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Stomach and duodenum diseases Flashcards

1
Q

What is dyspepsia?

A
  • common complaint w/ disorders of the stomach
  • features: indigestion, chronic/recurrent pain in upper abdomen, upper abdominal fullness, early satiety, bloating, belching, nausea, heartburn
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2
Q

Diff types of gastritis?

A
  • inflammatory changes in gastric mucosa
  • erosive and hemorrhagic gastritis: due to stress, NSAID and ETOH gastritis
  • nonerosive, nonspecific gastritis: H pylori, pernicious anemia, eosinophilic gastritis
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3
Q

Most common causes of erosive or hemorrhagic gastritis?

A
  • stress (from medical or surgical illness)
  • NSAIDs
  • ETOH
  • portal HTN
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4
Q

Sxs of gastritis?

A
  • most are asx
  • anorexia
  • epigastric pain
  • nausea
  • vomiting
  • upper GI bleeding
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5
Q

Presentation of upper GI bleed from erosive gastritis?

A
  • if due to erosive gastritis it is usually superficial
  • usually doesn’t lead to hemodynamically significant bleeding
  • melena (dark sticky feces containing partially digested blood) may be noted
  • coffee ground emesis
  • blood noted in nasogastric suction
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6
Q

Workup of erosive gastritis?

A
  • CBC, serum iron

- upper endoscopy

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7
Q

What is stress gastritis?

A
  • in critically ill pts may occur within 72 hrs of admission

at highest risks for bleeding due to stress induced ulcers:
-coag -
INR more than 1.5, and platelets less than 50K
- need for mechanical ventilation if more than 48 hrs
- trauma, burns, shock
- sepsis, liver failure, kidney disease
- multi-organ failure
- CNS injury

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8
Q

Best tx for stress gastritis?

A
  • enteral nutrition can decrease the risk
  • prophlyaxis should be routinely given to all critically ill pts:
    IV or oral PPIs (omeprazole, esomeprazole, iansoprazole, pantoprazole) are the best
    IV or oral H2 blockers (cimetidine, famotidine, ranitdine) help but are not as good as PPIs
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9
Q

Tx for GI bleeding secondary to stress induced gastritis?

A
  • IV PPI bolus followed by continuous infusion
  • sucralfate suspension given orally
  • endoscopy to look for treatable causes
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10
Q

How common is NSAID gastritis?

A
  • 20-50% of people on chronic NSAIDs develop gastritis
  • 10-20% have ulcers
  • approx 5% have sxs
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11
Q

Which NSAIDs have lower incidence of causing gastritis, but what is the downside to these?

A
  • COX-2 inhibitors have a lower incidence of significant ulcer formation
  • 75% less incidence of endoscopically visible ulcers
  • 50% less significant complications from ulcers
  • but COX-2 inhibitors have 2x risk of CV complications compared to nonselective NSAIDs
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12
Q

Red flags of dyspepsia/gastritis? What should you do?

A
  • severe pain
  • wt loss
  • vomiting
  • GI bleeding
  • anemia
  • refer for upper endoscopy
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13
Q

Tx of gastritis/dyspepsia?

A
  • if no red flag sxs - tx consists of d/c of NSAIDs if possible
  • trial of PPI for 2-4 wks
  • can use H2 blockers but not as effective
  • if no improvement in 2 weeks refer for endoscopy
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14
Q

PP of ETOH gastritis? What makes it worse?

A
  • ETOH disrupts the mucosal barrier

- ETOH and aspirin together increase permeability of the gastric mucosal barrier and cellular damage occurs

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15
Q

Sxs of alcoholic gastritis? Tx?

A
  • excessive ETOH consumption
  • sxs: dyspepsia, nausea, emesis, minor hematemesis
  • tx:
    H2 blockers or PPIs
    and sucralfate for 2-4 wks
    decrease ETOH consumption
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16
Q

What is portal hypertensive gastropathy?

A
  • portal HTN leads to congestion of gastric vessels
  • can cause chronic GI bleeding
  • tx with propranolol or nadolol to lower portal pressures
  • if failure of medical therapy may need a portal decompression procedure
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17
Q

Causes of nonerosive, nonspecific gastritis?

A
  • H. pylori
  • pernicious anemia
  • eosinophilic gastritis
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18
Q

What is H. pylori?

A
  • spiral gram negative rod
  • lives beneath gastric mucous layer next to gastric epithelial cells
  • secrete urease and enables them to produce ammonia to buffer the acid
  • causes gastric mucosal inflammation
  • prevalence:
    approx 2/3 of world’s pop infected, in US: older adults, African-Americans, hispanics
  • lower socioeconomic groups
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19
Q

How is H pylori spread? This leads to increase chance of what?

