TRANSKRIBEERI 🔗
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Hello, everyone.
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Welcome to Podbytes, where we break down complex medical topics into bite sized pieces, perfect for your commute, coffee break, or whenever curiosity calls.
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I'm Rafa Shaheen and today I'm joined by Raghda Adwan to discuss gastric disorders.
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Hi Rafa, I'm excited for today's topic.
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Gastric disorders can be a lot to digest, no pun intended, but I think we can break it down smoothly.
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I love the enthusiasm.
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So today we're unpacking a whole bunch of gastric conditions including acute and chronic gastritis, peptic ulcers, stress ulcers, gastric polyps, carcinomas, lymphomas, carcinoids, and finally mesenchymal tumors.
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We've got some interesting cases lined up, so let's jump right in! Alright! For our first case, we have a 55 year old man who presents with severe epigastric pain, nausea, and vomiting.
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He admits to drinking heavily and taking NSAIDs regularly for joint pain.
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After performing endoscopy, we found a reddish mucosa with small erosions.
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Oof, heavy drinking and NSAIDs? Girl, that's a lot.
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That sounds like a recipe for disaster.
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What's going on here? Now, this is a case of acute gastritis, which is an acute inflammatory process affecting the gastric mucosa.
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But luckily, it's usually transient and self limited.
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It often occurs when factors like alcohol, NSAIDs, or stress damage the stomach's protective mucus bicarbonate barrier.
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So what's happening behind the scenes? Are the stomach cells just waving white flags at this point? Pretty much.
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When the protective barrier is compromised, hydrogen ions can leak into the mucosa, causing inflammation, necrosis, and sometimes even bleeding.
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It can range from being asymptomatic to causing severe pain and hematomasis.
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All right, so if someone shows up clutching their stomach, how do you doctors figure out if it's acute gastritis and not something worse? That's actually a great question.
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There are clues that may point us toward a diagnosis
Load full transcript
of acute gastritis.
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Patients would usually present with sudden epigastric pain, nausea, vomiting, and possible hematomasis.
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Their endoscopy would show reddish mucosa with small superficial erosions.
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And if we perform biopsy, we would find neutrophilic infiltrates above the basement membrane.
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Okay, so what do you do then? Just cut out the alcohol and the NSAIDs? Well, yeah, pretty much.
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Stopping NSAIDs and alcohol is actually the first step.
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But you can also use proton pump inhibitors, or PPIs, to reduce acid and promote healing.
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And luckily, the prognosis is usually good if the offending agents are removed.
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All right, quiz time! Which histological finding is most characteristic of acute gastritis? The answer is neutrophilic infiltrate above the basement membrane.
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That's the hallmark of acute inflammation in gastritis.
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Our next case is a six year old man in the ICU with severe burns.
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He suddenly starts vomiting blood and his endoscopy shows multiple small ulcers in the stomach and duodenum, less than one centimeter in diameter.
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Yikes.
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Vomiting blood? That's terrifying.
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What's happening here? Yep, that's definitely a red flag.
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This is a case of stress ulcers, which are basically acute mucosal lesions that develop rapidly in critically ill patients due to severe stress, trauma, or shock.
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And we actually have two types of stress ulcers.
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The first type is curling's ulcers.
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They're usually found in the proximal duodenum and commonly occur in patients with severe burns, which is what we see in our patient here.
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The second type is Cushing's ulcers.
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These can appear in the stomach, duodenum, or esophagus and are linked to increased intracranial pressure.
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So it's like the stomach's throwing a fit because the body's under extreme stress.
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Exactly.
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The body's stress response can really throw things out of whack.
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Okay, so what's the reason behind these ulcers? Is it just too much acid? It actually depends on the type of stress ulcer.
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So for curling's ulcers, the severe burns cause hypovolemia and ischemia to the gastric mucosa.
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So you basically reduce blood flow to the stomach to the point that it impairs the protective barrier.
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However, for Cushing's ulcers, it's all about increased intracranial pressure.
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That high pressure triggers the vagus nerve.
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and causes a surge in gastric acid secretion.
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Because if you remember, the vagus nerve is a triggering factor for stomach acid release.
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All of this leads to acute ulceration of the mucosa.
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Aha, so curling's ulcers are due to the lack of blood flow, while cushing ulcers are more about too much acid.
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Exactly, two different roads to the same destination, ulcers.
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All right, so if a doctor suspects stress ulcers, What kind of clues are they looking for? The typical picture of curling's ulcers is a burn patient with hematemesis or melanoma.
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Think of getting burned by a curling iron to remember burns as a cause for curling's ulcers.
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As for Cushing's ulcers, it'll likely be a patient with a history of head trauma or neurosurgery who suddenly gets upper GI bleeding.
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A nice way to remember this is always cushion the brain.
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Okay, I like that.
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I don't think I'll ever confuse those two again.
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So what about more specific tests like endoscopy? Oh yeah, I was just getting to that.
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An endoscopy is used to further narrow down the diagnosis, where we can see multiple, small, round ulcers less than one centimeter in diameter with sharply demarcated edges.
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And these are often seen in different locations based on which type of ulcer it is.
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Remember, curling's ulcers are usually found in the proximal duodenum, while Cushing's ulcers can appear in the stomach duodenum or even the esophagus.
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And something important to remember is that these are
acute ulcers, so you would not see any scarring or fibrosis, and that's how you would know they're not chronic ulcers.
