stomach - GI Flashcards

1
Q

GERD- Gastroesophageal Reflux Disease

A

-GE reflux is normal a physiologic phenomenon
-GERD occurs when excessive gastric juice that refluxes into the esophagus causing symptoms with or without associated esophageal mucosal injury (ie, esophagitis).
-25-40% of healthy adult Americans experience symptomatic GERD at least once a month
-20% weekly symptoms
-7-10% daily symptoms
-Impairment of Lower Esophageal Sphincter (LES)
-Normal tone, but excessive relaxation
-Excessive intra-abdominal pressure
-Hypotonic/incompetent sphincter
-Factors contributing: Abnormal esophageal peristalsis
(Scleroderma), Diminished saliva production (Anticholinergic meds, Sjogren’s), Delayed gastric emptying (Gastroparesis, partial outlet obstruction)
-Hiatal Hernia: Increases likelihood of GERD, but not causative

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2
Q

GERD - sxs, dx

A

Most common
-Heartburn, regurgitation, dysphagia
Also
-Bronchospasm, laryngitis, chronic cough, hoarseness, sore throat, chest pain
-Nausea, hypersalivation, globus sensation
-Clinical Diagnosis
-Symptoms often worse at night
-Sleeping upright in bed or chair to reduce symptoms
-Symptoms worse after eating big meal, particular foods
-Symptoms worse when wearing constricting clothing
-Severity is related to how often and how long esophagus is exposed to acid
-Treatment is titrated to symptom severity
-Depending on presentation, either step up from lifestyle/dietary recommendations or down from potent antisecretory agents

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3
Q

GERD Lifestyle Modification

A
  • Head of bed elevation 6-8 inches with blocks or wedge - try not to increase abd pressure
  • Do not lie down shortly after eating or eat just prior to bed
  • Avoid tight fitting garments
  • Weight loss
  • Chew gum or use lozenges to promote salivation
  • Quit smoking (smoking reduces salivation)
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4
Q

GERD Dietary Modifications

A
  • Too stringent of recommendations insures non-compliance
  • Start with eliminating core LES-reducing foods
  • Fatty foods, chocolate, peppermint, alcohol
  • Low pH drinks - sodas, red wine, orange juice
  • Patient identified triggers (tomato sauce, garlic, onion, coffee, etc.)
  • Small, frequent meals
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5
Q

GERD Medications

A
  • Antacids - Gaviscon, TUMS, etc, chewable or liquid
  • After each meal and at bedtime
  • H2 Receptor Antagonists - ranitidine (Zantac), cimetidine (Tagamet), famotidine (Pepcid), and nizatidine (Axid)
  • Effective in healing mild esophagitis only
  • Good for maintenance
  • Proton Pump Inhibitors - omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex), and esomeprazole (Nexium)
  • Well tolerated long term but may interfere with calcium homeostasis and linked to hip fractures in postmenopausal women
  • No real difference between the meds, but higher doses more effective
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6
Q

GERD Surgical Management

A

Indications:

  • Incomplete control on PPIs
  • Barrett Esophagus
  • Extra-esophageal manifestations (Resp, ENT, Dental)
  • Young patients, elderly women with osteoporosis, cardiac conduction defects
  • Nissen fundoplication and Laparoscopic fundoplication
  • Both are 360 degree
  • Both as or more effective than PPIs
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7
Q

Gastritis

A
  • Inflammation of the gastric mucosa
  • Many causes
  • Drugs; alcohol; bile; ischemia; bacterial, viral, and fungal infections; acute stress (shock); radiation; allergy and food poisoning; and direct trauma.
  • Imbalance between the aggressive and the defensive factors that maintain the integrity of the gastric lining
  • Most commonly seen in alcoholic, critically ill or patients taking NSAIDs
  • Usually asymptomatic
  • Epigastric pain, nausea, vomiting, anorexia
  • Hematemesis “coffee ground” appearance, or bloody aspirate from NG tube – not hemodynamically significant
  • Symptom severity does not correlate with endoscopic finding severity
  • Labs not helpful, but if chronic iron deficiency anemia is possible
  • Upper GI Endoscopy helps distinguish from ulcers or esophageal varices
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8
Q

Erosive Gastritis

A

Stress Gastritis
-Critical illness can precipitate gastritis within a few days
-Prophylaxis - Enteral nutrition is as good or better than pharmacologic
-H2 Blockers, PPIs, Antacids
NSAID Gastritis
-NSAID users - 25-50% have gastritis, 10-20% ulcers at endoscopy
-But only 5% develop symptoms
-COX-2 selective decrease ulcers by 75%, but increase in CV complications
-D/C or reduce dose and administer with meals
-Treat with 2-4 weeks of PPI, endoscopy if not improved
Alcoholic Gastritis
-Dyspepsia, nausea, emesis, hematemesis
-Not necessarily erosive gastritis
-Treat with H2 Blockers, PPIs, or sucralfate for 2-4 weeks

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9
Q

Non-Erosive Gastritis

A

Helicobacter pylori Gastritis

  • Spiral gram neg rod between the epithelial layer and the mucous layer
  • Causes mucosal inflammation
  • Acute - Several days of nausea and abdominal pain
  • Chronic infection with gastritis results in 30-50%, but most are asymptomatic
  • 15% have inflammation in gastric antrum only … those people have
  • Increased gastrin
  • Increased acid production
  • Increased risk of development of peptic ulcers, esp duodenal ulcers
  • Few have inflammation of gastric body predominantly … and they have
  • Destruction of acid-secreting glands, mucosal atrophy
  • Decreased acid secretion, intestinal metaplasia
  • Increased risk of gastric ulcers and cancer
  • Best diagnosed with biopsy on UGI endoscopy
  • Treatment is with multiple antibiotics and PPI
  • Results in resolution of gastritis, peptic ulcer disease and reduces gastric cancer risk
  • Routine screening recommended in areas of high prevalence (Japan, Korea, China)
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10
Q

