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68 Cards in this Set
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53 year old Recently moved to US from E europe Pain in epigastrium for 2-3 years Wake him at night Helped by eating or taking antacids Uses OTC ranitidine when pain is bad Smokes 1 pack per day; modest alcohol intake No other medicines
What is the differential? What additional info is needed? What investigations are needed at this stage? |
GERD, CV issues, gastroparesis, cancer, chronic pancreatitis, idiopathic
Peptic ulcer, non-ulcer/functional dyspepsia, gastric cancer, pancreatic disease, gallstones, other causes? |
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Can we distinguish gastric ulcer form duodenal ulcer based on history? |
NO!!!! |
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What is dyspepsia? |
Pain or discomfort in the upper abdomen |
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What do we need to know about medications? |
Very important to know if on NSAIDS => 2nd most common cause of peptic ulcer disease (after H. pylori) => can also cause dyspepsia |
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What is the significance of being from Eastern Europe?
Family history? |
H. pylori! Higher prevalence in people coming to US than being born in US.
Grandfather died of stomach cancer |
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What are some investigations?
Upper endoscopy Barium X-ray Abdominal CT scan Gall bladder ultrasound Non-invasive test for H. pylori No tests just treat for ulcer |
Serological test for H. pylori positive Upper endoscopy showed ulcer in duodenal bulb Biopsy of gastric mucosa => chronic inflammation and the presence of H. pylori organisms |
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Should the ulcer in the duodenum have been biopsied? How does H. pylori cause duodenal ulcer? |
No! Duodenal ulcers are RARELY malignant. Hypersecretion of acid in stomach => duodenal ulcer. H. pylori can't survive in duodenum but can survive in the METAPLASIA in the duodenum! |
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What do you need to treat H. pylori infection? |
All ulcer patients with positive test must be treated for H. pylori!
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Do patients with duodenal ulcer get gastric cancer? (Hypersecreters)? |
No! |
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Do we need to re-endoscope to check for ulcer, H. pylori, and to exclude duodenal ulcer? |
No! = will heal with treatment and high probability (75%) that H. pylori will be eradicated. Never have a malignant duodenal ulcer |
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Negative urea breath test. Does this mean he's cured? What are the chances of reinfection? |
Probably yes. Likely that some of family is also infected, but it is unlikely he will ever get infected again IN ADULTS!
H. pylori is a pediatric infection almost ALWAYS acquired in childhood.
Risk factors: Low socio economic status Large family size Having infected parent (mother) Poor hygiene Children spread through gastric oral transmission... (child spits up on toys and other child picks up and puts in mouth)
If you reach 7th birthday without H. pylori => highly unlikely to ever get it. |
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How do ulcers often present in the elderly? |
If caused by NSAIDS => often asymptomatic |
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What do parietal cells produce? What do chief (peptic) cells secrete? What do mucus cells produce? What do G cells secrete? Where?
Draw where each is located. |
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Draw the pathway of cephalic phase of acid secretion.
What stimulates acetylcholine release via the vagal nerve? |
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Draw the pathway of the gastric phase of acid secretion. Chemical effects of food and dissension of stomach causes release of ________ by the ____ cells. |
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Draw the intestinal phase of acid secretion. Food and acid in small bowel cause release of _____ and ______ which inhibit acid production. |
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What is the effect of gastric acid secretion on the duodenum? |
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What causes a pH gradient in the stomach? What is it secreted by and what does it prevent? |
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What is a defect in an epithelial layer?
What is an ulcer in a site exposed to gastric secretions?
What is the difference between an ulcer and an erosion? |
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Does an erosion penetrate the muscular is mucosae? What about an ulcer?
Is lesion size useful to distinguish between the two?
Which is more likely to have perceptible depth at endoscopy? |
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What do 80% of people with PUD experience? Specifically where does it hurt? Timing? Relief?
What are two other non-specific symptoms commonly observed?
In which population are PUDs often asymptomatic and present with complications? |
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What are some risk factors for PUD? What must be present for PUD to occur? |
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What are some chronic diseases associated with PUD? Think ICU, liver, organs, smoking
What do you give these patients while in the ICU to prevent ulcers? |
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What is responsible for around 70% of ulcers? What percent of people with this develop ulcers? Is it associated with both duodenal and gastric ulcers? Which is more common in US?
What is the pathogenesis? |
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What does H. pylori contain that is responsible for its damage?
What is the appearance and gram stain of H. pylori? |
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What is the equation for the urea to ammonia? How can we test this? |
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Again, draw the principles of the urea breath test.
What are three causes of false negatives? |
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Where does H. pylori reside? What inflammatory cells are invoked?
Is the peptide heat, acid, and alkali stable? What do the inflammatory cells secrete? |
Mucus layer over the gastric epithelium. |
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What is the H. pylori infection mechanism that leads to DU? |
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Is H. pylori infection among families common? |
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Review |
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What component of the arachidonic acid pathway protect the gastric mucosa?
Would it be better to use a COX-2 selective inhibitor instead of a non-specific NSAID to protect the gastric mucosa? |
It is important to review that the salient difference in mechanisms of action between nonspecific NSAIDs and COX-2 inhibitors is that COX-2 inhibitors, at their clinical doses, do not inhibit the COX-1 enzyme, and therefore do not reduce the prostaglandins in the stomach that protect against injury. Also, in the platelet, COX-2 inhibitors do not inhibit prostaglandins that provide hemostasis and which are important for cardiovascular effects. Nonspecific NSAIDS, because they inhibit COX-1 and COX-2 have effects in the stomach as well as in the platelet. |
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What are the top three risk factors for serious GI adverse events with NSAIDs? |
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What are three things you need to do to diagnose PUD and exclude malignancy? |
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What are three complications of PUD (think bleeding)?