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Got it, got it.
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So the patient's history plus what we see on endoscopy really helps narrow it down.
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Exactly, you got it.
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And the absence of scarring is a big clue that these are acute, not chronic.
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Okay, so how do we treat these stress ulcers? Can they heal on their own or do you actually need to step in fast? You definitely need to step in.
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And here's what you do.
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First, you need to manage the underlying cause, whether that is shock, sepsis, trauma, or increased intracranial pressure.
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Then you go in with your classic PPI's or H2 blockers to reduce acid production and promote healing.
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Sometimes, in severe cases, you may need to intervene with endoscopic hemostasis or even surgery to fix any complications.
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Luckily, though, the prognosis is generally good if the underlying cause is treated quickly.
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Aha, so it is a race against time.
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Fix the underlying issue and calm the stomach down.
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Yep, exactly.
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The quicker you act, the better the outcome.
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Alright, quiz time! Which condition is the most commonly associated with Cushing's ulcers? The answer is intracranial injury.
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Cushing's ulcers are all about the vagal stimulation from increased intracranial pressure.
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Remember, you always cushion the brain.
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Yeah, right, right, right.
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Always cushion the brain.
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That really is a great mnemonic.
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Now, on to our next case.
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A 63 year old woman presents with fatigue, glossitis, and tingling in her hands and feet.
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Blood tests show megaloblastic anemia and low B12 levels.
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She has a history of thyroiditis.
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Her endoscopy reveals atrophic mucosa in the gastric body and fundus.
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Fatigue, a sore tongue, and tingling? And with a history of thyroiditis, it seems like there's more to the story, huh? Absolutely.
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This woman likely has autoimmune gastritis.
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It's a type of chronic gastritis that involves the autoimmune destruction of the gastric parietal cells and sometimes intrinsic factor.
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It primarily affects the body and fundus of the stomach, leading to atrophy, achlorhydria, and B12 deficiency.
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Okay, so her own immune system's causing the damage.
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Yep, you got it.
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Gotcha, gotcha.
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Okay, so what's the actual mechanism here? And how does the immune system end up causing this B12 deficiency? Well, it all comes down to autoantibodies.
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First, we have the anti intrinsic factor antibodies.
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These prevent the absorption of B12 in the terminal ileum, causing B12 deficiency and eventually megaloblastic anemia.
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Then, you have the antiparietal cell antibodies.
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And from their name, you know that they destroy parietal cells.
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So now the stomach cannot make acid, and you get achlorhydria.
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This destruction of the parietal cells causes G cells in the antrum to go crazy with gastrin secretion in an attempt to compensate.
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And that's how you get hypergastronemia.
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Over time, these G cells undergo hyperplasia and may lead to carcinoid tumors.
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Wow, so it is like a domino effect.
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You destroy the parietal cells, lose acid and intrinsic factor, then you don't have B12 anymore.
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Exactly.
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And that leads to the symptoms we're seeing.
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Alright, so if a doctor suspects autoimmune gastritis, what kind of clues should they be looking for? Well, first of all, the patient would present with symptoms of B12 deficiency.
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So think of fatigue, tingling in the hands and feet, ataxia, and a smooth, beefy red tongue.
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Then when you look at their lab results, you would see macrocytic anemia, low
B12 levels, high gastrin levels, and of course, positive antiparietal cell antibodies.
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Okay, and what about their endoscopy? On endoscopy, you would find atrophic mucosa with loss of rugal folds, specifically in the body and fundus of the stomach.
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And then if you take a biopsy, you would see a lymphocytic infiltrate, intestinal metaplasia, and loss of parietal cells.
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Got it, got it.
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So it's a whole collection of clues.
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Low B12, high gastrin.
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Positive antibodies and a biopsy confirming it.
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Yep, it's like piecing together all the puzzle pieces.
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Okay, so once they figure out it is autoimmune gastritis, how do they treat it? Are we talking lifelong meds? Pretty much, yeah.
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It's very important for these patients to take B12 supplements for the rest of their lives.
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They should also regularly monitor for gastric adenocarcinoma and carcinoid tumors because they are at a higher risk.
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Luckily, their prognosis is good if they maintain their B12, but unfortunately, they're still at risk of gastric cancer.
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Uh huh, so it is all about managing the damage and keeping an eye out for any bigger threats.
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Yep, you got it.
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Okay, Raghda, do you want to guess what time it is? Quiz time! You got it! Now, which of the following laboratory findings is the most characteristic of autoimmune gastritis? A.
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Low gastrin levels B.
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High gastrin levels and positive antiparietal cell antibodies C.
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Hyperchlorhydria or D.
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High B12 levels The answer is B.
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High gastrin levels and positive antiparietal cell antibodies.
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Those are the key markers for autoimmune gastritis.
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Nice, you got it.
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Let's go to the next case.
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Okay, a 50 year old male presents with burning epigastric pain that worsens after meals.
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And he says he's been experiencing this for months.
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There's no vomiting or weight loss, and a urea breath test is positive for H.
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pylori.
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An endoscopy shows erythematous mucosa in the antrum.
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Aha, so it is something to do with H.
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pylori, isn't it? Spot on.
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This patient has H.
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pylori associated chronic gastritis.
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This is actually the most common type of chronic gastritis worldwide, and it usually starts in the antrum but can progress to the whole stomach.
