Peptic ulcers develop in the lining of the stomach, duodenum, or esophagus when acidic digestive juices damage the protective mucus layer. Common symptoms include stomach pain relieved by food or antacids. While acid contributes to ulcer formation, infection with H. pylori bacteria is now the leading cause. Treatment focuses on reducing acid with H2 blockers or proton pump inhibitors, eliminating H. pylori, and counseling lifestyle changes.

1. Peptic Ulcer

2. aims
Definition
Location and symptoms
Causes
Types
Complication and treatment
Precautions
Patient counselling

3. Peptic ulcer
• Peptic ulcers are hole or open sore that develop on the inside lining of the
stomach, duodenum(beginning of the small intestine), or esophagus.
• The most common symptom of a peptic ulcer is stomach pain.
• An ulcer occurs when the lining of these organs is corroded by acidic
digestive juices secreted by the stomach cells.

4. Location of peptic ulcer
Ulcer may be found
• In esophagus
• Stomach and duodenum
• Jejunum at multiple levels(Zollinger Ellison Syndrome).

5. Different types of Ulcer
• Hyper acidity
• Gastroesophageal Reflux Disease(GERD)
• Stress induced ulcer( Curling’s Ulcer)
• NSAIDS induced ulcer
• Peptic ulcer
• Duodenal ulcer
• Ulcer due to H. pylori
• Zollinger Ellison Syndrome

6. Agents that increase HCl secretion

7. Agents which decrease the HCl secretion
• Somatostatin
• Secretin
• cholecystokinin

8. Natural defense mechanism of Stomach
• Naturally increase HCO3- secretion
• Increase the secretion of mucin
• Prostaglandins (PGE2)
• Increased mucosal blood flow
• Epithelial renewal

9. Causes of peptic ulcer
• While acid is still considered significant in ulcer formation, the leading cause
of ulcer disease is currently believed to be infection of the stomach by
bacteria called Helicobacter pyloridus (H.pylori)

10. • Stress increases HCl secretion.

11. • Chronic use of Anti-inflammatory medications, commonly referred to as
NSAIDs.

12. Cofactors
• Cigarette smoking
• Alcohol intake
• Coffee
• Colas
• Spicy foods
• Caffeine ,beer,

13. Symptoms
Abdominal discomfort usually occurs in epigastric area (upper middle part of
the abdomen) radiating to the back described as..
• Dull gnawing ache comes and goes for several days.The pain is often
epigastric and described as burning .
• A typical nocturnal pain may awaken patients from sleep, especially
between 12AM and 3 AM.
• Pain from Duodenal Ulcer occurs 1 to 3 hrs after meals. And is usually
relieved by food, where as food may precipitate or accentuate ulcer pain in
gastric ulcer.
• Pain is relieved by eating and antacid medication.

14. Other symptoms
• Weight changes
• fatigue

15. Other symptoms
• bloating

16. Other symptoms
• Chest pain
• burping

17. Other symptoms
• Nausea and Anorexia(common with gastric ulcer)
• Vomiting(relieves episodes of severe pain due to evacuation of gastric acid
content)

18. Less common symptoms
• Constipation and 5% of the patients with chronic duodenal ulcers has
predominantly colonic symptoms.
Heartburn and eructation are also commonly associated with ulcer activity.
Note- heartburn is so prominent that the primary disease is thought to be
esophageal.
This Photo by Unknown Author is licensed under
CC BY-NC-ND
This Photo by Unknown Author is

19. Emergency symptoms
• If you have an of these symptoms call the Doctor right away.
• Sharp sudden persistent stomach.
• Bloody or black stools.
• Bloody vomit or vomit that looks like coffee grounds.
They could be
signs of a serious
problem such as
perforation when
the ulcer burrows
through the
stomach or
duodenal wall.
Bleeding when the ulcer blocks
the path of food trying to leave
the stomach.
This Photo by Unknown Author is licensed under CC BY-
SA-NC
This Photo by Unknown Author is licensed
under CC BY
This Photo by Unknown Author is
licensed under CC BY

20. Gastric ATPase
• The Gastric Hydrogen potassium ATPase or H+/K+ATPase is the proton pump of
the stomach.
• It exchanges intestinal lumen with cytoplasmic hydronium ion.
• Function – Primarily responsible for the acidification of the stomach contents
and activation of the digestive enzyme pepsin.
• H+/K+ATPase found in Parietal cells.
Parietal cells are highly
specialized epithelial cells,
located in the inner cell lining of
the stomach called gastric
mucosa

