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84 Cards in this Set

  • Front
  • Back
what are the common forms of Peptic ulcer disease
H Pylori
NSAID
Stress ulcers
what are some less common causes of PUD
cig smoking
psychological stress
Zollinger Ellison syndrome
what type of ulcers are chronic and cause frequent ulcer recurrence
h pylori
nsaid
what are some factors for recurrence
h pylori
nsaid
cig smoking
alcohol
gastric acid hypersecretion
what are the aggressive factors of PUD
gastric acid (independent activity)
pepsin (proteolytic activity)
what pH is pepsin
-activation
-inactivated
-irreversibly
activation: 1.8-3.5
inactivated: 4
irreversibly destroyed: 7
what are the protective factors
mucus and bicarbonate secretion
endogenous prostaglandins (prevent deep mucosal injury)
what are the most common ways H pylori can be transmitted
person to person
gastro-oral
fecal-oral
what is the pathophysiologiy of H Pylori
adherence to pedestals
alters host inflammatory response
produces urease, lipases, proteases
produces acid inhibitory proteins
what does the production of urease and acid inhibitory proteins do for H pylori
urease converts urea to ammonia and CO2
-the ammonia can be used as a buffer to protect it from the acid

production of acid inhibitory proteins allows H pylori to adapt to low pH (protects it from low pH)
why are enterically coated NSAIDs still able to cause ulcers
cause systemic prostaglandin inhibiton
what does COX 1 do
produces protective prostaglandins
what does COX 2 do
produces prostaglandins that cause inflammation, fever, and pain
what induces COX 2
inflammatory stimuli
is NSAID related ulcers dose dependent?
yes, but may occur with low doses
what are some factors of NSAID use that can increase risk of ulcers and complications
potency
longer duration
COX 1 inhibitor vs COX 2
using multiple NSAIDS
concomitant use of certain drugs
what are complications of PUD
bleeding
perforation
penetration
gastric outlet obstruction
how does GI bleeding occur
how may it present
and what is the most important risk factor
occurs: ulcer moves into artery
present: melana (black stool), hematemesis (vomitting blood)
most important risk factor: NSAID use
how does perforation occur
what are the majority of them caused by
how does it present
occurs: ulcer opens up in the perotineal cavity
majority caused by NSAIDs
presents: sharp pain that starts in the gastric area but spreads to abdominal area
what is Penetration
ulcer moves into a nearby organ
-ex: pancrease, biliary tract, liver
what is Gastric outlet obstruction due to
what are the symptoms
due to: scarring, edema of duodenal bulb, muscular spasm
symptoms: ANOREXIA, WEIGHT LOSS, EARLY SATIETY, BLOATING, n/v
what complications are most often seen with chronic PUD
perforartion
penetration
gastric outlet obstruction
can you diffrentiate between an ulcer due to H. Pylori vs NSAID
no
what symptoms are more common in pts with gastric ulcer than duodenal ulcer
nausea
vomitting
anorexia
what are alarm symptoms that are signs of ulcer related complications
anemia
weight loss
loss of appetite (early satiety)
vomitting
symptoms in general may be described as
burning
what is the difference between duodenal ulcer pain and gastric ulcer pain
duodenal ulcer pain: 1-3 hours after meals, RELIEVED WITH FOOD

gastric ulcer pain: FOOD MAY CAUSE OR ACCENTUATE PAIN
when is H pylori testing recommended
when eradication is planned
what are the testing options for H Pylori
endoscopic
non endoscopic
when you are planning on doing endoscopic therapy what must you do first
hold antibiotics and bismuth salts for 4 weeks
hold PPI for 1-2 weeks
how are ulcer like symptoms in pts 55 years and up investigated
non endoscopic therapy
what are the non endoscopic tests
urea breath test
serologic test
fecal antigen test
what test is done to confirm that H pylori has been eradicated
Urea Breath Test
what non endoscopic test may be useful in children
fecal antigen test
-comparable to UBT in initial detection
why can't Serologic tests be used to see if eradication was successful
antibodies remain even after successful eradication
what does Serologic tests test for
antibodies
what non endoscopic test is good for initial diagnosis in untreated patients
serologic test
diagnosis of PUD depends on what? and what is used?
diagnosis depends on visualizing the ulcer

upper endoscopy is used to visualize.
what are the treatment goals of PUD, H pylori and NSAID also
relieve pain
heal ulcer
prevent recurrence
reduce complications

goals for H pylori + pts:
-eradicate H pylori
-heal ulcer
-cure the disease

goals for NSAID induced ulcers:
-heal ulcer as quickly as possible
what does treatment depend on
cause: H pylori vs NSAID
initial or recurrent infection
whether complications have occurred
what are the non pharmacological treatment for PUD
reduce/stop psychological stress
reduce/stop cig smoking
STOP USE OF NSAIDS ESPECIALLY ASA
avoid food/drinks that cause dyspepsia - spicy food, caffeine, alcohol
what can you use if you have pain due to PUD
acetaminophen or nonacetylated salicylate
what is an example of a nonacetylated salicylate
salsalate
what are the choices of therapy for H pylori erradication (1st course of treatment)
PPI triple therapy
Bismuth based quadruple therapy
Sequential therapy
what is PPI triple therapy
PPI + clarithromycin + amoxicillin or metronidazole for 10-14 days
why would you prefer using amoxicillin over metronidazole in PPI triple therapy
almost no bacterial resistance
few AE
leaves Metronidazole to be used as 2nd line treatment
what is the 1st line therapy for H Pylori eradication
PPI triple therapy
what is the Bismuth quadruple therapy
PPI or H2-RA + bismuth + tetracycline + metronidazole for 10-14 days
if someone has a penicillin allergy what treatment can you use for H pyloric eradication
Bismuth quadruple therapy
what is 2nd line therapy for H pylori erradication
bismuth quadruple therapy
what is sequential therapy for H pylori eradication
PPI and amoxicillin for 5 days
then
PPI clarithromycin and metronidazole for 5 days
if treatment failure occurs after trying the 1st line regimen what can you do
PPI 3 drug regimen with different ABx than before
bismuth quadruple regimen with PPI not H2RA
what are the antibiotics that are in the various regimens for H Pylori eradication and can they be substituted
metronidazole
amoxicillin
tetracyclin
clarithromycin

