Peptic Ulcer Drugs

Drug Presentation
On
Peptic Ulcer Disease
PRESENTED BY:
Ms. Navaneeta Kusum
M.Sc.Nsg.2nd Year,
CON-ILBS

PEPTIC ULCER DISEASE (PUD)
PUD is a break in the inner lining of the stomach, Duodenum or
sometimes the lower esophagus.
Gastric ulcer, Duodenal ulcer.
Symptoms:
DU - Upper abdominal pain at night that improves with eating.
GU- Pain may worsen with eating.

PEPTIC ULCER cont...
Causes: Helicobacter pylori and non-steroidal anti-inflammatory
drugs (NSAIDs), tobacco smoking, stress due to serious illness, Behcet
disease, Zollinger-Ellison syndrome, Crohn disease and liver cirrhosis.
Complications: Bleeding, perforation and blockage of the stomach.
Management:
Eradication therapy, NSAIDS induced ulcers, Fluid replacement with crystalloids

Goals
The goals of antiulcer therapy are:
• Relief of pain
• Ulcer healing
• Prevention of complications (bleeding, perforation)
• Prevention of relapse.

Classification of the Drug:
1. Reduction of gastric acid secretion
(a) H2 antihistamines: Cimetidine, Ranitidine, Famotidine, Roxatidine
(b)PPI: Omeprazole, Esomeprazole, Lansoprazole, Pantoprazole, Rabeprazole,
Dexrabeprazole
(c) Anticholinergic drugs: Pirenzepine, Propantheline, Oxyphenonium
(d) Prostaglandin analogue: Misoprostol

Classifications: cont...
2. Neutralization of gastric acid (Antacids)
(a) Systemic:
Sodium bicarbonate, Sodium citrate
(b) Nonsystemic:
Magnesium hydroxide, Mag. trisilicate, Aluminium hydroxide gel,
Magaldrate, Calcium carbonate

Classifications:
3. Ulcer protectives:
Sucralfate, Colloidal Bismuth subcitrate (CBS)
4. Anti-H. pylori drugs: Amoxicillin, Clarithromycin, Metronidazole,
Tinidazole, Tetracycline

(a) H2 antihistamines:
Cimetidine, Ranitidine, Famotidine, Roxatidine

Drug Name RANTIDINE CIMETIDINE FAMOTIDINE
Brand Name
Zantac,
Zantac – 75
Novocimetine ,
Peptol , Tagamet
Pepcid,
Pepcid AC
Drug Action
It blocks daytime and
nocturnal basal gastric
acid secretion stimulated
by histamine and
reduces gastric acid
release in response to
food and insulin.
It inhibit 50% of the
stimulated gastric acid
secretion.
By inhibition of histamine at
the H2-receptor sites, it
suppresses all phases of
daytime and nocturnal basal
gastric acid secretion in the
stomach. Indirectly reduces
pepsin secretion; it is not a
cholinergic.
Inhibits basal, nocturnal,
meal-stimulated and
pentagastrin-stimulated
gastric secretion; also
inhibits pepsin secretion.
It is 20–160 times more
potent than cimetidine
and 3–20 times more
potent than ranitidine.

Drug Name RANTIDINE CIMETIDINE FAMOTIDINEIndications
-Short-term treatment of
duodenal ulcer;
-Treatment of GERD,
gastric ulcer, GI hyper-
secretory conditions (e.g.,
Z- E syndrome) and in
heartburn.
Same as Rantidine Same as Rantidine

Drug
Name
RANTIDINE CIMETIDINE FAMOTIDINE
CONTRA..
- Hypersensitivity to
ranitidine;
-OTC administration in
children <12 yr
- Known
hypersensitivity to
cimetidine
-Lactation
-Pregnancy (cat B)
- Pregnancy
(category B)
ROUTE&DOSAGE
Adult:
PO 150/300 mg BD
IV 50 mg q6–8h
Child: PO 4–5 mg/kg/d
BD/TDS
IM/IV 2–4 mg/kg/d
TDS/QID
Adult: PO 300/ 400 mg
BD or 800 mg HS IM/IV
300 mg TDS/QID
Child:
PO/IM/IV 20–40
mg/kg/d in QID
Adult: PO 40 mg HS
or 20 mg BD
Child:
PO/IV 0.5 mg/kg
BD/TDS
(max: 40 mg/d)

