PUD Flashcards
3 common forms of PUD
H. pylori positive
NSAID-induced
Stress related mucosal damage
H. pylori site of damage
duodenum
NSAID site of damage
stomach
stress related site of damage
stomach
which type of PUD is more dependent on pH
H. pylori
which type/s of PUD are asymptomatic
NSAID
stress related
which type of PUD has deep ulcers
NSAID
Describe GI bleeding associated with H. pylori
less severe
single vessel
describe GI bleeding associated with NSAID
more severe
single vessel
describe GI bleeding associated with stress
more severe
superficial mucosal capillaries
PUD risk factors
H. pylori NSAIDs Stress Gastric acid hypersecretion Cigarette smoking Diet Chronic diseases Vascular insufficiency Chemo/radiation
Risk factors for NSAID induced ulcer
age >65 previous peptic ulcer, ulcer-related complications high dose NSAIDs Multiple NSAIDs Selection of NSAID Use of ASA, bisphosphonates, corticosteroids, anticoagulants, antiplatelets, SSRIs chronic debilitating disorders H. pylori infection Smoking Alcohol
Name nonselective NSAIDs
indomethacin piroxicam ibuprofen naproxen sulindac ketoprofen ketorolac
name partially selective NSAIDs
etodolac
meloxicam
nabumetone
diclofenac
PUD complications
Upper GI bleed
Perforation
Obstruction
PUD complications
Upper GI bleed
Perforation
Obstruction
PUD clinical presentation
Epigastric pain
Nocturnal pain
Duodenal ulcer (1-3 hours after eating, aggrevated by food)
Gastric ulcer (resolved by food)
Urease test requirements
Endoscopic
no PPIs x 2 weeks
no antibiotics/bismuth salts x 4 weeks
4 non-pharm treatments for PUD
reduce stress
smoking cessation
d/c NSAIDs
avoid aggrevating food/beverages
H2RA MOA
reversible inhibition of histamine receptor on parietal cells - acid production reduced 70%
Famotidine dosing
20 mg IV/PO BID or 40 mg HS
Famotidine dosing renal
CrCl
Ranitidine dosing
150 mg PO BID or 300 mg HS
50 mg IV Q6-8 hours
Ranitidine dosing renal
CrCl
H2RA AEs
Tolerance develops quickly
Thrombocytopenia
Neuro effects: somnolence, HA
PPI MOA
irreversibly inhibit proton pump, reduce acid up to 99%
Omeprazole dosing
20-40 mg PO daily
Esomeprazole dosing
40 mg PO/IV daily
Pantoprazole dosing
40 mg PO/IV daily
PPI AEs
Fractures C. diff Pneumonia Thrombocytopenia GI upset (N/V/D)
Antacids MOA
neutralize gastric acid
inhibit action of peptin
no effect on acid production
Antacids AEs
GI upset - diarrhea (magnesium), constipation (calcium)
Accumulation in renal dysfunction -> toxicity
frequent administration
drug interactions
Antacids AEs
GI upset - diarrhea (magnesium), constipation (calcium)
Accumulation in renal dysfunction -> toxicity
frequent administration
drug interactions
Sucralfate MOA
forms polyvalent bonds with damaged tissue and normal GI mucosa
Sucralfate AEs
Aluminum toxicity Cheap Decreased risk of pneumonia PO only Drug interactions Constipation Frequent administration
Misoprostol MOA
inhibits gastric acid secretion, increase in mucosal defense
synthetic prostaglandin analog
Misoprostol AEs
diarrhea
abdominal cramping
N/V
Misoprostal preg cat
X
Bismuth subsalicylate MOA
antibacterial effect
local gastroprotective effect
stimulation of endogenous prostaglandins
Bismuth subsalicylate AEs
Discoloration of the tongue
Gray/Black stools
tinnitus
Bismuth subsalicylate AEs
Discoloration of the tongue
Gray/Black stools
tinnitus
When is 14 day therapy for treatment of H. pylori preferred
1st line 3 drug regimen and recurrence
duration of therapy for treatment of H. pylori
10-14 days
