Inflammatory bowel disease: Epidemiology & pathology | NCLEX-RN | Khan Academy

Inflammatory bowel disease: Epidemiology & pathology | NCLEX-RN | Khan Academy


– [Voiceover] Inflammatory Bowel Disease is a group of disorders that includes both Crohn’s Disease
and Ulcerative Colitis. Now unfortunately, the exact cause of Inflammatory Bowel Disease
is not well understood. However, both types of
Inflammatory Bowel Disease are the result of an inappropriate
inflammatory response that results in chronic intestinal damage, as well as potentially serious and life-threatening complications. Now despite having considerable overlap in their clinical presentation, as well as a similar underlying mechanism, the two types of
inflammatory bowel disease have many important epidemiologic, as well as pathologic, distinctions. And these distinctions
are pretty important for the diagnosis and
treatment of the diseases. Now before we dive into the pathology of inflammatory bowel disease, let’s talk briefly about how
common these diseases are, and some of the risk factors. So, how common is
inflammatory bowel disease? Well, this may seem like
a fairly simple question, but it’s not quite as
easy as one might think. Because the prevalence, or the number of people with disease at any specific time, varies significantly
depending on the location. So, in countries that are more rural and less industrially developed, such as much of South America and Africa, the prevalence is much lower than in more well developed or well industrialized and more urban areas of the world, such as much of North America and Europe. So let’s focus on North
America and Europe, here. For Crohn’s disease, the
prevalence in North America and Europe is somewhere
between 250 and 300 per 100,000 individuals. Whereas ulcerative colitis has
a slightly lower prevalence, and that’s somewhere between
50 and 100 per 100,000 people. To put this into perspective,
in a city the size of London with a population of
about 8.3 million people, a prevalence of 300 per 100,000 would mean that about 25,000
people have Crohn’s disease, and that’s about the same amount of people as there are students at
King’s College in London. Whereas with Crohn’s disease, with a prevalence of
100 per 100,000 people, that means that in
London, there are probably somewhere around 8,300 people living with ulcerative colitis, which is about the number of people who visit Buckingham Palace everyday. Now as I mentioned
earlier, the exact cause of inflammatory bowel disease
is not really well understood. However, there are a few
distinct risk factors for both Crohn’s disease
and ulcerative colitis. And the first one to mention is age. In Crohn’s disease, the incidence, meaning the rate at which
people are diagnosed, is highest between the ages of 15 and 35. Now ulcerative colitis also tends to have a similar peak incidence
around the ages of 15 to 35, however, it is something known
as a bi-modal distribution. And this means that there’s a second peak, and this occurs during
the ages of 60 to 80 when, for some reason,
individuals once again become more likely to develop the disease. Now the next risk factor is
that of a family history. Now both types of
inflammatory bowel disease have an underlying genetic predisposition, which is made evident
in that an individual with an immediate family member, meaning one of their
brothers or their sisters or their parents, that person is going
to have a higher chance of developing either Crohn’s
disease or ulcerative colitis. Now for Crohn’s disease, this
risk is a little bit higher at 10 percent. Meaning that someone with
an immediate family member who has Crohn’s disease
has a 10 percent chance of also developing the disease, which is about 30 times higher than that of the general population. And with ulcerative
colitis, family history also is an important risk factor, but it’s not quite as significant, where the risk is about two percent, meaning that someone who has
an immediate family member with ulcerative colitis has
about a two percent risk of also developing ulcerative colitis sometime in their life. And that is about 10 times higher than that of the general population. And then there are a
few other risk factors that are important to mention. For Crohn’s disease, a
very important risk factor is a history of smoking, as well as what we talked about earlier in that someone living in urban areas, especially of industrialized countries, is at a high risk of
developing Crohn’s disease. Then with ulcerative colitis,
an important risk factor is having a diet that is
high in total fat intake and then also having a
history of salmonella or campylobacter infections. And salmonella and campylobacter
are types of bacteria that can cause an infection
of the G.I. tract. Now that we have a little
bit better understanding of what exactly inflammatory
bowel disease is, let’s discuss some of
the pathologic changes that occur in these two diseases, which are very important
for distinguishing Crohn’s disease from ulcerative colitis. And let’s start with the
location of the inflammation. Now if you break down the name
of many medical conditions, it will give you a better understanding of what the disease is. Unfortunately, with Crohn’s disease, it’s named after Burrill Bernard Crohn, who described the condition back in 1932. So it’s name doesn’t really
tell us much about the disease. Ulcerative colitis is
