317 PUD Flashcards
(138 cards)
1
Q
Lowest dose of aspirin leading to GI bleed
A
Aspirin 75 mg per day
2
Q
When to do endoscopy patient with GI bleed?
A
Most patients within 24 hours
3
Q
When to do endoscopy in patient with GI bleed with hemodynamic compromise?
A
Stabilize then do endoscopy within 12 hours
4
Q
What is the hemoglobin threshold to do blood transfusion?
A
Hemoglobin less than 7 mg/dl if without cardiac or respiratory compromise
Hemoglobin less than 10 mg/dl if with cardiac or Respiratory compromise (heart attack)
5
Q
disruption in the mucosal integrity of the stomach and duodenum leading to local defect or excavation due to active inflammation
A
peptic ulcer
6
Q
True or false. Majority of patient with peptic ulcer patients, about 90%, are asymptomatic
A
True.
7
Q
location of 75% of the gastric glands
A
oxyntic mucosa
8
Q
what are the gastric glands
A
mucous neck, parietel, chief, endocine, enterochromaffin, and enterochromaffin-like cells
9
Q
where are pyloric glands located
A
antrum
10
Q
what are the pyloric glands
A
mucous and endocrine cells
11
Q
also known as the oxyntic cells
A
parietal cell
12
Q
where does acid secretion occur
A
apical canalicular surface
13
Q
what are the mucosal defense system
A
three level barrier composed of preepithelial, epithelial, and subepithelial elements
14
Q
first line of defense
A
mucus bicarbonate phospholipid layer which serves as physiochemical barrier
15
Q
what is mucus made of
A
90% water and 10% mixture of phospholipids and glycoproteins
16
Q
second line of defense
A
surface epithelial cells
17
Q
true or false. Surface epithelial cells generate heart and shock proteins that prevent protein denaturation
A
True.
18
Q
True or false.epithelial cells also generate trefoil factor family peptides and cathelicidins which play a role in surface cell production
A
True.
19
Q
refers to the migration of gastric epithelial cells to restore a damaged region
A
restitution
20
Q
key component of the subepithelial defense/repair system providing HCO which neutralizes acid
A
elaborate microvascular system
21
Q
play a central role in gastric epithelial defense/ repair
A
prostaglandins
22
Q
contains abundant levels of prostaglandins
A
gastric mucosa
23
Q
from where is prostaglandin derived
A
esterized arachidonic acid
24
Q
controls the rate limiting step prostaglandin synthesis
A
cyclooxygenase
25
COX expressed in a host of tissues, including stomach, platelets, kidneys and endothelial cells
COX-1
26
COX inducible by inflammatory stimuli and is expressed in marcophages, leukocytes, fibroblasts and synovial cells
COX-2
27
Expounds the beneficial and toxicity effects of NSAIDs
beneficial effects: inhibition of COX-2 leads to reduction of inflammation toxic effect: inhibition of COX-1 isoform leading to GI mucosal ulceration and renal dysfunction
28
have the potential of providing the beneficial effect of decreasing tissue inflammation while minimizing toxicity in the GI tract
COX-2 selective NSAIDs
29
NSAIDs removed from the market and the reason for removal
valdecoxib and rofecoxib due to adverse effect on cardiovascular system
30
important in the maintenance of gastric mucosal integrity
nitric oxide
31
referred to as microbiota
bacterial communities consisting of hundreds of phylotypes
32
two principal gastric secretory products capable of inducing mucosal injury
Hcl and pepsinogen
33
basal acid production is highest during and lowest during?
basal acid products is highest at night and lowest during morning hours
34
principal contributors to basal acid secretion
cholinergic input via the vagus nerve and histaminergic input from local gastric sources
35
three phases of gastric acid secretion
cephalic, gastric, intestinal
36
components of cephalic phase
sight, smell and taste of food
37
when is gastric phase activated
when food enters stomach
38
true or false. Distention of the stomach wall also leads to gastrin release and acid production
True.
39
what is the last phase of acid secretion and how is mediated
intestinal phase is initiated as food enters the intestines and is mediated by luminal distention and nutrient assimilation
40
appetite regulating hormone
Ghrelin
41
inihibit acid production both direct and indirectly
somatostatin
42
responsible for generating large concentrations of H
H K ATPase
43
synthesize and secrete pepsinogen
chief cell
44
what are ulcers
breaks in mucosal surface of more than 5 mm in size with depth to the submucosa
45
most common risk for PUD
H pylori and NSAIDs
46
where does duodenal ulcer commonly located
first portion of the duodenum 95% and 90% located within 3 cm of the pylorus
47
True or false. Malignant duodenal ulcer are common
False. Malignant DU are extremely rare.
