Flashcards in Diseases of the Stomach and Duodenum Deck (78)
Dyspepsia features? 8
Common complaint with disorders of the?
2. chronic/recurrent pain in upper abdomen,
3. upper abdominal fullness,
4. early satiety,
Common complaint with disorders of the stomach
What is gastritis?
What are the two kinds of gastritis?
inflammatory changes in the gastric mucosa
1. Erosive and hemorrhagic gastritis
2. Nonerosive, nonspecific gastritis
What causes the following:
1. Erosive and hemorrhagic gastritis? 3
2. Nonerosive, nonspecific gastritis? 3
Most common causes of erosive and hemorrhagic gastritis
1. Stress (from a medical or surgical illness)
4. Portal hypertension
Most cases of gastritis are asymptomatic but may have what?
2. Epigastric pain
5. Upper GI bleeding
Upper GI Bleeding from erosive gastritis
1. If due to erosive gastritis it is probably what?
2. Usually does not lead to what?
3. What may be noted?
4. What might you find on nasogastric suction?
1. If due to erosive gastritis it is usually superficial
2. Usually does not lead to hemodynamically significant bleeding
3. Melena (dark sticky feces containing partially digested blood) may be noted
4. Coffee ground emesis
Blood noted in nasogastric suction
Work up for Upper GI Bleeding from erosive gastritis?
2. serum iron
3. Upper endoscopy
1. IN critically ill patients how soon may this occur?
2. Major risk factors for stress induced ulcers?
1. In critically ill patients may occur within 72 hours of admission
At highest risk for bleeding due to stress induced ulcers:
2. INR > 1.5 and platelets less than 50K
3. Need for mechanical ventilation > 48 h
4. Trauma, burns, shock
5. Sepsis, Liver failure, kidney disease
6. Multi-organ failure
7. CNS injury
1. Best treatment is what?
2. What can decrease the risk?
3. Prophylaxis should be routinely given to all critically ill patients. What would we do for this? 2
2. enteral nutrition
- IV or oral proton pump inhibitors (omeprazole, esomeprazole, lansoprazole, pantoprazole) are best
- IV or oral H2 blockers (cimetidine, famotidine, ranitidine) help but are not as good as PPIs
Treatment for GI bleeding secondary to stress induced gastritis
1. IV PPI bolus followed by continuous infusion
2. Sucralfate suspension given orally
3. Endoscopy to look for treatable causes
1. Which NSAIDs have a much lower incidence of significant ulcer formation?
1. COX-2 inhibitors
But COX-2 inhibitors have 2X the risk of what compared to nonselective NSAIDS?
How does the degree of symptoms does correlate with degree of mucosal abnormalities?
it does not
for NSAID gastritis
1. Severe pain
2. Weight loss
4. GI bleeding
Refer for upper endoscopy
1. 1. If no red flag symptoms… treatment consists of what?
2. Trial of what for 2-4 weeks?
3. If no improvement?
1. discontinuation of NSAIDs if possible
2. Trial of PPI for 2-4 weeks
-Can use H2 blockers but not as effective
3. If no improvement in 2 weeks refer for endoscopy
Pathophysiology of ETOH gastritis
1. Alcohol disrupts the mucosal barrier
2. Alcohol and aspirin together increase the permeability of the gastric mucosal barrier and cellular damage occur
1. Caused by?
2. Symptoms? 4
3. Treatment? 3
1. Excessive alcohol consumption
-H2 blockers or PPIs
-And sucralfate 2-4 weeks
-And decrease ETOH consumption
1. Portal hypertensive gastropathy
leads to what?