A
  • fecal oral spread
  • up to 80% of pop can be infected by 20 in areas of poor hygiene
  • increases risk of gastric cancer
  • if untx leads to lifelong infections
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20
Q

RFs for H pylori?

A
  • correlates inversely with socioeconomic status

- contaminated water supply

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21
Q

Chronic infection of H pylori presentation?

A
  • chronic infection with gastritis may be present in 30-50% of pop
  • most are asx and suffer no complications
  • others may have alteration in acid production and increased gastrin: 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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22
Q

Tests for H pylori?

A
  1. serology: IgG ab testing, can’t distinguish b/t active vs inactive infection (not that useful)
  2. urea breath test: sensitivity 88-95%, specificity 95-100%, tests for active infection, off abx for 4 weeks, PPI for 2 weeks
  3. stool antigen testing: tests for active infection, sensitivity 94%, specificity 86%
  4. endoscopic bx
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23
Q

Tx of H pylori gastritis?

A
  • eradication therapy:

2-3 abx + PPI or bismuth (triple or quadruple therapy)

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24
Q

What is pernicious anemia gastritis?

A
  • autoimmune gastritis: autoabs to gastric gland parietal cells and intrinsic factor
  • body and fundus of stomach mostly affected
  • gastric gland and mucosal atrophy causes loss of acid production
  • may be assoc with Hashimoto thyroiditis, addison disease, graves disease
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25
Q

What is eosinophilic gastritis? Dx, Tx?

A
  • infiltration of eosinophils into GI tissue
  • stomach is the area most commonly affected
  • sxs may include: abdominal pain, N/V, early satiety, and diarrhea
  • assoc with hx of allergies, asthma, atopy
  • dx: bx
  • tx: elimination diet, may need steroids
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26
Q

What is PUD? Most common ages for diff types?

A
  • break in gastric or duodenal mucosa
  • can be caused by too much acid or pepsin
  • more than 5 mm in diameter and extends through muscularis mucosae
  • lifetime prevalence: 10%
  • 5x more common in duodenum
  • gastric ulcers most common in antrum
  • duodenal ulcers: most common ages 30-55
  • gastric ulcers most common 55-70 years
  • most common in smokers and NSAID users
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27
Q

Etiology of PUD?

A
  • NSAIDs
  • chronic H. pylori infection
  • less than 10% hypersecretory states like zollinger-ellison syndrome or systemic mastocystosis, CMV, crohns, lymphoma, alendronate (fosomax), chronic medial illness or idiopathic
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28
Q

Clinical presentation of PUD?

A
  • dyspepsia
  • pain in epigastric area: gnawing, dull, aching, “hunger like”
  • pain may be relieved with food or antacids and return 2-4 hrs later
  • sometimes have nocturnal pain
  • periodicity
  • Nausea and anorexia may occur with gastric ulcers
  • less likely to have sxs other than GI bleeding in NSAID induced cases
29
Q

What will your physical exam of PUD pt show?

A
  • often normal
  • may have some epigastric tenderness to deep palpation
  • FOBT or FIT may be positive in 1/3 of pts
30
Q

Work up of PUD?

A
  • CBC, FOBT/FIT
  • upper endoscopy test of choice
  • barium upper GI series not as sensitive for detection of ulcers or GI malignancies
  • abdominal CT needed if ulcer perforation is suspected
  • bx samples are tested for H pylori infection and eval for malignancy
  • if ulcer dx w/o endoscopy then test for H pylori with fecal ag test or urea test:
    stop PPIs for 7-14 days prior to testing, otherwise false negatives
  • serologic testing for H pylori - approp where prevalence is greater than 30%, neg confirms absence of infection, can test positive for years after eradication of infection
  • stool ag tests: approp where the prevalence is less than 30%, a + stool test is highly predictive for active infection
31
Q

Tx for PUD?

A
  • PPIs
  • H2 blockers
  • 2nd line agents to enhance mucosal defenses:
    bismuth
    misoprostol (cytotec) - prostaglandin e1 analog
  • antacids
32
Q

Preferred tx for PUD?

A
  • PPIs
  • heal 90% of duodenal ulcers in 4 wks
  • heal 90% of gastric ulcers in 8 wks
  • provide faster sx relief and promote faster ulcer healing compared to H2 blockers
  • similar efficacy among all PPIs
  • encourage pts to stop smoking (smoking decreases ulcer healing rates and increases recurrence rates)
  • cut down on ETOH, moderation ok
  • encourage balanced diet
33
Q

Use of H2 blockers?

