Cram The Pance - S1E13 Esophageal Disorders Part 2 of 2

Episode Date: February 15, 2021

Hiatal Hernia, Zenkers Diverticulum, Mallory-Weiss Syndrome, Boerhaave Syndrome, Esophageal Varices, Esophageal Web/Ring review for your Pance, Panre, and Eor’s.►Paypal Donation Link: https://bit.ly/3dxmTql (Thank you!)--- Support this podcast: https://anchor.fm/scott--shapiro/supportBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

Okay, so today we're going to be going over the second part of esophageal disorders. This is again from the GI section of the NCCA blueprint for the pants. Today we're going to be going over hiatal hernias, esophageal strictures, zankers divertulum, esophageal tears and ruptures like Borhave syndrome, Mallory Weiss tear. And then we're also going to be going over esophageal varices. So this is part two of two. I already did the first part.

If you want to take a listen to that one, if you haven't yet, that'll definitely help. And I just wanted to mention one more time. if you don't mind leaving me a review, it really helps get the word out about the podcast, and I really appreciate it. So thank you so much for that. All right. So let's get into it. Let's start with hiatal hernias. So what a hiatal hernia is, is this occurs when a portion of the stomach herniates or slips through a portion of the diaphragm, which is known as the esophageal hiatus. Now, there's two types, and it all depends on where the stomach or the gastroasophageal junction is herniating into. So the first type is going to be known as sliding.

or type one. This is by far going to be your most common type. This is about 90 to 95% of patients. So this is the one you should really know. And again, sliding or type one. So in this case, it's not so much the stomach that's herniating, but the junction of the esophagus in the stomach, known as the gastroosophageal junction. And this is herniating straight up into the medial stym. So these patients are commonly going to present with reflux. And the reason that these patients have reflux is the lower esophageal sphincter is essentially being moved up and away from the diaphragm. And what does the diaphragm do to the lower esophageal sphincter? Well, the diaphragm actually augments and increases the strength of the lower asophageal sphincter. So they kind of work. The LES and the diaphragm are actually work in a synergistic

way to kind of help keep the gastric acid out of the esophagus. So when the LES herniates away from the diaphragm, it becomes more incompetent, which is going to lead to reflux and gird symptoms. So overall, that's a really long explanation. But just remember, sliding type 1 is going to be your most common type. And these patients are going to present with GERD symptoms. Again, type 1, 90 to 95 percent of patients. Let's move on to the second type, which is going to be parasophageal, also known as type 2. Again, not as common.

And this is where rather than the gastrosophageal junction herniating, it's going to be the funnus of the stomach now herniating through the diaphragm. So a little bit different than the other one. And this is considered a true hernia that has a hernia sac present. Most of these patients are asymptomatic. They may have some vague intermittent symptoms like nausea, post-pranile fullness, epigastric pain. But for the most part, they're not going to have the gird symptoms like we talked about in type 1. Now, how do you diagnose both of these? Well, Barium Swallow is going to be your most sensitive diagnostic test for both a type 1 and a type 2. And then treatment, it all depends on whether we're talking about a type 1 or a type 1. type 2. So sliding type 1, again, your most common type, there's not a lot you need to do. There's not a lot of

risks or complications with the type 1. It's mostly going to be medical management of their GERD symptoms. So PPI's H2 blockers, muscle may want to encourage weight loss because obesity increases the intra-abdominal pressure, which can worsen these hiatal hernias. Now, as far as treatment for parasophageal, this is a little bit more complicated because parasophageal actually have this risk of complications of developing complications like gastric volvulus and obstruction. So these patients actually a lot of times need to be treated surgically. If they're asymptomatic, it's kind of controversial because you have to weigh the risk of surgery versus the chances of them developing complications, which is about a little bit less than 2% of patients. So if they're asymptomatic, most of the time

