LECTURE 5 – GI DRUGS
1. Peptic Ulcer Diseasea. Diseases responsible for erosion of the gastric mucousa
b. Occur when there is an imbalance between protective mechanisms and those that intend to attack
c. Defenses:
i. Mucus – secreted by mucousa to protect the cells from pepsin and acid
ii. Bicarbonate – secreted by epithelial cells
1. Some is trapped in mucous and maintains alkalinity
2. Some neutralizes stomach acid
iii. Blood flow – perfuses gastric mucousa preventing ischemia
iv. Prostaglandins – several functions
1. Stimulate secretion of mucous and bicarbonate
2. Promote vasodilation and improve blood flow to stomach
3. Suppress gastric acid secretion
d. Damaging Effects:
i. Helicobacter pylori (H. pylori)
1. Bacteria that colonizes stomach
2. Promotes PUD by enzymatic action and by secreting ureaseurease changes to ammonia and is responsible for damaging the stomach tissue
ii. NSAIDS
1. Inhibit production of prostaglandins (from arachidonic acid) and increases erosion of the stomach (aka…NSAIDS block the COX pathway)
iii. Gastric acid
1. Direct mucosal damage and activation of pepsin
iv. Pepsin
1. Enzyme that damages mucousa
2. Drug Therapy used for Peptic Ulcer Disease:
a. Goal with drug therapy:
i. Alleviate symptoms
ii. Promote healing
iii. Prevent complications
iv. Prevent recurrence
b. If H. pylori is the presumed cause Triple therapy including 2-3 antibiotics and a proton pump inhibitor – KNOW THIS
c. If NSAIDS are the presumed cause Proton pump inhibitors are the best – no antibiotic necessary
3. Drug Therapy for PUD:
a. Eradicate H. pylori bacteria
b. Reduce gastric acid
c. Enhance protective effect of mucousa
4. Antibiotics:
a. Used to eradicate H. pylori
b. CANNOT BE USED INDIVIDUALLY- NEED AT LEAST 2 ANTIBIOTICS
c. Mechanisms of action for some antibiotics: FOCUS ON NAMES ONLY HERE
i. Drugs that inhibit protein synthesis:
ii. Drugs that destroy bacterial cell wall:
1. Clarithromycin (Biaxin)
1. Bismuth= PEPTO! It’s an
2. Tetracycline
antibiotic!
Drug Class
Example
Mechanism of Action
Histamine2
Receptor
Antagonists
Famotidine (Pepcid)
Cimetidine (Tagamet)
Ranitidine (Zantac)
Aka H2RA’s
-IDINE DRUGS
H2RA’s block H2 receptors
exclusively  blocking the
effect of H2  production of
gastric acid and hydrogen ion is
reduced.
Commonly
end in -IDINE
GI Drugs
Effects of Drug
Gastric acid buildup is
reduced but DOES NOT
improve symptoms of
allergy= minimal effect
on H1 receptors because
it only blocks H2
Drug InteractionsMost common with
cimetidine (Tagamet)
Inhibits hepatic drug
metabolism
Influences warfarin,
phenytoin, etc. Risk for
toxicity of these drugs.
Thrombocytopenia bleed risk
Misoprostol (Cytotec)
Stimulates prostaglandin
receptors on parietal cells to
suppress production of gastric
acid
iii. Drugs that destroy bacterial DNA:
1. Metronidazole (Flagyl)
Adverse Effects
Most common with
cimetidine (Tagamet)
(Don’t see many side
effects with Pepcid).
1. Anti-androgen effects
– binds to androgen
receptors, resulting in
gynecomastia, reduced
libido, impotence
2. CNS effects –
confusion
Clinical
Usefulness
1. Gastric and
duodenal
ulcers
2. GERD
3. ZollingerEllison
syndrome –
syndrome in
which
gastric acid
is hyper
secreted
from a
gastrinproducing
tumor
1. Diarrhea – smooth
1.
muscle contraction
2. Abdominal pain
3. Vaginal
spotting/dysmenorrhea
2.
Prevent
gastric
ulcers with
long term
use of
NSAIDS
Can induce
labor
Nursing
Considerations
Monitor male
patients for
development of
man boobs,
don’t give to
people on
warfarin,
phenytoin as it
can cause
toxicity of these
drugs. Monitor
platelet count.
GIVE TO
PREGNANT
WOMEN TO
ABORT THE
FETUS
Proton Pump
Inhibitors
Commonly
end in –
PRAZOLE OR AZOLE
Antacids
Osmotic
Laxatives
Pro-drug that is activated in
parietal cells of the stomach.
Active form blocks H+K+ATPase
a.k.a “the proton pump”
Protein embedded in the cell
membrane of parietal cells.
Generates gastric acid by
releasing H+ into gastric lumen in
exchange for K+.
