esophageal reflux versus peptic ulcer disease

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amestramgram

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Hi, could someone explain me how to tell the difference between gerd and peptic ulcer disease?
thanks for your help

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Hi, could someone explain me how to tell the difference between gerd and peptic ulcer disease?
thanks for your help

A simple way is to give a trial of acid suppression, if it helps then they probably have GERD (70ish% sensitivty and speicity) while it probably won't help PUD because PUD is usually secondary to infection
 
GERD is esophageal reflux due to transient lower esophageal relaxation. Stomach contents (acid) enter the esophagus and cause irritation/inflammaiton. This is remarkable because it can lead to intestinal metaplasia (amongst other types) leading to Barrett esophagus. Those with intestinal type metaplasia/Barrett esophagus are at a 30-40x risk of developing an adenocarcinoma.

PUD is a disease of the pyloric (antral) region of the stomach or the duodenum. Most gastric ulcers are related to NSAID use or H. pylori. Duodenal ulcers are mainly due to H. pylori and then NSAID use. NSAIDS block prostoglandin synthesis, which is a major secretagogue for gastric mucus. H pylori secretes urease, proteases, and phospholipases which directly damage the mucosa; in addition, chronic inflammation due to H pylori infection leads to the immune-mediated release of things like oxygen free radicals and proteases which further damage the mucosa.
 
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H pylori is in the stomach and most of the ulcers that it causes are in the duodenum. So I don't think it directly damages mucosa, I thought it led to increased acid secretion that then damaged the duodenal mucosa.

In terms of how to differentiate, the GERD patient will have heartburn, i.e. retrosternal chest pain in association with certain foods or in the first hour or two after eating, or constantly. The patient with duodenal ulcers will have their pain relieved by food and will experience the pain in the epigastric/abdominal region 2-3 hours after eating. Gastric ulcers though will cause pain upon eating; I think gastric ulcers should also be considered part of a malignancy until proven otherwise.
 
Endoscopy with biospy.
 
H pylori is in the stomach and most of the ulcers that it causes are in the duodenum. So I don't think it directly damages mucosa, I thought it led to increased acid secretion that then damaged the duodenal mucosa.

Well yes... the natural progression SEEMS to be: H pylori infection that becomes chronic in the antrum of the stomach. This causes an increase in gastrin secretion and, therefore, an increase in parietal cell activity and a decrease in pH. As this hyperacidic chyme passes into the duodenum it causes chronic irritation and inflammation leading to gastric metaplasia in the bulb (1st part) of the duodenum. Once the gastric mucosa has spread into the duodenum the H pylori can then infect those newly formed gastric pits. Then these small islands of gastric mucosa become ulcers due to the chronic inflammation.

Interestingly, acute H pylori infection causes an INCREASE in pH due to pangastric infection/damage. Because the infection is damaging the oxyntic glands they actually decrease the HCl secretion and cause a rise in pH. However, when there is a chronic antral-gastritis with H pylori there is a selective defect in D cells and a pro-gastrin secretion habit of H pylori that cause an extreme fall of pH. This then leads to the above pathology.

As for detection... there are numerous ways. Upper GI endo w/biopsy is great but you can also do a urea breath test, a stool test, an antigen test. Of course nothing is going to be as definitive as a positive CLO test.
 
H pylori is in the stomach and most of the ulcers that it causes are in the duodenum. So I don't think it directly damages mucosa, I thought it led to increased acid secretion that then damaged the duodenal mucosa.

In terms of how to differentiate, the GERD patient will have heartburn, i.e. retrosternal chest pain in association with certain foods or in the first hour or two after eating, or constantly. The patient with duodenal ulcers will have their pain relieved by food and will experience the pain in the epigastric/abdominal region 2-3 hours after eating. Gastric ulcers though will cause pain upon eating; I think gastric ulcers should also be considered part of a malignancy until proven otherwise.

