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.
2
Q
How are intermittent dyspeptic symptoms treated?
A
antacids
OTC H2 antagonists
3
Q
intermittent dyspeptic symptoms
A
occasional bloating
fullness
abdominal pain
heartburn
4
Q
What are intermittent dyspeptic symptoms associated with?
A
overeating or drinking or consumption of certain foods
5
Q
abdominal pain similar to gastritis, gastric ulcers or duodenal ulcers without demonstrable ulceration
A
non-ulcer dyspepsia
6
Q
What is non-ulcer dyspepsia associated with?
A
GI motility abnormalities
7
Q
How is non-ulcer dyspepsia treated?
A
antacids
OTC H2 antagonists
Rx H2 antagonists
8
Q
epigastric pain that can be accompanied by nausea/vomiting resulting from diffuse inflammation of the stomach
A
gastritis
9
Q
What is gastritis usually caused by?
A
H pylori
10
Q
How is gastritis treated?
A
discontinue NSAIDs
Antacids
OTC/Rx H2 antagonists
Antibacterial regimen
11
Q
diffuse gastric pain typically 1-3 hours after eating distinct ulcerations in stomach
A
gastric ulcers
12
Q
symptoms of gastric ulcers
A
ulcerations in stomach
nausea/vomiting
belching
anorexia
13
Q
How are gastric ulcers treated?
A
Discontinue NSAIDs Rx H2 antagonists Proton Pump Inhibitor Antibacterial regimen Misoprostol
14
Q
diffuse epigastric pain typically with empty stomach
A
duodenal ulcers
15
Q
What relieves duodenal ulcers?
A
eating
16
Q
treatment of duodenal ulcers
A
discontinue NSAIDs Rx H2 antagonists proton pump inhibitors antibacterial regimen succralfate
17
Q
symptoms of GERD
A
range from occasional heartburn to persistant burning substernal pain
18
Q
treatment of GERD
A
antacids
OTC/Rx H2 antagonists
proton pump inhibitors
prokinetic agents
19
Q
GERD alarm symptoms
A
dysphagia
odynophagia
anemia
weight loss
20
Q
classic symptoms of GERD
A
heartburn
regurgitation
water brash
21
Q
What is the treatment if a patient complains of alarm symptoms of GERD?
A
immediate upper endoscopy
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
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
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.
25
GERD treatment - Ulceration
consider causes of ulceration; e.g. acid
Peptic disease
viral or fungal infection
neoplasia
26
GERD treatment - erosive esophagitis
Intensify proton pump inhibitor therapy
27
GERD treatment - Barrett's esophagus
If dysphagia at initial endoscopy without inflammation, discuss utility of enrollment in endoscopic surveillance program.
28
GERD treatment - cancer
Referral to appropriate oncological service
29
GERD treatment - normal
Consider 24-hour pH probe to identify nonerosive reflux.
| Consider other causes of symptoms.
30
Sporadic uncomplicated heartburn, often in setting of known precipitating factor. Often not chief complaint. No additional symptoms
Stage I GERD
31
How many episodes per week are seen with Stage I GERD?
Less than 2-3.
32
Medical Management of Stage I GERD
Lifestyle modification, including diet, positional changes, weight loss, etc.
Antacids and/or histamine H2 receptor antagonists as needed.
33
Frequent symptoms with or without esophagitis.
Stage II GERD
34
How many episodes per week are seen in Stage II GERD?
More than 2-3.
35
Treatment of Stage II GERD
Proton pump inhibitors more effective than histamine H2 receptor antagonists
36
Chronic, unrelenting symptoms; immediate relapse off therapy. Esophageal complications (e.g., stricture, Barrett's metaplasia)
Stage III GERD
37
Treatment of Stage III GERD
Proton pump inhibitor either once or twice daily
38
Proton Pump Inhibitors
```
Omeprazole (Prilosec)
Esomeprazole (Nexium)
Lonsoprazole (Prevacid)
Pantoprazole (Protonix)
Rabeprazole (Aciphex)
Dexlansoprazole (Dexilant)
```
39
What do PPIs act on?
Parietal Cell - decreases production of acid.
40
Increasing acetylcholine in the stomach...
... increases the action of the parietal cells which increases acid production causing nausea.
41
What creates a mucous layer around the cells allowing them to have a pH of 7?
Prostogandins
42
Number 1 best selling drug in the US?
Esomeprazole - Nexium
43
Tmax of Prilosec
1-3 hours
44
Tmax of Prevacid
1.7 hours
45
Tmax of Aciphex
3.1 hours
46
Tmax of Nexium
1.6 hours
47
Tmax of Protonix
2-4 hours
48
Half-life of Prilosec
0.5-3 hours
49
Half-life of Prevacid
1-2 hours
50
Half-life of Aciphex
1-2 hours
51
Where do PPIs work?
