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