Week 10 Flashcards

1
Q

What is gastro-esophageal reflux disease?

A

Syndrome caused by overwhelmed lower esophageal defences. Caused by predisposing conditions including hiatal hernias, incompetent LES, decreased esophageal clearance.

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2
Q

What do acidic gastric secretions cause?

A

Esophageal irritation and inflammation,

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3
Q

What chemicals are corrosive to esophageal mucosa?

A

Pepsin, intestinal enzymes, and bile salts.

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4
Q

What is an incompetent LES?

A

A decrease in pressure in the distal portion of the esophagus. This allows gastric contents to move from an area of high pressure to an area of low pressure. Can be caused by certain foods (caffeine, chocolate, drugs).

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5
Q

What are the CM of GERD?

A

Heartburn, caused by irritation of esophagus from the gastric secretions.
Wheezing, coughing and dyspnea may also occur.
Regurgitation is common. Gastric symptoms like bloating, nausea, vomiting, also occur due to delayed gastric emptying.

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6
Q

What are complications of GERD?

A

Esophagitis, barrett’s esophagus (precancerous lesion =), Bronchospasm, laryngospasm, cricopharyngeal spasm and pneumonia, and dental errosion.

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7
Q

What diagnostic studies are used to diagnose GERD?

A

History and physical examination, barium swallow, motility, pH monitoring, upper GI endoscopy.

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8
Q

What collaborative therapies are used to treat GERD?

A

Elevate head of bed, high protein, low fat diet.

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9
Q

What drug therapies can be used for GERD?

A

Antacids, antisecretory drugs, cholinergic drugs, H2 receptor blockers, proton pump inhibitors, prokinetic drug therapy.

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10
Q

What surgical therapies may be used to treat GERD?

A

Belsey fundoplication, hill gastropexy, nissen fundoplication, toupet fundoplication.

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11
Q

What is a hiatal hernia?

A

Herniation of a portion of the stomach into the esophageous through an opening.

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12
Q

What is peptic ulcer disease?

A

Characterized by erosion of GI mucosa from action of HCl and pepsin. May cause ulcers in lower esophagus, stomach, duodenum.

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13
Q

What are the classifications of peptic ulcers?

A

Acute or chronic and gastric or duodenal.

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14
Q

What are acute ulcers?

A

Characterized by superficial erosion and minimal inflammation. Short in duration and resolve quickly.

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15
Q

What are chronic ulcers?

A

Long in duration, they erode through muscular wall and form fibrous tissue.

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16
Q

What do acids/bile salts/ ASA/ NSAIDS/alcohol/ischemia cause?

A

Breakdown of gastric mucosal barrier.

17
Q

What does the breakdown of the gastric mucosal barrier cause?

A

Acid back-diffusion into mucosa.

18
Q

What does the acid-back diffusion into the mucosa cause?

A

Destruction of mucosal cells, which leads to mucosal erosion, destruction of blood vessels, bleeding and ulceration.

19
Q

The acid back-diffusion into the mucosa causes histamine to be released. What does histamine cause?

A

Increased vasodilation, increased capilary permeability, which leads to loss of plasma proteins into gastric lumen, mucosal edema.

20
Q

What mechanisms protect against damage to the GI system?

A

Mucus is secreted by superficial mucous cells, forms a layer that traps and slows the diffusion of H+. Bicarbonate is secreted by gastric and duodenal mucosa which neutralizes HCl in the lumen of the GI tract.

21
Q

What causes the hypersecretion of HCl?

A

Increased vagal nerve stimulation.

22
Q

What are gastric ulcers?

A

Ulcers that occur in the stomach, less common than duodenal ulcers. May be caused by drugs (NSAIDs, ASA,), chronic alcohol abuse, chronic gastritis, and bile reflux gastritis.

23
Q

What are duodenal ulcers?

A

80% of peptic ulcers. Caused by COPD, cirrhosis, chronic pancreatitis, hyperparathyroidism, CKD. H. pylori is found in 90% of patients with duodenal ulcers.

24
Q

What is stress-related mucosal disease?

A

Ulcers caused by trauma or surgery. Gastric mucosa may be disturbed due to hypotension, severe burns, injury and surgery. Results as a compensatory mechanism to hypotension or shock

25
Q

What are the clinical manifestations of peptic ulcers?

A

Can be asymptomatic, because areas do not have sensory neurons to conduct pain. Ulcers located posteriorly may manifest as back pain.

26
Q

what are complications from gastric ulcers?

A

hemorrhage, perforation, gastric outlet obstruction.

27
Q

What is hemorrhage?

A

Most common complication of PUD. Develops as a result of erosion of the granulation tissue at the base of the ulcer during healing or erosion through a major blood vessel.

28
Q

What is perforation?

A

Most lethal complication. Common in large penetrating dudodenal ulcers that have not healed and are located on the posterior mucosal wall. Occurs when ulcer penetrates the serosal surface with spillage of gastric continents into periotenial cavity.

29
Q

What are the clinical manifestations of perforation?

A

Sudden severe upper abdominal pain that spreads, shoulder pain, shallow resps, bowel sounds absent, nausea and vomiting may occur.

30
Q

What is gastric outlet obstruction?

A

Obstruction near the pyloric areas of the stomach can cause increased contractile force, which causes scar tissue to form. CM include upper abdo pain, relief may be caused by belching, self induced vomiting, may have caused swelling, dilation of the stomach.

31
Q

What are some diagnositic studies used for PUD?

A

History, physical exam, CBC, h. pylori testing, liver enzyme measurements, serum electrolyte, upper GI endoscopy and biopsy, urinalysis.

32
Q

What is conservative therapy for PUD?

A

Adequet rest, bland diet, stop smoking, drug therapy, stress reduction.