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Gastroenterology > Diseases of the Stomach and Duodenum > Flashcards

Diseases of the Stomach and Duodenum Flashcards

1
Q

Dyspepsia features? 8

Common complaint with disorders of the?

A

Features

  1. Indigestion,
  2. chronic/recurrent pain in upper abdomen,
  3. upper abdominal fullness,
  4. early satiety,
  5. bloating,
  6. belching,
  7. nausea,
  8. heartburn

Common complaint with disorders of the stomach

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2
Q

What is gastritis?

What are the two kinds of gastritis?

A

inflammatory changes in the gastric mucosa

  1. Erosive and hemorrhagic gastritis
  2. Nonerosive, nonspecific gastritis
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3
Q

What causes the following:

  1. Erosive and hemorrhagic gastritis? 3
  2. Nonerosive, nonspecific gastritis? 3
A
    • Stress,
    • NSAID and
    • Alcoholic gastritis
    • H. pylori,
    • pernicious anemia,
    • eosinophilic gastritis
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4
Q

Most common causes of erosive and hemorrhagic gastritis

4

A
  1. Stress (from a medical or surgical illness)
  2. NSAIDs
  3. Alcohol
  4. Portal hypertension
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5
Q

Most cases of gastritis are asymptomatic but may have what?

5

A
  1. Anorexia
  2. Epigastric pain
  3. Nausea
  4. Vomiting
  5. Upper GI bleeding
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6
Q

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?
A
  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
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7
Q

Work up for Upper GI Bleeding from erosive gastritis?

3

A
  1. CBC,
  2. serum iron
  3. Upper endoscopy
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8
Q

Stress Gastritis
1. IN critically ill patients how soon may this occur?
2. Major risk factors for stress induced ulcers?
7

A
  1. In critically ill patients may occur within 72 hours of admission

At highest risk for bleeding due to stress induced ulcers:

  1. Coagulopathy
  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
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9
Q

Stress Gastritis

  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
A
  1. prevention
  2. enteral nutrition
    3.
    - 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
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10
Q

Treatment for GI bleeding secondary to stress induced gastritis
3

A
  1. IV PPI bolus followed by continuous infusion
  2. Sucralfate suspension given orally
  3. Endoscopy to look for treatable causes
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11
Q
  1. Which NSAIDs have a much lower incidence of significant ulcer formation?

`

A
  1. COX-2 inhibitors
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12
Q

But COX-2 inhibitors have 2X the risk of what compared to nonselective NSAIDS?

A

CV complications

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13
Q

How does the degree of symptoms does correlate with degree of mucosal abnormalities?

A

it does not

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14
Q

Red flags
for NSAID gastritis
6

A
  1. Severe pain
  2. Weight loss
  3. Vomiting
  4. GI bleeding
  5. Anemia

Refer for upper endoscopy

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15
Q 
NSAID gastritis
Treatment?
1. 1. If no red flag symptoms… treatment consists of what?
2. Trial of what for 2-4 weeks?
3. If no improvement?
A
  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
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16
Q

Pathophysiology of ETOH gastritis

2

A
  1. Alcohol disrupts the mucosal barrier

2. Alcohol and aspirin together increase the permeability of the gastric mucosal barrier and cellular damage occur

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17
Q

Alcoholic Gastritis

  1. Caused by?
  2. Symptoms? 4
  3. Treatment? 3
A
  1. Excessive alcohol consumption
  2. Symptoms:
    - dyspepsia,
    - nausea,
    - emesis,
    - minor hematemesis

Treatment

  • H2 blockers or PPIs
  • And sucralfate 2-4 weeks
  • And decrease ETOH consumption
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18
Q 
1. Portal hypertensive gastropathy
leads to what?
2. Can cause chronic what?
3. Treatment with what to lower pressures?
4. IF this fails?
A
  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
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19
Q

Nonerosive, nonspecific gastritis

3

A
  1. H. pylori
  2. Pernicious anemia
  3. Eosinophilic gastritis
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20
Q

Helicobacter pylori

  1. What kind of bacteria?
  2. Lives where in the GI tract?
  3. What is its normal function?
  4. Pathologically what can it cause?
A
  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
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21
Q

H. pylori

  1. Spread how?
  2. Increase risk of what from infection?
  3. If untreated it can lead to what?
A
  1. Fecal-oral spread
  2. Increases risk of gastric cancer
  3. If untreated leads to lifelong infections
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22
Q

Risk factors for H. pylori

2

A
  1. Correlates inversely with socioeconomic status

2. Contaminated water supply

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23
Q

H. pylori clinical presentation?

2

A
  1. most are asymptomatic and suffer no complications

2. Others may have an alteration in acid production and increased gastrin

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24
Q

H pylori:

Others may have an alteration in acid production and increased gastrin. Over time this may cause?

