going to have low estrogen amounts.
46:25Okay. And that basically renders you
46:26infertile because it's a vital hormone
46:28to basically prepare your body um to
46:31make the uh egg as well as to release
46:34the egg. Okay. Now, what estrogen goes
46:36from is something about 15 to 350
46:41pogs per milliliter. That's
46:43premenopausal. When you are
46:45postmenopausal, you have less than 15
46:48pigs per milliliter. So, it's a drastic
46:50drop in this hormone estrogen. Okay?
46:54Now, that can cause hot flashes, a
46:55variety of other very annoying symptoms.
46:58But one of the main things estrogen
46:59normally does if you have plenty of it
47:02is it stimulates osteoblast
47:06activity. Okay? So, if you have
47:08estrogen, it stimulates osteoblasts.
47:10These are your bone builder cells. They
47:12keep your bone strong and dense. It also
47:16inhibits Okay, so prevents from acting
47:20osteoclast activity. Okay? So it
47:23prevents the bone breakers from
47:25basically breaking down your bone too
47:26much. Now take estrogen out of the
47:29equation and the opposite's going to be
47:32true. So now instead of stimulating
47:34osteoblasts, now we have very low
47:37osteoblast activity. Now rather than
47:39inhibiting osteoclasts, we are now going
47:42to have higher osteoclast activity. And
47:44that's the key to the low bone density
47:49that occurs. we are basically amping up
47:52osteoclast activity due to the lack of
47:54estrogen and therefore boom low density
47:57because your osteoclasses are going
47:59crazy and they're just breaking down
48:00your bone constantly. So that's just
48:02another thing that postmenopausal women
48:04have to deal with. All right, here's a
48:07good quick easy application one. During
48:10surgery, a doctor cuts through the skin,
48:12connective tissue, and muscle to reach
48:14the bone. just list these layers in
48:16order and identify the primary tissue
48:19type for each. So, it obviously depends
48:21on where they're cutting into, but we'll
48:22just say they're cutting into like skin
48:24of your arm and then through. So, we
48:26know we've already talked about we've
48:28got that epidermis on the outside,
48:31right? We know the epidermis is made of
48:33long thin flat cells. So, we will call
48:37this many layers of flat cells.
48:40Stratified which means many layers.
48:43squamus, which means flat,
48:46uh, stratified squamus tissue, basically
48:48flat, tall, flat cells that are in a
48:52layer. So, they're cutting through this
48:54first. Next up, we've already talked
48:56about, we have the dermis, right? This
48:58is going to be the dermis. And we talked
49:01about how this is dense regular
49:03connective tissue. Okay? So, it's going
49:06to have some fibiberblast, those fiberb
49:08cells. It's going to have some collagen
49:10fibers all throughout keeping it strong.
49:12So we're cutting through dense regular
49:13connective tissue. Then we have the
49:15hypodermis or the subcutaneous layer.
49:18This is another type of connective
49:19tissue except it's going to be our
49:22atapost tissue. Atapost tissue. So
49:25basically fat tissue. And depending on
49:27the person, you might have a thicker
49:28layer or a thinner layer. Now underneath
49:30this, and this is where we can get into
49:32a little bit more of anatomy. If you
49:34were to actually peel the skin back, not
49:36only would you have atapost tissue, but
49:38you'd continue to have some areolar
49:40connective tissue. This is the classic
49:42connective tissue that usually connects
49:44bo most most parts of our body. So
49:46aerial connective tissue, it represents
49:49most of the fiber types. So we've got
49:50like elastic fibers and collagen fibers.
49:52Uh but it almost looks like if you're
49:54dissecting like a cat or a rat, it
49:56almost looks like um wispy uh tissue
49:58paper as it pulls apart. It's a really
50:00cool tissue. Now underneath that, that
50:03is when we're going to get into the
50:05muscle. So obviously if you got the
50:06muscle first, it's going to be a big
50:08muscular tissue.
50:11We could be [clears throat] specific
50:12with this is skeletal muscle tissue,
50:15okay, if it's attaching to the skeleton.
50:17And then last but not least, we have our
50:20bone tissue. So say here's a bone
50:22running along it [clears throat] and
50:24that would be bone connective tissue.
50:26Awesome. So those are all the layers.
50:28Fascinating, right? There's a lot in
50:29when a surgeon cuts through epidermis,
50:31stratified squamus, dense regular in the
50:33dermis, atapost tissue in the
50:35subcutaneous, areolar, and then the
50:36muscle and then to the bone. So, usually
50:39surgeons try to avoid hitting too many
50:41muscles if they're just fixing the bone
50:43because they don't want to cause a lot
50:44of scar tissue and damage. Hey, this has
50:47been organized biology. If this has been
50:48helpful for you, again, like the video,
50:50subscribe to the channel, watch these
50:51other videos that are related to these
50:53topics. Um, you can also watch my
50:55previous unit exam video here. Thanks
50:57again.