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pharmacology exam 3 > Gastroesophageal Reflux and PUD > Flashcards

Gastroesophageal Reflux and PUD Flashcards

(44 cards)

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1
Q

pathophysiology GERD

A
  • Results from the reflux of chyme from the stomach into the esophagus
  • The resting tone of the lower esophageal sphincter (LES) is less than normal  permits transient relaxation of the LES 1-2 hrs after eating
  • This relaxation allows gastric contents to regurgitate into the esophagus
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2
Q

hormones that increase LES resting tone

A

gastrin

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3
Q

hormones that decrease LES sphincter tone

A

 Estrogen
 Progesterone
 Glucagon
 Secretin
 Cholecystokinin

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4
Q

foods that decrease LES tone

A

 Tobacco
 Alcohol
 Peppermint
 Chocolate
 Foods with high concentrations of fat or carbohydrates

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5
Q

medications that increase LES tone

A

 bethanechol (Urecholine)
 metoclopramide (Reglan)
 pentobarbital (Nembutal)
 histamine
 antacids

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6
Q

medications that decrease LES tone

A

 Anticholinergics
 Theophylline
 Caffeine
 meperidine (Demerol)
 calcium channel blockers

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7
Q

reflux esophagitis causes inflammatory response in the esophageal wall, which results in:

A

o Hyperemia
o Increased capillary permeability
o Edema
o Tissue fragility
o Erosion
o Ulcerations
o Fibrosis and basal cell hyperplasia
o Long term consequence: precancerous lesions (Barrett’s esophagus)

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8
Q

medications can be used to treat GERD in various ways

A

o increase LES tone
o reduce the amount of acid in chyme
o improve peristalsis
- decrease the time chyme is available to produce reflux
- decrease the exposure of the mucosa to highly acid material

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9
Q

drugs that improve LES sphincter tone

A
  • metoclopramide and bethanechol
  • antacids
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10
Q

metoclopramide and bethanechol for GERD

A

o Improve LES tone
o Have a prokinetic function
o Not considered monotherapy for GERD
o Most useful in combination w/ acid suppression for gastroparesis
o Do not heal esophageal lesions

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11
Q

antacids for GERD

A

o Serve dual purpose
- Improve LES tone
- Increase gastric pH
o Usually, patient initiated

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12
Q

drugs to reduce the amount of acid

A

histamine2 receptor antagonists and PPIs

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13
Q

H2RA for GERD

A

 Act on parietal cells to decrease the amount of acid produced
 Available OTC - usually pt initiated
 Used as maintenance acid suppression or heartburn therapy in pts who do NOT have erosive GERD
 AGA guidelines -> Trial of nighttime H2RAs for pts taking daytime PPIs

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14
Q

PPIs for GERD

A

 1st line therapy for GERD
 Decrease acid secretion by almost 100%
 Improve esophageal healing by about 80%

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15
Q

drugs to improve peristalsis

A

Few patients continue to report s/s despite reduced acid secretion
o These patients may benefit from prokinetics
- Improve LES tone and peristalsis

Metoclopramide is used

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16
Q

drugs to decrease mucosal exposure in GERD

A

Two cytoprotective agents are available to decrease the exposure of the gastric mucosa to acid:
- Sucralfate (Carafate)
- misoprostol (Cytotec)

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17
Q

sucralfate (carafate) for GERD

A
  • Acts largely as a barrier to cover sites undergoing erosive damage
  • More often used with ulcers
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18
Q

misoprostol (Cytotec) for GERD

Study These Flashcards
A
  • Acts by increasing the production of cytoprotective mucus
  • Reserved for when NSAIDs are a contributing factor to the increased acid load
19
Q

goals of treatment for GERD

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A

o Reduce or eliminate s/s
o Heal any esophageal lesions
o Prevent relapse
o Manage or prevent complications such as:
- Stricture
- Barrett’s esophagus
- Esophageal carcinoma

20
Q

lifestyle modifications are central to the management of GERD

Study These Flashcards
A
  • antireflux maneuvers
  • dietary changes
  • cessation of smoking
  • GERD s/s can be reduced with weight loss
21
Q

antireflux maneuvers

Study These Flashcards
A

 Reduce back pressure on the LES from intra-abdominal contents
 Sleep with HOB elevated 6-8 inches
 Avoid the recumbent position within 3 hours after eating
 Avoiding bending over within 3 hours of eating
 Avoid exercise, especially strenuous exercise, within 3 hours of eating
 Attain and maintain appropriate body weight

22
Q

dietary changes for GERD

Study These Flashcards
A

 Reduce the total volume and acid content of the stomach
 Eat moderate amounts of food at each meal. Do not gorge yourself
 Avoid eating meals or bedtime snacks within 3 hours of going to bed