48
True or false. Gastric ulcer can represent a malignancy and should biopsied upon discovery
True.
49
where are gastric ulcer often found
distal to the junction between the antrum and the acid secretory mucosa
50
Type of gastric ulcers. Associated with low gastric acid production
Type I. Occur in the gastric body and Type IV cardia.
51
Type of gastric ulcer. Gastric acid can vary from low to normal
Type II. Occur in the antrum
52
Type of gastric ulcer. Normal or high acid production. Associated with duodenal ulcers
Type III. 3 cm from the pylorus
53
Type of gastric ulcer. Low gastric production.
Type IV. Found in the cardia
54
organism that play a role in the development of MALT and gastric adenocarcinoma
H pylori
55
True or false. H Pylori resides in the antrum but over time migrates towards the proximal segments of the stomach
True.
56
first step in infection by H Pylori is dependent on what factors
bacteria's motility and its ability to produce urease
57
how is H Pylori trasmitted
person to person following an oral-oral or fecal -oral route
58
True or false. H pylori infection is virtually always associated with chronic active gastritis
True.
59
True or false. Smoking appears to decrease healing rates, impair response to therapy and increase ulcer-related complications such as perforation
True.
60
potential susceptibility genes for NSAID induced PUD
cytochrome P450 2C9 and 2C8
61
chronic disorders to have strong association with PUD
advanced age, chronic pulmonary disease, chronic renal failure, cirrhosis, nephrolithiasis, alpha 1 antitrypsin deficiency, systemic mastocytosis
62
predominant causes of PUD
H pylori infection and NSAIDs
63
True or false. Abdominal pain has poor predictive value for presence of either DU and GU
True.
64
typical pain patter in DU
Occurs 90 mins to 3 hours after a meal and frequently relieved by antacids and food
65
most discriminating symptom of duodenal ulcer
pain that awakes the patient from sleep between midnight and 3 AM
66
typical pain patter in GU
discomfort precipitated by food
67
most frequent finding in patients with GU and DU
epigastric pain, right of midline
68
presence of what indicates retained fluid in the stomach and what does it suggest
succussion splash suggesting of gastric outlet obstruction
69
most common complication observed in PUD
GI bleeding
70
second most common ulcer related complications
perforation
71
True or false. DU tend to penetrate posteriorly into the pancreas leading to pancreatitis
True.
72
Where does GU tend to penetrate
penetrate into the left hepatic lobe
73
least common ulcer related complication
gastric outlet obstruction
74
refers to a group of heterogeneous disorders typified by upper abdominal pain without presence of ulcer
functional dyspepsia or essential dyspepsia
75
two subcategories of functional dyspepsia
postprandial distress syndrome and epigastric pain syndrome
76
True or false. Ulcers more than 3 cm in size or those associated with a mass are more often malignant
True.
77
Provides the most sensitive and specific approach for examining the upper GI tract
Endoscopy
78
3 types of studies for H Pylori
serologic, urea breath tests and fecal H pylori test
79
False negative with recent use of PPI, antibiotics or bismuth compounds
rapid urease
80
test for detection of H pylori. Inexpensive. Not useful for early follow up
serology
81
test for detection of H pylori. Simple. Rapid. Useful for early follow up
Urea breath test
82
test for detection of H pylori. Inexpensive. Conventient
stool antigen
83
antacid that can produce constipation and phosphate depletion
aluminum hydroxide
84
antacid that may cause loose stools
magnesium hydroxide
85
effect of long term use of calcium carbonate
milk alkali syndrome
86
effect of long term use of sodium bicarbonate
systemic alkalosis
87
first H2 receptor antagonist used for the treatment of acid peptic ulcer
cimetidine
88
side effect of cimetidine
reversible gynecomastia and impotense
89
systemic toxicities of H2 receptor antagonist
pancytopenia, neutropenia, anemia and thrombocytopenia
90
H2 receptor antagonist that bind to cytochrom P450
cimetidine and ranitidine
91
H2 receptor antagonists that does not bind to hepatic cytochrome P450
famotidine and nizatidine
92
substituted benzimadole derivatives that covalently bind and irreversible inhibit the H K ATPase
PPI such as omeprazole, esomeprazole, lansoprazole, rabeprazole, and pantoprazole
93
S enantiomer of omeprazole
esomeprazole
94
R isomer of lansoprazole
dexlansoprazole
95
most potent acid inhibitory agents available
PPIs
96
longest PPIs and are both acid labile
omeprazole and lansoprazole
97
pH PPIs are absorbed
pH of 6
98
advantageous for patient with dyphagia as it comes in oral disintegrating tablet and can be taken with to without water
lansoprazole
99
purpose of sodium bicarbonate in omeprazole
protect omeprazole from acid degradation and to promote rapid gastric alkalinization
100
half life of PPIs
about 18 hours
101
when gastric secretion to return to normal after cessation of PPIs
2-5 days before gastric secretion returns to normal
102
True or false. PPI efficacy is maximized if they are administered before a meal
True.