RANTIDINE CIMETIDINE FAMOTIDINEADVERSEEFFECTS(1%)
CNS: Headache,
dizziness, somnolence,
insomnia, vertigo
CV: Bradycardia (with
rapid IV push).
GI: Constipation, nausea,
abdominal pain, diarrhea.
Skin: Rash.
Hematologic:
Leukopenia,
thrombocytopenia.
GI: Diarrhoea;
constipation, abdominal
discomfort.
Hematologic: Increased
PT, Aplastic anemia.
Metabolic: Slight
increase in serum uric
acid, BUN, creatinine
CNS: Drowsiness,
dizziness, light-
headedness, depression
Skin: Rash, S-J
syndrome, alopecia.
CNS: Dizziness,
headache, confusion,
depression.
GI: Constipation,
diarrhoea.
Skin: Rash, acne,
pruritus, dry skin,
flushing.
Hematologic:
Thrombocytopenia.
Urogenital: Increases
in BUN and serum
creatinine.

Drug Name Rantidine Cimetidine FemotidineINTERACTIONS
It may reduce
absorption of
cefpodoxime,
cefuroxime,
ketoconazole,
itraconazole.
Cimetidine decreases
the hepatic
metabolism of
warfarin,
phenobarbital,
phenytoin, diazepam,
propranolol, lidocaine,
theophylline, thus
increasing their activity
and toxicity.
No clinically
significant
interactions
established.

Pharmacokinetics
Absorption:
Incompletely absorbed
from GIT (50%).
Peak: 2–3 h PO.
Duration: 8–12 h.
Distribution: Distribu
ted into breast milk.
Metabolism: Liver.
Elimination: Urine &
feces.
Half-Life: 2–3 h.
Absorption: GIT (70%).
Peak: 1–1.5 h.
Distribution: crosses
blood–brain barrier and
placenta.
Metabolism: Liver.
Elimination: Most of
drug excreted in urine in
24 h; excreted in breast
milk.
Half-Life: 2 h
Absorption: GIT(4
0–50%)
Onset: 1 h.
Peak: 1–3 h PO;
0.5–3 h IV.
Duration: 10–12
h.
Metabolism: Liver.
Elimination: Urin
e.
Half-Life: 2.5–4 h.
Drug
Name
Ranitidine Cimetidine Femotidine

Ranitidine Cimetidine FemtodineNURSINGIMPLICATIONS
- Monitor creatinine
clearance if renal
dysfunction is present.
-Long-term therapy
may lead to vitamin
B12 deficiency.
-- Be alert for early
signs of hepatotoxicity
- jaundice (dark urine,
pruritus, yellow sclera
and skin), elevated
transaminases.
- Report breast
tenderness or
enlargement.
- Mild bilateral
gynecomastia and
breast soreness may
occur after 1 mo of
therapy. It may
disappear
spontaneously or
remain throughout
therapy.
 Monitor for signs of GI
bleeding.
 Be aware that pain
relief may not be
experienced for
several days after
starting therapy.
 Do not breast feed
while taking this drug
without consulting
physician.

(b) PROTON PUMP INHIBITORS:
Omeprazole, Esomeprazole, Lansoprazole,
Pantoprazole, Rabeprazole, Dexrabeprazole

DRUG
NAME
PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE
SODIUM
BRAND
NAME
Protonix, Protonix
IV
Losec , Prilosec AcipHex
AVAILABILITY 40 mg enteric
coated tablets;
40 mg vial
10, 20, 40 mg
capsules; 20 mg
powder for oral
suspension
20 mg tablets

ACTIONS
Gastric acid pump
inhibitor, belongs to a
class of antisecretory
compounds.
Gastric acid
secretion is decreased
by inhibiting the H+,
K+-ATPase enzyme
system responsible for
acid production
An antisecretory compound
that is a gastric acid pump
inhibitor.
Suppresses gastric acid
secretion by inhibiting the
H+, K+-ATPase enzyme
system [the acid (proton
H+) pump] in the parietal
cells.
Gastric proton pump
inhibitor that specifically
suppresses gastric acid
secretion by inhibiting the
H+, K+-ATPase enzyme
system [the acid (proton
H+) pump] in the parietal
cells of the stomach.
DRUG NAME PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE
SODIUM

PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE SODIUM
INDICATIONS
Short-term treatment
of erosive
esophagitis
associated with
gastroesophageal
reflux disease
(GERD).
•Duodenal & gastric ulcer.
•Long-term treatment of
pathologic
hypersecretory conditions
ZES, multiple endocrine
adenomas.
•In combination with
clarithromycin to treat
duodenal ulcers
associated
with Helicobacter pylori.
•GERD;
•Healing of duodenal
ulcers
•Treatment of
hypersecretory
conditions.

SODIUM
CONTRAINDICATIONS
Hypersensitivity to
pantoprazole or
other proton
pump inhibitors
(PPIs);
severe hepatic
insufficiency,
cirrhosis.
Long-term use for GERD,
duodenal ulcers; PPIs,
hypersensitivity; children <2
y; use of OTC formulation in
children <18 y or GI
bleeding; pregnancy (cat C).
Hypersensitivity to
rabeprazole,
lansoprazole, or
omeprazole or proton
pump inhibitors
(PPIs), lactation.

SODIUM
RouteAndDosage
Adult: PO 40 mg QID
8–16 wk
IV 40 mg QID 7–10 d
Adult: PO 20 mg OD
for 4–8 wk
Gastric Ulcer
Adult: PO 20 mg BD X
4–8 wk
Hypersecretory
Disease
Adult: PO 60 mg OD
DU associated with H.
pylori, Adult: PO 40
mg OD x 14 d
GERD, Adult: PO 20
mg QID
Healing DU, Adult:
PO 20 mg QID x 4
wk

SODIUM
ADVERSEEFFECTS(1%)
GI: Diarrhoea,
flatulence, abdominal
pain.
CNS: Headache,
insomnia.
Skin: Rash
CNS: Headache,
dizziness, fatigue.
GI: Diarrhoea,
abdominal pain,
nausea, mild transient
increases in LFT.
Uro: Hematuria,
proteinuria.
Skin: Rash.
Body as a Whole:
Headache.
Skin: (Rare) Stevens-
Johnson syndrome,
toxic epidermal
necrolysis, erythema
multiforme.

SODIUM
INTERACTIONS
- May decrease
absorption of
ampicillin,
itraconazole,
ketoconazole;
increases INR
with warfarin.
- administration of
diazepam, phenytoin,
warfarin and
omeprazole may
increase their
concentrations.
- It may decrease
absorption of
ketoconazole; may
increase digoxin
levels.

PHARMACOKINETICS
Absorption: Well
absorbed with 77%
bioavailability.
Peak: 2.4 h.
Metabolism:
Metabolized in liver.
Elimination: 71%
excreted in urine, 18%
in feces.
Half-Life: 1 h.
Absorption: Poorly
absorbed from GI tract;
30–40% reaches
systemic circulation.
Onset: 0.5–3.5 h.
Peak: 5 d.
Metabolism: Liver.
Elimination: 80%
excreted in urine, 20% in
feces.
Half-Life: 0.5–1.5 h
Absorption: 52%
bioavailability.
Metabolism: Liver
Elimination:
Excreted primarily in
urine.
Half-Life: 1–2 h.
SODIUM

DRUG
NAME
SODIUM
NURSINGIMPLICATIONS
 Monitor for and
immediately report
S&S of angioedema
or a severe skin
reaction.
 Lab tests: Urea
breath test 4–6 wk
after completion of
therapy.
 Lab tests: Monitor
urinalysis for
hematuria and
proteinuria.
 Periodic liver
function tests with
prolonged use.
 Lab tests: Routine
serum chemistry;
serum gastrin in
long-term therapy.
 Coadministered
drugs: Monitor for
changes in digoxin
blood level.

DRUG
NAME
SODIUM
PATIENT&FAMILYEDUCATION
 Contact physician if
blistering, loosening
of skin; skin rash,
itching; swelling of
the face, tongue, or
lips; difficulty
breathing or
swallowing.
 Do not breast feed
while taking this
drug.
 Report any changes
in urinary elimination
such as pain or
discomfort
associated with
urination, Heamturia.
 Report severe
diarrhoea; drug may
need to be
discontinued.
 Report diarrhoea,
skin rash, other
adverse effects to
physician.
 Do not breast feed
while taking this
drug.

