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Pharmacology II > Disorders of the Upper GI Tract > Flashcards

Disorders of the Upper GI Tract Flashcards

1
Q

Goals of treatment of upper GI

A

Raise the pH of stomach fluid.
Get the stomach contents out quicker (preferably downward)
Eliminate any mysterious (or known) force(s) that may be increasing stomach irritation.

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2
Q

How are intermittent dyspeptic symptoms treated?

A

antacids

OTC H2 antagonists

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3
Q

intermittent dyspeptic symptoms

A

occasional bloating
fullness
abdominal pain
heartburn

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4
Q

What are intermittent dyspeptic symptoms associated with?

A

overeating or drinking or consumption of certain foods

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5
Q

abdominal pain similar to gastritis, gastric ulcers or duodenal ulcers without demonstrable ulceration

A

non-ulcer dyspepsia

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6
Q

What is non-ulcer dyspepsia associated with?

A

GI motility abnormalities

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7
Q

How is non-ulcer dyspepsia treated?

A

antacids
OTC H2 antagonists
Rx H2 antagonists

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8
Q

epigastric pain that can be accompanied by nausea/vomiting resulting from diffuse inflammation of the stomach

A

gastritis

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9
Q

What is gastritis usually caused by?

A

H pylori

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10
Q

How is gastritis treated?

A

discontinue NSAIDs
Antacids
OTC/Rx H2 antagonists
Antibacterial regimen

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11
Q

diffuse gastric pain typically 1-3 hours after eating distinct ulcerations in stomach

A

gastric ulcers

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12
Q

symptoms of gastric ulcers

A

ulcerations in stomach
nausea/vomiting
belching
anorexia

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13
Q

How are gastric ulcers treated?

A 
Discontinue NSAIDs
Rx H2 antagonists
Proton Pump Inhibitor
Antibacterial regimen
Misoprostol
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14
Q

diffuse epigastric pain typically with empty stomach

A

duodenal ulcers

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15
Q

What relieves duodenal ulcers?

A

eating

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16
Q

treatment of duodenal ulcers

A 
discontinue NSAIDs
Rx H2 antagonists
proton pump inhibitors
antibacterial regimen
succralfate
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17
Q

symptoms of GERD

A

range from occasional heartburn to persistant burning substernal pain

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18
Q

treatment of GERD

A

antacids
OTC/Rx H2 antagonists
proton pump inhibitors
prokinetic agents

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19
Q

GERD alarm symptoms

A

dysphagia
odynophagia
anemia
weight loss

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20
Q

classic symptoms of GERD

A

heartburn
regurgitation
water brash

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21
Q

What is the treatment if a patient complains of alarm symptoms of GERD?

A

immediate upper endoscopy

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22
Q

What if a patient only complains of classic symptoms of GERD?

A

Begin conservative antireflux measures.
Discuss use of OTC preparations
Provide pt education

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23
Q

If a patient attempts conservative management of GERD and patietnts still persist, what is the next level of treatment?

A

begin empirical trial of proton pump inhibitor

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24
Q

If a patient attempts conservative symptoms, attempts an empirical proton pump inhibitor, but symptoms still persist, what is the next step?

A

Perform upper endoscopy.

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25
Q

GERD treatment - Ulceration

A

consider causes of ulceration; e.g. acid
Peptic disease
viral or fungal infection
neoplasia

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26
Q

GERD treatment - erosive esophagitis

A

Intensify proton pump inhibitor therapy

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27
Q

GERD treatment - Barrett’s esophagus

A

If dysphagia at initial endoscopy without inflammation, discuss utility of enrollment in endoscopic surveillance program.

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28
Q

GERD treatment - cancer

A

Referral to appropriate oncological service

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29
Q

GERD treatment - normal

A

Consider 24-hour pH probe to identify nonerosive reflux.

Consider other causes of symptoms.