A
  • inhibit nocturnal acid secretion but don’t work as well against meal stimulated acid secretion
  • administer at bedtime
  • heal 85-90% of duodenal ulcers at 6 weeks
  • heal 85-90% of gastric ulcers at 8 weeks
  • avoid cimetidine due to drug interactions
34
Q

How common are ulcers in an H pylori infection?

A
  • ulcers develop in 10% of infections
  • causes 75-90% of duodenal ulcers
  • assoc with increased gastric acid secretion
  • w/o H pylori eradication ulcer recurrence rate is 85% at 1 yr and decreases to 5-20% at 1 yr after tx
35
Q

How can we tx H pylori?

A

combo therapy is necessary

  • 2-3 abx + PPI or bismuth
  • 50% of strains resistant to metronidazole
  • 13% of strains resistant to clarithromycin
  • eradication rates: 93% with quadruple therapy
  • 70% with triple therapy

typical: PPI bid + clarithromycin bid + amoxicillin bid

if PCN allergic:
PPI bid+clarithro+ metronidazole

36
Q

Goals of therapy for H pylori assoc ulcers?

A
  • relieve sxs
  • promote ulcer healing
  • eradicate infection
37
Q

Tx after triple or quadruple therapy for PUD?

A
  • if small ulcer (less than 1 cm) no further tx
  • large or complicated ulcer: continue PPI for up to 6 weeks post completion
  • if eradicated most pts don’t need further acid suppression therapy
38
Q

When should you retest for H pylori?

A
  • more than 4 wks post abx therapy and
  • more than 2 wks post d/c of PPI
  • urea breath test, fecal ag or endoscopy with bx
39
Q

Medical tx of NSAID induced ulcers?

A
  • stop offending agent whenever possible
  • H2 blockers or PPIs
  • 80% of ulcers heal at 8 wks even if they continue to take NSAIDs
40
Q

Prevention of PUD after NSAID ulcer healing?

A
  • long term PPI therapy if NSAIDs must be continued
  • rx NSAIDs at lowest dose and shortest duration possible
  • use cox-2 inhibitor instead of a nonselective NSAID if no significant CV risks identified
41
Q

Risk of recurrent bleeding on meds?

A
  • NSAID + PPI = 5% at 6 mo
  • low dose ASA alone= 15%
  • low dose ASA + PPI = 0-2%
  • clopidogrel = 9-14%
42
Q

RFs for NSAID ulcer related complications?

A
  • pts at highest risk for complications: older than 60
  • hx of PUD or complications
  • aspirin or other antiplatelet therapy
  • anticoag therapy
  • oral glucocorticoid use: long term
  • serious underlying medical illness
43
Q

What is zollinger-ellison syndrome (gastrinoma)?

A
  • gastrin secreting gut neuroendocrine tumor
  • causes hypergastrinemia from increase acid secretion
  • cause less than 1% of PUD
  • 2/3 are malignant
  • most are resectable
  • 25% of pts have small nonresectable gastrinomas assoc with MEN 1
44
Q

sites for primary GI tumors?

A
  • pancreas 25%
  • duodenal wall 45%***
  • lymph nodes 5-15%
  • unknown location
  • gastrinoma triangle: where most tumors are located
45
Q

Clinical presentation of zollinger-ellison syndrome?

A
  • dyspepsia
  • 90% have peptic ulcers
  • ulcers usually located in duodenum
  • no isolated gastric ulcers
  • diarrhea, steatorrhea, wt loss if pancreas affected
46
Q

screening for zollinger-ellison syndrome?

A

check fasting gastrin levels if:

  • refractory duodenal ulcers
  • large ulcers greater than 2 cm
  • ulcers distal to duodenal bulb
  • mult duodenal ulcers
  • frequent recurrent ulcers
  • ulcers assoc with diarrhea
  • ulcers+hypercalcemia
  • if ulcers+ negative for NSAID use + neg for H pylori (Big red flag!!)
47
Q

Imaging for zollinger-ellison syndrome?

A
  • CT and MRI to eval for hepatic mets and primary lesions
  • nuclear med study: SPECT somatostatin receptor scintigraphy (SRS):
    gastrinomas have somatostatin receptors that take up the radiolabeled somatostatin
    80% sensitivity: best imaging study to find tumors (gold std)
  • endoscopic US if SRS is negative: with + SRS more than 90% of primary tumors can be ID
48
Q

Tx of zollinger-ellison syndrome?

A

met disease: PPIs to decrease acid hyper secretion
biggest predictor of survival is degree of hepatic metastasis: 10 yr survival is 30%
- localized disease: resection b/f hepatic metastasis is only cure: 15 yr survival 95%

49
Q

What is gastroparesis?