Anticholinergic drugs:
Pirenzepine, Propantheline, Oxyphenonium
Prostaglandin analogue: Misoprostol

DRUG NAME PROPANTHELINE MISOPROSTOL
BRAND NAME Pro-Banthine, Propanthel Prostaglandin
AVAILABILITY 7.5 mg, 15 mg tablets 100 mcg, 200 mcg tablet
ACTIONS Decreases motility (smooth
muscle tone) in the GI, biliary,
and urinary tracts.
Results in antispasmodic action.
Synthetic prostaglandin
E1 analog, with both
antisecretory (inhibiting gastric
acid secretion) and mucosal
protective properties.
It Increases bicarbonate
and mucosal protective
properties also increases
bicarbonate and mucous
production.

USES  Peptic ulcer
 IBS
 Pancreatitis
 Urinary bladder spasm
- Prevention of NSAID (including
aspirin-induced) gastric ulcers in
patients at high risk of
complications from a gastric
ulcer (e.g., the older adult and
patients with a concomitant
debilitating disease or a history
of ulcers).
CONTRA.. Pregnancy (category C)
Lactation
Pregnancy, lactation.

ROUTE &
DOSAGE
Adult: PO 15 mg (Max: 120
mg/d)
Adult: PO 100–200 mcg QID.
ADVERSE
EFFECTS
(1%)
GI: Constipation, dry mouth.
EENT: Blurred vision, mydriasis,
increased intraocular pressure.
CNS: Drowsiness.
Urogenital: Decreased sexual
activity, difficult urination.
CNS: Headache.
GI: Diarrhoea, abdominal
pain, nausea, flatulence,
dyspepsia, vomiting,
constipation.
Urogenital: Dysmenorrhea,
uterine contractions.
INTERACTIO
N
Drug: Decreased absorption
of ketoconazole
Food: Food significantly
decreases absorption.
Drug: Magnesium-containing
antacids may increase
diarrhoea.

DRUG NAME PROPANTHELINE MISOPROSTOLPHARMACOKINETICS
Absorption: Incompletely
absorbed from GI tract.
Onset: 30–45 min.
Duration: 4–6 h.
Metabolism: 50% metabolized
in GI tract before absorption;
50% metabolized in liver.
Elimination: Excreted primarily
in urine; some excreted in bile.
Half-Life: 9 h.
Absorption: Readily absorbed
from GIT
Onset: 30 min.
Peak: 60–90 min.
Duration: At least 3 h.
Metabolism: Liver.
Elimination: Urine; small
amount excreted in feces.
Half-Life: 20–40 min.

Nursing Responsibility
- Assess bowel sounds, especially in presence of ulcerative colitis,
since paralytic ileus may develop.
- Be aware that older adult may respond to a usual dose with
agitation, excitement, confusion, drowsiness.
- Stop drug and report to physician if these symptoms are observed.

Patient & Family Education
- Void just prior to each dose to minimize risk of urinary hesitancy or
retention.
- Record daily urinary output.
- Relieve dry mouth by rinsing with water frequently, chewing sugar-free
gum or sucking hard candy.
- Maintain adequate fluid and high-fiber food intake to prevent
constipation.

Neutralization of gastric acid (Antacids)-
(a) Systemic: Sodium bicarbonate, Sodium citrate

DRUG
NAME
SODIUM BICARBONATE SODIUM CITRATE
CLASS
Gastrointestinal agent; antacid, fluid and
electrolyte balance agent
Gastrointestinal agent;
antacid
ACTIONS
-Neutralizes gastric acid to form sodium
chloride, CO2, and H2O.
-After absorption of sodium bicarbonate,
plasma alkali reserve is increased and
excess sodium and bicarbonate ions are
excreted in urine, thus rendering urine less
acid. Not suitable for treatment of peptic
ulcer because it is short-acting.
- a buffer and neutralizing
agent for gastric acid.
Sodium citrate is broken
down to sodium bicarbonate
which decreases the acidity
of urine, increasing the
excretion of substances that
cause kidney stones.