21. Gastric acid(HCl)
• Gastric acid, gastric juice or stomach acid, is a digestive fluid formed
within the stomach lining.
• A typical adult human will secrete about 1.5 liters of gastric acid daily.
• The production of gastric acid is tightly regulated by positive regulators and
negative feedback mechanisms.
• Four types of cells are involved in this process, parietal cells, G cells, D cells
and ECL cells.
• Nerve endings in the stomach secrete two stimulatory neurotransmitters-
acetylcholine, gastrin releasing peptide(Bombesin)
• Hypochlorhydria and achlorhydria, hypocholeremic metabolic alkalosis.

22. Mechanism of HCl Production

27. Test and diagnosis
• Non-invasive-Urea BreathTest, blood test
• Invasive –Histology, Biopsy UreaseTest
• Other tests- Culture, Stool antigen test, Endoscopy, Upper GI X-ray

28. Management
• Life style modification
• Hyposecretory drug therapy
• H.pylori eradication therapy
• Surgery

29. Goals ofTreatment
• Lowering the amount of acid that stomach makes
• Neutralizing the acid
• Protecting the injured area
• Stop smoking and drinking of alcohol
• Prevent complications (bleeding, perforation, penetration, Obstruction)
• Minimize recurrences.
• Reduce financial costs.

30. Life style and Home remedies
• Don’t smoke
• Limit or avoid alcohol
• Less coffee and carbonated beverages
• Use of olive oil
• Avoid NSAIDs
• Exercise
• Fruits and vegetables
• Stress relief

31. Treatment of Peptic Ulcer
1.Reduction of Gastric acid secretion
H2 antihistamines-Cimetidine, Ranitidine, Famotidine, Roxatidine
Proton Pump Inhibitors- Omeprazole, Lansoprazole, Pantoprazole,
Rabeprazole, Esomeprazole, Dexlanzoprazole
Anticholinergics-Pirenzepine, Propantheline,Oxyphenonium
Prostaglandin analogues- Misoprostol
2.Neutralization of Gastric acid (Antacids)
Systemic- Sodium bicarbonate, Sodium citrate
Non-systemic- Magnesium hydroxide, Mag.Trisilicate,Aluminium hydroxide
Gel, Magaldrate, Calcium Carbonate.
3. Ulcer Protetives- Sucralfate, Colloidal bismuth subcitrate
4. Anti-H Pylori drugs- Amoxicillin, Clarithromycin, Metronidazole,Tinidazole,
Tetracycline

32. H2 antagonist( H2RAs OR H2 BLOCKERS)
• These are drugs that block the action of histamine at the histamine H2
receptors of the parietal cells in the stomach.This decreases the production
of stomach acid.
• Prototype- Cimetidine--- Sir JamesW Black and C. Robin Ganellin at Smith,
Kline and French(GlaxoSmithKline) in 1960.
• First marketed in 1976. (Tagamet)
• H2 antagonists are a type of antihistamine, although in common use the
term “antihistamine” is often reserved for H1 antagonists.

33. History and Development
Nα-guanylhistamine-a partial H2 receptor antagonist
Burimamide – specific competitive antagonist
Metiamide- effective ( nephrotoxicity and
agranulocytosis)
Cimetidine

34. • Cimetidine
• Ranitidine
• Famotidine
• Nizatidine
• Roxatidine
• Lafutidine
• Lavoltidine(discontinued as carcinogen)
• Niperotidine (withdrawing as causing liver damage)

35. Pharmacology
• H2 blockade-The H2antagonists are competitive antagonists of histamine at
the parietal cell’s H2 receptor.They suppress the normal secretion of acid by
parietal cells and meal-stimulated secretion of acid.
• The only significant invivo action of H2 blockers is marked inhibition of gastric
secretion. All phases (basal, psychic, neurogenic, gastric)of secretion are
suppressed dose-dependently, but the basal nocturnal secretion is suppressed
more completely.
• The volume , pepsin content and intrinsic factor excretion are also reduced.
• They do not have effect on gastric or esophageal motility or on lower
esophageal sphincter (LES) tone.