23
Q

drug therapy for GERD step therapy

Study These Flashcards
A
  1. lifestyle modifications and OTC antacids
  2. H2RAs is s/s are mild and no erosive disease is evident
  3. PPIs are 1st line therapy for pts w/ moderate to severe GERD or erosive disease
  4. reassess in 4-8 weeks
24
Q

long-term use of PPI presents concerns

Study These Flashcards
A
  • Development of gastric cancer
  • Increase in hip fractures in pts who are on PPIs longer than 2 years
  • Vitamin B12 deficiency is a concern with chronic acid suppression
25
PUD pathophysiology
PUD is a chronic inflammatory condition of the stomach and duodenum, resulting from: o Increased acid and pepsin secretion o Impaired mucosal cytoprotection o Use of NSAIDs o H. pylori infections o Personal factors: - Genetics - Smoking - Heavy alcohol use - Stress
26
definitive diagnosis of PUD
made via endoscopy
27
peptic ulcers fall into two categories
1. duodenal ulcers 2. gastric ulcers
28
gastric ulcer disease
underlying defect -> a disruption that increases the gastric mucosal barrier's permeability to H+ ions another contributing factor -> increased duodenal gastric reflux of bile across an incompetent pyloric sphincter
29
incompetent pyloric sphincter causing gastric ulcer disease
An increased concentration of bile salts disrupts the gastric mucosa and decreases the electrical potential across the gastric mucosal membrane - Permits the diffusion of hydrogen ions into the mucosa - they disrupt permeability and cellular structure Once the barrier is broken, the damaged submucosal areas exposed to hydrogen ions release histamine
30
histamine in gastric ulcer disease
 Stimulates an increase in acid and pepsinogen production  Causes local vasodilation  Increases capillary permeability
31
pepsinogen in gastric ulcer disease
produces mucosal erosion, resulting in the formation of ulcers
32
pyloric stenosis is another possible cause of gastric ulcers
o Gastric emptying is poor - resulting in stasis and antral distention o Leads to increased gastrin release and gastric acid production
33
chronic gastritis has been associated w/ the development of gastric ulcers
- Limit the ability of the mucosa to secrete a protective layer of mucus - Decreased mucosal synthesis of prostaglandin may also create an ulcerogenic environment
34
duodenal ulcer disease - major cause
infection with H. pylori o Once attached to the mucosal layer -> H. pylori releases toxins, proteases, and phospholipase enzymes that promote inflammation and impair the integrity of the mucosal layer - The inflammatory process include the release of histamine, which acts the same on the duodenal mucosa and on the gastric mucosa - end result is ulceration
35
PUD pharmacodymanics
all patients with PUD should be started on a PPI to decrease gastric acid production and facilitate ulcer healing - omeprazole 20-40mg daily (or equivalent) will lead to faster control of s/s and promote healing eradication of H. pylori is critical to PUD tx
36
eradication of H. pylori for PUD tx
all recommended treatment regimens include a combination of PPI and antimicrobial therapy antimicrobial agents include:  clarithromycin  tetracycline  amoxicillin  levofloxacin  metronidazole
37
goals of treatment for PUD
o eradicate H. pylori o heal any ulcers o manage or prevent complications such as - GI bleeding - Development of gastric carcinoma o Prevent relapse o Reduce or eliminate symptoms
38
algorithm for PUD tx
1. lifestyle modifications and antacids 2. testing for H. pylori and PPI therapy 3. uncomplicated -> tx H. pylori w. abx and PPI 3. complicated (bleeding) -> refer to gastroenterologist and tx H.pylori
39
triple therapy for H. pylori
 PPI BID  Clarithromycin 500 mg BID  Amoxicillin 1 g  Treat for 10-14 days  Usual first-line therapy
40
triple therapy for H. pylori (PCN allergy)
 PPI BID  Clarithromycin 500 mg BID  Metronidazole 500 mg TID  Treat for 7-14 days  Used as first line therapy in PCN allergic patients
41
bismuth quadruple therapy for PUD
 PPI BID  Metronidazole 250 mg qid or 500 mg tid  Tetracycline 500 mg qid  Bismuth subcitrate 120–300 mg qid or subsalicylate 300 mg qid  Treat for 10-14 days  First-line therapy in patients w/ previous macrolide use or PCN allergy
42
levofloxacin-based triple therapy
 PPI bid  Levofloxacin 500 mg qday  Amoxicillin 1 g  Treat for 10-14 days
43
LOAD therapy for PUD
 Levofloxacin 250mg qday  Omeprazole  Nitazoxanide (Alinia) 500 mg bid  Doxycycline 200 mg qday
44
four weeks after completion of therapy, pts should have H. pylori testing to determine eradication
 Urea beath test  Fecal antigen testing  Endoscopic biopsy

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