USES
 Antacid
 Cardiac Arrest
 Metabolic Acidosis
 Metabolic acidosis
 Buffer agent to neutralize
gastric acidity.
 Systemic alkalinizer.
CONTRAINDICATION
• Hypertension
• Pregnancy (category C)
• Hypersensitivity to sodium
citrate, citric acid, severe renal
impairment; oliguria;
azotemia.
DRUG NAME SODIUM BICARBONATE SODIUM CITRATE

ROUTE &
DOSAGE
Adult: PO 0.3–2 g 1–4 times/d or
½ tsp of powder in glass of water
P. O. 10 to 30 mL QID
ADVERSE
EFFECTS
GI: Belching, gastric
distention, flatulence.
Metabolic: Metabolic alkalosis;
hypocalcemia, hypokalemia,
dehydration.
Skin: Severe tissue damage
following extravasation of IV
solution.
Urogenital: Renal calculi,
impaired kidney function.
- Hypocalcemia
- Metabolic alkalosis
- Diarrhoea, nausea, vomiting

INTERACTION - May decrease absorption
of ketoconazole;
-may decrease elimination
of dextroamphetamine, ephedri
ne, pseudoephedrine, quinidine;
-may increase the absorption of
Aluminum Hydroxide.
-Amantadine: Alkalinizing Agents
may increase the serum
concentration of Amantadine.
- Amphetamines: Alkalinizing
Agents may decrease the
excretion of Amphetamines.

PHARMACOKINETICS
- Absorption: Readily
absorbed from GI tract.
- Onset: 15 min.
- Duration: 1–2 h.
- Elimination: Excreted
in urine within 3–4 h.
- Metabolism
≥95% via hepatic oxidation to
bicarbonate; may be impaired in
patients with hepatic failure,
shock, or severe illness
- Excretion
Urine
DRUG NAME SODIUM
BICARBONATE
SODIUM CITRATE

NURSINGRESPONSIBILITY
•Be aware that long-term use of oral
preparation with milk or calcium can
cause Milk-alkali syndrome: Anorexia,
nausea, vomiting, headache, mental
confusion, hypercalcemia,
hypophosphatemia, metabolic alkalosis.
•Patient may experience diarrhoea, N/V.
• Educate patient about signs of a
significant reaction (eg: wheezing, chest
tightness; fever, itching, seizures,
swelling of face, lips, tongue, or throat).
• Monitor Serum creatinine, BUN,
LFTs, serum bicarbonate and
urinary pH in patients with renal
disease.
• Monitor the Patient for
diarrhoea, N/V.
• Educate patient about signs of
a significant reaction (eg:
wheezing; chest tightness; fever;
itching, seizures or swelling of
face, lips, tongue).
DRUG
NAME
SODIUM BICARBONATE SODIUM CITRATE

Patient & Family Education
- Do not take antacids longer than 2 wk except under advice and
supervision of a physician.
- Self-medication with routine doses of sodium bicarbonate or soda
mints may cause sodium retention and alkalosis, especially when
kidney function is impaired.

(b) Non-systemic:
Magnesium hydroxide, Aluminium hydroxide,
Calcium carbonate, Magaldrate, Magnesium
trisilicate

Class Gastrointestinal agent,
antacid
Gastrointestinal agent;
antacid
Fluid and electrolytic
balance agent, antacid
ACTIONS
Acts as antacid in low
doses and as mild saline
laxative at higher doses.
Decreases rate of
gastric emptying and
has demulcent and mild
astringent properties.
Rapid-acting antacid with
high neutralizing capacity
and relatively prolonged
duration of action.
Decreases gastric
acidity and also increases
lower esophageal
sphincter tone.
Drug
Name
Magnesium
hydroxide
Aluminium
hydroxide
Calcium carbonate

USES
Occasional
constipation, for relief
of GI symptoms
associated with
hyperacidity, and as
adjunct in treatment of
peptic ulcer.
-poisoning by mineral
acids & arsenic.
- mouthwash to
neutralize acidity.
-Hyperacidity associated
with gastritis,
- esophageal reflux
- hiatal hernia
- adjunct in treatment of
gastric and duodenal
ulcer.
More commonly
used in combination with
other antacids.
Hyperacidity as in
acid indigestion,
heartburn, and hiatal
hernia.
Drug
Name
Magnesium hydroxide Aluminium hydroxide Calcium carbonate