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30
Q

Sporadic uncomplicated heartburn, often in setting of known precipitating factor. Often not chief complaint. No additional symptoms

A

Stage I GERD

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31
Q

How many episodes per week are seen with Stage I GERD?

A

Less than 2-3.

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32
Q

Medical Management of Stage I GERD

A

Lifestyle modification, including diet, positional changes, weight loss, etc.
Antacids and/or histamine H2 receptor antagonists as needed.

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33
Q

Frequent symptoms with or without esophagitis.

A

Stage II GERD

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34
Q

How many episodes per week are seen in Stage II GERD?

A

More than 2-3.

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35
Q

Treatment of Stage II GERD

A

Proton pump inhibitors more effective than histamine H2 receptor antagonists

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36
Q

Chronic, unrelenting symptoms; immediate relapse off therapy. Esophageal complications (e.g., stricture, Barrett’s metaplasia)

A

Stage III GERD

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37
Q

Treatment of Stage III GERD

A

Proton pump inhibitor either once or twice daily

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38
Q

Proton Pump Inhibitors

A 
Omeprazole (Prilosec)
Esomeprazole (Nexium)
Lonsoprazole (Prevacid)
Pantoprazole (Protonix)
Rabeprazole (Aciphex)
Dexlansoprazole (Dexilant)
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39
Q

What do PPIs act on?

A

Parietal Cell - decreases production of acid.

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40
Q

Increasing acetylcholine in the stomach…

A

… increases the action of the parietal cells which increases acid production causing nausea.

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41
Q

What creates a mucous layer around the cells allowing them to have a pH of 7?

A

Prostogandins

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42
Q

Number 1 best selling drug in the US?

A

Esomeprazole - Nexium

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43
Q

Tmax of Prilosec

A

1-3 hours

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44
Q

Tmax of Prevacid

A

1.7 hours

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45
Q

Tmax of Aciphex

A

3.1 hours

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46
Q

Tmax of Nexium

A

1.6 hours

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47
Q

Tmax of Protonix

A

2-4 hours

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48
Q

Half-life of Prilosec

A

0.5-3 hours

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49
Q

Half-life of Prevacid

A

1-2 hours

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50
Q

Half-life of Aciphex

A

1-2 hours

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51
Q

Where do PPIs work?

A

Hydrogen - Potassium - ATPase pump

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52
Q

Half-life of Nexium

A

1.4 hours

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53
Q

Half-life of Protonix

A

1-1.9 hours

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54
Q

Binding of Prilosec

A

95%

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55
Q

Binding of Prevacid

A

99%

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56
Q

Binding of Aciphex

A

96%

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57
Q

Binding of Nexium

A

97%

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58
Q

Binding of Protonix

A

98%

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59
Q

Clearance of the PPIs is completed by

A

the Liver

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60
Q

Bioavailability of Prilosec

A

40-60%

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61
Q

Bioavailability of Prevacid

A

85%

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62
Q

The PPIs are pro-drugs which means…

A

they are not activated until they reach the stomach. DO NOT open up/crush capsule/pill.

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63
Q

Bioavailability of Aciphex

A

52%

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64
Q

Bioavailability of Nexium

A

90%

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65
Q

Bioavailability of Protonix

A

77%

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66
Q

Dosage form(s) of Prilosec

A

Capsule

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67
Q

Dosage form(s) of Prevacid

A

Capsule/Tab

68
Q

Dosage form(s) of Aciphex

A

Tablet

69
Q

Dosage form(s) of Nexium

A

Capsule / IV

70
Q

Dosage form(s) of Protonix

A

Tablet / IV

71
Q

Indications for Prilosec

A 
Short-term duodenal ulcer
H.Pylori eradication
Maintenance - duodenal ulcer
Short-term active benign gastric ulcer
Short-term-symptomatic GERD
Short-term erosive esophagitis
Maintenance-erosive esophagitis
Pathological hypersecretory disorders
72
Q

