Gastrointestinal Pathophysiology I

Now for a new Pathophysiology series! This series will probably be the hardest to write because the lectures, while interesting, weren't that well organised. But let's see how we go!

GI Tract Structure and Function

This series of lectures, like all of the series before it, starts out with a review of the anatomy and pathophysiology of the GI tract. Here's a link to all of my previous posts on this subject:

• Tubes
• Coelomic Cavities
• Gastrointestinal Tract: Mesenteries, Nerves and Blood Supply
• Gastrointestinal Function part 1
• Gastrointestinal Function part 2
• Gastrointestinal Function part 3

There is, however, one important topic that I did not cover in any of the above posts, and that is the innervation of the gut. As mentioned in my post on the autonomic nervous system, the gut has its own nervous system, known as the enteric nervous system. This nervous system has a lot of sensory and motor functions, and has a lot of reflexes which is why our gut can digest things without us even being aware of it. The one thing it doesn't do is pain- that's mediated by the autonomic nervous system (though we're not sure what exactly stimulates pain, whether it's wall distension, action of inflammatory factors or otherwise). Many GI diseases have their own unique "pain patterns."

Another important thing which got a brief mention in the previous posts is that there are plenty of immune cells in the mucosa of the gut. These help to defend against a whole range of antigens.

Gastroenteritis

Gastroenteritis is a general term referring to inflammation anywhere in the GI tract. It can be broken down further into gastritis (stomach inflammation), colitis (colon inflammation) and so on, but I'm going to start off by talking about it in more general terms.

Gastroenteritis is usually caused in response to some noxious stimulus, such as an infectious agent. Sometimes this might break down some of the mucosa and other barriers lining the gut, meaning that there is a risk of the damage escaping elsewhere if the pathogen isn't dealt with. The body's response to this is usually to try and get rid of everything, by causing symptoms such as nausea and diarrhoea (which might come with other fun stuff like stomach cramps), while trying to discourage you from taking anything else in with lovely symptoms such as anorexia (which in this case refers to a general loss of appetite, not the eating disorder), fever and malaise (i.e. just generally "not feeling good"). Inflammation can be acute, due to the short-term presence of some kind of irritant, or chronic, due to the long-term presence of an irritant or an extended response to a stimulus that isn't there any more.

One example of a stimulus that can cause gastroenteritis is the Norwalk virus, also known as norovirus (since it was originally named after a city that no longer wants to be associated with a shitty virus. Sorry for the pun). It can hit pretty much anyone, including otherwise healthy people.

Gastritis

Now let's get a little bit more specific and talk about gastritis, which is inflammation of the stomach! One common symptom of gastritis is vomiting, which is basically the body trying to get rid of the bad stuff by making it all come out the way it came. Aside from general irritation of the GI tract, other stimuli that can induce vomiting include certain drugs, motion sickness, intracranial pressure and being grossed out by stuff, but I'm sure you were pretty aware of all that already. Although vomiting helps the body get rid of bad stuff, it can be a problem if it persists because of the fluid loss as well as the risk of some of the fluid getting into the lungs. (The glottis usually closes during vomiting, but y'know, accidents do happen sometimes.) In order to vomit, the lower oesophageal sphincter relaxes, peristaltic waves reverse direction and the abdominal muscles contract to let it all come out.

Another common stimulus for vomiting is ulceration. Micro-organisms such as Helicobacter pylori can cause these. This nasty little bugger usually causes inflammation when it finds itself a nice home in the stomach, and is implicated in 70-98% of ulcers. Cruel bugger.

Well, that's where the slides for this lecture end, even though I don't think we actually got up to the end in the lecture itself. (These Pathophysiology lecturers all seem way too optimistic about how much content they can actually cover in one lecture.) Oh well, I think that means that there'll be less to cover in the next post. Yay?