PUD (exam 2) Flashcards
where in the layers of the GI tract is PUD most common?
inner layer (mucosa and mesentery)
peptic ulcer disease types of ulcers
gastric ulcer (stomach)
duodenal ulcer (duodenum)
esophageal ulcer
dyspepsia (gastritis)
persistent or recurrent abdominal pain or discomfort centered in the upper abdomen
how does gastritis differ from PUD?
it is more superficial erosions
PUD extends deeper into the GI layers
Zollinger-ellison syndrome
severe form of PUD
ulcers accompanied by extreme gastric hyperacidity and at least one gastrinoma
Zollinger-Ellison syndrome is usually present in the
pancreas or duodenum
three common forms of peptic ulcers
H. Pylori
NSAID-induced
stress-related mucosal damage (SRMD)
H. Pylori ulcers are ___________ and primarily in the _____________
chronic
duodenum of ambulatory patients
NSAID-induced ulcers are _________ and primarily in the _______________
chronic
stomach of ambulatory patients
SRMD ulcers are __________ and primarily in the ______________
acute
stomach in hospitalized patients
which ulcers are dependent on intragastric pH?
only H. Pylori ulcers
which ulcers are typically asymptomatic
NSAID induced and SRMD
which ulcers are deep?
superficial?
deep - NSAID induced
superficial - H. Pylori, SRMD
which ulcers have a more severe GI bleed?
NSAID induced and SRMD
which ulcers respond to acid suppression alone?
NSAID induced and SRMD
main factors of chronic PUD
H. Pylori infection
NSAID use
patient noncompliance
smoking
alcohol
long duration of PUD
gastric acid hypersecretion
chronic PUD is commonly associated with
frequent ulcer recurrence when therapy is stopped or dose is reduced
someone with chronic PUD may need _____________ therapy with _______________
continuous management
low dose PPI (preferred), H2RA or sucralfate
refractory ulcers
symptoms, ulcers, or both persist beyond 8 weeks (duodenal) or 12 weeks (gastric) despite treatment
people with refractory ulcers should undergo _______ to confirm a non healing ulcer
endoscopy
(refractory ulcers) if H. pylori positive
receive eradication therapy
(refractory ulcers) if H. pylori negative
higher PPI dosages
when aggressive factors become greater than protective factors,
there is a break in the lining of the stomach or duodenum which leads to PUD
compromise of mucosal integrity can cause
pain, bleeding, obstruction and perforation
what is the most common symptom of PUD?
is it always present?
abdominal pain
no
abdominal pain of PUD is often
epigastric (burning, abdominal fullness, cramping)
complications of PUD
hemorrhage
perforation
obstruction
stomach cancer
how to tell if someone has a hemorrhage from PUD
hematemesis
black tarry stools
weakness
how to tell if someone has a perforation from PUD
acute abdominal pain
absent or decreased bowel sounds
how to tell if someone has an obstruction from PUD
inflammatory edema, spasm and scarring
postprandial vomiting/bloating
appetite/weight loss
abdominal distention
pain from a duodenal ulcer
episodic
relieved with food
pain from a gastric ulcer
constant
precipitated by food
nausea/vomiting and anorexia
non pharmacological therapy for PUD
avoid foods and beverages that cause dyspepsia or worsen symptoms
eliminate/reduce psychological stress, cigarette smoking, and use of NSAIDs
take NSAIDs with food
diagnosis of PUD depends on
visualizing the ulcer crater upon upper GI radiography or endoscopy
what is the preferred method to diagnose uncomplicated PUD?
for complications?
uncomplicated - radiography
complicated - upper endoscopy
radiography contrast technique
iodinated (gastrografin)
barium swallow (less preferred)
what is the type of endoscopy used to visualize and inspect the inside go the GI tract for PUD?
esophago/gastro/duodenoscopy (EGD)
laboratory tests for PUD
CBC
coagulation studies
microbiologic studies
guaiac fecal occult blood test
if bleeding is suspected, which test for PUD should be done?
guaiac fecal occult blood test
H. Pylori infection
gram negative bacteria that lives in acid environment
pH sensitive
oral-oral or fecal-oral
how does H. pylori cause ulcers
direct mucosal damage
impairs mucosal defense by toxins and enzymes
increases gastrin release which increases acid secretion
H. pylori produces __________ which converts ___________
urease
urea into ammonia
H. pylori uses __________ to buffer the H+ and forms _________________ which creates a _______________ around the bacteria
ammonia
ammonium hydroxide
alkaline cloud
C urea breath test
detects presence of H. pylori
based on production of urease
endoscopic tests to diagnose H. pylori infection
endoscopy (invasive, can do a biopsy)
nonendoscopic tests to diagnose H. pylori infection
stool antigen test
blood antibody test
urea breath test
which is the preferred nonendoscopic tests to diagnose H. pylori infection?
stool antigen test
which is the less preferred nonendoscopic tests to diagnose H. pylori infection?
why?
blood antibody test
antibodies can be present in the blood 12-18 months after a successful treatment
when getting a stool antigen test or urea breath test what needs to be discontinued and for how long?