Indications for Prevacid

A 
Short-term duodenal ulcer
H.Pylori eradication
Maintenance - duodenal ulcer
Short-term active benign gastric ulcer
Short-term-symptomatic GERD
Short-term erosive esophagitis
Maintenance-erosive esophagitis
Pathological hypersecretory disorders
73
Q

Indications for Aciphex

A

Short-term duodenal ulcer

Short-term erosive esophagitis
Maitenance-erosive esophagitis
Pathological hypersecretory disorders

74
Q

Indications for Nexium

A

H.Pylori eradication
Short-term-symptomatic GERD
Short-term erosive esophagitis
Manitenance-erosive esophagitis

75
Q

How long does it take for PPIs to work?

A

3-4 days

76
Q

Indications for Protonix

A

Short-term erosive esophagitis
Maintenance-erosive esophagitis
Pathological hypersecretory disorders

77
Q

Acid levels peak…

A

at meal times and during the night

78
Q

Where to H2 blockers work well for acid inhibition?

A

Overnight acid production. Less successful for acid suppression around mealtimes.

79
Q

Which drugs work best for acid suppression?

A

PPIs

80
Q

True or False: PPIs are effected by first-pass metabolism

A

True

81
Q

True or False: PPIs are renally excreted and must be adjusted.

A

False

82
Q

What is the relationship between PPIs and fracture risk?

A

fracture risk in increased

83
Q

What is the relationship between PPIs and clopidogrel?

A

PPIs interfere with a necessary metabolic step for clopidogrel. Effects 2C19. Increases clotting risk.

84
Q

What is the relationship between PPIs and C.Diff?

A

May be associated with an increased risk of clostridium difficile - associated diarrhea.

85
Q

What are PPIs not approved for?

A

use of treatment of upper GI bleeding

86
Q

What PPI IV forms are available for quicker onset?

A

Protonix IV

Nexium IV

87
Q

Physiologic activity at pH >3.5

A

decreased incidence of stress-induced bleeding

88
Q

Physiologic activity at pH >4

A

Target pH- prevention of stress-related mucosal bleeding.

89
Q

Physiologic activity at pH >4.5

A

Pepsin inactivation

90
Q

Physiologic activity at pH 5

A

99.9% acid neutralization

91
Q

Where do you want the pH of the stomach for a GI bleed?

A

between 5.1 and 7

92
Q

Physiologic activity at pH 5.1 to 7

A

Alterations in caogulation and platelet aggregation

93
Q

Physiologic activity at pH >6

A

Target pH - prevention of peptic ulcer reoccurrence

94
Q

Physiologic activity at pH >7

A

Potential decrease in incidence of rebleeding.

95
Q

Physiologic activity at pH >8

A

Pepsin destruction

96
Q

Which PPIs have less drug interactions?

A

Prevacid & Protonix

97
Q

ADRs of PPIs

A

Diarrhea
Abdominal pain
Headache
Dizziness

98
Q

Possible long-term effects of PPIs

A

Inhibition of calcium absorption

Rise in gastrin levels

99
Q

Omeprazole

A

Omeprazole
20 mg
One capsule one daily

100
Q

Proton Pump Inhibitor Rx to know

A

Omeprazole

101
Q

H2 Receptor Antagonists

A

Cimetidine - Tagamet
Ranitidine - Zantac
Famotidine - Pepcid
Nizatidine - Axid

102
Q

Bioavailability of Cimetidine

A

~60%

103
Q

Bioavailability of Ranitidine

A

50%

104
Q

Bioavailability of Famotidine

A

40-45%

105
Q

Bioavailability of Nizatidine

A

> 70%

106
Q

Tmax of Cimetidine

A

0.75 to 1.5

107
Q

Tmax Rantidine

A

2-3

108
Q

Tmax of Famotidine

A

1-3

109
Q

Tmax of Nizatidine

A

0.5 - 3

110
Q

Instead of dosing a PPI twice a day…

A

… do a PPI in the morning and an H2 inhibitor at night.