36. Pharmacokinetics
• Cimetidine is adequately absorbed orally, though bioavailability is 60-80%
due to first hepatic metabolism.
• Absorption is not interfered by presence of food in stomach.
• It crosses placenta and reaches milk. But penetration in brain is poor.
• About 2/3 of a dose is excreted unchanged in urine and bile, the rest as
oxidized metabolites.
• The elimination half life is 2-3 hrs.
• Dose reduction is needed in renal failure.

37. ADR
• Headache , dizziness, bowel upset, dry mouth, rashes
• CNS effects like confusional state, restlessness, convulsions and coma have
occurred infrequently in elderly patients in those with renal impairment.
• Always be given by slow infusion.
• Antiandrogenic effects,-gynecomastia, loss of libido, impotence and temporary
decrease in sperm count.
• Transient elevation of plasma aminotransferases.

38. Drug interactions
• Cimetidine is an inhibitor of Cytochrome P450(CYP) enzymes and reduces
hepatic blood flow. So cimetidine may increase their serum concentrations to
toxic levels of drugs are warfarin, theophylline, phenytoin, lidocaine, quinidine,
propranolol, labetalol, metoprolol, methadone, tricyclic antidepressants, some
benzodiazepines, dihydropyridine calcium channel blockers, sulfonylureas,
metronidazole and some recreational drugs as ethanol and methylene dioxy
methamphetamine(MDMA).
• Metabolism of propranolol and diazepam is also retarded.(No significant)
• Antacid reduce the absorption of all H2 blockers. When used concurrently a gap
of 2hrs should be allowed.
• Ketoconazole absorption is decreased by cimetidine.
Dose –for ulcer healing400mg BD or 800mg at bed
time. Maintenance dose- 400mg
For stress ulcer- 50mg/hr i.v infusion

39. RANITIDINE
Furan ring
About 5 times more potent than cimetidine.
t1/2 2-3hr similar to cimetidine.(pharmacokinetic profile)
A longer duration of action with greater 24hr acid suppression is obtained.
No androgenic action
Lesser permeability into the brain.
Does not significantly inhibit hepatic metabolism of other drugs.
Overall incidence of side effects is lower- headache, diarrhoea/constipation, dizziness
Dose
300mg at bed time or 150mg BD,
For maintenance 150mg at bed time
Parenteral dose 50mg i.m or slow i.v( rapid i.v injection can cause hypotension.)
For Gastrinoma 300mg 3-4 times a day.

40. Famotidine
A thiazole ring containing H2 blocker.
Longer duration of action.
Elimimation t1/2 2.5-3.5 hr
5-8 times more potent than ranitidine
and no androgenic action.
Oral bioavailability is 40-50%.
Excreted by the kidney, 70% in the
unchanged form.
ADR is low- headache, dizziness, bowel
upset, rarely disorientation and rash.
Dose – 40mg at bed time or 20mg
BD,ZES- 480mg/day,
High potency and
longer duration- ZES
and for prevention of
aspiration Pneumonia.

41. Roxatidine
Similar to Ranitidine
Twice as potent and longer acting.
No antiandrogenic action.
Dose – 150mg at bed time or 75 mg BD.

42. ADR
• Hypotension (Infrequent)
• Rare ADRs-headache, tiredness, dizziness, confusion, diarrhea,
constipation, rash.
• In addition cimetidine- gynocomastia, loss of libido, impotence(more than
one month or longer)
• Risk of pneumonia.

43. Clinical uses
Duodenal
ulcer
Gastric
ulcer
Stress
ulcer and
gastritis
Zollinger-
Ellison
Syndrome
Gastroeso
phageal
Reflux
Diseases(
GERD)
Prophylax
is of
aspiration
pneumoni
a
Other
uses-
adjuvant
in case of
urticaria.

44. Patient counseling
• These products have been approved for the relief of “heartburn associated
with acid indigestion, and sour stomach”.They should not be taken for
longer than 2 weeks and are not recommended for children < 12 years of
age.

45. PROTON PUMP INHIBITORS(PPIs)

47. PPIs
• Proton Pump Inhibitors (PPIs) block the gastric hydrogen potassium
ATPase(H+/K+ ATPase) and inhibit gastric acid secretion.