acid suppressors and antibiotics for 2-4 weeks prior to test
first line therapy to treat H. pylori ulcer
Pylera or Helidac:
PPI BID
bismuth subsalicylate
metronidazole
tetracycline
(for 14 days)
alternative treatments for H. pylori ulcer
Talicia
PCAB dual or triple therapy
Talicia treatment regimen
omeprazole
amoxicillin
rifabutin
(for 14 days)
patients with a salicylate allergy should not be given
bismuth subsalicylate
Voquenza Dual Pak
vonoprazan
amoxicillin
(all for 14 days)
Voquenza Triple Pak
Vonoprazan
amoxicillin
clarithromycin
(all for 14 days)
is the voquenza triple pak or dual pak preferred?
why?
dual pak
high resistance to macrocodes (clarithromycin)
PrevPac
amoxicillin
clarithromycin
lansoprazole
(for 10 days)
after finishing their medication, all patients treated for H. pylori infection should undergo _________
when should the test be performed?
breath or stool test
30 days after treatment complete (2-4 weeks off PPI, pepto bismol, antibiotic)
persistence or recurrence of symptoms after several weeks of HP eradication treatment suggests
failure of ulcer healing or HP eradication
alternative diagnosis such as GERD
when should a patient be given a maintenance PPI if they had an ulcer from H. pylori infection?
they’ve been:
treated with a PPI for 14 days with antibiotic regimen
repeat upper endoscopy
persistent ulcer found
giant ulcer and above 50 or comorbidities
recurrent peptic ulcers
long term ASA/NSAID use
failure of eradication
____________ of long term NSAID uses have PUD on endoscopy
5-20%
NSAIDs increase PUD risk _______ fold and risk _____________________ in first month of therapy and long term therapy
2
increases with increased dose
mechanisms where NSAIDs cause ulcers
direct/topical injury of gastric epithelium
systemic effects due to decreased mucosal PG synthesis through inhibition of COX1
risk factors for NSAID PUD
choice of NSAID
over 60 years old
chronic illness
previous ulcer (with or without complication)
high dose/long duration of NSAID
multiple NSAID use or ASA plus NSAID use
additional risk factors of NSAID PUD include concomitant use of
corticosteroids
anticoagulant or coagulopathy
other anti platelet drugs such as plavix
oral bisphosphonates
selective serotonin reuptake inhibitors
which nonselective NSAIDs are partially selective COX2?
Dolobid
Disalcid
Triisate
etodolac (Lodine)
Meloxicam (mobic)
nabumetone (relafen)
which NSAID is least problematic?
celecoxib - selective COX2
which NSAID is most problematic?
nonselective traditional agents
Celebrex has an increased risk for
MI and stroke
the FDA requires all NSAIDs to include a
black box warning to highlight the increased risk of CV events
high risk factors for GI toxicity for NSAIDs
(can have 1 of the following to get prophylactic meds)
history of ulcer disease
on dual antiplatelet therapy
on anticoagulant therapy
high risk factors for GI toxicity for NSAIDs
(can have 2-3 of the following to get prophylactic meds)
age over 60
glucocorticoid use
dyspepsia or GERD symptoms
high risk patients for developing NSAID induced ulcers should receive
prophylactic cotherapy with misoprostol or a PPI/H2RA
FDA combination regimens for prevention of NSAID induced ulcers
Arthotec (misoprostol/diclofenac)
vimovo (esomeprazole/naproxen)
duexis (famotidine/ibuprofen)
nonselective NSAIDs should be ___________ if an active ulcer is confirmed
stopped
what are the drugs of choice for treatment of NSAID induced ulcers and why?
PPIs
rapid relief of symptoms and ulcer healing
if NSAIDs need to be continued after treatment of an NSAID indused ulcer then
dose should be reduced
switched to acetaminophen
nonacetylated salicylate
partially selective COX2 inhibitor
selective COX2 inhibitor
why are PPIs preferred over H2RA?
heal over shorter treatment
maintain a higher intragastric pH
fewer side effects
smaller doses work
when using a PPI for long term, what are the risks?
kidney disease
dementia
vertebral fractures
CV disease - MI
infections
calcium, iron, magnesium, vitamin b12 deficiencies
GI malignancies
types of infections that can be from long term use of PPIs
small growth of bacteria in GI
salmonella
clostridium dificile
pneumonia
stress related mucosal bleeding ulcer
in critically ill patients
due to lack of blood flow which leads to necrosis of GI mucosa
what is used as prophylaxis for a stress ulcer?
PPI or H2RA
major risk factors to place a patient on a PPI for SRMD
mechanical ventilation over 48 hours
coagulopathy
risk factors than need to be 2 or more to place a patient on a PPI for SRMD
sepsis
NSAIDs
anti platelet agents
ICU stay over a week
occult bleeding for 6 or more days
other factors to place a patient on a PPI for SRMD
shock
hepatic failure
renal replacement therapy
trauma
burns over 35% BSA
organ transplant
history of PUD, or upper GI bleed
three or more coexisting diseases
when to place a patient on a maintenance PPI if they had an ulcer secondary to aspirin/NSAID use
avoid aspirin/NSAIDs
giant ulcer and over 50 or comorbidities
history of frequent peptic ulcers
condition requiring long term aspirin/NSAID use
