Week 2 Flashcards

1
Q

signs and symptoms of gastroesophageal reflux disease

A

o Heartburn (mimics cardiac chest pain): burning sensation –>after meals or when lying flat
o Asthma (adult-onset) and cough
o Damage to enamel of teeth
o Dysphagia: difficult to swallow
o Ulceration w stricture (acid damages mucosa–>ulceration of mucosa–>knock out stem cells–>fibrosis–>stricture) and Barrett’s esophagus are late complications

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2
Q

risk factors for the development of, or exacerbation of GERD.

A
  • increase your risk of GERD include: Obesity, hiatal hernia, Pregnancy, Connective tissue disorders, such as scleroderma, Delayed stomach emptying
  • Factors that can aggravate acid reflux include: Smoking (Nicotine: an agonist for nicotinic Ach receptors.Nn receptors–>inc in parasympathetic–>increase GI secretions), Eating large meals or eating late at night (duodenal G cells–> intestinal gastrin production–> stimulates parietal cells to make more H+), Eating certain foods (triggers) such as fatty or fried foods, Drinking certain beverages, such as alcohol or coffee, Taking certain medications (aspirin)
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3
Q

relationship between Lower Esophageal Sphincter (LES) tone and gastroesophageal reflux.
- what triggers transient?

A
  • Functional (frequent transient LES relaxation) or mechanical (hypotensive LES) problem of LES is the most common cause of GERD.
  • Transient relaxation of LES can be caused by foods (coffee, alcohol, chocolate, fatty meals), medications (beta-agonists,nitrates, calcium channel blockers, anticholinergics), hormones ( progesterone), and nicotine.
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4
Q

alarm (red flag) symptoms for esophagogastroduodenoscopy

A
  • older than 55 with new onset
  • FH of GI cancer
  • unintended weight loss
  • GI bleeding
  • progressive dysphagia
  • odynophagia
  • unexplained iron deficiency anemia
  • persistent vomiting
  • palpable mass
  • jaundice
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5
Q

behavioral and lifestyle modification that may aid in the alleviation of GERD

A

· Mediterranean diet, exercise, quit smoking, stress reduction, sleep hygiene, smaller meals, chew gums after meal
· Losing weight (if overweight)
· Avoiding alcohol, chocolate, citrus juice, and tomato-based products
· Avoiding peppermint, coffee, and possibly the onion family
· Eating small, frequent meals rather than large meals
· Waiting 3 hours after a meal to lie down
· Refraining from ingesting food (except liquids) within 3 hours of bedtime
· Elevating the head of the bed 8 inches
· Avoiding bending or stooping positions
· Avoid thigh clothing, belts, or anything that can increase abdominal pressure

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6
Q

Contrast the therapeutic efficacy of omeprazole to esomeprazole in the treatment of Barrett’s esophagus

A
  • both bind H+/K+ ATPaseenzyme system
  • Omeprazole: Racemic mixture of isomers amd Esomeprazole is only the S isomer form not racemic mixture—>this helps better control acidic production, more selective
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7
Q

mechanisms of action and indications of agents that reduce intragastric acidity

  • antacids containing aluminum hydroxide or magnesium hydroxide).
  • ranitidine
A

o Aluminum hydroxide: Reacts w HCL—–> AlCl3 +H2O; Overuse: can halts diarrhea—>can lead to constipation–> not significantly absorbed in the bowel
o Magnesium hydroxide : Reacts w HCL—–>MgCl2 + H2O; Overuse: Can cause massive diarrhea–> not significantly absorbed in the bowel
- ranitidine: Reversible H2 antagonists in parietal cells—->decrease H+ secretion

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8
Q

Define Barrett’s Esophagus and recognize its association with the development of dysplasia and malignancy

  • what causes it?

- what can it progress to?

A

· Metaplasia of lower esophageal mucosa from stratified squamous epithelium to nonciliated columnar epithelium w goblet cells

  • Response of lower esophageal stem cells to acidic stress; GERD can erode the esophageal mucosa, promote inflammatory cell infiltrate, and ultimately cause epithelial necrosis. This chronic damage is believed to promote the replacement of healthy esophageal epithelium with the metaplastic columnar cells of Barrett esophagu
  • May progress to dysplasia and adenocarcinoma
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9
Q

epidemiology and relative risk of progression from Barrett’s esophagus to adenocarcinoma

A
  • malignant proliferation of glands
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