CONTRAINDICATIONS
- Pregnancy (category B)
and in children <2 y
- pregnancy (category C). Hypercalcemia and
hypercalciuria (e.g.,
hyperparathyroidism,
vitamin D overdosage,
pregnancy (cat c).
Drug
Name
Magnesium
hydroxide
Aluminium hydroxide Calcium carbonate

ROUTE&
DOSAGE
- PO: 2.4–4.8 g (30–60
mL)/d OD/BD
- PO 600 mg TDS or QID PO 1–2 g BD or TDS
ADVERSEEFFECTS
GI: N/V, diarrhoea.
Metabolic: Electrolyte
imbalance with
prolonged use.
CV: Hypotension,
bradycardia
Resp: Respiratory
depression.
GI: Constipation, fecal
impaction, intestinal
obstruction.
Metabolic: Hypophosphat
emia, hypomagnesemia.
GI: Constipation,
Nausea
Metabolic: Hypercalc
emia with alkalosis,
hypercalciuria,
hypomagnesemia,
Uro: Polyuria, renal
calculi.
Drug
Name
Magnesium
hydroxide

PHARMACOKINETICS
Onset: 3–6 h
Absorption: 15–30% of
magnesium is absorbed.
Distribution: Small
amounts of magnesium
distributed in saliva and
breast milk.
Elimination: Excreted
in feces; some renal
excretion.
Absorption: Minimal
absorption.
Duration: 2 h when taken
with food; 3 h when taken
1 h after food.
Elimination: Excreted in
feces.
Absorption: Approxi
mately 1/3 of dose
absorbed from small
intestine.
Distribution: Cross
placenta.
Elimination: through
feces; small amounts
excreted in urine,
pancreatic juice, saliva,
breast milk.
Drug
Name
Magnesium
hydroxide

- Monitor S. Mg2++
with signs of hyper-
magnesemia such as
bradycardia.
- Note number and
consistency of stools.
Constipation is common
and dose related.
- Monitor periodic serum
calcium and phosphorus
levels with prolonged
high-dose therapy or
impaired renal function.
 Note number and
consistency of
stools.
 Determine serum
and urine calcium
weekly in patients
receiving prolonged
therapy and in
patients with renal
dysfunction.
Drug
Name
Magnesium hydroxide Aluminium
hydroxide
Calcium carbonate

Patient&FamilyEducation
 Report if persistent or
recurrent constipation.
 Do not breast feed
while using this drug.
• Increase phosphorus in
diet when taking large
doses of these antacids
for prolonged periods;
hypophosphatemia can
develop within 2 wk of
continuous use of these
antacids.
• Antacid may cause
stools to appear whitish.
•Do not take other oral
drugs, generally, within
1–2 h of an antacid.
•Do not breast feed
while taking this drug
without consulting
physician.
Drug
Name
Magnesium hydroxide Aluminium hydroxide Calcium carbonate

3. Ulcer protectives:
Sucralfate, Colloidal Bismuth subcitrate (CBS)

CLASSIFICATIONS
Gastrointestinal agent, antiulcer - It is water soluble but
precipitates at pH < 5.
- It is not an antacid but heals
60% ulcers at 4 weeks and 80–
90% at 8 weeks.
AVAILABI
LITY
1 g tablets; 10 mL suspension
DRUG
NAME
SUCRALFATE COLLOIDAL BISMUTH
SUBCITRATE (CBS)

ACTIONS
Sucralfate and gastric acid
react to form a viscous, adhesive,
paste-like substance that resists further
reaction with acid.
This "paste" adheres to the GI
mucosa with a major portion binding
electrostatically to the positively
charged protein molecules in the
damaged mucosa caused by alcohol or
other drugs.
The mechanism of action
of CBS is not clear; probabilities
are:
• May increase gastric mucosal
PGE2, mucus and HCO3 ¯
production.
• May precipitate mucus
glycoproteins and coat the ulcer
base.
• May detach and inhibit H.pylori
directly
DRUG
NAME
SUBCITRATE (CBS)