2. Can cause chronic what?
3. Treatment with what to lower pressures?
4. IF this fails?
1. Portal hypertension leads to congestion of gastric vessels.
2. Can cause chronic GI bleeding
3. Treatment with propranolol or nadolol to lower the portal pressures
4. If failure of medical therapy may need a portal decompression procedure
Nonerosive, nonspecific gastritis
1. H. pylori
2. Pernicious anemia
3. Eosinophilic gastritis
1. What kind of bacteria?
2. Lives where in the GI tract?
3. What is its normal function?
4. Pathologically what can it cause?
1. Spiral gram negative rod
2. Lives beneath the gastric mucous layer next to the gastric epithelial cells
3. Secrete urease and enables them to produce ammonia to buffer the acid
4. Causes gastric mucosal inflammation
1. Spread how?
2. Increase risk of what from infection?
3. If untreated it can lead to what?
1. Fecal-oral spread
2. Increases risk of gastric cancer
3. If untreated leads to lifelong infections
Risk factors for H. pylori
1. Correlates inversely with socioeconomic status
2. Contaminated water supply
H. pylori clinical presentation?
1. most are asymptomatic and suffer no complications
2. Others may have an alteration in acid production and increased gastrin
Others may have an alteration in acid production and increased gastrin. Over time this may cause?
Over time may cause cellular changes and lead to duodenal or gastric ulcers, gastric cancer and low grade B cell gastric lymphoma
Testing for H. pylori
2. Urea breath test
3. Stool antigen testing
4. Endoscopic biopsy
1. What kind of serology?
2. Disadvantage of this?
3. Breath test is the test for?
4. Must be off of what for the breath test? 2
5. Stool antigen test is for what?
1. IgG antibody testing
2. Can’t distinguish between active vs. inactive infection
3. Tests for active infection
4. Off abx for 4 weeks, PPIs for 2 weeks
5. Tests for active infection
Sensitivity 94%, Specificity 86%
Treatment for H pylori gastritis
2-3 antibiotics + PPI or bismuth (“Triple or Quadruple Therapy”)
1. What is Pernicious anemia gastritis?
2. What areas of the stomach are most affected? 2
3. Gastric gland and mucosal atrophy causes what?
4. May be associated with what?3
1. Autoimmune gastritis
---Autoantibodies to gastric gland parietal cells and intrisic factor
2. Body and fundus of stomach mostly affected
3. loss of acid production
1. Eosinophilic gastritis is what?
2. What organ is most commonly affected?
3. Symptoms may include what?
4. Associated with a history of what?
6. Treatment? 2
1. Infiltration of eosinophils into GI tissue
2. Stomach is the area most common affected
3. Symptoms may include:
4. Associated with a history of
5. Diagnosis: biopsy
-May need steroids
1. What is peptic ulcer disease?
2. Can be caused by what? 2
3. Size and extends through where?
4. 5x more likely where in the intestine?
5. Gastric ulcers are most common where?
1. Break in the gastric or duodenal mucosa
2. Can be caused by too much acid or pepsin
3. > 5 mm in diameter and extend through the muscularis mucosae
--Lifetime prevalence 10%
4. 5X more common in the duodenum
5. Gastric ulcers most common in the antrum
1. Duodenal ulcers….. most common ages are ______?
2. Gastric ulcers most common _____ years
3. Most common in who? 2
3. smokers and NSAID users
Etiology of PUD
(two most common)
2. Chronic H. pylori infection
Clinical presentation of PUD
2. Pain in the epigastric area
3. Gnawing, dull, aching, “hunger like”
4. Pain may be relieved with food or antacids and return 2-4 hours later
5. Sometimes have nocturnal pain
7. Nausea and anorexia may occur with gastric ulcers
8. Less likely to have symptoms other than GI bleeding in NSAID induced cases
PE for PUD?
1. Often normal
2. May have some epigastric tenderness to deep palpation
3. FOBT or FIT may be positive in 1/3 of patients
(whats the test of choice?)
3. Upper endoscopy is the test of choice
4. Abdominal CT needed if ulcer perforation is suspected
5. Biopsy samples are tested for H pylori infection and evaluated for malignancy
Barium upper GI series is not as sensitive or specific for the detection of ulcers or GI malignancies
If ulcer diagnosed without endoscopy then test for H pylori with what? 2
1. a fecal antigen test or
2. urea breath test
For fecal antigen testing or urea breath test:
