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Gastroenterology > 317 PUD > Flashcards

317 PUD Flashcards

1
Q

Lowest dose of aspirin leading to GI bleed

A

Aspirin 75 mg per day

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2
Q

When to do endoscopy patient with GI bleed?

A

Most patients within 24 hours

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3
Q

When to do endoscopy in patient with GI bleed with hemodynamic compromise?

A

Stabilize then do endoscopy within 12 hours

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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)

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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

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6
Q

True or false. Majority of patient with peptic ulcer patients, about 90%, are asymptomatic

A

True.

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7
Q

location of 75% of the gastric glands

A

oxyntic mucosa

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8
Q

what are the gastric glands

A

mucous neck, parietel, chief, endocine, enterochromaffin, and enterochromaffin-like cells

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9
Q

where are pyloric glands located

A

antrum

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10
Q

what are the pyloric glands

A

mucous and endocrine cells

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11
Q

also known as the oxyntic cells

A

parietal cell

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12
Q

where does acid secretion occur

A

apical canalicular surface

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13
Q

what are the mucosal defense system

A

three level barrier composed of preepithelial, epithelial, and subepithelial elements

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14
Q

first line of defense

A

mucus bicarbonate phospholipid layer which serves as physiochemical barrier

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15
Q

what is mucus made of

A

90% water and 10% mixture of phospholipids and glycoproteins

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16
Q

second line of defense

A

surface epithelial cells

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17
Q

true or false. Surface epithelial cells generate heart and shock proteins that prevent protein denaturation

A

True.

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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.

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19
Q

refers to the migration of gastric epithelial cells to restore a damaged region

A

restitution

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20
Q

key component of the subepithelial defense/repair system providing HCO which neutralizes acid

A

elaborate microvascular system

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21
Q

play a central role in gastric epithelial defense/ repair

A

prostaglandins

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22
Q

contains abundant levels of prostaglandins

A

gastric mucosa

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23
Q

from where is prostaglandin derived

A

esterized arachidonic acid

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24
Q

controls the rate limiting step prostaglandin synthesis

A

cyclooxygenase

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25
Q

COX expressed in a host of tissues, including stomach, platelets, kidneys and endothelial cells

A

COX-1

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26
Q

COX inducible by inflammatory stimuli and is expressed in marcophages, leukocytes, fibroblasts and synovial cells

A

COX-2

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27
Q

Expounds the beneficial and toxicity effects of NSAIDs

A

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

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28
Q

have the potential of providing the beneficial effect of decreasing tissue inflammation while minimizing toxicity in the GI tract

A

COX-2 selective NSAIDs

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29
Q

NSAIDs removed from the market and the reason for removal

A

valdecoxib and rofecoxib due to adverse effect on cardiovascular system

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30
Q

important in the maintenance of gastric mucosal integrity

A

nitric oxide

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31
Q

referred to as microbiota

A

bacterial communities consisting of hundreds of phylotypes

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32
Q

two principal gastric secretory products capable of inducing mucosal injury

A

Hcl and pepsinogen

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33
Q

basal acid production is highest during and lowest during?

A

basal acid products is highest at night and lowest during morning hours

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34
Q

principal contributors to basal acid secretion

A

cholinergic input via the vagus nerve and histaminergic input from local gastric sources

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35
Q

three phases of gastric acid secretion

A

cephalic, gastric, intestinal

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36
Q

components of cephalic phase

A

sight, smell and taste of food

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37
Q

when is gastric phase activated

A

when food enters stomach

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38
Q

true or false. Distention of the stomach wall also leads to gastrin release and acid production

A

True.

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39
Q

what is the last phase of acid secretion and how is mediated

A

intestinal phase is initiated as food enters the intestines and is mediated by luminal distention and nutrient assimilation

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40
Q

appetite regulating hormone

A

Ghrelin

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41
Q

inihibit acid production both direct and indirectly

A

somatostatin

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42
Q

responsible for generating large concentrations of H

A

H K ATPase

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43
Q

synthesize and secrete pepsinogen

A

chief cell

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44
Q

what are ulcers

A

breaks in mucosal surface of more than 5 mm in size with depth to the submucosa

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45
Q

most common risk for PUD

A

H pylori and NSAIDs

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46
Q

where does duodenal ulcer commonly located

A

first portion of the duodenum 95% and 90% located within 3 cm of the pylorus

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47
Q

True or false. Malignant duodenal ulcer are common

A

False. Malignant DU are extremely rare.

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48
Q

True or false. Gastric ulcer can represent a malignancy and should biopsied upon discovery

A

True.

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49
Q

where are gastric ulcer often found

A

distal to the junction between the antrum and the acid secretory mucosa

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50
Q

Type of gastric ulcers. Associated with low gastric acid production

A

Type I. Occur in the gastric body and Type IV cardia.

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51
Q

Type of gastric ulcer. Gastric acid can vary from low to normal

A

Type II. Occur in the antrum

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52
Q

Type of gastric ulcer. Normal or high acid production. Associated with duodenal ulcers

A

Type III. 3 cm from the pylorus

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53
Q

Type of gastric ulcer. Low gastric production.