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Eventually, it leads to atrophy and intestinal metaplasia.
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with an increased risk of ulcers, mouth lymphoma, and adenocarcinoma.
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Alright, so what makes H.
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pylori such a troublemaker? H.
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pylori shows up, makes a whole mess, and doesn't leave.
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It uses urease to convert urea into ammonia, which neutralizes stomach acid, allowing it to survive.
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But that's not all! It also releases cytotoxins such as CAG A that cause chronic inflammation and mucosal damage, leading to atrophy and intestinal metaplasia.
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Patients with H.
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pylori infection are at risk of peptic ulcers due to increased gastrin secretion and acid production.
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And unfortunately, long term infection can lead to malt lymphoma by promoting lymphoid tissue hyperplasia.
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Wow, so it's not just crashing the party.
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It's trashing the whole house.
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It's got urease, allowing it to survive, and cytotoxins, damaging the mucosa, both increasing the risk of peptic ulcers and cancer.
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Exactly.
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That's why it's so dangerous if left untreated.
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Right.
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And how do doctors spot these patients? Well, they present with burning epigastric pain and tenderness that worsens with meals, nausea, and sometimes bloating.
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Their endoscopy would show an erythematous specifically in the antrum.
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On biopsy, you would see neutrophilic infiltrate, lymphoid aggregates, and most importantly, H.
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pylori visible with special stains.
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But since endoscopy and biopsy are too invasive, these patients are usually just diagnosed with a positive urea breath test or stool antigen test.
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We can also detect anti H.
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pylori IgG antibodies on serology, but this method is not useful for active infection.
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Got it.
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So urea breath test or stool antigen test for the diagnosis.
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And how do you get rid of H.
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pylori? Do you need to go for antibiotics? Yes, you need to use antibiotics, but not alone.
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The go to is something called triple therapy.
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which is made up of PPI plus clarithromycin plus amoxicillin for 10 to 14 days.
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But sometimes, if the H.
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pylori is found to be resistant to clarithromycin, you would need to go for quadruple therapy, which involves bismuth, metronidazole, tetracycline, and a PPI.
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After that, you need to follow up with your patient four weeks after stopping therapy to confirm eradication.
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That sounds like an intense therapy regimen.
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Do they usually respond well? Well, luckily, yes.
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If treated early, these patients have a good prognosis.
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But the main issue comes when they're left untreated because that increases the risk of ulcers and gastric cancer.
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Okay, so the sooner you get rid of it, the better.
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Now, let's go for a practice question.
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Which complication is most commonly associated with H.
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pylori infection? The answer is malt lymphoma.
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Long term H.
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pylori infection increases the risk of malt lymphoma due to chronic inflammation and lymphoid hyperplasia.
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Now, on to our next case.
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Here we have a 48 year old man who presents with burning epigastric pain
that gets worse 2 3 hours after eating, and often wakes him up at night.
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The pain is temporarily relieved by antacids.
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He admits to taking NSAIDs regularly for chronic back pain.
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He does not have weight loss or vomiting.
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Endoscopy reveals a single ulcer on the anterior wall of the duodenum.
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Oof, being woken up by stomach pain sounds awful.
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What's your take on this one? Yeah, it's definitely not fun.
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This patient has peptic ulcer disease, or PUD.
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It's characterized by deep focal defects in the mucosa.
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PUD actually has two main types of ulcers, and those are either gastric or duodenal.
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Duodenal ulcers are more common and are usually benign, while gastric ulcers are less common and have a higher risk of being malignant.
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Got it, so duodenal ulcers are more common and more benign than gastric ulcers.
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Exactly.
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That's why gastric ulcers may sometimes need a closer look.
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Okay, and what's causing these ulcers? Is it too much acid, not enough protection, or both? Both, actually.
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Peptic ulcers form when there's an imbalance between mucosal defense mechanisms and aggressive factors like gastric acid and pepsin.
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The two main causes of PUD are H.
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pylori infection and NSAID use.
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In duodenal ulcers, excess acid secretion is usually the main problem, while in gastric ulcers, it's more about impaired mucosal defense.
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Aha, okay.
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So, again, we need to watch out for H.
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pylori and the NSAIDs.
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Yep, and remember that NSAIDs inhibit COX enzymes and prostaglandin synthesis, which impairs mucosal defenses by reducing mucus, bicarbonate secretion, and blood flow.
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Alright, but if someone shows up with these symptoms, how do you end up diagnosing PUD? Well, in order to tell if the problem is in the stomach or the duodenum, the key here is the timing of the pain.
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The pain in duodenal ulcers actually improves when you eat, and then gets worse again 2 3 hours later or at night.
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But the pain in gastric ulcers gets worse with eating.
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Then, if you go in with endoscopy, you would see an ulcer in the stomach or duodenum.
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For gastric ulcers specifically, you need to assess the risk of malignancy.
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Just by looking at it on endoscopy, a benign gastric ulcer will appear more clean and punched out, while a malignant one will have more heaped up margins.
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But to confirm or rule out malignancy in gastric ulcers, you will need a biopsy.
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Aha, so it is all about connecting the symptoms, timing, and what they see on the scope.
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Exactly.
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Plus, labs might show a positive urea breath test or stool antigen test for H.
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pylori and iron deficiency anemia if there's a chronic blood loss from the ulcer.