a little bit different on the other hand. So itis stands for inflammation, and col is for the colon,
which is just another way of saying the large intestine. So ulcerative colitis is an ulcerative or an inflammatory ulcer of the colon, which is this part of the
G.I. tract right here. Now in ulcerative colitis, the lesions almost invariably begin here in the rectum and then they move backwards
through the intestine in a continuous fashion and
are completely contained within the large intestine. So about 50 percent of
people who have also colitis will have inflammation
that starts in the rectum and then moves just a little ways back into the sigmoid colon. So this is the sigmoid colon. It’s called the sigmoid because
it kind of looks like an S. Then about 30 percent of
people with ulcerative colitis will have what’s called subtotal colitis. This means that the inflammation extends beyond the rectum and the sigmoid colon back into the descending and
maybe into transverse colon, but not the entire colon. It’s subtotal or less than total, less than all of the colon. And the last 20 percent of people will have total colitis, meaning that the inflammation
is going to extend all the way back through
their entire colon. So it’s going to include the
ascending, the transverse, the descending, the
sigmoid and the rectum. So they have total inflammation. Now in Crohn’s disease,
the inflammation can occur anywhere from the mouth to the anus, but it doesn’t occur in
this continuous fashion that ulcerative colitis does. In Crohn’s disease, it’s discontinuous, meaning that someone may have inflammation in the terminal ileum or the last part of the small intestine, maybe here in the colon. Another spot in the small intestine. They could have it in the
esophagus and in the mouth, but they’ll have gaps
between these inflamed areas with normal G.I. tract and then another area of inflammation, then
normal G.I. and so on. And so these are known as skip lesions because they’ll skip over
normal segments of bowel. Now the most common place
for the inflammation to occur in Crohn’s disease is the terminal ileum, which is the very last segment
of the small intestine. And the second most common place that these inflammatory lesions
occur in Crohn’s disease is the large intestine. Now aside from the
location of inflammation, the microscopic pathology
of Crohn’s disease and ulcerative colitis are
distinct from one another. So here we have a diagram of the wall of a segment of the intestine here. So imagine this is the
inside of the intestine where the food kind of travels through and then gets absorbed through the wall of the intestine into the bloodstream. Now there are three distinct
layers to the intestinal wall. The one closest to the
inside of the intestine is known as the mucosa. Then below that is the submucosa, which is named submucosa
because it’s below the mucosa, and then the third and innermost layer is known as the muscularis externa, and this is because it
contains the muscle fibers that help move food along
through our digestive tract. Now the exact mechanism and
cause of the inflammation in inflammatory bowel disease
isn’t well understood, but what seems to happen
is that individuals have a genetic predisposition for developing inflammatory bowel disease. That’s we mentioned they’re hereditary, or that family history as a risk factor. But this genetic predisposition
isn’t quite enough. In addition, there’s some sort of trigger. And this trigger here
is the part that’s not quite as well understood. It could be caused by some sort of change in the composition of the normal
intestinal bacterial flora within the large and small intestine, or it could be the result of some sort of G.I. infection, like the
campylobacter or the salmonella that we talked about earlier. But what happens is when
you get this combination of the genetic predisposition
and some sort of environmental trigger, that
causes the immune system to attack and damage the G.I. tract. Now so far, this part of the mechanism is the same for both Crohn’s
disease and ulcerative colitis. However, over time, the damage that occurs to this intestinal wall at
a microscopic level differs. So let’s take a look at this. Now over here on the
left, we have a picture of the intestinal wall in
someone with Crohn’s disease. And I have a couple of cells here and they’re a little bit out of scale but the idea is that this is a macrophage and this here is a neutrophil. Now macrophages and
neutrophils are normal cells that are part of the immune system. But for some reason in Crohn’s disease and ulcerative colitis,
they begin to attack the intestinal wall. And overtime, this inflammatory response causes damage to the intestinal wall. And as you can see here
in Crohn’s disease, this inflammation extends,
these lesions extend through all three layers
of the intestinal wall. So this is known as
transmural inflammation. And in Latin, transmural
literally means through the wall. So the inflammation is
going all the way through the intestinal wall. And in addition to these immune
cells causing this damage, there’s infiltration of
the wall of the intestine with another type of immune cell. It’s known as a lymphocyte,
which I have demonstrated here with these kind of loop, little blue dots that are infiltrating the wall. So you have transmural inflammation with lymphocytic infiltration. And in addition, the
