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Flashcards in Stomach and duodenum diseases Deck (68)

What is dyspepsia?

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


Diff types of gastritis?

- 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


Most common causes of erosive or hemorrhagic gastritis?

- stress (from medical or surgical illness)
- portal HTN


Sxs of gastritis?

- most are asx
- anorexia
- epigastric pain
- nausea
- vomiting
- upper GI bleeding


Presentation of upper GI bleed from erosive gastritis?

- 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


Workup of erosive gastritis?

- CBC, serum iron
- upper endoscopy


What is stress gastritis?

- 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


Best tx for stress gastritis?

- 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


Tx for GI bleeding secondary to stress induced gastritis?

- IV PPI bolus followed by continuous infusion
- sucralfate suspension given orally
- endoscopy to look for treatable causes


How common is NSAID gastritis?

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


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

- 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


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

- severe pain
- wt loss
- vomiting
- GI bleeding
- anemia

- refer for upper endoscopy


Tx of gastritis/dyspepsia?

- 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


PP of ETOH gastritis? What makes it worse?

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


Sxs of alcoholic gastritis? Tx?

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


What is portal hypertensive gastropathy?

- 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


Causes of nonerosive, nonspecific gastritis?

- H. pylori
- pernicious anemia
- eosinophilic gastritis


What is H. pylori?

- 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


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

- 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


RFs for H pylori?

- correlates inversely with socioeconomic status
- contaminated water supply


Chronic infection of H pylori presentation?

- 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


Tests for H pylori?

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


Tx of H pylori gastritis?

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


What is pernicious anemia gastritis?

- 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


What is eosinophilic gastritis? Dx, Tx?

- 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


What is PUD? Most common ages for diff types?

- 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


Etiology of PUD?

- 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


Clinical presentation of PUD?

- 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


What will your physical exam of PUD pt show?

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


Work up of PUD?

- 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


Tx for PUD?

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


Preferred tx for PUD?

- 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


Use of H2 blockers?

- 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


How common are ulcers in an H pylori infection?

- 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


How can we tx H pylori?

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


Goals of therapy for H pylori assoc ulcers?

- relieve sxs
- promote ulcer healing
- eradicate infection


Tx after triple or quadruple therapy for PUD?

- 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


When should you retest for H pylori?

- 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


Medical tx of NSAID induced ulcers?

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


Prevention of PUD after NSAID ulcer healing?

- 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


Risk of recurrent bleeding on meds?

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


RFs for NSAID ulcer related complications?

- 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


What is zollinger-ellison syndrome (gastrinoma)?

- 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


sites for primary GI tumors?

- pancreas 25%
- duodenal wall 45%***
- lymph nodes 5-15%
- unknown location

- gastrinoma triangle: where most tumors are located


Clinical presentation of zollinger-ellison syndrome?

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


screening for zollinger-ellison syndrome?

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!!)


Imaging for zollinger-ellison syndrome?

- 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


Tx of zollinger-ellison syndrome?

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%


What is gastroparesis?

- delayed gastric emptying in absence of mechanical obstruction


What is gastroparesis usually secondary to?

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

other etiologies:
neuro disease


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

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


Presentation of viral gastroparesis? Causes?

- 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


What meds can delay gastric emptying?

- 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


How can postsurgical gastroparesis occur?

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


Neuro diseases that can cause gastroparesis?

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


Autoimmune causes of gastroparesis?

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


Other causes of gastroparesis?

- mesenteric ischemia
- scleroderma (infiltration o muscular layer of stomach)


Sxs of gastroparesis?

- nausea
- vomiting
- early satiety
- bloating
- upper abdominal pain


PE of gastroparesis?

-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)


Work up of gastroparesis?

1. upper endoscopy
2. CT enterography or MRI to rule out mechanical obstruction
3. assessment of gastric motility with scintigraphic gastric emptying

further workup:
fasting plasma glucose
serum total protein
HbA1C in pts with DM to assess glucose control


What is scintigraphic gastric emptying?

- 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


Tx of gastroparesis?

- dietary modifications
- hydration
- vitamin supplementation may be needed
- optimize glycemic control
- prokinetics (enhance GI motility)


Dietary modifcations to help with gastroparesis?

- small frequent meals 4-5x daily
- low fat
- avoid:
insoluble fiber
carbonated drinks


Types of prokinetics?

- metaclopramide (reglan)
- macrolides


Metoclopramide as a prokinetic?

- 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


Erythromycin as a pro kinetic?

-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


Use of antiemetics?

- 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


What is tx of refactory cases of gastroparesis?

- surgical: gastrostomy tube for decompression and jejunostomy for feeding