Quiz 2 Study Guide: GI
Disease States
1. Constipation
● bowel movements become less frequent and stools become difficult to pass.Common
affliction caused by everything from lack of sufficient fluids, fiber, and exercise to serious
GI diseases to iatrogenic causes secondary to adverse reactions to drugs
● Treatment- adults and children
● Six classes of laxatives
● Stimulants: cascara, senna, bisacodyl, and castor oil
● Osmotics: magnesium hydroxide, magnesium citrate, sodium phosphate, polyethylene
glycol electrolyte solution, and polyethylene glycol (PEG) 3350
● Bulk-producing laxatives: psyllium, methylcellulose, and polycarbophil
● Lubricants: mineral oil
● Surfactants: docusate compounds – docusate sodium, docusate calcium, and docusate
potassium
● Hyperosmolar laxatives: glycerine, lactulose
● Chloride channel activators: lubiprostone
● Opioid-receptor antagonists: methylnaltrexone
1. Diarrhea, including traveler’s diarrhea
● Diagnosis
● Causes of diarrhea in primary care: Infections, Food or drug induced, Inflammatory bowel
disease
● Acute (less than 2 weeks and usually self limiting) vs chronic (more than 2 weeks)
● Children can become dehydrated quickly as a result of diarrhea
● Medication not required in most cases
● Treatment- adults and children
1. PUD (H-Pylori)
a. Increased acid and pepsin secretion
b. Impaired mucosal cytoprotection
c. Use of nonsteroidal anti-inflammatory drugs (NSAIDs), Helicobacter pylori
d. Gastric: antral stomach region erosion, raised gastrin
e. Duodenal: H. pylori releases toxins, phospholipase enzymes promoting inflammation and
erosion
f. Disease of the upper GI tract characterized by mucosal damage caused by pepsin and
gastric secretion
g. Pathophysiology: Normal mucosal lining and healing mechanisms are disrupted in the
presence of gastric acid and pepsin
h. Most common causes are H. pylori (known carcinogen) and chronic NSAID use
i. Most peptic ulcers occur in the stomach and upper duodenum
j. Complication from PUD: bleeding, gastric outlet obstruction, perforation
● Presentation
● Clinical presentation: heartburn like symptoms, epigastric pain, weight loss, abdominal
fullness ( can differ with location)
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, ● Gastric ulcer: nausea, vomiting, anorexia with pain resulting from food consumption
● Duodenal ulcer: pain usually follows food consumption 1-3hours afterwards and normally
relieved with food
● Diagnosis
● Diagnostic test for H. pylori: no gold standard and based on symptom presentation
● Endoscopic testing (invasive)
● Rapid urease test (RUT)
● Histology-limited use due to sampling error
● Tissue culture- 100% specific but time consuming and costly
● Polymerase chain reaction (PCR) not commercially available
● Non-endoscopic testing (non-invasive) for patients with uninvestigated dyspepsia, or
under 60 years old or without alarming symptoms
● Serum antibody testing: rapid, low cost, but low sensitivity/specificity
● Urea breath test (UBT): allows accurate post-treatment testing
● Recent antibiotics and PPIs may cause false negative
● Discontinue medications 2 weeks before UBT or 4 weeks after treatment
● Fecal antigen test (FAT): less validated than UBT but can be used to make diagnosis and
confirm eradication
● Bismuth, antibiotics, or PPI can cause false negative
● Discontinue medication 2 weeks before FAT or 4 weeks after treatment
● Treatment- including second line therapy
● Step 1 Lifestyle modifications and over-the-counter antacids or H2 blockers
● Step 2 H. pylori testing, Treatment with PPIs
● Step 3 Treatment for H. pylori
i. All regimens include a PPI plus antibiotics to treat H. pylori.
ii. Triple therapy: PPI plus
1. Clarithromycin: 500 mg twice daily, or
2. Metronidazole: 500 mg twice daily
3. Amoxicillin: 1 gm twice daily
4. Treatment for 10 to 14 days
iii. Quadruple therapy: PPI plus
1. Metronidazole: 250 mg four times/day
2. Tetracycline: 500 mg four times/day
3. Bismuth subsalicylate: 525 mg four times/day
4. Treatment for 14 days
5. Usually used as second-line therapy in patients who fail first-line therapy
iv. Levofloxacin-based triple therapy
1. PPI: twice daily
2. Levofloxacin: 250 to 500 mg twice daily
3. Amoxicillin: 1 g twice daily
4. Treatment for 10 to 14 days
5. Second-line or rescue therapy
v. Consider adding probiotics (Lactobacillus and Bifidobacterium) as adjuvant
therapy
vi. Treatment Outcomes
vii. After treating for H. pylori, continue PPI for 8 to 12 weeks to promote healing.
viii. If the patient is at low risk, no further treatment is needed.
ix. If a patient is at high risk, consider chronic acid suppression therapy.