you'll kind of just observe. But when they do become symptomatic, obviously if they develop complications like a volvulus or an obstruction, they need to have surgical repair. So that's parasophageal again. You need to sometimes have surgery, sliding type 1, just medical management, weight loss, etc., those types of things. So that's Heidel hernia. Not a lot to know for you. Let's move on to Zincers diverticulum. So Zincers diverticulum is this false diverticulum or an out-pouching of the mucosa and the sub-mucosa through a weakened area of the junction of the pharynx and the esophagus, which is known as Killian's triangle. So again, Zincers diverticulum is this outpouching of a weakened area between the pharynx and the esophagus known as Killian's triangle. So with Zincers diverticulum, it's going to be most common

in males, about a one to five ratio, so very common in males. It's going to be more common in patients in their seventh and eighth decade of life. So patients in their 70s and 80s. As far as clinical manifestation, it really depends on the size. Small diverticula often will be asymptomatic. but when they become larger, they're going to start to have some symptoms. They may have dysphasia. And then a key one that you need to know is these patients, when it gets larger, they may start to develop palatosis, also known as bad breath. Now, why do they develop a bad breath? Well, what you need to know is these larger diverticular, you have this outpouching at the posterior aspect of the esophagus.

And what happens is these patients eat and the food literally goes into this outpouching. and sits there. And the food ferments and it starts to smell after a while and they may develop halitosis. Sometimes they'll actually regurgitate some of the food. So you need to remember that because that one always comes up in the vignette. And that's the way for you to differentiate this disorder from other esophageal conditions. So remember halotosis. That's really, really important for Zincers diverticulum. Definitely need to know that. As far as diagnosing, you're going to do barium swallow, also known as a barium esophagram. This is just basically going to show the barium collecting at the posterior ed. of the esophagus. So that's pretty easy for diagnosis. As far as treatment, if they're asymptomatic,

it's a small diverticular less than a centimeter. Just going to observe, there's really not, doesn't really warrant treatment. Now, if it becomes symptomatic or it's larger than a centimeter, they need to have a surgical procedure to remove the diverticula. Typically, it's minimally invasive transoral endoscopic approach, and it's called a diverticulectomy, literally just removing the diverticula. So that's only if they're symptomatic or it's a large diverticula over a centimeter. So that's a Zengro's diverticulum. Let's move on to a couple different things known as Mallory Weiss syndrome or Mallory Weiss tear and Borjave syndrome. These are two different conditions, just differing in severity, and they're both a laceration of the esophagus. Now Mallory Weiss is going to be a more superficial

laceration. It's not going to be all the way through the esophagus. It's a superficial laceration, a partial thickness. And Borhave syndrome is going to be a full thickness. through the entire esophagus. So it's obviously much more serious. Now the way I remember this, because a lot of times you'll have a vignette and you'll have both of these answers on there. You need to remember which is which. So I remember this is Mallory Weiss syndrome. I take the name Mallory. And to me, Mallory just sounds like a little girl. So Mallory isn't going to be able to cause a lot of damage to your esophagus. Mallory is going to have a partial thickness laceration. Now Boar Have syndrome, Boar Have, I think of a boar, which is that wild pig with the tusks coming out.

out of the side of its mouth, and that tusk is just going to rip through your esophagus, and it's going to cause a full thickness laceration. So remember that, Mallory Weiss, Mallory's a little girl, she can't cause a lot of damage. Boar Have is a bore ripping through the esophagus with its tusks, causing a full thickness tear. So that's how I remember, which is the more severe one. Now let's start with Mallory Weiss syndrome. This is going to be a longitudinal mucosal laceration of the distal esophagus and the proximal stomach. Again, no perforation. It's just a partial thickness laceration. What you need to really know for Mallory Wyss syndrome is that most commonly this is going to be caused from persistent vomiting or retching after an alcohol