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Okay, and how do they fix it? Can they just cut back on the hot sauce or is there much more to it? There's definitely more involved.
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For H.
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pylori positive ulcers, it's the triple or quadruple therapy for 14 days like we mentioned earlier.
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For NSAID induced ulcers, stopping NSAIDs and starting a PPI for 8 weeks usually does the trick.
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In cases of complications like bleeding or perforation, endoscopic hemostasis or even surgery might be needed.
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Luckily though, prognosis is great if treated properly.
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Nice, sounds like a pretty straightforward plan.
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Kick out the bacteria or cut out the meds.
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You got it.
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Catch it early and you're good to go.
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Alright Radha, do you really, really want to guess what time it is? Quiz time! You got it.
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Now, which of the following is the most common complication of peptic ulcer disease? A, gastric outlet obstruction, B, perforation, C, bleeding, or D, fistula formation? The answer is C, bleeding.
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It's the most common complication occurring in about 15 to 20
percent of cases.
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Now should we move on to the gastric tumors? Not yet! We discussed a lot of diseases, so let's quickly recap the important points we mentioned before moving on to the next segment.
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Okay, let's do it.
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Alright.
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Starting off with acute gastritis, acute gastritis can be caused by alcohol, NSAIDs, or stress.
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Endoscopy reveals reddish mucosa with small erosions.
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And biopsy shows neutrophilic infiltrates seen above the basement membrane.
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It is treated by PPIs and the stopping of the offending agent.
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Next up is stress ulcers.
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Krilling's ulcers are caused by severe burns and are often found in the proximal duodenum.
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Cushing's ulcers are a result of increased intracranial pressure and are often found in the stomach, duodenum, or even the esophagus.
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Endoscopy of stress ulcers reveals multiple small ulcers less than 1 cm with sharply demarcated edges.
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Alright.
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Chronic autoimmune gastritis is characterized by autoantibodies targeting parietal cells and intrinsic factor.
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This leads to achlorhydria, B12 deficiency, megaloblastic anemia, and high gastrin levels.
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This increases the risk of carcinoid tumors.
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And our main character of today's episode.
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H.
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pylori is a gram negative bacteria that uses urease and causes chronic gastritis.
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It poses a long term risk for malt lymphoma and adenocarcinoma.
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Diagnosis can be achieved by a positive urea breath test or stool antigen test.
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Treatment involves triple therapy of PPIs with clarithromycin and amoxicillin.
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Now, last but not least, we have peptic ulcers disease.
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This can either present as gastric ulcers or, more commonly, duodenal ulcers.
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Duodenal ulcers are usually benign, while the gastric ulcers carry a higher risk of malignancy.
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They're mostly caused by NSAIDs or H.
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pylori.
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The classic symptom is a burning pain in the stomach which worsens with meals in gastric ulcers and improves with meals in duodenal ulcers.
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The most common complication in both types is bleeding.
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This carries a risk of perforation and gastric outlet obstruction.
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That was quite the recap.
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Let's jump into our next case.
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Here, we have a 70 year old man who presents for a routine endoscopy due to a history of chronic gastritis.
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Endoscopy reveals multiple small polyps in the antrum.
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Biopsies confirm they are hyperplastic polyps with no dysplasia.
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Ooh, polyps.
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Those always sound a bit ominous.
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How worried should this guy be? Not too much in this case.
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These hyperplastic polyps are usually benign unless they're larger than 1.
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5 centimeters.
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Gastric polyps are mucosal protrusions that develop due to epithelial or stromal hyperplasia.
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Okay, so more like harmless bumps on the road, unless they start getting too big.
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Exactly.
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But adenomatous polyps are the ones to worry about since they carry a higher malignant potential.
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Okay, and how do these polyps form? Just too much cell growth, or is there more to it? Yup, it's mostly too much cell growth due to chronic inflammation.
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Hyperplastic polyps arise from regenerative hyperplasia of the gastric epithelium, while fundic gland polyps, on the other hand, are linked to increased gastrin levels due to long term PPI use.
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Uh huh, okay, so it's like overgrowth, but without the usual checks and balances.
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Yep.
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Okay, so if you find these polyps, do you take them out, or do you just keep an eye on them? That's actually a great question.
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Small hyperplastic polyps usually just need endoscopic surveillance.
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However, adenomatous polyps should be removed due to their malignant
potential.
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For fundigland polyps, no treatment is needed unless they're large or dysplastic.
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Got it, so it is a case of watchful waiting unless they look sketchy.
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Exactly.
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Now let me guess.
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Quiz time! You got it! So, which type of gastric polyp has the highest risk of malignant transformation? A.
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Hyperoplastic polyp.
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B.
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Fundic gland polyp.
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C.
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Adenomatous polyp.
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D.
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Inflammatory polyp.
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The answer is C.
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Adenomatous polyp.
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They have a high malignant potential, especially if larger than 2 centimeters.
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Noted.
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Let's keep it moving.
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Now, our next case is a 65 year old man who presents with weight loss, early satiety, and epigastric pain.
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He also reports melanoma for a few weeks.
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Endoscopy shows a large ulcerated mass in the antrum, and biopsies confirm adenocarcinoma.
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Yikes.
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Weight loss and melanoma? That's definitely alarming.
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What's the story here? Yeah, those symptoms are definitely concerning.
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This is gastric adenocarcinoma, which is the most common gastric malignancy, accounting for over 90 percent of stomach cancers.
