GI: GERD & PUD Flashcards
Pathophys of GERD (6)
- decreased salivation
- decreased basal LES pressure
- LES relaxation
- impaired esophageal clearance
- dec acid clearance
- delayed gastric emptying
Severity of GERD is related to:
amount of time esophagus is exposed to acid and pepsin
aggravating factors for GERD (6)
diet exercise pregnancy tight clothing cigarettes alcohol
substances which “cause” GERD
nicpotine iron potassium alcohol narcotics
complications of GERD (4)
Erosive esophagitis
strictures
barrett’s esophagus
esophageal adenocarcinoma
Peptic ulcer disease consists of
2
gastric ulcers
duodenal ulcers
duodenal ulcers may result from
h pylori
3 common forms of PUD
H pylori
NSAID induced
stress related
non pharm therapy for PUD
dietary change
lifestyle change
pharmacologic goals for PUD
eradicate h pylori
relieve pain
heal ulcers/erosions
how to “heal” ulcers and erosions of PUD
PPI
step up management for PUD/GERD
treat with OTC antacids and escalate to rx H2 blockers and PPIs
step down treatment for PUD/GERD
starting with highest treatment and going down
Rx H2 blockers or PPI first, de escalate.
when is metocloperamide prescribed for GERD?
only after confirmed diagnosis
follow up for GERD/PUD
additional drugs and lifestyle changes like PPIs or misoprostol
MoA Antacids
3
- neutralize acid by increasing intragastric pH
- inhibits conversion of pepsinogen to pepsin
- may also stimulate production of mucosal prostaglandins and LES tone
stimulating prostaglandins: antacids
protective to GI mucosa
types of antacids (4)
aluminum
magnesium
calcium
bismuth
antacids for ulcers
symptomatic relief but do not provide healing
antacid suspensions vs pills
suspensions are better
AE aluminum based antacid
constipation
AE of magnesium based antacid
diarrhea
antacids decrease absorption of drugs which require
an acidic environment to work
solution for antacid drug interactions
separate drugs and antacids by 2 hours
aluminum plus magnesium
maalox
mylanta
calcium carbonate
tums
sodium bicarb / bismuth
peptic bismol
ae pepto bismol
black tongue
dark stool
antacid duration/dosing
quick onset, short duration, many doses per day
antacids in renal disease
watch for accumulation
histamine-2 receptor antagonists MoA
inhibit histamine receptors on parietal cells in stomach, decreasing secretion of H+ ions
MoA PPI
allow acid to be made but inhibit the final step of secretion by inhibiting H+/K+ ATPase on parietal cells
H2 blockers are 1st line for
mild to moderaste PUD or GERD
H2 blockers/PPI may be used for (6)
tx of ulcers maintenance of remission tx of h pylori tx of nsaid ulcers erosive/non erosive esophagitis PUD/GERD
h2 blockers or PPI for duodenal ulcer duration of therapy
4-8 wks
h2 blockers/PPI for gastric ulcers: duration of therapy
4-8 wks
h2 blockers/PPI for GERD: duration of therapy
8 weeks
monitoring parameters for h2 blockers (4)
relief of symptoms
healing of ulceration
adverse effects
renal function
4 common h2 blockers
cimetidine
nizatidine
ranitidine
famotidine
cimetidine interacts c
warfarin
lidocaine
theophylline
ranitidine interacts with
warfarin
diazepam
H2 blockers are first line for _, while PPIs are first line for _
h2: mild to mod PUD/GERD
ppi: mod to severe PUD/GERD
patient teaching for PPI
do not chew or crush
take before 1st meal of day
risks in long term use of PPI
fractures
hypomagnesemia
c diff
short term risk of PPI
CAP
pt with osteoporosis who needs a PPI
limit dose/duration
ensure adequate ca/vit d
bone density screening
hypomagnesemia with PPIs
comes into play with patients who are on meds which also waste mag
PPI drug examples
dexlansoprazole lansoprazole omeprazole rabeprazole pantoprazole esomeprazole
safest PPI in terms of drug interactions
pantoprazole
common AE of PPIs (3)
nausea
diarrhea
HA
metoclopramide MoA
stimulates motility of upper GI and increases LES tone
metoclopramide increases
anal contractions and peristalsis
dosing time: metoclopramide
30 min before meals and sleep
AE of metoclopramide
galactorrhea diarrhea EPS depression drowsiness
metoclopramide is contraindicated with
parkinsons
bowel obstruction
monitoring for metoclopramide
renal function
metoclopramide interacts with
anti cholinergics
MAOI
levodopa
sucralfate MoA
promotes mucosal defenses by reacting with HCl in stomach to form a paste and bind to ulcer, allowing it to heal.
sucralfate does not
have acid-reducing capacity
sucralfate should be given as
adjunct, not on its own
NSAID induced ulcers
adverse effect related to inhibition of COX 1 or seen dose dependently with cox 2 inhibitors
cox sites
cox 1: GI, kidney
cox 2: inflammation sites
tx of nsaid induced ulcer
dc nsaid, start PPI or H2 blocker.
nsaid induced ulcer in the pt who needs to continue nsaid
use PPI and see if the NSAID can be changed to either celecoxib or meloxicam
prevention of NSAID induced ulcers:
misoprostol
PPI
using misopristol prophylactically is indicated for patients who are
> 60 y/o
prior hx GIB
high dose NSAID therapy
receiving anticoags/steroids
MoA misoprostol
prostaglandin E1 analog
stimulates production of mucous/HCO3
cytoprotective
AE misoprostol (4)
diarrhea
abd pain
spontaneous abortion
postmenopausal bleeding
Misoprostol is CI in
women of childbearing age
h pylori and nsaid induced ulcers
tx of h pylori is recommended for pts taking NSAIDs who have ulcers and h pylori
tx of h pylori (2 options)
clarithromycin, amoxicillin, PPI
clarithromycin, metronidazole, PPI
depending on previous hx of macrolide exposure (resistance)
if you can’t use clarithromycin in triple therapy, what are your next 3 options for h pylori tx?
bismuth quadruple therapy:
bismuth, metronidazole, tetracycline, PPI
concomitant: ppi/clarith/amox/metro
levo triple therapy:
PPI, levo, amoxicillin
bismuth quadruple therapy
bismuth/metro/tetra/ppi
concomitant therapy for h pylori in areas where clarithro resistance is high
PPI, clarithro, amox, metro
levo triple therapy for H pylori
PPI, levo, amox