I though Duodenal Ulcers have increased pain with food, 2-3 hrs after eating.

Gastric Ulcers will have pain relieved by food.?

Also duodenal ulcers are always always due to hyper secretion of acid (90% of the time do to H.Pylori)... but gastric ulcers are not necessarily due to hypersecretion of acid (can occur in normal and even low gastric acid levels). For stomach ulcers it is important to compare basal acid output to maximal acid output to determine the relation of acid to the ulcer.
 
I though Duodenal Ulcers have increased pain with food, 2-3 hrs after eating.

Gastric Ulcers will have pain relieved by food.?

No, pain from duodenal ulcers should always be relieved by eating. Gastric ulcer pain is most often relieved by eating, but may be exacerbated.
 
No, pain from duodenal ulcers should always be relieved by eating. Gastric ulcer pain is most often relieved by eating, but may be exacerbated.
Gastric ulcer pain is most often exacerbated by eating.
 
What I wrote above was verbatim what our professor taught during GI pathophys. Up to date has this: "Gastric ulcer (GU) has classically been associated with more severe pain occurring soon after meals, with less frequent relief by antacids or food." (whatever that means?)

Further review seems to indicate that symptomatology is not sensitive, specific or diagnostically accurate in the workup of peptic ulcer disease.
 
Regarding gastric ulcers

boards and wards:
"worse with food intake" p56

Step up to med:
"eating does not relieve pain" p146t

FA for the wards:
"pain from dudenal ulcers can be alleviated with food and antacids but usually recurs roughly three hours later. Pain from gastric ulcers can worsen with food intake, leading to weight loss." p147

Pocket Medicine:
"epigastric pain: relieved by food (duodenal) or worsened by food (gastric)" p3-2
 
Last edited:
I'm not trying to impress you. I am just saying you were wrong.
 
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What I wrote above was verbatim what our professor taught during GI pathophys. Up to date has this: "Gastric ulcer (GU) has classically been associated with more severe pain occurring soon after meals, with less frequent relief by antacids or food." (whatever that means?)

Further review seems to indicate that symptomatology is not sensitive, specific or diagnostically accurate in the workup of peptic ulcer disease.

last i checked thats exactly what those 4 review sources are saying. meaning you didn't understand what your professor said. if youre eating, theres an increase in acid in the stomach. if theres more acid in the stomach its going to irritate the ulcer

ps. in case you trust wikipedia:

duodenal ulcers are classically relieved by food, while gastric ulcers are exacerbated by it
 
Hi, could someone explain me how to tell the difference between gerd and peptic ulcer disease?
thanks for your help
The difference is in the pathophysiology of the diseases and the subsequent long term complications.

Are you asking questions just for the hell of it?
GERD is esophageal reflux due to transient lower esophageal relaxation. Stomach contents (acid) enter the esophagus and cause irritation/inflammaiton. This is remarkable because it can lead to intestinal metaplasia (amongst other types) leading to Barrett esophagus. Those with intestinal type metaplasia/Barrett esophagus are at a 30-40x risk of developing an adenocarcinoma.

PUD is a disease of the pyloric (antral) region of the stomach or the duodenum. Most gastric ulcers are related to NSAID use or H. pylori. Duodenal ulcers are mainly due to H. pylori and then NSAID use. NSAIDS block prostoglandin synthesis, which is a major secretagogue for gastric mucus. H pylori secretes urease, proteases, and phospholipases which directly damage the mucosa; in addition, chronic inflammation due to H pylori infection leads to the immune-mediated release of things like oxygen free radicals and proteases which further damage the mucosa.
This is a really good explanation - describes the manifestation of disease --> MOA of disease process & contributing factors --> long term complications.
 
Thank you all for your help - this was very useful =)

Are you asking questions just for the hell of it?

No, I had a question about something in my class - which was not explained in great detail, so I went here to get an explanation in more detail so I wouldn't get it wrong on the test and learn it well for the future.
 
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