What complication requires surgery? What complication may penetrate into adjacent organs?
What can a gastric obstruction cause? |
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What are some characteristics of BENIGN gastric ulcers?
What can be used to diagnose the lesion with a high sensitivity?
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Large, well circumscribed, symmetrical, healed on followup, projection away from the lumen, absence of mass effect or nodularity, rugal folds are normal.
Barium radiography |
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What is the chance of the stigmata rebleeding? |
50% with a visible vessel like the one shown here |
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How do you know? |
Patient present with acute severe abdominal pain => notice the air present under the right hemidiaphragm |
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Pyloric outlet obstruction and peripyloric ulcer disease is ___ (common or uncommon). Acutely, obstruction may result from _____. In some patients, however, ______ results in fixed fibrosis and outlet obstruction. In this patient presenting with ______ and vomiting and a ______ splash on physical examination, endoscopy demonstrates the pyloric obstruction with an active ulcer ______ seen in the ______ channel. Nasogastric suction and intravenous H2-receptor antagonists resulted in a clinical cure. In some patients, ______ may be required. _____ has been useful in some patients with fixed obstruction without active ulcer disease. |
Pyloric outlet obstruction and peripyloric ulcer disease is uncommon. Acutely, obstruction may result from edema. In some patients, however, chronic disease results in fixed fibrosis and outlet obstruction. In this patient presenting with nausea and vomiting and a succussion splash on physical examination, endoscopy demonstrates the pyloric obstruction with an active ulcer crater seen in the pyloric channel. Nasogastric suction and intravenous H2-receptor antagonists resulted in a clinical cure. In some patients, surgery may be required. Endoscopic balloon dilation has been useful in some patients with fixed obstruction without active ulcer disease. |
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What is shown here? |
Pyloric outlet obstruction related to peripyloric ulcer disease. Plain film of the abdomen in the patient presenting with nausea and vomiting and a succussion splash on |
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What is the treatment of PUD? Should you test for H. pylori infection in ALL patients with PUD? Should you treat it if present?
What three things should you avoid (bad habit and drugs)? What may be needed for complications? |
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What is a PATHOLOGICAL diagnosis of gastric inflammation of mucosa? Can it be acute or chronic? What may it be caused by? |
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The observation of multiple erosive and hemorrhagic lesions may be defined endoscopically as ______. This figure is an example of endoscopic erosive ______. Common settings that may lead to endoscopic gastritis include use of ______ drugs, alcohol abuse, and the physiologic ______ associated with serious illnesses (______ gastritis). Other less common causes include ingestion of corrosives, ______ agents, or irradiation. There may also be no known demonstrable associated factor present (idiopathic). |
The observation of multiple erosive and hemorrhagic lesions may be defined endoscopically as gastritis. This figure is an example of endoscopic erosive gastritis. Common settings that may lead to endoscopic gastritis include use of nonsteroidal anti-inflammatory drugs, alcohol abuse, and the physiologic stress associated with serious illnesses (stress gastritis). Other less common causes include ingestion of corrosives, chemotherapeutic agents, or irradiation. There may also be no known demonstrable associated factor present (idiopathic). |
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Alcohol consumption can result in endoscopic mucosal abnormalities termed ______ gastritis. As shown in this figure, endoscopically such patients will have multiple subepithelial ______ without any visible breaks in the mucosa. The appearance has been described as that of “______”. These lesions are mainly confined to the body and ______ of the stomach and are infrequently seen in the ______. |
Alcohol consumption can result in endoscopic mucosal abnormalities termed alcoholic hemorrhagic gastritis. As shown in this figure, endoscopically such patients will have multiple subepithelial hemorrhages without any visible breaks in the mucosa. The appearance has been described as that of “blood under plastic wrap”. These lesions are mainly confined to the body and fundus of the stomach and are infrequently seen in the antrum. |
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What is shown here? What are three causes? |
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What is shown here? |
Acute hemorrhagic gastritis |
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ACUTE HEMORRHAGIC GASTRITIS
associated with _____, non-steroidal typically have numerous ______, |
ACUTE HEMORRHAGIC GASTRITIS associated with alcohol, non-steroidal typically have numerous petechiae, |
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What can chronic gastritis lead to? Again, what are the three top causes? |
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Is helicobacter pylori gastritis common? Does its prevalence increase with age? What part of the stomach is it more severe in? Commonly has what two things on histology? What special type of inflammation is this? Where will the spiral bacteria be located?
What are two ways to diagnose?
What percent progress to gastric adenocarcinoma? What percent to low grade lymphoma? |
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What is the condition? What stain makes H. pylori easier to see What part of the gastric glands to H. pylori favor? |
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What is shown here? |
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Identify the intestinal metaplasia!
Identify the numerous inflammatory cells in the lamina propria! |
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What is the most important HP toxin? What does it cause degradation of? What components of the cell proliferation pathway are activated?
How is this toxin injected into cells? |
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What is shown here that is less than 10% of chronic gastritis? What do antibodies attack that leads to what two conditions?
Can you get metaplasia and hyperplasia? |
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What is the name for the condition that causes these small, round, deep, and punched out lesions? |
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Identify each letter shown here for chronic peptic ulcer disease. |
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Which is a benign ulcer? Which is a malignant ulcer? |
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Is this benign or malignant? How do you know? |
I want to say benign... |
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When do stress ulcers usually occur?
Describe their depth, number, and size. What are they associated with? |
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What is shown here? |
Stress ulcer |
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Again, what are the three major complications of ulcer disease? |
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