A
  • delayed gastric emptying in absence of mechanical obstruction
50
Q

What is gastroparesis usually secondary to?

A

diabetes
post surgical
idiopathoc: most common - 1/2 all cases

other etiologies:
viral
meds
neuro disease
autoimmune
other
51
Q

Diabetic gastroparesis is more common in 1 or 2? How common?

A
  • type 1 more common than type 2
  • 11-18% of diabetics
  • chronic hyperglycemia can lead to neuropathy
  • autonomic dysfxn and abnormal intrinsic nervous system
52
Q

Presentation of viral gastroparesis? Causes?

A
  • sudden onset of sxs post a viral prodrom
  • norwalk and rotavirus
  • sxs usually improve within a year
  • CMV, EBV, and varicella zoster virus may lead to severe long term sxs
53
Q

What meds can delay gastric emptying?

A
  • oxycodone
  • clonidine (alpha-2-adrenergic agonist)
  • TCAs
  • CCBs
  • dopamine agonists
  • muscarinic cholinergic receptor antagonists: scopolamine, atropine
  • ocreotide (used to tx acromegaly and also diarrhea assoc with certain tumors)
  • phenothiazines: antipyschotics, antiemetics
  • cyclosporine
  • GLP-1 agonists and amylin analogues: Byetta, victoza
54
Q

How can postsurgical gastroparesis occur?

A
  • injury to vagus nerve
  • gastrectomy
  • fundoplication (surgery for intractable reflux) - most common causes
  • lung or heart transplantation
  • variceal sclerotherapy
  • botox injection
55
Q

Neuro diseases that can cause gastroparesis?

A
  • loss of extrinsic neural control - examples:
    MS, brainstem stroke or tumor, diabetic or amyloid neuropathy
  • myenteric plexus: AIDS, diabetes, parkinsons
56
Q

Autoimmune causes of gastroparesis?

A
  • idiopathic or part of a paraneoplastic syndrome (small cell lung cancer)
57
Q

Other causes of gastroparesis?

A
  • mesenteric ischemia

- scleroderma (infiltration o muscular layer of stomach)

58
Q

Sxs of gastroparesis?

A
  • nausea
  • vomiting
  • early satiety
  • bloating
  • upper abdominal pain
59
Q

PE of gastroparesis?

A
  • epigastric tenderness but no guarding or rigidity
  • may not abdominal distension
  • look for signs of underlying disorder:
    scleroderma: skin taut over hands and chest, telangiectasis
    diabetes: signs of autonomic dysfxn (ortho hypotension, lack of pupillary response to light with delayed response to accommodation)
60
Q

Work up of gastroparesis?

A
  1. upper endoscopy
  2. CT enterography or MRI to rule out mechanical obstruction
  3. assessment of gastric motility with scintigraphic gastric emptying
further workup:
hemoglobin
fasting plasma glucose
serum total protein
albumin
TSH
ANA
HbA1C in pts with DM to assess glucose control
61
Q

What is scintigraphic gastric emptying?

A
  • nuclear medicine study
  • overnight fast
  • eat breakfast of eggs and toast with dash of isotope
  • imaging at timed intervals up to 4 hrs to determine degree of gastric emptying
62
Q

Tx of gastroparesis?

A
  • dietary modifications
  • hydration
  • vitamin supplementation may be needed
  • optimize glycemic control
  • prokinetics (enhance GI motility)
63
Q

Dietary modifcations to help with gastroparesis?

A
  • small frequent meals 4-5x daily
  • low fat
  • avoid:
    insoluble fiber
    ETOH
    carbonated drinks
    tobacco
64
Q

Types of prokinetics?

A
  • metaclopramide (reglan)

- macrolides

65
Q

Metoclopramide as a prokinetic?

A
  • use liquid formulation 15 min prior to eating
  • variety of sie effects and serious drug interactions that can lead to irreversible tardive dyskinesia
  • 12 wk rx with 2 wk holiday to make certain of efficacy
66
Q

Erythromycin as a pro kinetic?

A
  • indcues gastric contraction and stimulates fundic contractility
  • liquid formulation 40-250 mg TID
  • use no longer than 4 wks at a time otherwise efficacy decreases
67
Q

Use of antiemetics?

A
  • use if persistent N/V
  • diphenhydramine (benadryl) 12.5 mg po q 6-8 hrs
  • promethazine 25 mg po q 6-8 hrs
  • if no relief of N/V can use a 1st gen 5HT3 antagonist: zofran, kytril, and anzemet
  • caution due to QT prolongation
68
Q

What is tx of refactory cases of gastroparesis?

A
  • surgical: gastrostomy tube for decompression and jejunostomy for feeding

GI (21 decks)

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