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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.
PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE
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.
PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE
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
DRUG NAME PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE
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.
DRUG NAME PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE
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.
PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE
SODIUM
DRUG
NAME
PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE
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
PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE
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.
DRUG NAME PROPANTHELINE MISOPROSTOL
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.
DRUG NAME PROPANTHELINE MISOPROSTOL
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
DRUG NAME SODIUM BICARBONATE SODIUM CITRATE
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.
DRUG NAME SODIUM BICARBONATE SODIUM CITRATE
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
Aluminium hydroxide Calcium carbonate
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
Aluminium hydroxide Calcium carbonate
NURSINGRESPONSIBILITY
- 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
SUCRALFATE COLLOIDAL BISMUTH
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
SUCRALFATE COLLOIDAL BISMUTH
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
SUCRALFATE COLLOIDAL BISMUTH
SUBCITRATE (CBS)
NURSINGRESPONSIBILITY
- 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
SUCRALFATE COLLOIDAL BISMUTH
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.
THANK YOU

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Peptic Ulcer Drugs

  • 1. Drug Presentation On Peptic Ulcer Disease PRESENTED BY: Ms. Navaneeta Kusum M.Sc.Nsg.2nd Year, CON-ILBS
  • 2. 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.
  • 3. 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
  • 4. Goals The goals of antiulcer therapy are: • Relief of pain • Ulcer healing • Prevention of complications (bleeding, perforation) • Prevention of relapse.
  • 5. 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
  • 6. 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
  • 7. Classifications: 3. Ulcer protectives: Sucralfate, Colloidal Bismuth subcitrate (CBS) 4. Anti-H. pylori drugs: Amoxicillin, Clarithromycin, Metronidazole, Tinidazole, Tetracycline
  • 8. (a) H2 antihistamines: Cimetidine, Ranitidine, Famotidine, Roxatidine
  • 9. 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.
  • 10. 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
  • 11. 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)
  • 12. 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.
  • 13. 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.
  • 14. 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
  • 15. 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.
  • 16. (b) PROTON PUMP INHIBITORS: Omeprazole, Esomeprazole, Lansoprazole, Pantoprazole, Rabeprazole, Dexrabeprazole
  • 17. 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
  • 18. 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
  • 19. 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.
  • 20. PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE 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.
  • 21. PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE 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
  • 22. DRUG NAME PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE 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.
  • 23. DRUG NAME PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE 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.
  • 24. 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. PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE SODIUM
  • 25. DRUG NAME PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE 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.
  • 26. DRUG NAME PANTOPRAZOLE OMEPRAZOLE RABEPRAZOLE 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.
  • 27. Anticholinergic drugs: Pirenzepine, Propantheline, Oxyphenonium Prostaglandin analogue: Misoprostol
  • 28. 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.
  • 29. DRUG NAME PROPANTHELINE MISOPROSTOL 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.
  • 30. DRUG NAME PROPANTHELINE MISOPROSTOL 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.
  • 31. 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.
  • 32. 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.
  • 33. 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.
  • 34. Neutralization of gastric acid (Antacids)- (a) Systemic: Sodium bicarbonate, Sodium citrate
  • 35. 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.
  • 36. 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
  • 37. 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 DRUG NAME SODIUM BICARBONATE SODIUM CITRATE
  • 38. 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. DRUG NAME SODIUM BICARBONATE SODIUM CITRATE
  • 39. 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
  • 40. 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
  • 41. 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.
  • 42. (b) Non-systemic: Magnesium hydroxide, Aluminium hydroxide, Calcium carbonate, Magaldrate, Magnesium trisilicate
  • 43. 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
  • 44. 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
  • 45. 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
  • 46. 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 Aluminium hydroxide Calcium carbonate
  • 47. 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 Aluminium hydroxide Calcium carbonate
  • 48. NURSINGRESPONSIBILITY - 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
  • 49. 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
  • 50. 3. Ulcer protectives: Sucralfate, Colloidal Bismuth subcitrate (CBS)
  • 51. 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)
  • 52. 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 SUCRALFATE COLLOIDAL BISMUTH SUBCITRATE (CBS)
  • 53. 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 SUCRALFATE COLLOIDAL BISMUTH SUBCITRATE (CBS)
  • 54. 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 SUCRALFATE COLLOIDAL BISMUTH SUBCITRATE (CBS)
  • 55. NURSINGRESPONSIBILITY - 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 SUCRALFATE COLLOIDAL BISMUTH SUBCITRATE (CBS)
  • 56. 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.
  • 57. 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
  • 58. 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.
  • 59. 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.
  • 60. 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.