binge. Now, up to 80% of patients with Mallory Wyss syndrome or Mallory Wice tear have a history of heavy alcohol use associated with vomiting. So as far as you are concerned, Mallory Yis syndrome is from a patient who's been drinking a lot and vomiting all day. That's how you need to remember it. It's how it's going to be on the vignette. And that's most likely how it'll be in real life, too. So, and the reason that happens is when these patients vomit, they have all this increase in intra-abdominal pressure, and it leads to lacerations and also bleeding from some of the ruptures of the subnecosal arteries. It can also be caused from hyodal hernias, but I wouldn't even worry about that because it's much more rare. And as far as the boards are concerned, and, you know, in real

life, about 80% is going to be from vomiting or retching after an excessive amount of alcohol. alcohol. As far as clinical manifestations, they're going to have upper GI bleeding with hematomiesis if they do rupture one of those subunucal arteries. Remember, just because they're lacerating the esophagus doesn't necessarily mean there's going to be a lot of bleeding. Really, it's only going to be in the patients, about 8 to 15 percent of patients that have a rupture of a subunucal artery, which is definitely possible. They may also have epigastric or back pain, and then patients with significant bleeding may have symptoms of hypovolemia. So they're going to have hemodynamic instability like tachycardia hypotension.

And those are, so those are some of the main things you'll see in Mallory Wyss syndrome or tear. As far as diagnosing, you're going to use an upper endoscopy to identify the area of the laceration and to locate and treat any ruptured arteries, if that were the case. Now, treatment, it depends if they're bleeding or they're not bleeding. Again, did they lacerate or did they rupture an artery? or not. So if they're bleeding, they're going to be pretty unstable. They may be hypovalimic. So first, you need to stabilize them. So IV fluids, blood transfusions may be necessary. And then once they're stabilized, you want to go ahead and go with your endoscopy, locate and treat the active bleed.

It can be performed with either thermal coagulation, which is just really like a heated probe that singes the bleeding artery closed or they can also use hemoclips. I wouldn't worry so much about the specific options. Just know you need to locate and treat. the bleed. Now, if they're not bleeding, what you're going to do is you're going to use PPI to suppress the acid in the esophagus. PPIs promote hemostasis by neutralizing gastric acid. It's stabilized blood clots, and it's normally used for about two weeks after an incident of Malory Weiss tear. And of course, if they're still actively vomiting when they come in to see you, you can use antimetics like metaclopramide or odansetron. So that's Mallory Weiss Ter or Malloryeis

syndrome. Now let's move on to the more severe one. Remember, Borhave syndrome, a bore. This is full thickness tear. So Borjave syndrome is full thickness rupture of the esophagus, and it's much more severe. It has a high morbidity and mortality rate, and essentially, Borhave syndrome is fatal without intervention. So the rupture or perforation of the esophagus is most common in the left posterior lateral aspect of the lower esophagus. So again, Borjafeus syndrome, most common in the left posterior lateral aspect of the lower esophagus. May come up, may not, but it's good to know. What are some of the causes?

So retching and vomiting again is a common cause, but it's not as common as in Mallory Weiss tear. It may actually be iatrogenic. So it may be caused from an endoscopic examination that actually perforated the esophagus. That's one of the causes. It can actually be caused during childbirth, seizures, prolonged, laughing, coughing, weightlifting, all of this due to the increased intraosophageal pressure, because these patients are bearing down in a lot of these activities combined with the negative intratheracic pressure.

So there's a lot of different causes, but remember the itrogenic causes, remember, retching of vomiting can happen, and then some of the other ones, too, childbirth, prolonged laughing, which are less common. And as far as clinical manifestation and exam, it all depends on the location of the rupture, time elapsed, you know, how severe these patients are. but really there's a few things that you need to know for the boards. One of the main things that these patients are going to present with is really like excruciating retro-sternal chest pain.

They have a ruptured esophagus. So these patients are going to be a lot of pain. And then there's two other key things that you need to know, really for the boards. They're not so common in real life. And a lot of patients will not present with this, but these are things that the boards like to ask. So definitely know this. So they may have crepitous on chest palpitation or auscultation. And then I have a key term for you.

so definitely listen up. They may have something called Hammond sign. And what Hammond sign is a medistinal crackling when you're auscultating with each heartbeat. So again, it's important to know Hammonsign, medistinal crackling with each heartbeat. Again, these things are not very common in real life, but you need to know them for the boards. That's just kind of how it is. Diagnosing, you're going to use a contrast esophogram. That's going to be your treatment of choice.