A

Type IV. Found in the cardia

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54
Q

organism that play a role in the development of MALT and gastric adenocarcinoma

A

H pylori

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55
Q

True or false. H Pylori resides in the antrum but over time migrates towards the proximal segments of the stomach

A

True.

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56
Q

first step in infection by H Pylori is dependent on what factors

A

bacteria’s motility and its ability to produce urease

57
Q

how is H Pylori trasmitted

A

person to person following an oral-oral or fecal -oral route

58
Q

True or false. H pylori infection is virtually always associated with chronic active gastritis

A

True.

59
Q

True or false. Smoking appears to decrease healing rates, impair response to therapy and increase ulcer-related complications such as perforation

A

True.

60
Q

potential susceptibility genes for NSAID induced PUD

A

cytochrome P450 2C9 and 2C8

61
Q

chronic disorders to have strong association with PUD

A

advanced age, chronic pulmonary disease, chronic renal failure, cirrhosis, nephrolithiasis, alpha 1 antitrypsin deficiency, systemic mastocytosis

62
Q

predominant causes of PUD

A

H pylori infection and NSAIDs

63
Q

True or false. Abdominal pain has poor predictive value for presence of either DU and GU

A

True.

64
Q

typical pain patter in DU

A

Occurs 90 mins to 3 hours after a meal and frequently relieved by antacids and food

65
Q

most discriminating symptom of duodenal ulcer

A

pain that awakes the patient from sleep between midnight and 3 AM

66
Q

typical pain patter in GU

A

discomfort precipitated by food

67
Q

most frequent finding in patients with GU and DU

A

epigastric pain, right of midline

68
Q

presence of what indicates retained fluid in the stomach and what does it suggest

A

succussion splash suggesting of gastric outlet obstruction

69
Q

most common complication observed in PUD

A

GI bleeding

70
Q

second most common ulcer related complications

A

perforation

71
Q

True or false. DU tend to penetrate posteriorly into the pancreas leading to pancreatitis

A

True.

72
Q

Where does GU tend to penetrate

A

penetrate into the left hepatic lobe

73
Q

least common ulcer related complication

A

gastric outlet obstruction

74
Q

refers to a group of heterogeneous disorders typified by upper abdominal pain without presence of ulcer

A

functional dyspepsia or essential dyspepsia

75
Q

two subcategories of functional dyspepsia

A

postprandial distress syndrome and epigastric pain syndrome

76
Q

True or false. Ulcers more than 3 cm in size or those associated with a mass are more often malignant

A

True.

77
Q

Provides the most sensitive and specific approach for examining the upper GI tract

A

Endoscopy

78
Q

3 types of studies for H Pylori

A

serologic, urea breath tests and fecal H pylori test

79
Q

False negative with recent use of PPI, antibiotics or bismuth compounds

A

rapid urease

80
Q

test for detection of H pylori. Inexpensive. Not useful for early follow up

A

serology

81
Q

test for detection of H pylori. Simple. Rapid. Useful for early follow up

A

Urea breath test

82
Q

test for detection of H pylori. Inexpensive. Conventient

A

stool antigen

83
Q

antacid that can produce constipation and phosphate depletion

A

aluminum hydroxide

84
Q

antacid that may cause loose stools

A

magnesium hydroxide

85
Q

effect of long term use of calcium carbonate

A

milk alkali syndrome

86
Q

effect of long term use of sodium bicarbonate

A

systemic alkalosis

87
Q

first H2 receptor antagonist used for the treatment of acid peptic ulcer

A

cimetidine

88
Q

side effect of cimetidine

A

reversible gynecomastia and impotense

89
Q

systemic toxicities of H2 receptor antagonist

A

pancytopenia, neutropenia, anemia and thrombocytopenia

90
Q

H2 receptor antagonist that bind to cytochrom P450

A

cimetidine and ranitidine

91
Q

H2 receptor antagonists that does not bind to hepatic cytochrome P450

A

famotidine and nizatidine

92
Q

substituted benzimadole derivatives that covalently bind and irreversible inhibit the H K ATPase

A

PPI such as omeprazole, esomeprazole, lansoprazole, rabeprazole, and pantoprazole

93
Q

S enantiomer of omeprazole

A

esomeprazole

94
Q

R isomer of lansoprazole

A

dexlansoprazole

95
Q

most potent acid inhibitory agents available

A

PPIs

96
Q

longest PPIs and are both acid labile

A

omeprazole and lansoprazole

97
Q

pH PPIs are absorbed

A

pH of 6

98
Q

advantageous for patient with dyphagia as it comes in oral disintegrating tablet and can be taken with to without water

A

lansoprazole

99
Q

purpose of sodium bicarbonate in omeprazole

A

protect omeprazole from acid degradation and to promote rapid gastric alkalinization

100
Q

half life of PPIs

A

about 18 hours

101
Q

when gastric secretion to return to normal after cessation of PPIs

A

2-5 days before gastric secretion returns to normal

102
Q

True or false. PPI efficacy is maximized if they are administered before a meal

A

True.