111
Q

Cmax of Cimetidine

A

2-3

112
Q

Cmax of Ranitidine

A

0.44 - 0.55

113
Q

Cmax of Nizatidine

A

0.7 - 1.8

114
Q

Half-life of Cimetidine

A

~2

115
Q

Half-life of Ranitidine

A

2.5-3

116
Q

Half-life of Famotidine

A

2.5 - 3.5

117
Q

Half-life of Nizatidine

A

1-2

118
Q

Indications for Cimetidine

A

Short-term treatment of active duodenal ulcers and benign gastric ulcers.
Maintenance therapy of duodenal ulcer.
Treatment of gastric hypersecretory states.
Treatment of GERD.

119
Q

Indications for Rantidine

A

Short-term and maintenance therapy of duodenal ulcer, gastriculcer, GERD, active benign ulcer, erosive esophagitis, and pathological hypersecretory conditions.

*As part of a multidrug regimen for H.pylori eradication to reduce the risk of duodenal ulcer recurrence.

120
Q

Indications for Famotidine

A

Maitenance therapy and treatment of duodenal ulcer.
Treatment of GERD.
Treatment of active benign gastric ulcer.
Treatment of pathological hypersecretory conditions.

121
Q

Indications for Nizatidine

A

Treatment of maintenance of duodenal ulcer.
Treatment of benign gastric ulcer.
Treatment of GERD.

122
Q

Do H2-receptor antagonists require renal dosing adjustment?

A

Yes (look up thresholds in book)

123
Q

What are the differences between the Rx and OTC H2-blockers?

A

10 hours of 50% acid inhibition at Rx dosing.

Less than 6 hours of 50% acid inhibition at OTC dosing.

124
Q

MOA of H2 receptor antagonists

A

he H2 antagonists are competitive antagonists of histamine at the parietal cell H2 receptor. They suppress the normal secretion of acid by parietal cells and the meal-stimulated secretion of acid. They accomplish this by two mechanisms: Histamine released by ECL cells in the stomach is blocked from binding on parietal cell H2 receptors, which stimulate acid secretion; therefore, other substances that promote acid secretion (such as gastrin and acetylcholine) have a reduced effect on parietal cells when the H2 receptors are blocked.

125
Q

H2 receptor antagonists are usually dosed twice per day. In what instance would they be dosed once per day?

A

If given in the evening in combination with a PPI. Double the dose of the H2 receptor antagonist.

126
Q

ADRs of H2 receptor antagonists

A

Mental status changes - cimetidine; critical care; intravenous.
Thrombocytopenia.
Endocrine issues - cimetidine.

127
Q

What is a common drug interaction with H2 receptor antagonists?

A

Cimetidine

128
Q

Hw receptor antagonist to know

A

Famotidine

129
Q

Famotidine

A

Famotidine
20 mg
one tablet twice a day

130
Q

MOA of gastric protectant

A

complexes with protein-like exudate located at ulcerations.

Covers ulcer area.

131
Q

ADRs of gastric protectant

A

Constipation major (2%) with all others at less than 0.5% incidence rate including rash, vertigo, headache, insomnia.

132
Q

gastric protectant class drug

A

sucralfate - Carafate

133
Q

Sucralfate

A

Sucrafate
1 g
Take 4 times a day on an empty stomach for 4-8 weeks.

134
Q

MOA of antacids

A

neutralize or reduce gastric acidity
protects gastric mucosa
increases gastric pH, inactivates pepsin
stimulates production of prostaglandins

135
Q

ADRs of antacids

A

GI - diarrhea, constipation, nausea/vomiting

136
Q

antacids class drug

A

aluminum/magnesium hydroxide (Maalox)

137
Q

Is sucralfate absorbed systemically?

A

No - goes in the mouth and out of the body.

138
Q

What does sodium bicarbonate do?

