Peptic ulcer disease Flashcards

1
Q

Erosion of GI mucosa from HCl acid and pepsin

A

Peptic Ulcer Disease (PUD)

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2
Q

superficial erosion and minimal inflammation

A

acute

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3
Q

Erosion of muscular wall with formation of fibrous tissue; present continuously for long duration

A

Chronic

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4
Q

two types of ulcers

A

gastric (less common) & duodenal

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5
Q

gastric is felt

duodenal is felt

A

right after eating

2-5 hours after meal

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6
Q

Gastric characteristics

A

increased obstruction
increase mortality
high recurrence
more in females older than 50

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7
Q

Duodenal characteristics

A

35-45 y/o
High HCL secretion
occur, disappear, recur

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8
Q

Risk Factors

A

a. H. pylori
i. Major risk factor
ii. 80% gastric
iii. 90% duodenal
b. Transmission
i. Oral-oral or fecal-oral
ii. Black and Hispanic
c. Long survival (activates immune response)
i. Never develops ulcer, it just lays there
d. Produce urease
e. Medication-Induced Injury
i. NSAIDs; especially with
ii. Corticosteroids or anticoagulants

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9
Q

Epigastric discomfort 1 to 2 hours after meal; burning or gaseous pain; food may worsen

A

Gastric

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10
Q

Burning or cramp like pain in midepigastric or back; 2 to 5 hours after meal
c. Other: bloating, nausea, vomiting, early satiety

A

Duodenal

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11
Q

Diagnostic studies

A

Endoscopy-direct visualization (obtain specimens for H. pylori

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12
Q

Gastric Ulcer labs

A

CBC, liver enzymes, serum amylase

Stool-blood

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13
Q

Conservative care for gastric ulcers

A

i. Adequate rest, no smoking or alcohol, stress management, dietary modifications
ii. Pain management. No NSAIDs or aspirin 4 to 6 weeks unless administered with PPI, H2 receptor blocker, or misoprostol
iii. Endoscopic evaluation and follow-up; 3 to 6 months for healing

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14
Q

Drug therapy for gastric ulcers

A

i. Reduce gastric acid secretion (PPI)

ii. Eliminate H. pylori (antibiotics and PPI)

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15
Q

Three major complications for gastric ulcers

A

hemorrhage, perforation, gastric outlet obstruction

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16
Q

Perforation s/s

A

severe abdominal pain
bowel sounds absent
respirations shallow
pulse increased & weak

17
Q

If perforation untreated

A

Bacterial peritonitis occurs

18
Q

Edema, inflammation, pylorospasm, or scar tissue cause obstruction in distal stomach and duodenum

A

Gastric Outlet Obstruction

19
Q

Gastric outlet obstruction: if residual is less than

A

200 mL after clamped for 8-12 hrs..begin oral intake

20
Q

Gastric risk factors

A

H. Pylori
NSAIDs
Bile reflux

21
Q

Duodenal etiology

A

H. Pylori

22
Q

Antibiotic Therapy

A

H. pylori 14 days of PCN; if allergic, metronidazole

23
Q

i. Protects esophagus, stomach, and duodenum

ii. Works best in low pH; give 1 to 2 hours before or after antacid

A

Sucralfate (cytoprotective drug therapy)

24
Q

acute care

A

i. NPO, NGT, IV fluids, VS, monitor for shock
ii. Gastric content analysis; check pH, blood, or bile
iii. Monitor labs
iv. Manage pain and anxiety; restful environment

25
Q

Hemorrhage acute care

A

i. Monitor VS, NG aspirate
ii. See interventions for upper GI bleeding
iii. Will have a decrease in pain bc the blood neutralizes acids in stomach

26
Q

gastric outlet treatment

A
  1. Treatment: decompress with NGT; PPI or H2 receptor blocker; pain management; fluid and electrolyte replacement; surgery or balloon dilation