Hydrogen - Potassium - ATPase pump
52
Half-life of Nexium
1.4 hours
53
Half-life of Protonix
1-1.9 hours
54
Binding of Prilosec
95%
55
Binding of Prevacid
99%
56
Binding of Aciphex
96%
57
Binding of Nexium
97%
58
Binding of Protonix
98%
59
Clearance of the PPIs is completed by
the Liver
60
Bioavailability of Prilosec
40-60%
61
Bioavailability of Prevacid
85%
62
The PPIs are pro-drugs which means...
they are not activated until they reach the stomach. DO NOT open up/crush capsule/pill.
63
Bioavailability of Aciphex
52%
64
Bioavailability of Nexium
90%
65
Bioavailability of Protonix
77%
66
Dosage form(s) of Prilosec
Capsule
67
Dosage form(s) of Prevacid
Capsule/Tab
68
Dosage form(s) of Aciphex
Tablet
69
Dosage form(s) of Nexium
Capsule / IV
70
Dosage form(s) of Protonix
Tablet / IV
71
Indications for Prilosec
```
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
Indications for Prevacid
```
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
Indications for Aciphex
Short-term duodenal ulcer
Short-term erosive esophagitis
Maitenance-erosive esophagitis
Pathological hypersecretory disorders
74
Indications for Nexium
H.Pylori eradication
Short-term-symptomatic GERD
Short-term erosive esophagitis
Manitenance-erosive esophagitis
75
How long does it take for PPIs to work?
3-4 days
76
Indications for Protonix
Short-term erosive esophagitis
Maintenance-erosive esophagitis
Pathological hypersecretory disorders
77
Acid levels peak...
at meal times and during the night
78
Where to H2 blockers work well for acid inhibition?
Overnight acid production. Less successful for acid suppression around mealtimes.
79
Which drugs work best for acid suppression?
PPIs
80
True or False: PPIs are effected by first-pass metabolism
True
81
True or False: PPIs are renally excreted and must be adjusted.
False
82
What is the relationship between PPIs and fracture risk?
fracture risk in increased
83
What is the relationship between PPIs and clopidogrel?
PPIs interfere with a necessary metabolic step for clopidogrel. Effects 2C19. Increases clotting risk.
84
What is the relationship between PPIs and C.Diff?
May be associated with an increased risk of clostridium difficile - associated diarrhea.
85
What are PPIs not approved for?
use of treatment of upper GI bleeding
86
What PPI IV forms are available for quicker onset?
Protonix IV
| Nexium IV
87
Physiologic activity at pH >3.5
decreased incidence of stress-induced bleeding
88
Physiologic activity at pH >4
Target pH- prevention of stress-related mucosal bleeding.
89
Physiologic activity at pH >4.5
Pepsin inactivation
90
Physiologic activity at pH 5
99.9% acid neutralization
91
Where do you want the pH of the stomach for a GI bleed?
between 5.1 and 7
92
Physiologic activity at pH 5.1 to 7
Alterations in caogulation and platelet aggregation
93
Physiologic activity at pH >6
Target pH - prevention of peptic ulcer reoccurrence
94
Physiologic activity at pH >7
Potential decrease in incidence of rebleeding.
95
Physiologic activity at pH >8
Pepsin destruction
96
Which PPIs have less drug interactions?
Prevacid & Protonix
97
ADRs of PPIs
Diarrhea
Abdominal pain
Headache
Dizziness
98
Possible long-term effects of PPIs
Inhibition of calcium absorption
| Rise in gastrin levels
99
Omeprazole
Omeprazole
20 mg
One capsule one daily
100
Proton Pump Inhibitor Rx to know
Omeprazole
101
H2 Receptor Antagonists
Cimetidine - Tagamet
Ranitidine - Zantac
Famotidine - Pepcid
Nizatidine - Axid
102
Bioavailability of Cimetidine
~60%
103
Bioavailability of Ranitidine
50%
104
Bioavailability of Famotidine
40-45%
105
Bioavailability of Nizatidine
>70%
106
Tmax of Cimetidine
0.75 to 1.5
107
Tmax Rantidine
2-3
108
Tmax of Famotidine
1-3
109
Tmax of Nizatidine
0.5 - 3
110
Instead of dosing a PPI twice a day...
... do a PPI in the morning and an H2 inhibitor at night.
111
Cmax of Cimetidine
2-3
112
Cmax of Ranitidine
0.44 - 0.55
113
Cmax of Nizatidine
0.7 - 1.8
114
Half-life of Cimetidine
~2
115
Half-life of Ranitidine
2.5-3
116
Half-life of Famotidine
2.5 - 3.5
117
Half-life of Nizatidine
1-2
118
Indications for Cimetidine
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
Indications for Rantidine
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
Indications for Famotidine
Maitenance therapy and treatment of duodenal ulcer.
Treatment of GERD.
Treatment of active benign gastric ulcer.
Treatment of pathological hypersecretory conditions.
121
Indications for Nizatidine
Treatment of maintenance of duodenal ulcer.
Treatment of benign gastric ulcer.
Treatment of GERD.