Now, remember, I normally say barium asophogram, but in this case, case I'm saying contrast asophogram because you're not going to be using barium. And let me explain why. So normally you use barium in an esophagram because it has superior contrast. It just looks a lot better than some of the other contrast agents. But in this case, you suspect a perforation. And any time you suspect a perforation, you use something called gastrographin instead of barium instead of barium. So why do you use gastrographin over barium? Well, one, because gastrograffin is actually water soluble. So if it leaks through this rupture you have in the esophagus, it can be readily absorbed back into the body.

And two, the reason you use it over barium is because barium, in the case of a perforation, if barium leaks out into the medius steinum, it can actually cause inflammation. And it's actually caustic to the body. So it can cause a lot of problems if it's anywhere outside of the GI tract. So remember that. You're going to do a contrast to softgram, but you're going to use gastrographin. You also may do a CT of the chest, but it's really only used if a contrast esophogram is contraindicated or in patients that have, you suspect any free air in the mediastinum known as a pneumomomedeasthenum. It's a way to be able to visualize that.

That's how you diagnose mainly contrast isophanophram treatment. Initially, like I said, these patients are normally going to be very, very severely ill. They're losing a lot of blood. So initially you need to stabilize these patients. This has a really high mortality. rate. So initially, what do you do when these patients first come in? So initially, IV fluids right away. I want to do IV PPI to suppress all the gastric acid. And you also want to give them IV broad spectrum antibiotics. This is the prevent sepsis because you have this rupture releasing all the gastric contents,

since the media stym in the rest of the body, you can certainly have these pretty bad infections. So you want to give them antibiotics too. And then also make sure that their MPO. I can't imagine anybody's going to be coming in. You're going to be feeding them or they're going to be drinking anything with an esophageal rupture, but it just needs to be mentioned as well. So initially, IV broad spectrum antibiotics, IV fluids, IV PPIs, NPO. Now, this may be enough for patients who come in that are fairly stable in some of these patients that have a smaller rupture. These treatments may be enough.

But more severe ruptures, these patients or patients with a number of comorbidities, these patients are likely going to require surgical treatment. Or if they're non-surgical candidates, they can use an endoscopic approach. and they can do suturing, resection, et cetera. So overall, stabilize patients and then go ahead and treat the perforation, whether it's surgical or an endoscopic approach. Okay, so now I'm going to move on to something that's kind of similar in a way because it is bleeding in the esophagus, but it's not a laceration.

And this is called esophagealvarices. And what esophagealverases is, is an enlarged or dilated veins in the distal esophagus, which is caused by portal vein hypertension, specifically the veins that are enlarged is the gastroasophageal collateral submucosal veins. These veins are susceptible to rupture, which can be life-threatening with esophageal varices. Okay. Now, one of the most important things that you need to know, one of the most important risk factors seen in almost all patients with esophagealveris is cirrhosis. Half of patients with cirrhosis will develop esophageal varices.

And patients with cirrhosis, are actually typically screened with an endoscope about every two to three years for esophagealvarices to check and prevent any rupture if they do find this in the endoscope. So why does cirrhosis cause esophagealvarices? Well, cirrhosis causes scarring in the liver that can lead to obstruction of some of the vessels throwing through the liver, flowing through the liver. And when that happens, the blood flow can back up into other nearby blood vessels, like the vessels in the esophagus, which leads to the engorgement of these esophageal veins

and leads to increased pressure. And ultimately, in some cases, this can lead to these vessels rupturing an esophagealvarices. So that's why cirrhosis causes this. Well, as a side note, really, this isn't very important because it's not common. But it is possible for children to develop esophageal varices as well. Children that have something, you know, as portal vein thrombosis can develop this as well. So again, remember, you should really just remember, remember cirrhosis, but that is a little side note. It's important to know that that exists as well. As far as clinical manifestations, it all depends. If these patients that have stable esophagealvarices, just these engorged veins, they're probably going to be asymptomatic.