A

provides a bicarbonate ion which in turn neutralizes hydrogen ion concentrations.

139
Q

What does calcium carbonate do?

A

neutralizes gastric acid like aluminum and/or magnesium.

140
Q

What does a gastric protectant need to work?

A

An acidic environment - do not give with antacids

141
Q

What makes up sodium bicarbonate?

A

Formation of carbon dioxide and sodium chloride.

142
Q

What can sodium bicarbonate potentially effect?

A

It is well absorbed and has potential to affect blood pH and sodium levels.

143
Q

Compare calcium carbonate to sodium bicarbonate.

A

Calcium carbonate is less soluble and slower reacting than sodium bicarbonate.

144
Q

Aluminum/magnesium Hydroxide suspension

A

Aluminum/magnesium Hydroxide suspension

30 ml every 4 hours as needed for epigastric pain relief.

145
Q

MOA of prostaglandins

A

Synthetic prostaglandin E1 analog that replaces gastric prostaglandin.

Decreases gastric acid secretion.

146
Q

ADRs of prostaglandins

A

diarrhea
abdominal pain

*avoid use during pregnancy - miscarriage/spontaneous abortion

147
Q

prostaglandins class drug

A

misoprostol - Cytotec

148
Q

Cytotec

A

Cytotec
200 mcg
one tablet 4 times a day with food

149
Q

MOA of prokinetics

A

stimulation of release of acetylcholine at nerve ending to increase LES tone

improve esophageal peristalsis

150
Q

ADRs of prokinetics

A

CNS effects including restlessness, fatigue, drowsiness, mental depression at higher doses.

Neuroleptic malignant syndrome very rare.

151
Q

prokinetics class drug

A

metoclopramide - Reglan

152
Q

Metoclopramide

A

Metoclopramide
10 mg
one tablet 4 times a day 30 minutes before meals and at bedtime.

153
Q

How do antispasmodics work?

A

anticholinergic activity

154
Q

ADRs of antispasmodics

A

may cause drowsiness and/or blurred vision.

impair physical or mental abilities - patients must be cautioned about performing tasks which require mental alertness like operating machinery or driving.

155
Q

Antispasmodic products

A 
Clidinium
chlordiazepoxide - Librad
Hyoscyamine
atropine
scopolamine
phenobarbitol - Donnatal
156
Q

Regional bacterium (5 main genetic groups) that likely migrated from mice and sheep (European strains) and cats, pigs, and gerbils (Asian strains)

A

Helicobacter pylori

157
Q

How long does a h.pylori infection last?

A

Lifelong infection unless eradicated through drugs.

80% infected are asymptomatic
20% infected develop gastrointestinal disease

158
Q

Nearly 100% of duodenal ulcers, unless NSAID-induced or gastromas are associatd with…

A

H.pylori infection.

159
Q

If H.pylori is eradicated, duodenal ulcer rate recurrence…

A

… drops from 67% to 6%.

160
Q

How many approved H.pylori regimens exist?

A

multiple

161
Q

length of h.pylori eradication regimens

A

range from 10-14 days

162
Q

Most complicated h.pylori eradication regimen

A

PeptoBismol, metronidazole, and tetracycline all 4 times a day for 2 weeks and an H2 blocker for 4 weeks.

163
Q

Least complicated h.pylori eradication regimen

A

Prevacid, Biaxin, and amoxicillin twice a day for 10 days

164
Q

downside to h.pylori eradication

A

People carrying H.pylori have a higher risk of developing peptic ulcers and stomach cancer (and Barrett’s esophagus)

165
Q

People carrying H.pylori have a higher risk of developing peptic ulcers and stomach cancer (and Barrett’s esophagus) but…

A

They may also have a lower risk of acquiring diseases of the esophagus including esophageal adenocarcinoma which has been growing at a rate of 7-9% every year. Once diagnosed, 5 year survival is 10%.

Pharmacology II (9 decks)

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