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There are two main types.
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The first one is the intestinal type, where you have gland like structures.
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It is linked to H.
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pylori infection, chronic gastritis, and nitrosamines.
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The second type is the diffuse type, which has signet ring cells and does not form glands.
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It's linked to E cadherin mutations and is characterized by a leather bottled stomach, also known as linitis plastica.
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Got it.
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And how do these types of gastric cancers actually form? Are they both related to inflammation? Now, for the intestinal type, it usually starts with chronic inflammation, often from H.
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pylori infection.
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That leads to intestinal metaplasia and dysplasia, whereas for the diffuse type, it's more about genetic mutations, particularly in E.
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cadherin, which messes up cell adhesion and leads to that thickened, stiff stomach wall we call linitis plastica.
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Okay, so one's more of a slow buildup from inflammation, and the other is a genetic sneak attack.
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Exactly.
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Two different paths, same dangerous destination.
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Alright, so what kind of clues might point the doctors towards this diagnosis? So symptoms like weight loss, early satiety, epigastric pain, and melanoma are big red flags for malignancy.
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When you go in with endoscopy, you might find an ulcerated mass, or in the case of the diffuse type, a thickened stomach wall.
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Then we can continue with biopsy to distinguish the types.
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The intestinal type would have gland formation, and the diffuse type would have signet ring cells.
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And finally, we do a CT scan for staging and spotting metastases, like Burkhaus node or Sister Mary Joseph nodule.
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Okay, so once we've made the diagnosis, what's the treatment plan? Are we talking surgery, chemo, or both? Usually it's both.
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Surgical resection or gastrectomy is the main treatment if it's localized, but for more advanced stages, we would go for chemotherapy and radiation.
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When it comes to prognosis, a localized mass has a 5 year survival of up to 90%, but unfortunately, an advanced disease has less than 20%.
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Wow, so catching it early really makes a huge difference.
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Absolutely.
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Early detection is everything.
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Alright, Rahda, do you want to tell me what time it is? Quiz time! You got it! Which of the following is a characteristic finding of diffuse type gastric adenocarcinoma? A.
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Gland formation, B.
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Cygnet ring cells, C.
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Lymphoid aggregates, or D.
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Intestinal metaplasia? The answer is B, signet ring cells.
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Those are the hallmark of the diffuse type of gastric adenocarcinoma.
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Got it.
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Let's keep on moving.
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Next up, we have a 58 year old woman who presents with weight loss, abdominal discomfort, and early satiety.
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Endoscopy reveals thickened gastric folds and multiple ulcers in the body of the stomach.
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Biopsies show lymphocytic infiltrates with evidence of monoclonal B cell proliferation.
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Lymphomas in the stomach.
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I thought those were more of a lymph node thing.
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You're right, lymphomas usually start in lymph nodes, but gastric lymphomas are actually the most common type of extra nodal lymphoma.
348
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Most are malt lymphomas linked to h pylori infection, or we even have diffuse large B-cell lymphomas, which are more aggressive.
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Uh huh, so the stomach's playing host to some unwelcome guests.
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Got it.
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Exactly.
352
00:24:58,429.6901773 --> 00:25:01,139.6901773
And it's all about that chronic inflammation inviting the men.
353
00:25:01,459.6901773 --> 00:25:02,159.6901773
So how does H.
354
00:25:02,189.6901773 --> 00:25:07,779.6901773
pylori manage to turn stomach tissue into a lymphoma breeding ground? Well, chronic H.
355
00:25:07,799.6901773 --> 00:25:12,409.6901773
pylori infection causes continuous inflammation, leading to lymphoid tissue proliferation.
356
00:25:12,959.6901773 --> 00:25:18,179.6901773
Over time, this inflammation can trigger genetic changes, like the T1118 translocation.
357
00:25:18,679.6901773 --> 00:25:24,639.6901773
These changes activate NF kappa B, promoting B cell survival and eventually leading to malt lymphoma.
358
00:25:25,49.6891773 --> 00:25:28,99.6901773
Okay, so lymphoid tissue proliferation from chronic H.
359
00:25:28,139.6891773 --> 00:25:34,179.6901773
pylori leading to the T1118 translocation leading to the B cell malt lymphoma.
360
00:25:34,539.6901773 --> 00:25:35,849.6901773
Exactly, you got it.
361
00:25:36,259.6901773 --> 00:25:39,29.6901773
Alright, and how do we treat this? Do you just treat the H.
362
00:25:39,59.6901773 --> 00:25:40,929.6901773
pylori? Great question.
363
00:25:41,39.6901773 --> 00:25:42,729.6901773
For malt lymphoma, getting rid of H.
364
00:25:42,759.6901773 --> 00:25:45,459.6901773
pylori with antibiotics can actually induce remission.
365
00:25:45,769.6901773 --> 00:25:55,129.5901773
But, for more aggressive lymphomas, like diffuse large B cell lymphoma, it's all about CHOP chemotherapy, or CHOP, which includes cyclophosphamide.
366
00:25:55,299.6901773 --> 00:25:59,369.6901773
Doxorubicin, vincristine, and prednisone, often with rituximab.
367
00:25:59,789.6901773 --> 00:26:01,759.6901773
Okay, so it depends on the severity.
368
00:26:02,39.6901773 --> 00:26:02,649.6901773
Exactly.