Peptic Ulcer Disease

A

-Defects in the gastrointestinal mucosa that extend through the muscularis mucosae
-Protective mechanisms - secretory, defense, and repair - make this uncommon
-H pylori and NSAIDs are biggest offenders
-BUT still, incidence is only 1% yearly in these patients
Risk Factors:
-Acid Hypersecretion - H pylori related or not
-Bicarb undersecretion in the duodenum
-Familial - some genetic predisposition
-Smoking + H pylori

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11
Q

Peptic Ulcer Disease - Clinical Presentation

A

-Epigastric pain, indigestion, or asymptomatic
-Classic epigastric pain when acid secreted in absence of food buffer
-Burning, gnawing, hunger-like, vague, or crampy
-May have radiation to back, RUQ, or LUQ
-2-5 hrs after meal or empty stomach;11 pm - 2am
-Food-provoked indigestion - epigastric discomfort and fullness, nausea, early satiety
-Other symptoms
-High incidence of GERD with PUD
-Constipation, Irritable bowel like symptoms
-Asymptomatic in 43-87% of bleeding duodenal ulcers
Complications
-Most often in chronic peptic ulcers with fibrosis, present for months
-Penetration - more intense pain, radiating to back
-Perforation - sudden, severe,diffuse abd pain
-Pyloric Outlet Obstruction - vomiting
-Hemorrhage - nausea, hematemesis, melena, dizziness

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12
Q

Peptic Ulcer Disease - dx, tx

A

Dx: Upper GI endoscopy with biopsies

tx:
- Antisecretory therapy - PPIs or H2 blockers
- PPIs are faster (2-4 weeks vs 4-8 weeks)
- Treat H pylori if present
- Withdraw offending or potentiating agents: NSAIDs, smoking, alcohol
- In non-H pylori, non-NSAID users, explore other causes
- Maintenance therapy (H2 blockers or PPIs) decreases recurrence - use in complicated or higher risk groups
- Withdraw from PPIs gradually to prevent rebound
- Controversial as to which need follow up UGI endoscopy
- Uncomplicated duodenal ulcers do not
- High risk for cancer do

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13
Q

Pyloric Stenosis

A
  • Post-natal hypertrophy of the pylorus
  • Progressive gastric outlet obstruction in children under 12 weeks (mean age 43 days)
  • Cause unknown
  • 1-8 per 1000 births; 4:1 male predmoninance
  • Family history in 13%
  • Projectile post-prandial vomiting, beginning at 2-4 weeks or as late as 12 weeks
  • Non-bilious, may be blood-streaked
  • Hungry, avid nursers
  • Constipation, weight loss
  • Dehydration
  • Gastric peristaltic waves L to R can be seen
  • Oval mass 5-15 mm on deep palpation in RUQ, especially after vomiting in 14%
  • Electrolytes/BMP: Hypochloremic alkalosis (14%) with potassium depletion (23%)
  • CBC - Dehydration may cause elevated hemoglobin and hematocrit
  • Barium Upper GI Series: Retention of contrast in stomach and long, thin pyloric canal
  • Ultrasound: Hypoechoic muscle ring
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14
Q

Pyloric Stenosis - Tx

A

-Admit to hospital for IV rehydration, IV cimetidine
-Consult Pediatric Surgeon
-Pyloromyotomy
-Post Op barium xray stays abnormal for months despite symptom relief
Children more likely to have chronic abdominal pain
- will see on X-ray string sign

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15
Q

Gastric Adenocarcinoma

A

Gastric Adenocarcinoma

  • Second most common cause of cancer death worldwide - Still high incidence in Japan and many developing regions
  • US - 21,500 new dx/yr; higher incidence in Latinos, African and Asian Americans
  • Asymptomatic until advanced
  • Vague epigastric pain, dyspepsia, anorexia, early satiety, weight loss
  • Ulcerating lesions lead to hematemesis or melena
  • Pyloric obstruction - postprandial vomiting
  • PE - gastric mass in 20%
  • Anemia - iron deficiency or anemia of chronic disease
  • LFTs (Alk Phos) may be elevated if liver mets
  • UGI Endoscopy essential
  • Obtain in ALL pts over 55 with new onset dyspepsia or anyone who fails antisecretory therapy
  • Curative Surgical Resection
  • Palliative Therapies
  • Long-term survival: <15%
  • 45% for patients who have successful curative resection
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16
Q

Gastric Lymphoma

A
  • May be primary (arising from gastric mucosa) or secondary (patients with nodal lymphomas)
  • Presentation similar to adenocarcinoma
17
Q

Gastric Carcinoid

A
  • Rare neuroendocrine tumors, < 1% of gastric neoplasms
  • Sporadic (20%); or
  • Secondary to hypergastrinemia -> hyperplasia -> transformation of enterochromograffin cells in fundus
  • Most solitary, over 2 cm
  • Strong propensity for metastatic spread
  • Tumors release hormone products, which cause symptoms
  • Profuse diarrhea
  • Flushing - hot, red face
  • Telangiectasias on cheeks
  • Wheezing, SOB, Cardiac arrhythmias
  • R-sided valvular disease, heart failure
  • Above make up carcinoid syndrome
    tx:
  • Usual cancer treatments ineffective due to slow growth
  • Presentation usually quite late
  • Mainstay is Octreotide, which mimics somatostatin, to control symptoms