When they ask you a question about this, they're not asking about a patient with a stable esophagealvaracy. They're asking about the ones who ruptured. So patients with ruptured asophageal varices are going to have hematomis. They're going to be vomiting all this blood up. They're going to have melana because they're swallowing large quantities of blood. So melanin, us, that dark, sticky stool from all the broken down red blood cells that they're swallowing. And all depending on how severe the bleed is, they may be tachycardic, altered mental status, hypotension, all due to being volume depleted from the loss of blood. Diagnosis, very simple.

You're going to do an upper endoscopy. And an upper endoscopy is not only going to be used to diagnose, but also to treat. So upper endoscopy is diagnostic and therapeutic. So endoscopy is going to be the test you need to know, because, it's used for treatment and diagnosing. Now, going on to treatment, first thing that you need to do when these patients come in is stabilize these patients. They're going to be very volume depleted.

And again, we're not talking about patients with stable esophagealverices. We're talking about the ones that ruptured. So you need to stabilize these patients. They are losing a serious amount of blood very, very fast. So you need to replenish fluids and you need to do it fast. So how are you going to do that? You're going to do IV fluids. What you're going to do is you're going to use a large bore.

So you're going to use these really thick gauge needles. So 14 to 16 gauge needles in each arms. You're trying to get as much blood in as you can. So both arms, IV fluids, large bore 14 to 16 gauge. And then they're also likely going to need blood transfusions. That's initially. Once they're somewhat stable, you need to treat the ruptured vessel. And you can do this with something known as an endoscopic varic seal banding or ligation.

This is going to be your treatment of choice. So once you stabilize them with fluids, blood transfusion, you're going to do an endoscopic varic varicil ligation. And the way this works is with endoscopy, you visualize the rupstered vessel. And then once you visualize, you go ahead and you put this elastic ring placed around the vessel and it cuts off the blood supply and stops the bleed. So that's going to be your treatment of choice. If for some reason that doesn't work or it's contradicated, there's another treatment called

in endoscopic sclerotherapy. And what this is is you inject the sclerosing agent into the ruptured vein. And it causes this local inflammation, decrease blood flow. And in many cases, a collapse of the vein and resolves the bleeding. It's not as effective as endoscopic ligation. And it's really going to be your second line treatment. It's actually the same way they treat varicose veins. So those are a couple options there. And there is some pharmacosal. pharmacologic agents that you can use as an adjunct to the actual endoscopic intervention. So the one you really need to know, the pharmacological agent that you need to know, and this can be used, like I said, while you're getting them ready for the endoscopic procedure. The first one that you need to know, this is going to be your first line pharmacological agent, and it's going to be okreotide.

So ocriotide is a somatostatin analog, and it reduces portal venous flow by causing vasoconstriction, decreasing overall pressure. and decreases blood loss. So again, when you're using meds for these patients, okriotide is going to be your first line by far. You can also use vasopressin. This is going to be a second line, really only if okreotide is contradicated. Now, when all else fails,

you did your aniscopic ligation. You gave them okreotide that's not working. You have a couple other options. You can do a balloon tamponade or something called a tips procedure, which is a transjugular intra-hypatic portosystemic shunt. So there's some other options you should be aware of as well. but really you're going to do endoscopic ligation, okriotide, stabilize these patients. That's going to be your main treatment.

And then once these patients are stable, everything's all fixed, they're doing well. You want to prevent these patients from having a bleed again, which can happen in a good portion of patient with esophagealvarices. So how do you prevent a re-bleed? Well, the main treatment of choice is going to be non-selective beta blockers. Natalol and propranol are going to be the two that you need to know. And these meds block the adrenergic dilation of the mesenteric arteries, and it leads to vasoconstriction of the vessels and decrease portal inflow. So preventing rebleed is going to be with non-selective beta blockers, natalol and propranol.