103
PPIs that do not inhibit hepatic cytochrome P450
rabeprazole, pantoprazole, esomeprazole
104
Long term acid suppression esp with PPI has been associated with a higher incidence of what diseases
CAP and clostridium difficile associated disease
105
True or false. PPIs may exert negative effect on antiplatelet effect of clopidogrel
True.
106
Mechanism on the negative effect of PPI on clopidogrel
competition of PPI and clopidogrel with the same cytochome P450 (CYP2C19)
107
hour separation between administration of clopidogrel and PPI
12 hour separation; PPI 30 mins before breakfast and clopidogrel at bedtime
108
PPI containing imidazopyridine ring instead of the benzimidazole ring
tentoprazole, irreversible proton pump inhibition
109
examples of potassium competitive acid pump antagonist (P-CAB)
revaprazan and venoprazan
110
complex sucrose salt in which the hydroxyl groups have been substituted by aluminum hydroxide and sulfate
sucralfate
111
most common toxicity of sucralfate
constipation
112
mechanism of action of sucralfate
1. physiochemical barrier
2. stimulation mucus
3. promoting trophic action by binding growth factors
4. enhancing mucosal repair and defense
113
standard dosing of sucralfate
sucralfate 1 gram QID
114
short adverse effect of bismuth
black stool and darkening of the tongue
115
most common side effect of prostaglandin analogues
diarrhea
116
mechanism of action of prostaglandin analogues
enhancement of mucosal defense and repair
117
provides the greatest efficacy in eradicating H pylori
14 days combination therapy
118
two prepacked H pylori regimens
Prevpac (lansoprazole, clarithromycin, amoxicillin) 2x a day
| Helidac (BBS, tetracycline, metronidazole) 4x a day
119
What are the recommended first line therapies for H pylori infection
```
8 regimens
Clarithromycin triple
Bismuth quadruple
Concomitant
Sequential
Hybrid
Levofloxacin triple
Levofloxacin sequential
LOAD
```
120
Clarithomycin triple
PPI
Clarithomycin 500 mg
Amoxicillin 1 gram or metronidazole 500 mg TID
121
Bismuth quadruple
PPI
Bismuth 120--300 mg QID
Tetracycline 500 mg QID
Metronidazole 250 mg QID 500 mg TID
122
Concomitant
PPI BID
clarithromycin 500 mg
Amoxicillin 1 g
nitroimidazole 500 mg
123
Sequential
PPI BID x 5-7 days
| PPI, Clarithromycin Nitroimidazole BID x 5-7 days
124
Hybrid
PPI + Amox 1 gram BIX x 7 days
| PPI, Amox, Clarithromycin , nitroimidazole
125
Levofloxacin triple
PPI + Amox 1 g BID x 5-7 days
Levofloxacin 500 mg QD
Amox 1 g
126
Levofloxacin sequential
PPI + Amox 1 g IX x 5-7 days
| PPI + Amox + Levox 500 mg OD, Nitroimidazole BID x 5-7 days
127
LOAD
Levofloxacin 250 mg QD
PPI double dose
Nitazoxanide 500 mg BID
Doxycyline 100 mg QD
128
FDA approved first line treatment for H Pylori infection
clarithomycin triple
129
most feared complication of amoxicillin
pseudomembranous colitis
130
True or false. Concomitant use of probiotics may ameliorate some of the antibiotic side effects
True
131
most common cause for treatment failure in compliant patients
antibiotic resistant strains
132
Next step in failure of triple therapy
salvage therapy
133
what are the the salvage therapies for H Pylori
```
bismuth quadruple
levofloxacin triple
Concomitant
Rifabutin triple
high dose dual
```
134
salvage therapy. bismuth quadruple
PPI
Bismuth 120--300 mg QID
Tetracycline 500 mg QID
Metronidazole 250 mg QID 500 mg TID
135
salvage therapy. Levofloxacin triple.
PPI + Amox 1 g BID
Levofloxacin 500 mg QD
Amox 1 g
x 14 days
136
salvage therapy. Concomitant
```
PPI BID
clarithromycin 500 mg BID
Amoxicillin 1 g BID
nitroimidazole 500 mg BID or TID
x 10-14 days
```
137
salvage therapy. rifabutin triple.
PPI BID
rifabutin 300 mg QD
Amox 1 g
x 10 days
138
salvage therapy. High-dose dual
PPI TID or QID
Amox 1 g TID or 750 mg QID
x 14 days