A

Over time may cause cellular changes and lead to duodenal or gastric ulcers, gastric cancer and low grade B cell gastric lymphoma

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25
Q

Testing for H. pylori

A
  1. Serology
  2. Urea breath test
  3. Stool antigen testing
  4. Endoscopic biopsy
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26
Q

H. pylori

  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?
A
  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%
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27
Q

Treatment for H pylori gastritis

2

A

Eradication therapy

2-3 antibiotics + PPI or bismuth (“Triple or Quadruple Therapy”)

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28
Q
  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
A
  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
    • Hashimoto thyroiditis,
    • Addison disease,
    • Graves disease
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29
Q
  1. Eosinophilic gastritis is what?
  2. What organ is most commonly affected?
  3. Symptoms may include what?
  4. Associated with a history of what?
  5. Diagnosis?
  6. Treatment? 2
A
  1. Infiltration of eosinophils into GI tissue
  2. Stomach is the area most common affected
  3. Symptoms may include:
    - abdominal pain,
    - nausea,
    - vomiting,
    - early satiety
    - diarrhea
  4. Associated with a history of
    - allergies,
    - asthma,
    - atopy
  5. Diagnosis: biopsy
  6. Treatment:
    - elimination diet.
    - May need steroids
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30
Q
  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?
A
  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
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31
Q
  1. Duodenal ulcers….. most common ages are ______?
  2. Gastric ulcers most common _____ years
  3. Most common in who? 2
A
  1. 30-55
  2. 55-70
  3. smokers and NSAID users
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32
Q

Etiology of PUD
3
(two most common)

A
  1. NSAIDs
  2. Chronic H. pylori infection
    3.
33
Q

Clinical presentation of PUD

8

A
  1. Dyspepsia
  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
  6. Periodicity
  7. Nausea and anorexia may occur with gastric ulcers
  8. Less likely to have symptoms other than GI bleeding in NSAID induced cases
34
Q

PE for PUD?

3

A
  1. Often normal
  2. May have some epigastric tenderness to deep palpation
  3. FOBT or FIT may be positive in 1/3 of patients
35
Q

Work Up
for PUD?
5
(whats the test of choice?)

A
  1. CBC,
  2. FOBT/FIT
  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

36
Q

If ulcer diagnosed without endoscopy then test for H pylori with what? 2

A
  1. a fecal antigen test or

2. urea breath test

37
Q

For fecal antigen testing or urea breath test:
1. Stop PPIs for ____ days prior to testing, otherwise false negatives

  1. Serologic testing for H pylori….appropriate where the prevalence is > ___%….neg confirms absence of infection.
  2. Can test _______ for years after eradication of infection
  3. Stool antigen tests…appropriate where the prevalence ___%….+ ________ highly predictive for active infection
A
  1. 7-14
  2. 30%
  3. positive
  4. less than 30%, stool test
38
Q

Treatment for PUD

5

A
  1. Proton pump inhibitors
  2. H2 blockers

Second line agents to enhance mucosal defenses

  1. Bismuth
  2. Misoprostol (Cytotec)….prostaglandin e1 analog
  3. antacids
39
Q
  1. PUD preferred treatment?
  2. duodenal
  3. gastric
  4. Advantages over H2 blockers?
A
  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
40
Q
  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?
A
  1. Inhibit nocturnal acid secretion but do not work as well against meal stimulated acid secretion
  2. Administer at bedtime
  3. 6
  4. 8
  5. Avoid cimetidine due to drug interactions
41
Q

H pylori eradication

  1. Combination therapy?
  2. 50% of strains resistant to what?
  3. 13% of strains resistant to what?
A
  1. 2-3 antibiotics + PPI or bismuth (“Triple or Quadruple Therapy”)
  2. metronidazole
  3. clarithromycin

Eradication rates
93% with quadruple therapy
70% with triple therapy

42
Q

Medical treatment of PUD

  1. How does smoking affect ulcers?
  2. ETOH?

Encourage a balanced diet

A
  1. Smoking decreases ulcer healing rates and increases recurrence rates
  2. Moderate ETOH is ok
43
Q

H pylori associated ulcers
Goals of therapy?
3

A
  1. Relive symptoms
  2. Promote ulcer healing
  3. Eradicate infection
44
Q

Treatment after Triple or Quadruple therapy depends on ulcer severity:
1. Small ulcer?

  1. Large or complicated ulcer? 2
A
  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
45
Q

Retesting for H pylori
2

With what tests? 3

A
  1. > 4 weeks post antibiotic therapy and
  2. > 2 weeks post discontinuation of PPI
  3. Urea breath test,
  4. fecal antigen
  5. endoscopy with biopsy
46
Q

Medical treatment of NSAID induced ulcers

2

A
  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

47
Q

Prevention after NSAID ulcer healing

3

A
  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
48
Q

Risk factors for NSAID ulcer related complications

6

A
  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
49
Q
  1. What is Zollinger-Ellison Syndrome (Gastrinoma)?

2. What does it cause?

A
  1. Gastrin secreting gut neuroendocrine tumor

2. Causes hypergastrinemia from increase acid secretion

50
Q

Zollinger-Ellison Syndrome (Gastrinoma)

Sites of primary tumors? 4

A
  1. Pancreas 25%
  2. Duodenal wall 45%
  3. Lymph nodes 5-15%
  4. Unknown location
51
Q

Whats the gastrinoma triangle?