All right. So esophageal verices has a lot of things that you need to remember, but really I feel like there's only six things that I would really memorize and really know well. And those six things that I feel that you need to know is this. So I feel you need to know cirrhosis is going to be your most common cause. You need to know endoscopy is both going to be the way you diagnose and treat these patients. You need to know that if you are using medications, okreotide is going to be your first line. You need to know that beta blockers are used for preventing rebleeds. You need to know that this is a complication of portal vein hypertension.

And then you need to know finally that esophagealveris leads to excessive amount of bleeding. So excessive upper GI bleed. So those are the six things I think you need to know. And how do you remember those six things? Well, if you can remember the sentence, you can remember that. So the sentence I came up with is beta blockers prevent continual occurrence of esophageal bleeds. Again, beta blockers prevent continual occurrence of esophageal bleeds. So all of the first letters from those words is how you're going to remember each thing.

The only word that doesn't actually have a letter that means anything is of. It's just kind of like a placeholder. So beta blockers prevent continual occurrence of esophageal bleeds. B for beta blockers stands for beta blockers, which again is going to be your prophylaxis against rebleeds. Prevent, the P and Prevent is going to stand for portal vein hypertension, which is a complication of. C, continual stands for cirrhosis, which is your most common cause.

O occurrence stands for ocreatide, which is going to be your first line medical agent. E for esophageal stands for endoscope, which is going to be. your both your diagnostic and your therapeutic agent for this. And then B, which stands for bleed, is going to stand for bleed because you need to remember that this is a serious cause of bleeding. And it can also stand if you want. The B can also stand for balloon tamponotat, which is another agent. So again, beta blockers prevent continual occurrence of asofobleeds. Stans for beta blockers, portal vein hypertension, cirrhosis, ochreotide, endoscope, and then bleeds or balloon tamponad. So that's the way I remember.

The six things I feel are really important for this. Now let's bring it home with two other things I think you should know that aren't as high yield, but I feel like they're important as well. So esophageal web and esophageal ring. So these are the two last topics. And these are thin membranes or diaphragms of tissue that protrude into the esophagus and cause obstruction. Let's start with the esophageal web. This is a thin, fibrous mucus membrane. And it's most commonly found in the upper or the proximal esophagus, the cervical

area of the esophagus it's known as. So esophageal web, thin fibrous, mucous membrane, most commonly found in the proximal or upper esophagus, the cervical area of the esophagus. So how are these patients going to present? Well, whether it's esophageal web or a sophagial ring, it's the same way. Most of these patients are going to be asymptomatic. But when they do develop symptoms, it's going to be dysphasia, mostly to solids, not to liquids. Now remember when we went over in the previous podcast, we went over a motility disorders like acalasia. These, These patients had dysphasia to both solids and liquids, but an esophageal web and ring, these are obstructive causes.

And this is going to be dysphasia just to solids. So remember that. You need to be able to differentiate. Sophageal web dysphasia just to solids. Diagnosing, going to be the same for both. It's going to be a barium swallow, also known as a barium esophogram. And this is, you know, going to be your go-to test. It can be up to 100% sensitive when it's performed properly.

So this is definitely going to be your diagnosis. your way to diagnose this and you're just going to see a narrowing in the area of the esophageal web. An endoscopy can be used, but it's more invasive and it's actually less sensitive than barium swallow. So why would you ever use it if you didn't have to? As far as treatment with esophageal web, you can do an esophageal dilation in symptomatic patients. And after you do the esophageal dilation to open up the area of the esophagus, you're going to treat these patients with PPI to prevent recurrence. And patients who use PPI's post-asophagus. And patients who use PPI's post-es diallation only have about a 7% recurrence compared to patients who did not use PPI have about a 47% recurrence.