122
Do H2-receptor antagonists require renal dosing adjustment?
Yes (look up thresholds in book)
123
What are the differences between the Rx and OTC H2-blockers?
10 hours of 50% acid inhibition at Rx dosing.
| Less than 6 hours of 50% acid inhibition at OTC dosing.
124
MOA of H2 receptor antagonists
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
H2 receptor antagonists are usually dosed twice per day. In what instance would they be dosed once per day?
If given in the evening in combination with a PPI. Double the dose of the H2 receptor antagonist.
126
ADRs of H2 receptor antagonists
Mental status changes - cimetidine; critical care; intravenous.
Thrombocytopenia.
Endocrine issues - cimetidine.
127
What is a common drug interaction with H2 receptor antagonists?
Cimetidine
128
Hw receptor antagonist to know
Famotidine
129
Famotidine
Famotidine
20 mg
one tablet twice a day
130
MOA of gastric protectant
complexes with protein-like exudate located at ulcerations.
Covers ulcer area.
131
ADRs of gastric protectant
Constipation major (2%) with all others at less than 0.5% incidence rate including rash, vertigo, headache, insomnia.
132
gastric protectant class drug
sucralfate - Carafate
133
Sucralfate
Sucrafate
1 g
Take 4 times a day on an empty stomach for 4-8 weeks.
134
MOA of antacids
neutralize or reduce gastric acidity
protects gastric mucosa
increases gastric pH, inactivates pepsin
stimulates production of prostaglandins
135
ADRs of antacids
GI - diarrhea, constipation, nausea/vomiting
136
antacids class drug
aluminum/magnesium hydroxide (Maalox)
137
Is sucralfate absorbed systemically?
No - goes in the mouth and out of the body.
138
What does sodium bicarbonate do?
provides a bicarbonate ion which in turn neutralizes hydrogen ion concentrations.
139
What does calcium carbonate do?
neutralizes gastric acid like aluminum and/or magnesium.
140
What does a gastric protectant need to work?
An acidic environment - do not give with antacids
141
What makes up sodium bicarbonate?
Formation of carbon dioxide and sodium chloride.
142
What can sodium bicarbonate potentially effect?
It is well absorbed and has potential to affect blood pH and sodium levels.
143
Compare calcium carbonate to sodium bicarbonate.
Calcium carbonate is less soluble and slower reacting than sodium bicarbonate.
144
Aluminum/magnesium Hydroxide suspension
Aluminum/magnesium Hydroxide suspension
| 30 ml every 4 hours as needed for epigastric pain relief.
145
MOA of prostaglandins
Synthetic prostaglandin E1 analog that replaces gastric prostaglandin.
Decreases gastric acid secretion.
146
ADRs of prostaglandins
diarrhea
abdominal pain
*avoid use during pregnancy - miscarriage/spontaneous abortion
147
prostaglandins class drug
misoprostol - Cytotec
148
Cytotec
Cytotec
200 mcg
one tablet 4 times a day with food
149
MOA of prokinetics
stimulation of release of acetylcholine at nerve ending to increase LES tone
improve esophageal peristalsis
150
ADRs of prokinetics
CNS effects including restlessness, fatigue, drowsiness, mental depression at higher doses.
Neuroleptic malignant syndrome very rare.
151
prokinetics class drug
metoclopramide - Reglan
152
Metoclopramide
Metoclopramide
10 mg
one tablet 4 times a day 30 minutes before meals and at bedtime.
153
How do antispasmodics work?
anticholinergic activity
154
ADRs of antispasmodics
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
Antispasmodic products
```
Clidinium
chlordiazepoxide - Librad
Hyoscyamine
atropine
scopolamine
phenobarbitol - Donnatal
```
156
Regional bacterium (5 main genetic groups) that likely migrated from mice and sheep (European strains) and cats, pigs, and gerbils (Asian strains)
Helicobacter pylori
157
How long does a h.pylori infection last?
Lifelong infection unless eradicated through drugs.
80% infected are asymptomatic
20% infected develop gastrointestinal disease
158
Nearly 100% of duodenal ulcers, unless NSAID-induced or gastromas are associatd with...
H.pylori infection.
159
If H.pylori is eradicated, duodenal ulcer rate recurrence...
... drops from 67% to 6%.
160
How many approved H.pylori regimens exist?
multiple
161
length of h.pylori eradication regimens
range from 10-14 days
162
Most complicated h.pylori eradication regimen
PeptoBismol, metronidazole, and tetracycline all 4 times a day for 2 weeks and an H2 blocker for 4 weeks.
163
Least complicated h.pylori eradication regimen
Prevacid, Biaxin, and amoxicillin twice a day for 10 days
164
downside to h.pylori eradication
People carrying H.pylori have a higher risk of developing peptic ulcers and stomach cancer (and Barrett's esophagus)
165
People carrying H.pylori have a higher risk of developing peptic ulcers and stomach cancer (and Barrett's esophagus) but...
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%.
