Gastroesophageal Reflux Disease (GERD) Flashcards

1
Q

What is the function of the lower esophageal sphincter (LES)?

A

Ring of smooth muscle at the lower end of the esophagus. Usually constricted to prevent gastric reflux, and relaxes when swallowing to allow the passage of food from the esophagus into the stomach.

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2
Q

Why is it important that the lower esophageal sphincter is aligned with the esophageal hiatus?

A

The esophagus, at the level of the LES, passes through a hole in the diaphragm = esophageal hiatus. When the diaphragm contract and flattens during inhalation, abdominal pressure increases, pushing gastric content upward. The pressure on teh LES by diaphragm contraction helps prevent gastric reflux while breathing.

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3
Q

What are transient relaxations of the LES?

A

After swallowing, LES will relax transiently a number of times causing some reflux (30-60 mins after eating) which is normal as they help to release swallowed air.

Any reflux of gastric contents gets cleared by secondary peristalsis, a partial wave of peristalsis that starts from the point of distention or irritation to remove any remaining food or refluxed contents from the espohagus. Plus, saliva helps to neutralize any acid that remains in the esophagus.

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4
Q

What is a hiatal hernia?

A

The displacement of a portion of the stomach through the esophageal hiatus into the thoracic cavity.

D/t:
- weakening of diaphragm with age
- congenital = enlarged esophageal hiatus
- congenital or scarring = sortening of the esophagus
- conditions that persistently increase intraabdominal pressure (e.g. obesity)

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5
Q

What is the most common cause of reflux?

A

Sliding hiatal hernia = 90% of cases

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6
Q

How does a hiatal hernia contribute to GERD?

A

The LES slides into the thoracic cavity temporarily which means the LES and diaphragm don’t align and the loss of pressure on the LES allows reflux to occur more easily.

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7
Q

What is an incompetent LES?

A

1) LES weakening
- unable to maintain a sufficient resting pressure to prevent gastric reflux. Gastric contents move from an area of higher to lower pressure (from the stomach to esophagus) when the patient is supine or when there is an increase in the abdominal pressure

2) abnormal transient LES relaxations
- transient LES relexations are normal for a short time period after eating and fucntion to release swallowed air. In some, these relaxations occur spontaneously and inappropriately.

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8
Q

What are some conditions thought to decrease LES pressure?

A
  • age
  • foods (caffeine, alcohol, chocolate, peppermint, fatty foods)
  • nicotine
  • medications (anticholinergics, Ca+ channel blockers)
  • hormones (progesterone)
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9
Q

How does delayed gastric emptying contribute to GERD?

A

Prolonging the time when reflux might occur and increasing intragastric pressure on the LES.

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10
Q

What are conditions that impair gastric motility (gastroparesis)?

A

Diabetic neuropathy, damage to the vagus nerve, certain medications

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11
Q

What are conditions that cause gastric outlet obstruction?

A

Gastric ulcers (d/t edema and/or scarring), tumour, congenital pyloric stenosis

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12
Q

What effect do fatty meals have on gastric emptying?

A

Slows it down in order to allow duodenum to digest fats

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13
Q

How does increased abdominal pressure contribute to GERD?

A

Intrabdominal pressure causes an increase in intragastric pressure, and thus pressure placed on the LES. Reflux may occur when intraabdominal pressure overcomes LES and intraesophageal pressures (a pressure gradient favours reflux)

In some cases increased intraabdominal pressure may contribute to hiatal hernia development.

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14
Q

What are some causes of increased abdominal pressure?

A
  • obesity
  • pregnancy
  • persistent coughing
  • lifting heavy objects
  • straining to have a bowel movement
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15
Q

How does impaired esophageal motility or saliva production contribute to GERD?

A

Impaired esophageal peristalsis - unable to effectively clear refluxed contents.

Impaired saliva syntesis - unable to neutralize refluxed contents.

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16
Q

What can cause impaired esophageal motility or saliva production?

A
  • stroke, esophageal stricture
  • radiation therapy to the head or neck, medications
17
Q

Describe the pathogenesis of GERD.

A
  1. Reflux causing esophageal injury
  2. inflammation (esophagitis), and possibly erosion
  3. Erosive esophagitis = formation of superficial erosions in the esophageal mucosaW
18
Q

What are characteristics of epigastric/chest pain d/t GERD?

A
  • burning pain (r/t esophageal irritation and injury)
  • starts over the sternum and radiates upwards to the neck
  • starts after eating (30-40 mins) and may last for several hours (pain associated with increased gastric secretion and pressure on the LES, and potentially lasts the duration of gastric emptying)
  • worse with coffee or spicy food (increase stomach acidity and caffeine in coffee is suggested to decrease LES tone)
  • some relief with antacids (decreases acidity)
  • sour taste in the morning = regurgitation of gastric contents into the mouth
  • voice hoarseness - aspiration of gastric contents into the upper airways causing inflammation of the larynx
19
Q

Why is difficulty swallowing relevant in diagnosing GERD?

A

Esophageal scarring caused by chronic irritation and inflammation of the esophagus wall. When the scar tissue contracts the esophagus lumen narrows (forms a stricture) causing dysphagia.

20
Q

What are the benefits of PPIs and H2 receptor antagonists?

A

Decrease gastric acid production and thus decrease stomach acidity. they won’t prevent reflux but they will reduce esophageal injury when reflux occurs.

21
Q

How can GERD lead to esophageal Ca?

A

Repeated irritation of the distal esophagus by gastric reflux may cause metaplasia. The stratified sqaumous epithelium of the esophagus is converted to a simple columnar epithelium similar to that found in teh stomach that will better withstand exposure to refluxed gastric ontents (called Barrett’s esophagus). Continued irritation can progress to dyslpasia and neoplasia.

Barrett’s esophagus is a risk factor of esophageal Ca (40x risk)