stomach disorders Flashcards
Dyspepsia
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?
Psychotherapy?
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)
gastritis
Gastritis
The most common cause of erosive gastropathy include:
Medications – especially NSAIDs (esp. w.out meals)
Alcohol
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.
H.pylori
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
resistance??
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”
mainstay
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)
PUD
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