48. History and Basic structure
• At the end of 1970s–Timoprazole-it is a pyridylmethylsulfinyl benzimidazole
compound.
• High degree of anti-secretory activity.
• PPIs can be divided into two groups based on their basic structure.
• Omeprazole (1979)- first new class of drug., Marketed in 1988.
• Pantoprazole
• Esomeprazole
• Lansoprazole
• Rabeprazole
Substituted
pyridine part
Benzimidazoles

49. PPIs are prodrugs- activate in acid environment.
In acidic solutions, the sulfenic acid is isolated before reaction with one or more
cysteines from the luminar surface of the enzyme, a tetracyclic sulfenamide.
The effectiveness of PPIs derives from
1. The target, H+/K+ATPase which is responsible for the last step in acid secretion.
2. Covalent binding of the activated drug to the enzyme , resulting in a duration of
action that exceeds their plasma half life.

50. Mechanism

54. Omeprazole
• It is the prototype member of Substituted benzimidazoles which inhibit the final
common step in gastric acid secretion.
• Dose dependent suppression of gastric acid secretion without anticholinergic and
H2 blocking action.
• Omeprazole is inactive at neutral pH , but at pH<5 rearranges to two charged
cationic forms( a sulphenic acid and a sulphenamide configurations) that react
covalently with SH groups of th H+K+ATPase enzyme and inactivate irreversibly.
• It also inhibits gastric mucosal carbonic anhydrase.

55. • The oral absorption of Omeprazole is ~50%, because of instability at acidic PH.
• Bioavailability of all PPIs is reduced by food, they should be taken in empty
stomach, followed I hr later by a meal to activate the H+K+ATPase and make it
more susceptible to PPIs.
• Omeprazole is highly plasma protein bound, rapidly metabolized in liver by
CYP2C19 andCYP3A49 (Plasma half life ~1 hr) and metabolites are excreted in
urine.
• No dose modification is needed in elderly or in renal/ hepatic impairment.
Because tight binding to its target enzyme.
• Inhibition of HCl secretion occurs within 1 hr, reaches maximum at 2hr, is still
half maximal at 24hr and last for 3 days.
• Dose- 20-40mg OD
• Available as enteric- coated tablets, capsules, powder for oral suspensions,
powder for i.v injection.

56. Interactions
• Omeprazole inhibits the oxidation of certain drugs- diazepam, phenytoin
and warfarin levels may be increased.
• Clarithromycin inhibits omeprazole metabolism and increases its plasma
concentration.

57. Lanzoprazole
• More potent than Omeprazole
• It was the second of PPIs drugs to reach market.(Europe, US)
• inhibition of H+K+ ATPase by lansoprazole is partly reversible.
• Higher oral bioavailability, faster onset of action and slightly longer t1/2 than
omeprazole.
• It inhibits the absorption of Atazanavir, digoxin, ketoconazole, iron salts,
amoxicillin esters, theophylline.
• Dose should be reduced in liver disease.
• Dose- 15-30 mg OD
• Available as capsule, tablet as well as chewable tablets.

58. Pantoprazole
• Similar in potency and clinical efficacy to omeprazole.
• Third PPI introduced in German Market in 1994.
• More acid stable and has higher oral bioavailability.
• It has lower affinity for Cytochrome P450 than omeprazole and lansoprazole.
• Available as gastroresistant or delayed release tablets and as lyophilized
powder for I.V use.
• Dose- 40 mg OD
• S-Pantoprazole – It is the active single enantiomer, twice as potent as the
racemate., Dose 20mg tab

59. Rabeprazole
• Fastest acid suppression (due to higher pKa it is more rapidly converted to
the active species) and to aid gastric mucin synthesis.
• It sis a novel benzimidazole compound on market 1999 USA.
• Dose- 20mg OD
• It is available as enteric coated tablets.

60. Esomeprazole
• It is the S(-)-enantiomer of omeprazole.
• In 2001 launched in USA.
• High oral bioavailability and to produce better control of intragastric pH than
omeprazole in GERD patients because longer t1/2.
• Higher healing rates of erosive esophagitis and better GERD symptoms relief
have been reported.
• Dose – 20-40mg OD, pellet form in capsules.

