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Flashcards in stomach disorders Deck (37):


Epigastric pain or burning, early satiety, sensation of fullness after eating
-Pain is in the upper abdomen, often recurrent
-With or without concurrent reflux symptoms
-EGD is warranted in patients over age 55yo with persistent symptoms
Why? worry about cancer


Dyspepsia tx

PPI trial (OTC PPIs OK) can be initiated
-Usually over a period of 4 weeks to determine if symptoms improve ("purple pill challenge")
-H. pylori testing to be considered


Dyspepsia etiology

“Indigestion” caused by overeating, eating high fat or spicy foods, or drinking too much alcohol or coffee
Medications such as ASA, NSAIDs, antibiotics, etc.
Up to ¾ of all patients have no obvious organic cause for their symptoms
Stress, anxiety, food sensitivity, delayed gastric emptying


what is also present with Dyspepsia ??

PUD present in 5-15% of patients with dyspepsia
-H.pylori an unlikely cause *unless in the presence of PUD*
Pancreatic cancer ("sneaky jerk", by time present, may already be advanced, takes time to enlarge, vague symptoms)


Dyspepsia dx

EGD should be performed, especially if over age 55yo
-Testing for celiac disease, parasites, fecal fat studies for malabsorption or pancreatic insufficiency
-CT for volvulus or pancreatic/biliary disease can be considered (threshold for getting CT lowered for older pop)


Dyspepsia tx

Empiric therapy should be initiated with a PPI
-If PUD is known, testing and treatment for H.pylori can be considered
-Consideration for antidepressants, especially if visceral sensitivity
Herbal therapies?


case 1: 20 yo gymnast, gnawing epigastric pain, N.V, bright red blood in vomit, otherwise healthy, v. aggressive physical training schedule
consider eating disorder, ask about strict diets

mallory weiss tear in ddx (but she's alarmed there's blood)



The most common cause of erosive gastropathy include:
Medications – especially NSAIDs (esp. w.out meals)
Stress – including medical and surgical too
And portal hypertension


Patients on ventilators should be given ??

Hospitalized patients are often given PPIs empirically – the draw back to the liberal use of *PPIs is an increased incidence of what other GI issue?

enteral feedings whenever possible to “coat” the stomach and reduce the risk of stress related bleeding

*C. diff* (now more selective)


gastritis s/s

Erosive gastritis is often asymptomatic
-When symptoms do occur they include epigastric pain, nausea, anorexia, vomiting, hematemesis, coffee ground emesis
-Hemodynamically significant bleeding is rare


gastritis lab findings

most sensitive test?

Lab findings are nonspecific, Possibly low HCT or iron deficiency

EGD is the most sensitive test for diagnosis
Intervention can be performed if there is a significant source of bleeding as well


case 2: 64 yo, nausea abdominal pain, now resolved, gastritis like symps, vague abd. discomfort esp. in morning
-suspect ??
You should consider testing for what else?

Suspecting an erosive gastritis, an EGD is performed and does not show any mucosal damage or inflammation.



Helicobacter pylori Gastritis

a gram-negative rod that resides beneath the mucosal layer adjacent to the gastric epithelial cells
-It is not an invasive organism but does cause mucosal inflammation
-vacA and cagA genes contribute to inflammatory properties


H. pylori presentation

Acute infection with H.pylori may cause a transient clinical illness followed by gastritis-like symptoms
-The majority of patients may have no symptoms at all of ongoing H.pylori infection, Mild diffuse disease only


H. pylori presentation 2

Around 15% of patients have involvement of the gastric antrum only but spares the omentum
-These patients are at increased risk of peptic ulcer disease
-Even less commonly some may have infection in the gastric body which can lead to destruction of acid-secreting glands and intestinal metaplasia: Association with MALT lymphoma (tx with PPIs and abx)


H. pylori noninvasive testing

what's more sensitive and specific ??

what will reduce the accuracy of the urea breath test and fecal antigen studies ??

Serologic testing is available, however most guidelines don’t include serologic testing
Less accurate than non-invasive tests, ELISA testing 80% accurate

Fecal antigen immunoassay and urea breath test

Use of PPIs or antibitoics
PPIs should be held 7-14 days, antibiotics should be completed a month prior to testing


H. pylori more dx: endoscopic testing

Not routinely indicated for the testing of H.pylori
-When performed for other reasons (ie PUD), biopsies can be taken for H.pylori testing
-Yield still high when patient have been on PPIs or antibiotics


H. pylori tx


Eradication of H.pylori is difficult, tx regimens usually contain a PPI + 2 or 3 antibiotics used in a 10-14 day total regimen
-In the US up to 50% of all strains are resistant to metronidazole (shy away from) and a fraction are resistant to clarithromycin as well


H. pylori Standard “Triple Therapy”

PPI orally 2x a day
Clarithromycin 500mg p.o. BID
Amoxicillin 1gm p.o. BID (or metronidazole if PCN allergic)


H. pylori Standard “Quadruple Therapy”

PPI orally 2x a day
Bismuth subsalicylate – 2 tablets QID
Tetracycline 500mg p.o. QID
Metronidazole 250mg p.o. QID or 500mg p.o. BID

("hot mess" Taormino usually doesn't go into this but sometimes makes her own tx with resistant/refractory pts)



A peptic ulcer is a break in the gastric mucosa that can occur when usual defense factors are impaired or there is a hypersecretion of acid/low pH environment
-Ulcers extend through the muscularis mucosa and are over 5mm in diameter.
-May be singular or multiple
Lifetime prevalence in adults is 10%
Gastric ulcers are located most commonly in the antrum of the stomach (60%)
More common in smokers, drinkers, and men aged 30-55yo.