This study source was downloaded by 100000846529857 from CourseHero.com on 05-06-2022 12:57:17 GMT -05:00
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Disease States
1. Constipation
● bowel movements become less frequent and stools become difficult to pass.Common
affliction caused by everything from lack of sufficient fluids, fiber, and exercise to serious
GI diseases to iatrogenic causes secondary to adverse reactions to drugs
● Treatment- adults and children
● Six classes of laxatives
● Stimulants: cascara, senna, bisacodyl, and castor oil
● Osmotics: magnesium hydroxide, magnesium citrate, sodium phosphate, polyethylene
glycol electrolyte solution, and polyethylene glycol (PEG) 3350
● Bulk-producing laxatives: psyllium, methylcellulose, and polycarbophil
● Lubricants: mineral oil
● Surfactants: docusate compounds – docusate sodium, docusate calcium, and docusate
potassium
● Hyperosmolar laxatives: glycerine, lactulose
● Chloride channel activators: lubiprostone
● Opioid-receptor antagonists: methylnaltrexone
1. Diarrhea, including traveler’s diarrhea
● Diagnosis
● Causes of diarrhea in primary care: Infections, Food or drug induced, Inflammatory bowel
disease
● Acute (less than 2 weeks and usually self limiting) vs chronic (more than 2 weeks)
● Children can become dehydrated quickly as a result of diarrhea
● Medication not required in most cases
● Treatment- adults and children
1. PUD (H-Pylori)
a. Increased acid and pepsin secretion
b. Impaired mucosal cytoprotection
c. Use of nonsteroidal anti-inflammatory drugs (NSAIDs), Helicobacter pylori
d. Gastric: antral stomach region erosion, raised gastrin
e. Duodenal: H. pylori releases toxins, phospholipase enzymes promoting inflammation and
erosion
f. Disease of the upper GI tract characterized by mucosal damage caused by pepsin and
gastric secretion
g. Pathophysiology: Normal mucosal lining and healing mechanisms are disrupted in the
presence of gastric acid and pepsin
h. Most common causes are H. pylori (known carcinogen) and chronic NSAID use
i. Most peptic ulcers occur in the stomach and upper duodenum
j. Complication from PUD: bleeding, gastric outlet obstruction, perforation
● Presentation
● Clinical presentation: heartburn like symptoms, epigastric pain, weight loss, abdominal
fullness ( can differ with location)
This study source was downloaded by 100000846529857 from CourseHero.com on 05-06-2022 12:57:17 GMT -05:00
https://www.coursehero.com/file/131569803/NURS-6234-Quiz-2-Study-Guide-Spring-2021pdf/
, ● Gastric ulcer: nausea, vomiting, anorexia with pain resulting from food consumption
● Duodenal ulcer: pain usually follows food consumption 1-3hours afterwards and normally
relieved with food
● Diagnosis
● Diagnostic test for H. pylori: no gold standard and based on symptom presentation
● Endoscopic testing (invasive)
● Rapid urease test (RUT)
● Histology-limited use due to sampling error
● Tissue culture- 100% specific but time consuming and costly
● Polymerase chain reaction (PCR) not commercially available
● Non-endoscopic testing (non-invasive) for patients with uninvestigated dyspepsia, or
under 60 years old or without alarming symptoms
● Serum antibody testing: rapid, low cost, but low sensitivity/specificity
● Urea breath test (UBT): allows accurate post-treatment testing
● Recent antibiotics and PPIs may cause false negative
● Discontinue medications 2 weeks before UBT or 4 weeks after treatment
● Fecal antigen test (FAT): less validated than UBT but can be used to make diagnosis and
confirm eradication
● Bismuth, antibiotics, or PPI can cause false negative
● Discontinue medication 2 weeks before FAT or 4 weeks after treatment
● Treatment- including second line therapy
● Step 1 Lifestyle modifications and over-the-counter antacids or H2 blockers
● Step 2 H. pylori testing, Treatment with PPIs
● Step 3 Treatment for H. pylori
i. All regimens include a PPI plus antibiotics to treat H. pylori.
ii. Triple therapy: PPI plus
1. Clarithromycin: 500 mg twice daily, or
2. Metronidazole: 500 mg twice daily
3. Amoxicillin: 1 gm twice daily
4. Treatment for 10 to 14 days
iii. Quadruple therapy: PPI plus
1. Metronidazole: 250 mg four times/day
2. Tetracycline: 500 mg four times/day
3. Bismuth subsalicylate: 525 mg four times/day
4. Treatment for 14 days
5. Usually used as second-line therapy in patients who fail first-line therapy
iv. Levofloxacin-based triple therapy
1. PPI: twice daily
2. Levofloxacin: 250 to 500 mg twice daily
3. Amoxicillin: 1 g twice daily
4. Treatment for 10 to 14 days
5. Second-line or rescue therapy
v. Consider adding probiotics (Lactobacillus and Bifidobacterium) as adjuvant
therapy
vi. Treatment Outcomes
vii. After treating for H. pylori, continue PPI for 8 to 12 weeks to promote healing.
viii. If the patient is at low risk, no further treatment is needed.
ix. If a patient is at high risk, consider chronic acid suppression therapy.
This study source was downloaded by 100000846529857 from CourseHero.com on 05-06-2022 12:57:17 GMT -05:00
https://www.coursehero.com/file/131569803/NURS-6234-Quiz-2-Study-Guide-Spring-2021pdf/