A

Gastrinoma triangle: bounded by the porta hepatis, the neck of the pancreas and the 2nd/3rd portion of the duodenum

52
Q

How many of the Zollinger-Ellison Syndrome are malignant?

A

2/3 are malignant
Most are resectable
25% of patients have small nonresectable gastrinomas associated with MEN 1

53
Q

Clinical presentation
of Zollinger-Ellison Syndrome (Gastrinoma)?
5

A
  1. Dyspepsia
  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
54
Q

Screening
for Zollinger-Ellison Syndrome (Gastrinoma): When should we check fasting gastrin levels?
8

A
  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
55
Q

Imaging for Zollinger-Ellison Syndrome (Gastrinoma)?

3

A
  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
56
Q

What is the best imaging test to find gastrinoma tumors? why?

A

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

57
Q

Treatment of gastrinomas:

  1. Malignant? 1
  2. Localized disease? 1
A
  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%
58
Q

What is gastroparesis?

A

Delayed gastric emptying in the absence of a mechanical obstruction

59
Q

Gastroparesis is usually secondary to what?

3

A
  1. Diabetes
  2. Post surgical
  3. Idiopathic….
    Most common – about ½ of all cases
60
Q

Other etiologies of gastroparesis?

4

A
  1. Viral
  2. Medications
  3. Neurologic disease
  4. Autoimmune
    Other
61
Q

Diabetic gastroparesis

  1. MOre common in what type?
  2. Chronic hyperglycemia can lead to what?
  3. What is abnormal? 2
A
  1. Type 1 > Type 2
    11-18% of diabetics
  2. Chronic hyperglycemia can lead to neuropathy
  3. Autonomic dysfunction and abnormal intrinsic nervous system
62
Q

Viral gastroparesis

  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
A
  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
63
Q

Several medications can delay gastric emptying

11

A

1 Oxycodone (narcotic)

  1. Clonidine (alpha-2 adrenergic agonist)
  2. TCAs
  3. Calcium channel blockers
  4. Dopamine agonists
  5. Muscarinic cholinergic receptor antagonists
    - Scopolamine, atropine
  6. Ocreotide (used to treat acromegaly and also diarrhea associated with certain tumors)
  7. Phenothiazines
    - -Antipsychotics, antiemetics
  8. Cyclosporine
  9. GLP-1 agonists and amylin analogues
    - -Byetta, Victoza
64
Q 
Postsurgical gastroparesis
6 causes (one most common)
A
  1. Injury to the vagus nerve
  2. Gastrectomy
  3. Fundoplication (surgery for intractable reflux)
    - -*most common cause
  4. Lung or heart transplantation
  5. Variceal sclerotherapy
  6. Botulinum toxin injection
65
Q

Neurologic disease

that could cause gastroparesis?

A
  1. Loss of extrinsic neural control…examples:
    - Multiple sclerosis,
    - brainstem stroke or
    - tumor,
    - diabetic or amyloid neuropathy
  2. Myenteric plexus
    - AIDS,
    - diabetes,
    - Parkinson’s
66
Q

Autoimmune causes of gastroparesis?

A

Idiopathic or part of a paraneoplastic syndrome (small cell lung cancer)

67
Q

Other causes of gastroparesis?2

A
  1. Mesenteric ischemia

2. Scleroderma (infiltration of the muscular layer of the stomach)

68
Q

Gastroparesis…Symptoms

5

A
  1. Nausea
  2. Vomiting
  3. Early satiety
  4. Bloating
  5. Upper abdominal pain
69
Q

Gastroparesis PE?

3

A
  1. Epigastric tenderness but no guarding or rigidity
  2. May note abdominal distention
  3. Look for signs of the underlying disorder
70
Q

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)?

A
  1. Schleroderma

2. Diabetes

71
Q

Workup for gastroparesis?

3

A
  1. Upper endoscopy
  2. CT enterography or MRI to rule out mechanical obstruction
  3. Assessment of gastric motility with scintigraphic gastric emptying
72
Q

Describe scintigraphic gastric emptying?

A

Nuclear medicine study
Overnight fast
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

73
Q

Further work up to help determine the etiology
of gastroparesis?
7

A
  1. Hemoglobin
  2. fasting plasma glucose
  3. serum total protein
  4. albumin
  5. TSH
  6. ANA
  7. HbA1C in patients with DM to assess glucose control
74
Q

Treatment of gastroparesis

5

A
  1. Dietary modifications
  2. Hydration
  3. Vitamin supplementation may be needed
  4. Optimize glycemic control
  5. Prokinetics (enhance GI motility)
75
Q

Dietary modifications for gastroparesis?

6

A
  1. Small frequent meals 4-5 times daily
  2. Low fat
    Avoid
  3. Insoluble fiber
  4. ETOH
  5. Carbonated drinks
  6. Tobacco
76
Q

What are prokinetics?

2 meds

A
  1. Metaclopramide (Reglan)

2. Macrolide antibiotics

77
Q

MOA of erythromycin?

A
  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

78
Q

Refractory cases of gastroparesis warrant what?

A

Surgical treatment

Gastrostomy tube for decompression and jejunostomy for feeding

Gastroenterology (20 decks)

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