369
00:26:02,969.6901773 --> 00:26:05,499.6901773
Different levels of intervention based on the threat level.
370
00:26:05,929.6891773 --> 00:26:08,419.6891773
Okay, we have another practice question rolling in.
371
00:26:08,829.6901773 --> 00:26:16,829.6901773
Which of the following infections is most commonly associated with gastric malt lymphoma? A, Epstein Barr virus, B, H.
372
00:26:16,859.6901773 --> 00:26:18,414.6901773
pylori, C.
373
00:26:18,424.6901773 --> 00:26:20,151.3901773
Cytomegalovirus or D.
374
00:26:20,151.3901773 --> 00:26:27,24.6901773
Hepatitis C virus? The answer is, of course, B.
375
00:26:27,64.6901773 --> 00:26:27,324.6901773
H.
376
00:26:27,354.6901773 --> 00:26:27,894.6901773
pylori.
377
00:26:28,174.6901773 --> 00:26:31,84.6901773
Chronic infection is the key risk factor for malt lymphoma.
378
00:26:31,464.6891773 --> 00:26:33,754.6891773
Nice! On to the next case.
379
00:26:34,919.0752452 --> 00:26:39,959.0752452
A 62-year-old woman with a history of pernicious anemia presents with abdominal pain and flushing.
380
00:26:40,349.0752452 --> 00:26:44,399.0752452
Endoscopy reveals a submucosal yellow 10 nodule in the gastric body.
381
00:26:44,909.0752452 --> 00:26:48,299.0752452
Biopsy confirms a well differentiated neuroendocrine tumor.
382
00:26:48,504.5854493 --> 00:26:54,144.5854493
Ooh, a neuroendocrine tumor? That sounds a bit different from the other stuff we've talked about.
383
00:26:54,424.5854493 --> 00:26:57,854.5854493
What's going on here? Now this is a gastric carcinoid tumor.
384
00:26:58,164.5844493 --> 00:27:04,964.5844493
There are well differentiated neuroendocrine tumors that arise from enterochromaffin like cells or ECL cells in the gastric mucosa.
385
00:27:05,434.5854493 --> 00:27:07,84.5854493
They're characterized into three types.
386
00:27:07,394.5854493 --> 00:27:11,314.5854493
Type 1 is linked to chronic atrophic gastritis and hypergastronemia.
387
00:27:11,804.5854493 --> 00:27:14,164.5854493
This type is the most common and least aggressive.
388
00:27:14,717.9187826 --> 00:27:18,817.9187826
Type 2 is associated with Zollinger Ellison syndrome and MEN1 syndrome.
389
00:27:19,107.9187826 --> 00:27:21,327.9187826
This type usually involves multiple lesions.
390
00:27:21,947.9187826 --> 00:27:23,677.9187826
Type 3 is the most aggressive one.
391
00:27:23,987.9187826 --> 00:27:26,247.9187826
It's sporadic and not linked
to hypergastronemia.
392
00:27:26,847.9187826 --> 00:27:32,7.9187826
Okay, so type 1 is mild, type 2 is in the middle, and type 3 is the most severe.
393
00:27:32,97.9187826 --> 00:27:36,567.9187826
Exactly, and they're all neuroendocrine tumors arising from anterior chromaffin like cells.
394
00:27:37,497.9187826 --> 00:27:41,167.9187826
So how do these carcinoid tumors form? Well, it depends on the type.
395
00:27:41,397.9187826 --> 00:27:43,717.9187826
Type 1 starts with chronic atrophic gastritis.
396
00:27:43,947.9187826 --> 00:27:47,237.9187826
If you remember, we said this has low stomach acid and high gastrin levels.
397
00:27:47,587.9187826 --> 00:27:52,187.9187826
All of this basically causes ECL cell hyperplasia and eventually carcinoid tumors.
398
00:27:52,657.9177826 --> 00:28:00,657.9187826
Whereas type 2 is driven by a gastrin secreting tumor called a gastrinoma that also elevates gastrin, leading to ECL cell hyperplasia.
399
00:28:01,77.9187826 --> 00:28:06,657.9177826
And finally, type 3 arises spontaneously with no connection to gastrin levels and tends to be more aggressive.
400
00:28:07,12.9187826 --> 00:28:13,542.9187826
Okay, so it's either too much gastrin causing cell overgrowth, or just bad luck with type 3.
401
00:28:14,42.9187826 --> 00:28:14,692.9187826
Exactly.
402
00:28:14,802.9187826 --> 00:28:16,602.9187826
Different pathways to the same problem.
403
00:28:16,892.9187826 --> 00:28:29,529.5854493
Alright, so if a doctor is trying to figure out if someone has a carcinoid tumor, what should they look for? Carcinoid tumors usually present with abdominal pain, flushing, and sometimes diarrhea if serotonin is secreted.
404
00:28:30,19.5854493 --> 00:28:35,129.5854493
Endoscopy would show submucosal yellow tan nodules, usually in the body and fundus of the stomach.
405
00:28:35,749.5854493 --> 00:28:42,889.5854493
If you perform biopsy, you would see uniform, round cells with salt and pepper chromatin positive for chromogranin A and synaptophysin.
406
00:28:43,209.5854493 --> 00:28:50,999.5854493
And finally, lab results would show high serum gastrin for types 1 and 2, and urinary 5 HIAA if serotonin is being secreted.