103
Q

PPIs that do not inhibit hepatic cytochrome P450

A

rabeprazole, pantoprazole, esomeprazole

104
Q

Long term acid suppression esp with PPI has been associated with a higher incidence of what diseases

A

CAP and clostridium difficile associated disease

105
Q

True or false. PPIs may exert negative effect on antiplatelet effect of clopidogrel

A

True.

106
Q

Mechanism on the negative effect of PPI on clopidogrel

A

competition of PPI and clopidogrel with the same cytochome P450 (CYP2C19)

107
Q

hour separation between administration of clopidogrel and PPI

A

12 hour separation; PPI 30 mins before breakfast and clopidogrel at bedtime

108
Q

PPI containing imidazopyridine ring instead of the benzimidazole ring

A

tentoprazole, irreversible proton pump inhibition

109
Q

examples of potassium competitive acid pump antagonist (P-CAB)

A

revaprazan and venoprazan

110
Q

complex sucrose salt in which the hydroxyl groups have been substituted by aluminum hydroxide and sulfate

A

sucralfate

111
Q

most common toxicity of sucralfate

A

constipation

112
Q

mechanism of action of sucralfate

A
  1. physiochemical barrier
  2. stimulation mucus
  3. promoting trophic action by binding growth factors
  4. enhancing mucosal repair and defense
113
Q

standard dosing of sucralfate

A

sucralfate 1 gram QID

114
Q

short adverse effect of bismuth

A

black stool and darkening of the tongue

115
Q

most common side effect of prostaglandin analogues

A

diarrhea

116
Q

mechanism of action of prostaglandin analogues

A

enhancement of mucosal defense and repair

117
Q

provides the greatest efficacy in eradicating H pylori

A

14 days combination therapy

118
Q

two prepacked H pylori regimens

A

Prevpac (lansoprazole, clarithromycin, amoxicillin) 2x a day

Helidac (BBS, tetracycline, metronidazole) 4x a day

119
Q

What are the recommended first line therapies for H pylori infection

A 
8 regimens
Clarithromycin triple
Bismuth quadruple
Concomitant
Sequential
Hybrid
Levofloxacin triple
Levofloxacin sequential
LOAD
120
Q

Clarithomycin triple

A

PPI
Clarithomycin 500 mg
Amoxicillin 1 gram or metronidazole 500 mg TID

121
Q

Bismuth quadruple

A

PPI
Bismuth 120–300 mg QID
Tetracycline 500 mg QID
Metronidazole 250 mg QID 500 mg TID

122
Q

Concomitant

A

PPI BID
clarithromycin 500 mg
Amoxicillin 1 g
nitroimidazole 500 mg

123
Q

Sequential

A

PPI BID x 5-7 days

PPI, Clarithromycin Nitroimidazole BID x 5-7 days

124
Q

Hybrid

A

PPI + Amox 1 gram BIX x 7 days

PPI, Amox, Clarithromycin , nitroimidazole

125
Q

Levofloxacin triple

A

PPI + Amox 1 g BID x 5-7 days
Levofloxacin 500 mg QD
Amox 1 g

126
Q

Levofloxacin sequential

A

PPI + Amox 1 g IX x 5-7 days

PPI + Amox + Levox 500 mg OD, Nitroimidazole BID x 5-7 days

127
Q

LOAD

A

Levofloxacin 250 mg QD
PPI double dose
Nitazoxanide 500 mg BID
Doxycyline 100 mg QD

128
Q

FDA approved first line treatment for H Pylori infection

A

clarithomycin triple

129
Q

most feared complication of amoxicillin

A

pseudomembranous colitis

130
Q

True or false. Concomitant use of probiotics may ameliorate some of the antibiotic side effects

A

True

131
Q

most common cause for treatment failure in compliant patients

A

antibiotic resistant strains

132
Q

Next step in failure of triple therapy

A

salvage therapy

133
Q

what are the the salvage therapies for H Pylori

A 
bismuth quadruple
levofloxacin triple
Concomitant
Rifabutin triple
high dose dual
134
Q

salvage therapy. bismuth quadruple

A

PPI
Bismuth 120–300 mg QID
Tetracycline 500 mg QID
Metronidazole 250 mg QID 500 mg TID

135
Q

salvage therapy. Levofloxacin triple.

A

PPI + Amox 1 g BID
Levofloxacin 500 mg QD
Amox 1 g
x 14 days

136
Q

salvage therapy. Concomitant

A 
PPI BID
clarithromycin 500 mg BID
Amoxicillin 1 g BID
nitroimidazole 500 mg BID or TID
x 10-14 days
137
Q

salvage therapy. rifabutin triple.

A

PPI BID
rifabutin 300 mg QD
Amox 1 g
x 10 days

138
Q

salvage therapy. High-dose dual

A

PPI TID or QID
Amox 1 g TID or 750 mg QID
x 14 days

Gastroenterology (13 decks)

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