Welcome to our last lecture on development of the gastrointestinal system.
Specifically, we’re going to look at the hindgut
and how it forms from a common structure called the cloaca.
The hindgut is basically the remaining portion of the gastrointestinal tract
and its development is gonna be intimately tied with development of the urogenital system
and we’ll discuss that specifically in another set of talks.
The hindgut is gonna be the continuation of the gut tube
and it’s gonna comprise the descending colon, sigmoid colon, and rectum,
and they’re all supplied blood by the inferior mesenteric artery,
the last unpaired branch coming off the aorta in the abdominal cavity.
Initially, we have a common chamber receiving all the products of the urinary,
the genital, and the gastrointestinal system and this is called the cloaca.
It’s a normal feature for several animals
but in our case, we want to subdivide it and separate those systems a bit.
And the cloacal membrane is gonna be the only mark we see of it on the surface.
So it’s not in contact with the outside cavity yet
but sooner or later, we will have rupture of that membrane
and its derivatives allowing movement of fluid and food
through the gastrointestinal tract.
The cloaca is subdivided into an anterior and posterior chamber
by a wall of mesoderm that comes down and pushes the two away from each other.
This is called the urorectal septum and it appears in most pictures as though
that septum is pushing its way straight down the midline.
In reality, the left and right mesoderm are pinching together progressively
more inferiorly creating that urorectal septum
and separating the cloaca into two separate components.
You’ll note we have initially a single cloacal membrane covering the cloaca
but as the separation continues,
the urorectal septum is going to push the two portions away from each other
creating the urogenital sinus in the front, that’s going to be where the urinary
and reproductive tracts will thereafter be emptying
and the rectum posteriorly which is simply the end of the gastrointestinal tract
lined by the endoderm that developed off the initial early gut tube.
The perineal body is a connective tissue structure
that we can see on the surface from where that urorectal septum grew out
and finally met the body wall.
And in the process, it’s subdivided that cloacal membrane
into an anal membrane posteriorly and a urogenital membrane anteriorly.
These membranes are intact
and do not actually rupture until a little further on in development.
The anal membrane, it would make sense if it simply ruptured
and that was the emptying of the gastrointestinal tract
but what happens is actually a bit more complex.
The rectum meets the anal membrane and is sealed off by it.
The skin on the underside of it actually invaginates
and moves into the body forming what’s called an anal pit.
And the anal pit meets the rectum at the anal membrane
and the line marking where those two systems come together is called the pectinate line
and it’s within the anal canal and it actually marks where the skin moved in to form the anus
and the rectum came down to meet it.
And that pectinate line also marks a distinct series of structures within.
There’s separate blood supply to each area
and there’s separate blood drainage from each area.
So the divisions between anus and rectum is actually more significant
than it might appear where we have blood drainage of the rectum
drain into the portal system, specifically through the superior mesenteric vein
to the inferior mesenteric vein, to the splenic vein, to the liver,
and below, branches of the internal iliac vein pull blood away from the anus.
And if we have backup of blood in any of those systems,
we can develop hemorrhoids or other problems related to that region.
Now, problems that can occur in this process is that we can have the anal pit form,
we can have the rectum mitted, but we can have the anal membrane fail to rupture.
This is known as an imperforate anus and essentially,
our gastrointestinal system is unable to expel any fecal material out of the body.
This does have to be corrected surgically,
otherwise, the affected infant will eventually die
because there can be no movement of fecal material out of the body.
Similar but more severe is what’s called anal atresia.
Failure of the anal pit to form at all.
So there’s simply a smooth covering.
This also has to be corrected surgically but because there’s no anus moving in,
and therefore, no muscular sphincters surrounding it to control the release of fecal material,
the surgery’s a bit more complex and has to be done in multiple stages.
This is a picture of an infant who was born
and we can see that there is actual anal atresia where no anus is present.
If an imperforated anus is present, the anus may appear normal
but that membrane will not allow fecal material to pass through.
Hence, the importance of a good, well baby exam right after delivery.
So malformations associated with this urorectal septum moving down
and subdividing the cloaca into the urogenital sinus
and the rectum can be very interesting
and thankfully, have a very well described nomenclature.
If we have a connection of the rectum to the vagina instead of to the anus,
we have what’s called a rectovaginal fistula
and this presents exactly the way you think it would.
That there will be fecal material draining into the vagina and released from there.
This obviously can happen only in women because men do not have a vagina.
Also, women could have what’s known as a persistent cloaca.
While this is very rare, it is a common chamber
receiving both the urogenital sinus
and therefore, the urinary and reproductive tracts, and the rectum,
and once again, has to be repaired surgically.
In males where there’s no intervening uterus and vagina,
a similar set of fistulas can occur where the rectum instead of connecting to the anus,
connects to the urinary bladder.
That would be a rectovesical fistula
and if we have that same inappropriate connection a little further down,
we can have a rectourethral fistula
and if you use your imagination, I’m sure you don’t want to
but if you do, you can imagine exactly how these are going to pronounce,
are going to present in a child.
You will have leakage of rectal material, a.k.a. feces from the urethra of the penis.
Alright, last but not least,
we have a series of problems related to the innervation of the hindgut.
The neural crest cells that migrate into all regions of the gut
are going to form the nerve cell plexi that continuously allow peristalsis to occur.
So as food and fecal materials move through the intestines,
it’s because peristalsis and coordinated peristaltic movements
from these nerve cells cause it to happen.
If the neural crest cells fail to migrate into the hindgut during weeks five to seven,
we can wind up with an area that is deprived of its nerve supply.
And failure of that migration to occur
is gonna cause congenital megacolon, also known as Hirschsprung's megacolon.
It is the most common form of colonic obstruction in newborns.
It happens once in every 5.000 births or so.
If there’s no ganglion cells within the smooth muscle of the gut,
specifically, the hindgut, the muscle there really doesn’t know how to do anything else
but contract and the affected area will be very tightly contracted
causing backup of fecal material into the intestines and severe expansion of it.
Hence the name, megacolon.
So the normal colon that’s proximal to the denervated region will expand tremendously
and bowel movements may be very limited, very small, and very infrequent.
A famous case of congenital megacolon
is demonstrated in Philadelphia’s Mütter Museum
and the affected person was said to have a bowel movement once every month
and his colon was roughly the size of a tuba.
So very severe, needs to be corrected surgically,
and hopefully, caught much earlier than it was in that particular individual.
Thank you very much for you attention and I’ll see you at our next talk.