Requires ATP → ADP…This
mechanism is shut off
Acid suppression is
greater than H2RAs; well
tolerated.
Drug InteractionsReducing acid secretion
can influence the
absorption of
antiretrovirals
Usually uncommon (<1%)
1. Headache, diarrhea
2. Pneumonia – by
changing flora and
inhibiting acid
secretion
3. Rebound
hypersecretion – after
stopping the
PPIhyper-acidic
state from not taking
the pill.
Used to
decrease acid
secretions
within the
stomach to
reduce gastric
ulcer risk and
prevent excess
acid
Milk of Magnesia
(Magnesium
Hydroxide)
Maalox (aluminum
Hydroxide/magnesium
hydroxide combo)
Alkaline compounds that react
with gastric acid to produce
neutral salts (water and salt).
Treatment raises pH, reduces
destruction of gut wall and
reduces pepsin activity
The alkaline drug reacts
with hydrogen within
the stomach to
neutralize stomach
contents and prevent
further destruction of
the stomach wall.
Usually affect the colon
 Magnesium hydroxide
causes diarrhea
 Aluminum hydroxide
and calcium carbonate
cause constipation
Sucralfate (Carafate)
Ingested as a “slurry” in
acidic environments, converts
to a gel that coats the stomach
and adheres to ulcers= COATS
YOUR STOMACHHHH!!!
NO ACID REDUCING
CAPACITY
Poorly absorbed salts or
carbohydrates that pull water
into intestineSoftens fecal
massFeces expands and
stretches colonStimulates
peristalsis
Helps pull water into
colon to poop!
No known serious adverse
effects
Concomitant use of
antacids can reduce
effectiveness – need acid
to turn them into a gel
1. Loss of water
2. Nausea
3. Flatulence
4. Magnesium
contraindicated in
renal patient due to
risk of toxicity
Used to prevent
hydrogen within
stomach acid to
further cause
destruction to
stomach wall
and prevent
more damage.
Used for
heartburn as
well
Used to coat the
stomach and
provide relief
from gastric
ulcer/acid
Omeprazole (Prilosec)
Esomeprazole
(Nexium)
Pantoprazole
(Protonix)
-AZOLE DRUGS
Magnesium
Hydroxide (Milk of
Magnesia)
Polyethylene Glycol
(Miralax)
Lactulose
Golytely
Moviprep
ACTS AS A PHYSICAL
BARRIER
Used to help
poop!
Monitor patient
for adverse side
effects such as
pneumonia, HA,
diarrhea and
advise patient
to take
medication for
complete
course of
treatment to
prevent
rebound
hypersecretion.
Monitor for
constipation
and or diarrhea.
Don’t use
together with
antacids
Monitor
electrolyte
levels and don’t
give to a renal
patient because
it can cause
toxicity
Bulk forming
laxatives
Surfactant
laxatives
Psyllium
(fiber-like)
Docusate Sodium
(Colace)
Acts like natural fiberSwells
in water that’s already in colon
at the time of taking the
medicationTransforms into a
gelSoftens stool and increases
bulk Swelling stretches
intestine stimulating peristalsis
SHOULD DRINK A FULL GLASS
OF WATER!!!! – none there =
doesn’t work
Lowers surface tension of
stoolallows influx of water
into the stoolalso inhibits
reabsorption of water from
colon
Non-digestible and nonabsorbable compounds
Adverse effects are rare.
Used to help
poop!
Monitor for
constipation
and impaction
and advise
client to drink a
FULL glass of
water!!
Constipation and
impaction if GI motility is
interrupted (can occur if
water isn’t consumed with
the medication)
Helps us poop by
decreasing surface
tension of stool and
promoting water into
stool
Adverse effects are rare.
Used to help
poop!
Advise patient
to take
medication
with a full glass
of water
Stimulates the colon to
help stool move out!
Usually only with repeated
use:
Dependency
Proctitis-inflammation of
the rectum/anus
Helps us poop!
Monitor for
diarrhea and
Proctitis
SHOULD DRINK A FULL GLASS
OF WATER – same reason as
above
Stimulant
laxatives
Bisacodyl (Dulcolax,
Feen-a-mint)
Senna (Senokot)
Castor Oil
Stimulate the intestinal motility
and peristalsis of colon and
increase secretion of water and
electrolytes into colon
1. Antiemetic’sa. Drugs used to reduce nausea and vomiting
b. Emesis is a complex reflex
i. Requires activation of vomiting center in medulla
ii. Once activated, the vomiting center (in the medulla) signals stomach, diaphragm, and abdominal muscles to expel contents
2. Emesisa. Vomiting center may be triggered
i. Directly (sight, smell, pain, fear, vestibular stimulation)
1. Vestibular stimulation of the vomiting center due to stimulation of H1 receptors and muscarinic receptors in the brain
ii. Indirectly (vomiting center stimulated by the chemoreceptor trigger zone in response to chemotherapy, opioids, ipecac, vagal stimulation from the
stomach)
1. Stimulation of serotonin and dopamine receptors enhances this effect
Antiemetics
Drug Class
Serotonin receptor
antagonists
Examples
Ondanestron
(Zofran)
Mechanism of Action
Exerts effects by blocking
serotonin in the pathway
to the vomiting center
Effects of Drug
Prevents patient
from vomiting
Adverse Effects
Clinical
Usefulness
Used to
stop N & V
Nursing
Considerations
Monitor V/S
and watch for
heart
arrhythmias
Usually only with high-dose or prolonged
use:
*Tardive dyskinesia
*Sedation
Used to
stop N & V
Monitor for
tardive
dyskinesia and
sedation
1.