So treatment again, esophageal dilation followed by PPI's to prevent recurrence. Now there's one other thing that you need to know about esophageal web. And this is pretty important because this does come up sometimes. So esophageal web is actually one of the three components of the triad in something called Plummer Vincent syndrome. And Plummer Vincent's syndrome consists of three things. Plummer Vincent syndrome consists of dysphasia, cervical esophageal webs, and iron deficiency anemia. Again, Plummer Vincent's syndrome, you need to know this syndrome because it does come up. Plummer Vincent syndrome is a triad of dysphasia, cervical asophageal webs, and iron deficiency anemia. Now, how do you remember that? So the way I remember

Plummer Vincent syndrome and what's in it is plumbers inspect clogged toilets. Plumbers inspect clogged toilets. First letter of each is PICT, plumbers inspect clogged toilets, and that helps me remember plumbers, which is Plummer Vincent syndrome, inspect. The I stands for iron deficiency anemia, clogged, which is a C, stands for cervical esophageal webs, and then toilets, which is a T, stands for trouble swallowing, also known as dysphasia. So again, plumbers inspect clogged toilets. That's going to be Plummer Vincent syndrome, iron deficiency anemia, cervical esophageal webs, and trouble swallowing, also known as dysphasia. Okay, so just a quick recap on esophageal webs, thin protruding membrane in the upper or cervical region of the esophagus. Patients are going to have dysphasia to

swallowing or dysphasia to solids, diagnosed with the barium esophagogram, true with endoscopic dilation followed by PPI's, and then it's one of the three components of Plummer Vincent Triad or Plummer Vincent's syndrome. Okay, last thing that you need to know is esophageal ring, also known as a Shatsky's ring. So this is a diaphragm of obstructive. tissue in the esophagus, which is found at the lower esophagus, at the squamo-columinar junction. Now, if you remember when we went over esophageal webs, we said esophageal webs were at the top of the esophagus. Now, esophageal ring is an obstruction at the bottom of the esophagus. And I actually remember in school getting this one confused and forgetting which was at which

end of the esophagus. And it was actually important to be able to figure out the vignette. So I came up with a way. I didn't have it back then, but I have it now. to remember which occurs in the upper or the lower. So, asophageal web, think of, an asophageal web, you think of a spider, a spider web. So, asophageal web think of the itsy-bitsy spider climbs up the water spout. So web equals spider, spider climbs up the water spout. So you think of the top, or the esophageal web is at the top of the esophagus. So asophageal web, itsy-bitsy spider climbs up the water spout.

He's at the top of the water spout. So asophageal web is at the top of the top. of the esophagus. Now, asophageal ring, I think of a ring. When you put a ring on a finger, you don't put it at the top of the finger and just leave it there. When you put a ring on a finger, you push it all the way down to the bottom of the finger. So asophageal ring is at the bottom of the esophagus. So that's how I remember. Saofageal ring. When you put a ring on, you put it all the way at the bottom of the esophagus. It's at the lower end of the esophagus, at the squamo Columina junction. That's how I remember which is at which end of the esophagus. Now,

let's go back to asophageal ring into the specifics of that. And then so one really important thing you need to know for esophageal ring, aka Shatsky's ring, is that esophageal ring is almost always associated with hyatal hernias. About 97% of patients with hiatal hernias, or sorry, about 97% of patients with asophageal rings will also have hiatal hernias. So you need to know that esophageal rings always think of hiatal hernias.

That's really important. Everything else is pretty much the same. name as esophageal web, clinical manifestations. They're going to have, most patients are going to be asymptomatic. The symptomatic ones, we're going to have dysphagias to solids. Diagnosis, again, barium swallow esophagram. And then treatment. If they're symptomatic, you can do esophageal dilation, followed with PPI's,

would be your treatment of choice. And that's pretty much it. And that's your entire esophagus, part one and part two. I know that was a lot. I hope some of those different mnemonics help you to remember it. And I hope that was helpful overall. So again, good luck on your exams. Good luck in PA school.

Good luck on your pants. Good luck on your panery. And thank you so much for listening to the podcast.