9am - Upper GI
10am- Malnutrition, Appetite and Abdo. pain
11am- GI Cancers and Infections
12pm- GI surgery
This on-demand session offers a comprehensive overview of the upper gastrointestinal tract, focusing on the esophagus, its function, and key disorders. It starts with a case study of a patient presenting symptoms of esophageal perforation, leading to a discussion around Boerhaave syndrome. It goes into depth explaining the structure of the esophagus, its muscular composition, and the role of the upper and lower esophageal sphincters. There's a deep dive into how swallowing works and the role these sphincters play. Additionally, there's a thorough analysis of esophageal motility disorders and conditions such as achalasia. This class uses relatable examples, employs quizzes, offers clinical tips, and provides key terminologies, all beneficial to the medical professional seeking to expand their knowledge in gastroenterology.
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The following transcript was generated automatically from the content and has not been checked or corrected manually.
Great, thank you. Uh Come on here. Um First Lech of the day is gonna be on upper gi um And this lecture I think is actually fairly straightforward and well done. Um So hopefully, uh this will be a nice recap for, for a lot of you. So these are the learning objectives which we quickly pass, skip past. Um And this is the lecture timeline. So this is I structure all my lectures. I start with an ask me and function and then hopefully, this like builds on this. Uh we build on this into disorders and the pathophysiology and those can often say the features like the signs and symptoms uh and the management. Um So let's start with an FDA uh just to see where you guys are. So it's a 19 year old female sending to A&E um with extreme sudden chest pain. After vomiting earlier, they've been eating and drinking three hours ago at a restaurant when the patient felt unwell patients taking short rapid breaths and has a fever of 38 degrees. Um and chest X ray shows an enlarged mediastinum and is in line with the diagnosis of esophageal perforation. So what's the most likely cause of presentation? Uh Just give you a few seconds to answer. I can't see the chat unfortunately. But um, ok, the answer is uh a Bo syndrome and hopefully lecture will understand why. Um But just key things to point out on this is relatively young, chest pain, sudden onset chest pain, uh sorry, relatively young person with sudden onset chest pain after vomiting, um, a fever, taking short rapid breaths and a chest X ray. Uh all at all points that we should be looking out for. Uh uh in this question. So, exactly what is the upper gi tract? Now, this is actually slightly controversial. So, embryologically and the upper gi tract is the mouth, the major papilla in the Georgianum clinically, er we just say mouth to ileum. Um and when we're talking about upper gi bleeds versus lower gi bleeds, um an upper gi bleed is anything that's uh any blood that's been uh produced from the mouth to the er Du du du, the no Juin junction. I can't say that but the DJ junction basically. Um so we tend to use the mouth to ileum. Um most of the time it's quite simple, quite straightforward. Um And basically is everything, what we're gonna be looking at is the esophagus, um the stomach, uh and that's about it. So, um in terms of the esophagus, uh it's a vertical muscular tube, the next thoracic abdomen. Um and it lies between the trachea and the viral bodies. It's therefore divided into three sections, the cervical thoracic and abdominal section and it starts at the level of T five and goes to T 10. And in terms of muscle composition, it's mainly skeletal at the cervical level. And uh this turns into smooth towards the abdomen. There are two sphincters present. Why are they present because to prevent entry of air and reflux of gastric contents? Um And uh we can do and these two sphincters are called upper esophageal sphincter and the lower esophageal sphincter. Um So let's talk about these sphincters which are really important for the following uh disorders. Um So we have the upper esophageal sphincter. Um This is an anatomical striated muscle sphincter where at the junction between the pharynx and the esophagus and the lower esophageal sphincter is interesting because there's no specific muscle which makes it a physiological sphincter. So what what this means is usually sphincters have muscles that literally contract and relax to open or close them. However, some spincter is like this one, the low esophageal sphincter is a physiological sphincter, which means that other things other than a specific muscle is closing up. So how does this work? There are four factors, the fact that there's an acute angle, the ie the esophagus