1. Stop PPIs for ____ days prior to testing, otherwise false negatives
2. Serologic testing for H pylori….appropriate where the prevalence is > ___%....neg confirms absence of infection.
3. Can test _______ for years after eradication of infection
4. Stool antigen tests…appropriate where the prevalence ___%....+ ________ highly predictive for active infection
4. less than 30%, stool test
Treatment for PUD
1. Proton pump inhibitors
2. H2 blockers
Second line agents to enhance mucosal defenses
4. Misoprostol (Cytotec)….prostaglandin e1 analog
1. PUD preferred treatment?
4. Advantages over H2 blockers?
1. Preferred treatment
2. Heal 90% of _________ ulcers in 4 weeks
3. Heal 90% of ______ ulcers in 8 weeks
4. Provide faster symptom relief and promote faster ulcer healing compared to H2 blockers
1. H2 blockers MOA?
2. Administer when?
3. Heal 85-90% of duodenal ulcers at_ weeks
4. Heal 85-90% of gastric ulcers at __ weeks
5. What should we avoid?
1. Inhibit nocturnal acid secretion but do not work as well against meal stimulated acid secretion
2. Administer at bedtime
5. Avoid cimetidine due to drug interactions
H pylori eradication
1. Combination therapy?
2. 50% of strains resistant to what?
3. 13% of strains resistant to what?
1. 2-3 antibiotics + PPI or bismuth (“Triple or Quadruple Therapy”)
93% with quadruple therapy
70% with triple therapy
Medical treatment of PUD
1. How does smoking affect ulcers?
Encourage a balanced diet
1. Smoking decreases ulcer healing rates and increases recurrence rates
2. Moderate ETOH is ok
H pylori associated ulcers
Goals of therapy?
1. Relive symptoms
2. Promote ulcer healing
3. Eradicate infection
Treatment after Triple or Quadruple therapy depends on ulcer severity:
1. Small ulcer?
2. Large or complicated ulcer? 2
1. Small ulcer (less than 1 cm) no further treatment
-continue PPI for up to 6 weeks post completion
- If eradicated most patients don’t need further acid suppression therapy
Retesting for H pylori
With what tests? 3
1. > 4 weeks post antibiotic therapy and
2. > 2 weeks post discontinuation of PPI
1. Urea breath test,
2. fecal antigen
3. endoscopy with biopsy
Medical treatment of NSAID induced ulcers
1. Stop offending agent whenever possible
2. H2 blockers or PPIs
80% of ulcers heal at 8 weeks even if they continue to take NSAIDs
Prevention after NSAID ulcer healing
1. Long term PPI therapy if NSAIDs must be continued
2. Prescribe NSAIDs at the lowest dose and shortest duration possible
3. Use cox-2 inhibitor instead of a nonselective NSAID if no significant CV risks identified
Risk factors for NSAID ulcer related complications
1. > 60 y/o
2. History of PUD or complications
3. Aspirin or other antiplatelet therapy
4. Anticoagulation therapy
5. Oral glucocorticoid use
6. Serious underlying medical illness
1. What is Zollinger-Ellison Syndrome (Gastrinoma)?
2. What does it cause?
1. Gastrin secreting gut neuroendocrine tumor
2. Causes hypergastrinemia from increase acid secretion
Zollinger-Ellison Syndrome (Gastrinoma)
Sites of primary tumors? 4
1. Pancreas 25%
2. Duodenal wall 45%
3. Lymph nodes 5-15%
4. Unknown location
Whats the gastrinoma triangle?
Gastrinoma triangle: bounded by the porta hepatis, the neck of the pancreas and the 2nd/3rd portion of the duodenum
How many of the Zollinger-Ellison Syndrome are malignant?
2/3 are malignant
Most are resectable
25% of patients have small nonresectable gastrinomas associated with MEN 1
of Zollinger-Ellison Syndrome (Gastrinoma)?
2. 90% have peptic ulcers
3. Ulcers usually located in the duodenum
4. No isolated gastric ulcers
5. Diarrhea, steatorrhea, weight loss if pancreas affected
for Zollinger-Ellison Syndrome (Gastrinoma): When should we check fasting gastrin levels?
1. Refractory duodenal ulcers
2. Large ulcers > 2 cm
3. Ulcers distal to the duodenal bulb
4. Multiple duodenal ulcers
5. Frequent recurrent ulcers
6. Ulcers associated with diarrhea
7. Ulcers + hypercalcemia
8. If ulcers + negative for NSAID use + negative for H pylori
Imaging for Zollinger-Ellison Syndrome (Gastrinoma)?