THESE CAN NOT BE SUBSTITUTED WITH DRUGS OF THE SAME CLASS
what is the treatment for NSAID induced ulcers
test for H pylori
IF POSITIVE: do PPI triple therapy
IF NEGATIVE: STOP NSAID, tx with either PPI, H2RA, or sucralfate
why is PPI prefered for NSAID induced ulcers that are negative for H pylori
accelerate healing process
if pt has NSAID induced ulcer and NSAID is necessary what is the course of treatment
if H pylori positive initiate therapy with PPI triple regimen

if H pylori negative initiate therapy with PPI (PPI should be extended for 8-12 weeks)
-reduce NSAID dose
-Switch to APAP or Nonacetylated Salicylate (salsalate)
-use more selective COX 2 inhibitor
what is the drug of choice in NSAID induced ulcers if the NSAID still needs to be continued
PPI (PPI should be extended for 8-12 weeks)
what can you use to reduce risk of NSAID ulcer and Ulcer related complications
Misoprostol cotherapy
PPI cotherapy
switch to selective COX 2 inhibitor
what is the dose of Misoprostol
200 mcg by mouth 4x/day (switch to 3x/day if intolerable)
what is the SE of Misoprostol
diarrhea
what is the fixed combo for misoprostol cotherapy
misoprostol 200 mcg and diclofenac 50 mg or 75 mg max
what kind of NSAID related ulcer are H2RA cotherapy ok for
reduces NSAID related duodenal ulcer NOT GASTRIC ULCER
what drug can you use to relieve NSAID related dyspepsia
H2RA
why is H2RA cotherapy not recommended as prophylactic cotherapy
not as effective
how do PPI work
inhibit basal and stimulated gastric acid secretion

DOSE DEPENDENT
when are PPI most effective
30 - 60 mins before meals
with PPI the duration of suppression is a function of binding to _____ of parietal cell, longer than elimination half lives
with PPI the duration of suppression is a function of binding to H/K ATPase of parietal cell, longer than elimination half lives
name the generic
prilosec
zegerid
prevacid
aciphex
protonix
nexium
prilosec - omeprazole
zegerid - omeprazole sodium bicarbonate
prevacid - lansoprazole
aciphex - rabeprazole
protonix - pantoprazole
nexium - esomeprazole
what PPI is not labeled as an antiulcer agent
dexlansoprazole
is there renal dosing for PPI
no renal dosing
consider dose adjustment in severe hepatic disease
what is the issue with immediate release formulations of PPI
contain sodium bicarbonate therefore
contrindicated in metabolic alkalosis, hypokalemia, and must watch Na content in Na restricted diets
what are the Drug interactions with PPI
increase gastric pH
inhibit CYP2C19
increase metabolic clearance and decrease GI absorption of levothyroxine
reduce effectiveness of clipidogrel
what drugs are affected by PPI increasing gastric pH
this may alter bioavailability of some drugs that depend on pH to work

example: ketoconazole, digoxin
what PPI inhibit CYP2C19 and what drugs are affected by this
omeprazole and esomeprazole inhibit CYP2C19

this may decrease elimination of phenytoin, warfarin, diazepam, carbamazepine
what occurs due to PPI affect on levothyroxine
increase TSH
increase dose of levothyroxine must be given
what PPI aren't given with clopidogrel and why
esomeprazole, omeprazole, omeprazole/sodium bicarbonate

reduce its effectiveness
PPI in general may attenuate antiplatelet effect
do you have to adjust the dose renally in H2 Rc antagonist
yes
name the generic
Tagamet
Pepcid
Axid
Zantac
Tagamet - cimetidine
Pepcid - famotidine
Axid - nizatidine
Zantac - ranitidine
what AE occurs in all H2 Rc Antagonist
thrombocytopenia
what H2 RcA inhibits CYP450 isoenzymes and what drugs are affected
tagamet (cimetidine)
theophyline, lidocaine, phenytoin, warfarin, clopidogrel can be affected
how does Sucralfate work
promotes healing by improving mucosal repair
-forms a viscous adhesive substance that coats stomach against peptic acid, pepsin, bile salts

MAY ALSO SUPPRESS H PYLORI INFECTION
what antiulcer agent is contraindicated in women and why
Misoprostol b/c produces uterine contractions
what antiulcer agent CAN NOT BE USED FOR TREATMENT AND IS ONLY USED FOR PREVENTION
misoprostol
what are the bismuth agents
do they inhibit or neutralize acid
pepto-bismol
do not inhibit or neutralize acid
often contain salicylates so must watch to see what other salicylates pt is on