enters, uh the diaphragms are stomach and acute angle, um which already constricts. Uh this portion a little bit more, there's distal esophagus, uh esophagus in within the abdomen. Um uh the fact that the diaphragm surrounds the lower esophageal sphincter and then there's an intact uh ligament. Um So let's talk about swallowing. Then how do these two sphincters aid in swallowing. So, swallowing, I've taken this er picture from the lecture which is very, very helpful and a lot of other images are actually from the lecture as well. But swallowing is a complicated and highly coordinated event and it's all relying on the muscles in the sphincter, er the muscles in the esophagus and the two sphincters. So, in stage zero, this is where uh we're chewing our food and we're preparing a bolus and then we'll start the action of swallowing. This is where we get to stage one, er the fal musculature guides the food bonus towards esophagus. Um and the sphincter opens reflexively. So this means without like um like this is just a uh if, if we go back to our neuro uh knowledge, a reflex is something that doesn't er ever really go into the central nervous system, it just goes straight back to peripheral to the peripheral nervous system. So that's what er this means. And so the upper esophageal sphincter opens and so does the lower at the same time and the lower is opened by the vasovagal reflex, also known as a receptive relaxation reflex. And this is actually really important just in terms of um um exam knowledge because this keeps coming and popping up and popping up. So when you see that the lowest sohal sphincter is opened, uh, think receptive relaxation reflex in stage two, the food BS has now entered the esophagus. Um, and the upper sphincter closes. And now how do we actually get this P bolus down from the top of the esophagus to the bottom? Well, um, above the food bolus, uh the circular muscle, circular muscle rings contract. So they kind kind of push the food bs down whereas the ones at the bottom dilate. So this creates a lot, a nice tube and pushing motion and all the longitudinal muscles of the esophagus, uh they contract as well in a similar fashion um to help guide the few boats down and then as it passes through the lower esophageal sphincter, um this sphincter closes. Um Now, how can this go wrong? Well, we can have disorders of the esophageal uh contraction where there can be hyper motility, hypo motility. So, more motility, less motility or disorders coordination. And this, this um all relies on this kind of definition of esophageal motility, which is defined by a manometry and the pressure within the esophagus. So, during peristaltic waves, er the pressure is about 40 mg of mercury and the lowest of your resting pressure is about 20 this decreases by five during that receptive uh uh relaxation reflex. Um And all of this is mediated by inhibitory, non choleric, noncholinergic, non adrenergic uh neurons of the mesenteric plexus also known as N CNA neurons. Now again, that's actually quite a key point that comes up in the exam, they love throwing in er, that set of neurons and we'll, and we'll see it more in, in one of these conditions. So let's first talk about hypermotility. Uh The condition which we focus on is achalasia and this is again due to a loss of the ganglionic cells in a a backs mm myenteric plexus in the lower esophageal wall. And again, this is just something that you need to kind of ro learn and it comes off er in exams. I will say for example, what plexus um are cells lost er in achalasia or um what type of cells you know. So just just remember that first sentence um and this leads to a decreased activity of the inhibitory N TNA neurons. So, if we lose inhibitory neurons, this means we have more action because we've lost the inhibition. So then this more action means that the resting pressure of the lowest of your sphincter like the gold star thing I have in the yellow is increased massively. What's really helpful is this diagram on the left showing um a bare and swallow where basically patient will swallow some um barium and this will show up very brightly uh on an X ray. So we can quite easily see the digestive tract on X ray. And what you can see here is towards the bottom, there should be a nice opening. Um If you go to the right image as well, there's a red circle on, on the parlor. I mean, um and this is uh a sign of uh an abnormality and it's called the bird beak sign. Um So it kind of looks like a, a bird's beak and this is very indicative of achalasia. So, what are some of the causes of achalasia? Um or primary achalasia? We actually don't know, but secondary eye stuff that might actually cause um major abnormalities is Chagas disease, protozoa infection or uh amyloid sarcoma is on the esophagitis. I was meant to say um the.