USES Short-term (up to 8 wk) treatment of
duodenal ulcer.
Gastritis and nonulcer dyspepsia
associated with H. pylori
CONTRA. Pregnancy (category B). Milk and antacids should not be
taken concomitantly.
ROUTE &
DOSAGE
Adult: PO 1 g QID. 120 mg taken ½ hr before 3
major meals
PHARMA.. Absorption: Minimally absorbed from
GI tract (<5%).
Duration: Up to 6 h (depends on
contact time with ulcer).
Elimination: 90% Excreted in feces.
Most of the ingested CBS passes
in the faeces.
Small amounts absorbed are
excreted in urine.
DRUG
NAME
SUBCITRATE (CBS)

ADVERSE
EFFECTS
GI: Nausea, gastric
discomfort, constipation,
diarrhoea.
Diarrhoea, Headache and
Dizziness.
INTERACTIONS
Drug: May decrease absorption of
QUINOLONES (e.g., ciprofloxacin,
norfloxacin), digoxin, phenytoin,
tetracycline.
DRUG
NAME
SUBCITRATE (CBS)

- Although healing has occurred within
the first 2 wk of therapy, treatment is
usually continued 4–8 wk.
- Be aware that constipation is a drug-
related problem.
- Increase water intake to 8–10 glasses
per day; increase physical exercise,
increase dietary bulk.
- Do not breast feed while taking this
drug without consulting physician.
-Patient acceptance of CBS is
compromised by blackening of
tongue, dentures and stools; and
by the inconvenience of dosing
schedule.
DRUG
NAME
SUBCITRATE (CBS)

4. Anti-H. pylori drugs: Amoxicillin, Clarithromycin,
Metronidazole, Tinidazole, Tetracycline
H. pylori infection starts with a neutrophilic gastritis lasting 7–10
days which is usually asymptomatic. Once established, H. pylori generally
persists for the life of the host. Up to 90% patients of duodenal and gastric
ulcer have tested positive for H. pylori. Antimicrobials that are used clinically
against H. pylori are: amoxicillin, clarithromycin, tetracycline and
metronidazole/tinidazole.

Cont.
◦ However, any single antibiotic is ineffective. Resistance develops rapidly,
especially to metronidazole/ tinidazole and clarithromycin, but amoxicillin
resistance is infrequent. In tropical countries, metronidazole resistance is
more common than clarithromycin resistance

Research Study
A study is conducted by Huang and Lee (2014) on
“Diagnosis, Treatment, and Outcome in Patients with Bleeding Peptic Ulcers
and Helicobacter pylori Infections”. They have searched Pubmed (to 15
March 2014) “ in which 129 articles were selected, and their reference lists
were checked for other possible studies for inclusion.

Result
Hp infection and NSAID use are two independent factors related to bleeding
peptic ulcers. PPI treatment is usually administered to patients with bleeding
peptic ulcers, even before endoscopic examination. This treatment can
facilitate the endoscopic hemostatic effect in reducing short-term rebleeding.
PPI treatment also has benefits for Hp eradication. One study demonstrated
that intravenous omeprazole can decrease the risk of peptic ulcer rebleeding
and may even improve the Hp eradication rate .
Confirmation of Hp eradication after completion of antibiotic treatment in
peptic ulcer bleeding is cost effective.

References
Audrey, J. (2012). Fundamentals of nursing. 9th ed. United state: Pearson Education
Inc. p. 565-576.
Thomas, L. (2010). Foye’s Principles of medicinal chemistry. 6th ed. New York: Wolter
Kluwer,.p.722-735.
Tripathi, K.D. (2009). Essential of Medical pharmacology. 6th edition. Jaypee Brother Medical
publisher, p.629-30.
Huang & Lee (2014). Diagnosis, Treatment, and Outcome in Patients with Bleeding Peptic
Ulcers and Helicobacter pylori Infections. BioMed Research International , 10.

Peptic Ulcer Drugs

More Related Content

What's hot

Similar to Peptic Ulcer Drugs

More from NAVANEETA KUSUM

Recently uploaded

Peptic Ulcer Drugs