1. CT and MRI to evaluate for hepatic metastases and primary lesions
2. Nuclear med study : SPECT Somatostatin receptor scintigraphy (SRS)
3. Endoscopic ultrasound if SRS is negative
What is the best imaging test to find gastrinoma tumors? why?
Nuclear med study : SPECT Somatostatin receptor scintigraphy (SRS)
Gastrinomas have somatostatin receptors that take up the radiolabled somatostatin
80% sensitivity…. the best imaging study to find the tumors
Treatment of gastrinomas:
1. Malignant? 1
2. Localized disease? 1
1. Metastatic disease
-PPIs to decrease acid hypersecretion
-Biggest predictor of survival is degree of hepatic metastasis
10 year survival is 30%
2. Localized disease
-Resection before hepatic metastasis is the only cure
15 year survival 95%
What is gastroparesis?
Delayed gastric emptying in the absence of a mechanical obstruction
Gastroparesis is usually secondary to what?
2. Post surgical
Most common – about ½ of all cases
Other etiologies of gastroparesis?
3. Neurologic disease
1. MOre common in what type?
2. Chronic hyperglycemia can lead to what?
3. What is abnormal? 2
1. Type 1 > Type 2
11-18% of diabetics
2. Chronic hyperglycemia can lead to neuropathy
3. Autonomic dysfunction and abnormal intrinsic nervous system
1. How does it present?
2. Two examples?
3. Symptoms usually improve with in how long?
4. Which viruses may lead to severe long term symptoms? 3
1. Sudden onset of symptoms post a viral prodrome
2. Norwalk and Rotavirus
3. Symptoms usually improve within a year
4. Cytomegalovirus, Epstein-Barr virus and varicella-zoster virus may lead to severe long term symptoms
Several medications can delay gastric emptying
1 Oxycodone (narcotic)
2. Clonidine (alpha-2 adrenergic agonist)
4. Calcium channel blockers
5. Dopamine agonists
6. Muscarinic cholinergic receptor antagonists
8. Ocreotide (used to treat acromegaly and also diarrhea associated with certain tumors)
11. GLP-1 agonists and amylin analogues
6 causes (one most common)
1. Injury to the vagus nerve
3. Fundoplication (surgery for intractable reflux)
--*most common cause
4. Lung or heart transplantation
5. Variceal sclerotherapy
6. Botulinum toxin injection
that could cause gastroparesis?
1. Loss of extrinsic neural control…examples:
-brainstem stroke or
-diabetic or amyloid neuropathy
2. Myenteric plexus
Autoimmune causes of gastroparesis?
Idiopathic or part of a paraneoplastic syndrome (small cell lung cancer)
Other causes of gastroparesis?2
1. Mesenteric ischemia
2. Scleroderma (infiltration of the muscular layer of the stomach)
3. Early satiety
5. Upper abdominal pain
1. Epigastric tenderness but no guarding or rigidity
2. May note abdominal distention
3. Look for signs of the underlying disorder
What would cause skin taut over the hands and chest, telangiectasias?
What would cause signs of autonomic dysfunction (orthostatic hypotension, lack of pupillary response to light with delayed response to accommodation)?
Workup for gastroparesis?
1. Upper endoscopy
2. CT enterography or MRI to rule out mechanical obstruction
3. Assessment of gastric motility with scintigraphic gastric emptying
Describe scintigraphic gastric emptying?
Nuclear medicine study
Eat a breakfast of eggs and toast sprinkled with a dash of isotope
Imaging at timed intervals up to 4 hours to determine degree of gastric emptying
Further work up to help determine the etiology
2. fasting plasma glucose
3. serum total protein
7. HbA1C in patients with DM to assess glucose control
Treatment of gastroparesis
1. Dietary modifications
3. Vitamin supplementation may be needed
4. Optimize glycemic control
5. Prokinetics (enhance GI motility)
Dietary modifications for gastroparesis?
1. Small frequent meals 4-5 times daily
2. Low fat
3. Insoluble fiber
5. Carbonated drinks
What are prokinetics?
1. Metaclopramide (Reglan)
2. Macrolide antibiotics
MOA of erythromycin?
1. Induces gastric contraction and stimulates fundic contractility
Liquid formulation 40-250mg TID
Use no longer than 4 weeks at a time otherwise efficacy decreases