407
00:28:51,429.5844493 --> 00:28:58,559.4854493
Okay, so the cells are positive for chromogranin A and synaptophysin, and there is urinary 5 HIAA.
408
00:28:59,549.5854493 --> 00:29:04,459.5854493
Alright, so now what? Surgery, meds, or both? Both.
409
00:29:04,834.5854493 --> 00:29:05,994.5854493
Again, depending on the type.
410
00:29:06,454.5854493 --> 00:29:09,624.5854493
Type 1 and 2 can be resected endoscopically if the tumor is small.
411
00:29:10,4.5854493 --> 00:29:12,664.5854493
Then they can also be given octeotride for symptoms.
412
00:29:12,974.5854493 --> 00:29:18,357.9187826
These two types have a good prognosis, whereas type 3 has a poor prognosis due to its aggressive nature.
413
00:29:18,677.9187826 --> 00:29:21,517.9177826
This type needs surgical resection and often chemotherapy.
414
00:29:22,50.9620628 --> 00:29:22,770.9620628
Okay, got it.
415
00:29:22,820.9620628 --> 00:29:25,150.9630628
So, resection plus some sort of pharmacotherapy.
416
00:29:25,200.9630628 --> 00:29:25,820.9630628
Exactly.
417
00:29:26,715.9630628 --> 00:29:26,945.9630628
Hold on.
418
00:29:27,815.9630628 --> 00:29:38,185.9630628
You want to guess what time it is? Quiz time! You got it! Now, which type of gastric carcinoid tumor is associated with chronic atrophic gastritis and hypergastronemia? A.
419
00:29:38,245.9630628 --> 00:29:39,875.9630628
Type 1 B.
420
00:29:39,945.9630628 --> 00:29:41,265.9620628
Type 2 C.
421
00:29:41,265.9620628 --> 00:29:42,675.9620628
Type 3 or D.
422
00:29:42,725.9620628 --> 00:29:47,476.9541017
Type 4 The answer is A.
423
00:29:47,526.9551017 --> 00:30:03,824.7806591
Type 1 It's the one linked to chronic atrophic gastritis and high gastrin levels Nice! Let's move on to the last segment Okay, we're almost done A 55 year old man presents with abdominal pain and a palpable mass CT scan shows a well circumscribed submucosal mass in the stomach.
424
00:30:04,414.7806591 --> 00:30:09,349.6806591
Biopsy reveals spindle cells positive for a CD117 secant mutation.
425
00:30:10,189.7806591 --> 00:30:11,389.7806591
A genetic mutation.
426
00:30:11,449.7806591 --> 00:30:29,639.7806591
What's the story here? This is a gastrointestinal stromal tumor, or just for short, and is the most common mesenchymal tumor of the stomach just originates from the interstitial cells of Kal, which are the pacemakers of Paracelsus, and the tumor is driven by mutations in the CD one 17 C kit gene, or sometimes in P-D-G-F-R-A.
427
00:30:30,519.7806591 --> 00:30:30,929.7806591
Got it.
428
00:30:30,979.7806591 --> 00:30:33,89.7806591
So, GIST from CKIT mutation.
429
00:30:33,139.7806591 --> 00:30:38,519.7806591
But what's the deal with these CKIT mutations? Are they just random bad luck? Pretty much.
430
00:30:38,559.7806591 --> 00:30:44,939.7796591
Mutations in CKIT, or PDGFRA, lead to tyrosine kinase activation, causing uncontrolled cell proliferation.
431
00:30:45,409.7806591 --> 00:30:49,999.7806591
GISTs can range from benign to highly malignant based on their size and how fast they're dividing.
432
00:30:50,379.7806591 --> 00:30:50,979.7806591
I see.
433
00:30:51,29.7806591 --> 00:31:02,999.7806591
And how do doctors spot a GIST? The patient would present with abdominal pain, early satiety, and sometimes GI bleeding, prompting doctors to perform an endoscopy where they would see a submucosal mass that sometimes ulcerates.
434
00:31:03,399.7806591 --> 00:31:08,839.7806591
Then on biopsy, there are spindle cells positive for CD117 or CKIT and PDGFRA.
435
00:31:09,809.7796591 --> 00:31:10,179.7806591
Got it.
436
00:31:10,189.7806591 --> 00:31:15,669.7806591
So a submucosal mass with spindle cells that has a CKIT or PDGFRA mutation.
437
00:31:15,859.7806591 --> 00:31:16,689.7806591
Exactly.
438
00:31:16,839.7806591 --> 00:31:17,219.7806591
All right.
439
00:31:17,579.7806591 --> 00:31:28,134.7806591
And how do you get rid of these tumors? Surgery is the mainstay of treatment if it's resectable, but for unresectable or metastatic gists, you can use imatinib since it targets the CKIP pathway.
440
00:31:28,264.7806591 --> 00:31:30,464.7806591
Uh huh, so cut them out or use imatinib.
441
00:31:30,584.7796591 --> 00:31:31,204.7796591
Exactly.
442
00:31:31,294.7796591 --> 00:31:33,554.7806591
Different scenarios prompt different approaches.
443
00:31:33,814.7806591 --> 00:31:37,384.7796591
Alright, now we're approaching our last final question for today.
444
00:31:37,684.7796591 --> 00:31:49,924.7806591
Which marker is most commonly positive in a gastrointestinal stromal tumor? A CD 20 B, CD one 17 C, kit C, CD three, or D CD 30.