2.
3.
4.
Used to
treat N & V
from
motion
sickness
Monitor for dry
mouth,
constipation,
urinary
retention and
drowsiness
Monitor for dry
mouth,
sedation,
constipation,
urinary
retetnion
Dizziness
Risk for arrhythmia-tosades de pointes
(treat with magnesium)
CTZ pathway only
Serotonin/Dopamine
antagonists
Muscarinic
Antagonists
Antihistamines
Metoclopramide Suppresses emesis by
(Reglan)
blocking serotonin AND
dopamine in emesis
pathway.
Also enhances effect of
acetylcholine in upper GI
tract to increase upper GI
motility.
Scopolamine
(Scopoderm)
Meclizine
(Antivert)
Dimenhydrinate
(Dramamine)
Can help a patient
on chemo
Prevents patient
from vomiting
CTZ pathway only
Can help a patient
on chemo
Blocks pathway from
vestibular apparatus to
vomitingblocks the
pathway to the vomiting
center
Used for MOTION
SICKNESS
Blocks the pathway from
vestibular apparatus to
vomiting center by
blocking histamine; also
blocks muscarinic
receptors to a lesser
degree
Helps reduce N & V
Cannot help a
patient with chemo
Dry mouth
Constipation
Urinary retention
Drowsiness
1. Sedation
2. Dry mouth
3. Constipation
4. Urinary retention
Basically the same as above
1. Inflammatory Bowel Diseasea. Crohn’s disease and Ulcerative colitis- Drugs are NOT curativethey only treat the symptoms
i. Autoimmune attack against normal intestinal flora
ii. Inflammation
Used to
treat N & V
Inflammatory Bowel Disease Drugs
Drug Class
5- aminosalicylates
Glucocorticoids
Example
Sulfasalazine
(Azulfidine)
Many specific agents
(see analgesics slide)
Mechanism of Action
Effects of Drug
Adverse Effects
Reduces inflammation by
suppressing prostaglandin
synthetic by inhibiting COX; used
for the treatment of acute attacks
Inhibit synthesis of chemical
mediators (prostaglandins,
leukotrienes, histamine)
Reduced swelling (decreases
capillary permeability and inhibits
vasodilation) and pain (fewer
prostaglandins and histamine)
Reduced infiltration by
phagocytes Less damage from
enzymes
Helps to
reduce
inflammation
1. Nausea
2. Fever
3. Rash
Antiinflammatory
actions
Usually, only due to
long-term use:
Neutralizes TNF-alpha (tumor
necrosis factor) and reduces
inflammation
Reduces
inflammation
Immunomodulators
Infliximab
(Remicade)
Mono-clonal
antibody
Immunomodulators
Cyclosporine (Neoral, Suppresses production of
Sandimmune)
Interleukins and other cytokines.
Reduces proliferation of B cells and
cytotoxic T cells.
Immunomodulators
Adalimumab
(Humira)
Binds to and neutralizes TNF-α
Reduces inflammation
- SUBQ INJECTION ONLY – ROTATE
SITES AND AVOID RED BRUISED
AREAS
Laxatives: used to ease or stimulate defecation
1. Softening stool
2. Increasing stool volume
3. Hasten passage through intestine
4. Facilitate evacuation
Clinical
Usefulness
Reduces
inflammation
in relation to
IBD
Antiinflammatory
actions
Nursing Considerations
Monitor for adverse
reactions to the drug
Monitor for adverse
reaction of the drug
*Adrenal
suppression – TAPER
THE DOSE
*Osteoporosis fractures
*Immunosuppressio
n
Reduces
inflammatory
response
Immunosuppression
increases risk for
infection including TB
Also infusion
reactions
Increased risk of
infection – less
immune response
Nephrotoxicity
Reduces
inflammation
seen in IBD
Monitor for infection
and use with caution in
patients who are
immunocompromised.
Reduces
inflammatory
response
Check BUN, creatinine
levels and use with
caution in patient with
kidney impairments.
Infection + Injection
site reactions
(itching and rash)
Reduces
inflammation
Monitor for adverse
reaction of the drug