immune system over time forms another type of microscopic lesion, which is known as a
non-caseating granuloma, which is a sign of chronic inflammation. Now in ulcerative colitis, the
macrophages and neutrophils are also causing damage
to the intestinal wall, but the microscopic appearance
is somewhat different. In ulcerative colitis, this inflammation doesn’t extend all the
through the intestinal wall as it does in Crohn’s disease. It only extends through the
mucosa and the submucosa. So in ulcerative colitis, you have mucosal and submucosal inflammation. So this distinction between
transmural inflammation and mucosal and submucosal inflammation is one of the most important
pathologic distinctions between Crohn’s disease
and ulcerative colitis. Now overtime, these lesions can worsen and they can cause many
different complications. And some of them are the same
with for both Crohn’s disease and ulcerative colitis,
although some of them are characteristic of one form
of inflammatory bowel disease or the other. So let’s take a look at that. So the first pathologic
complication we’ll discuss is something known as a crypt abscess. And occasionally, what
happens is this inflammation, as it progresses, will
result in kind of this walled off pocket of space. And if that pocket includes some bacteria, that can get infected and form an abscess. And these crypt abscesses
aren’t just in Crohn’s disease, they can also occur in ulcerative colitis. Now often times, these
abscesses, they may not cause a whole lot of symptoms other than perhaps just a mild fever. But if they rupture and they spill this kind of infective fluid
out into the abdominal cavity, they can cause a very serious or potentially even
life-threatening complication known as peritonitis. So if these abscesses are found, they’re normally treated
with IV antibiotics as well as drainage. And by treating that,
it prevents the rupture and the development of the peritonitis. So another one of these
pathologic complications that occurs primarily in Crohn’s disease is something known as a fistula. So imagine here that you have section of the bowel or maybe
it’s the small intestine that has a Crohn’s disease lesion. Now it’s in the abdominal cavity, so it’s bumping up next to
another section of bowel. Maybe this is the large intestine. But what can happen
overtime is eventually, this inflammation gets worse and worse and forms almost a tunnel between the two structures. So you can see that the
lumen of one section of bowel is actually in communication with another section of bowel. So this communication of this tunnel is known as a fistula. Now these fistulas
don’t just occur between two segments of the bowel, they can occur between pretty much anything
that a Crohn’s lesion is bumped up next to. So that can include things like the skin, the bladder and the vagina. Now these fistulas can cause
a significant amount of pain, as well as severe infection. So you can imagine that
if there’s a fistula between a segment of the
bowel and the bladder, what happens is the bladder,
which is normally sterile, now has a direct
connection to the bacteria of the intestine. So you can get a very
serious bladder infection. So if a fistula is found in
someone with Crohn’s disease, it’s usually going to
be removed with surgery. Now for ulcerative
colitis, there’s another one of these pathologic findings
that is important to note, and this is known as a pseudopolyp. Now overtime, as the inflammation of the intestinal wall worsens, the flattening out or thinning of the mucosal and the submucosal layers can occur in an uneven pattern. And what it leaves is
these kind of pseudopolyps, or it looks like a polyp sticking out of the intestinal wall, but
it’s called a pseudopolyp because it isn’t a growth out, it’s actually that everything
around that structure has been thinned out. And so that is a pseudopolyp, which is a characteristic
of ulcerative colitis. So inflammatory bowel disease
is a group of disorders that’s caused by an appropriate
inflammatory response that results in this
chronic intestinal change. But the two types, Crohn’s
disease and ulcerative colitis, although they have a similar
underlying mechanism, they can be defined
pathologically based on location of the lesions, as well as
the microscopic appearance of the pathology. So in Crohn’s disease,
the lesions can be located anywhere from the mouth to the anus, and they occur in this
discontinuous, skip lesion pattern. Whereas in ulcerative colitis, the inflammation nearly
always begins in the rectum and continues in a continuous fashion backwards through the colon and almost never exits
the large intestine. Now for the microscopic
findings on the pathology, Crohn’s disease is defined by inflammation that goes through all three
layers of the intestinal wall, which is known as that
transmural inflammation, as well as these non-caseating granulomas. Then ulcerative colitis, the
inflammation is contained only within the first two
layers of the intestinal wall, which is known as the mucosal
and submucosal inflammation. This is important
because it’s the location of the lesions that is going to define the clinical presentation of the disease in terms of the signs and symptoms, as well as the means for diagnosis. Whereas the microscopic pathology is going to have an effect on
the potential complications, as well as the treatment of the disease.

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