445
00:31:53,668.9274773 --> 00:31:59,358.9274773
The answer is B, CD one 17 or C kit, if you remember, it's the hallmark of gist.
446
00:31:59,448.9274773 --> 00:32:00,78.9274773
Nice.
447
00:32:00,348.9274773 --> 00:32:02,808.9274773
I feel like we've really covered the whole stomach today.
448
00:32:03,18.9274773 --> 00:32:05,748.9274773
Let's recap the gastric tumors to make sure we're good to go.
449
00:32:05,748.9274773 --> 00:32:06,588.9274773
All right, let's do it.
450
00:32:07,707.0595968 --> 00:32:12,87.0595968
Firstly, gastric polyps in the stomach are due to epithelial or stromal hyperplasia.
451
00:32:12,497.0595968 --> 00:32:15,587.0595968
They can either be hyperplastic polyps, which are the most common type.
452
00:32:15,917.0595968 --> 00:32:18,557.0595968
Or fund gland polyps or adenomatous polyps.
453
00:32:18,917.0595968 --> 00:32:28,957.0595968
Hyperplastic polyps are linked to chronic inflammation and are usually benign fund gland Polyps are often from PPI use, whereas adenomatous polyps carry a high risk of malignant transformation.
454
00:32:29,257.605883 --> 00:32:33,907.605883
Gastric polyps are usually asymptomatic unless they're really large, they might even cause bleeding.
455
00:32:34,512.9064075 --> 00:32:35,382.9064075
Alright, moving on.
456
00:32:35,382.9064075 --> 00:32:39,912.9064075
Gastric andino carcinomas includes the intestinal and diffuse types.
457
00:32:40,182.9064075 --> 00:32:42,342.9064075
The intestinal type is linked to h pylori.
458
00:32:42,772.9064075 --> 00:32:46,992.9064075
chronic gastritis and nitrosamines and forms gland like structures.
459
00:32:47,392.9064075 --> 00:32:56,222.9064075
The diffuse type involves signet ring cells and e cadherin mutations and may cause linidus plastica or a thick, stiff stomach.
460
00:32:56,282.9064075 --> 00:32:59,972.9074075
They usually spread to Virchow's nodes or sister Mary Joseph nodules.
461
00:33:00,468.8865061 --> 00:33:02,48.8875061
Now on to gastric lymphomas.
462
00:33:02,313.8875061 --> 00:33:05,503.8875061
These are classified into the more common Malt lymphoma linked to H.
463
00:33:05,523.8875061 --> 00:33:10,233.8875061
pylori infection and the less common, more aggressive, diffused large B cell lymphoma.
464
00:33:10,803.8875061 --> 00:33:12,853.8875061
Malt lymphoma is related to chronic H.
465
00:33:12,873.8875061 --> 00:33:19,183.8875061
pylori and a T1118 translocation, which activates NF kappa B and promotes B cell survival.
466
00:33:19,283.8875061 --> 00:33:21,333.8875061
Biopsy shows monoclonal B cells.
467
00:33:21,983.8875061 --> 00:33:29,93.8875061
Alright, now, gastric carcinoid tumors originate from ECL cells in the gastric mucosa and are of three types.
468
00:33:29,393.8875061 --> 00:33:33,623.8875061
Type one is linked to the chronic atrophic gastritis and is the least aggressive.
469
00:33:33,923.8875061 --> 00:33:41,393.8875061
Type two is linked to zore sison syndrome in MEN one syndrome, type three is sporadic and is the most aggressive type.
470
00:33:41,673.8875061 --> 00:33:48,33.8875061
Carcinoid tumors are submucosal tumors that stain positive for synaptophysin and chromogranin A and finally.
471
00:33:48,283.8875061 --> 00:33:53,93.8875061
GIST or gastrointestinal stromal tumors, which are the most common mesenchymal tumors in the stomach.
472
00:33:53,593.8875061 --> 00:34:03,891.0973904
These originate from the interstitial cells of KHAL and have spindle cells with either CKIT or CD117 or PDGFRA mutations causing excessive tyrosine kinase activity.
473
00:34:04,993.8865061 --> 00:34:13,153.8875061
Phew, we covered a lot today, from simple inflammation to polyps, cancers, lymphomas, and even some rare tumors.
474
00:34:13,333.8875061 --> 00:34:17,293.8875061
Yep, now our listeners know everything they need to know on gastric disorders.
475
00:34:17,788.8875061 --> 00:34:19,838.8875061
Thank you so much for the breakdown, Rada.
476
00:34:20,148.8875061 --> 00:34:23,818.8875061
And to all of our listeners, thank you for sticking with us and see you soon.
477
00:34:24,48.8875061 --> 00:34:24,548.8875061
Bye bye.
478
00:34:26,263.9671727 --> 00:34:27,283.9671727
Bloop, please.
479
00:34:28,368.9671727 --> 00:34:29,18.9671727
Quiz time.
480
00:34:29,263.9671727 --> 00:34:29,773.9671727
Quiz time.
481
00:34:30,523.9671727 --> 00:34:33,373.9671727
It's gonna get so annoying to whoever's listening to, I swear.
482
00:34:33,373.9671727 --> 00:34:38,863.9671727
Do you wanna get, do you wanna guess? Do, do you know what time, time, time.