Two major causes of peptic ulcer disease are ??

NSAID use and H.pylori infection


NSAID-induced ulcers

10-20% prevalence in long-term NSAID users
Coxibs decreased the incidence of ulcers by 75%
-COX-2 inhibitors block the inflammatory prostaglandins of COX-2 but spare the protective COX-1
-Drugs like ASA are non-selective and pose a greater risk for ulcer development
-Even low-dose cardioprotective ASA has an increased risk of GI bleeding complication


H.pylori associated ulcers

Almost a necessary factor in non NSAID induced ulcers
-Even greater association ~75-90% with duodenal ulcers
-85% will reoccur in 1 year without H.pylori treatment


case 3: 51yo epigastric pain, gnawing, improved after eating/tums comes back, wakes up with pain, mild discomfort reproducible, FOBT is +



?? is the test of choice to evaluate for both gastric and duodenal ulcers


Duodenal ulcers are virtually never malignant and don’t generally require biopsy
3-5% of gastric ulcer are malignant, especially if non-healing


more ulcer diagnostic testing

CT abdomen should be performed if there is any suspected complication from the ulcer disease
-H.pylori testing should be performed: Biopsy specimens can be obtained for rapid urease testing and histology
Positive urease testing is diagnostic


case 3 cont'd: patient now reports sudden, severe epigastric pain
Vitals are taken and he is found to have a HR of 121 and BP of 92/70
IV fluids are started and he is taken to CT scan

perforated ulcer

CT slide 23


Perforated ulcer tx

In the case of our fictitious patient, surgery would be required for repair of the perforated ulcer
-Moderate course IV antibiotics should be given as there is now effectively communication between the GI tract and sterile abdominal cavity


more perforated ulcer tx

PPI therapy should be initiated
-H2 blocker therapy is effective in the treatment of PUD, however PPIs have superior efficacy
-Caveat – H2 blockers remain the drugs of choice for patients taking other medications that require an acidic gastric environment (certain HIV medications, for example)
-Appropriate triple or quadruple H.pylori therapy if indicated


case 4: A 68yo woman with *known duodenal peptic ulcer disease* for many years, on *chronic PPI therapy*, is seen in your office with *diarrhea and weight loss*
Patient reports stools appear *greasy* and float on the top of the toilet water
You order a fasting *serum gastrin level* and suspect a diagnosis of?



Zollinger-Ellison Syndrome

FA: Gastrin-secreting tumor (gastrinoma) of pancreas or duodenum. Acid hypersecretion causes recurrent ulcers in duodenum and jejunum. Presents with abdominal pain (peptic ulcer disease, distal ulcers), diarrhea (malabsorption). Positive secretin stimulation test: gastrin levels remain elevated after administration of secretin, which normally inhibits gastrin release. May be associated with MEN 1.

chart on 26
listen 24


Zollinger-Ellison Syndrome2

Patients with known severe, atypical peptic ulcer disease
-Caused by gastrin-secreting neuroendocrine tumors which result in hypergastrinemia and acid hypersecretion
-80% of these tumors arise from the “gastrinoma triangle” bounded by the porta hepatis, neck of the pancreas, and the third portion of the duodenum
-2/3rds are malignant, 1/3 with liver mets at the time of presentation


more ZES

Diarrhea is common, relieved by NGT suctioning of gastric acid
-Screening for Zollinger-Ellison syndrome should occur in all patients with ulcers refractory to standard therapies and in those with large >2cm ulcers distal to the duodenal bulb


ZES dx: Most sensitive test is ??

Why do CT ??

demonstration of an increased serum gastrin concentration >150pg/mL
-H2 blockers should be held for 24 hours, PPIs should be held for 6 days
-Withdrawal of PPI may cause massive gastrin hypersecretion and miserable results for the patient
-Concurrent elevated serum calcium suggests hyperparathyroidism and a possible diagnosis of MEN-I
-CT scan should be performed in an attempt to determine the site of the primary tumor and possible metastasis


ZES tx For local disease

Cure can be achieved only if the gastrinoma can be resected
If no liver metastasis present, laparotomy should be performed


ZES tx For metastatic disease

In patient with multiple hepatic metastases, initial therapy should be directed toward hypersecretory symptoms
-PPIs should continue aggressively
-Overall very slow growing tumors and 1/3 of patients with hepatic metastases will have a favorable 10 year survival