61. Dexlansoprazole
• Introduced in 2009.
• It is the R(+)- enantiomer of Lansoprazole.
• The advantage is the Pharmaceutical formulation of the drug, which is
based on a dual release technology.
• Dose – 30mg OD

62. Uses
• GERD
• Helicobacter pylori infection
• Peptic ulcer- gastric, duodenal
• Prevention and treatment of NSAIDs induced lesions
• Functional dyspepsia
• Increased Gastric acid- ZES
• Stress gastritis prevention.
• Barrett’s esophagitis.

63. DIRECTION FOR USE
 Do not split, crush, or chew Delayed-Release Tablets.
 Swallow Delayed-Release Tablets whole, with or without food in the stomach.
 Concomitant administration of antacids does not affect the absorption of Delayed-Release
Tablets.
 Take a missed dose as soon as possible. If it is almost time for the next dose, skip the missed
dose and take the next dose at the regular scheduled time. Do not take 2 doses at the same
time.

64. Drugs to Avoid:
o Ampicillin, atazanavir, dasatinib, digoxin, erlotinib, itraconazole, ketoconazole,
methotrexate, mycophenolate mofetil, nelfinavir, nilotinib, saquinavir, sofosbuvir,
o Blood thinner (including warfarin)
o Diuretic
o Iron supplements
o Diazepam , citalopram, phenytoin

65. Possible side effects
• Gastrointestinal-abdominal pain, diarrhea, nausea, vomiting
• Neurologic- headache, dizziness

66. Rare
• Git –constipation, dry mouth, hepatitis
• Blood problems-low white blood cell count, thrombocytopenia
• Immunologic- stevens-johnson syndrome, toxic epidermal necrolysis
• Metabolic- elevated creatine kinase, elevated cholesterol levels, elevated
liver enzymes(AST/ALT), swelling
• Musculoskeletal-muscle disorders, bone fractures and infection, clostridium
difficile infection, osteoporosis- related hip fracture, rhabdomyolysis.

67. Warnings While Using This Medicine (long term side effects)
• Tell your doctor if you are pregnant or breast feeding, or if you have kidney disease, liver
disease, lupus, or osteoporosis.
• Avoid scheduled use of proton pump inhibitors for longer than 8 weeks in older adults, due to
risk of Clostridium difficile infection and bone loss and fractures, unless needed for high-risk
patients (eg, oral corticosteroids, chronic NSAID use), erosive esophagitis, Barrett's esophagitis,
pathological hypersecretory condition, or need for maintenance treatment (eg, due to failure of
drug discontinuation or histamine-2 blockers)
• Endocrine and Metabolic: Hypomagnesemia has been reported in patients treated with proton
pump inhibitors for at least 3 months; tetany, arrhythmias, and seizures may occur; monitoring
recommended with prolonged use or concomitant drugs that may cause hypomagnesemia;
discontinuation may be required. Vitamin B12 deficiency may occur with prolonged use (eg
greater than 1 to 2 years); monitoring recommended

68. CONTID……..
• Gastrointestinal: Use is associated with an increased risk of fundic gland polyps that increases with
long-term use, especially beyond one year; use shortest duration of therapy appropriate to the
condition being treated
• Hematologic: Thrombophlebitis has been reported with IV administration
• Immunologic: Anaphylaxis and other serious reactions, including erythema multiforme, Stevens-
Johnson syndrome, and toxic epidermal necrolysis have been reported with IV administration.
• Musculoskeletal: Osteoporosis-related bone fracture of hip, wrist, or spine may occur, especially
with higher (multiple daily) doses or longer duration of therapy (1 year or longer); use lowest dose
and shortest treatment duration
• Renal: Acute tubulointerstitial nephritis has been reported with proton pump inhibitor use; may
occur at any point during therapy. Discontinue use if suspected
• Dermatologic: New or worsening cutaneous lupus erythematosus has been reported within weeks
to years after continuous drug therapy; avoid using for longer than medically indicated and
discontinue use if suspected

69. When This Medicine Should Not Be Used:
• This medicine is not right for everyone. Do not use it if you had an allergic reaction to
pantoprazole or similar medicines.
• Do not use if you have angioedema, bronchospasm, acute tubulointerstitial nephritis, and
urticaria.
• Concomitant use with atazanavir or nelfinavir is not recommended. Do not use
with rilpivirine-containing products

70. • Monitoring: Monitor serum magnesium and serum Vit. B12 periodically if you are on long
term treatment with pantoprazole
• Missed dose: Take a dose as soon as you remember. If it is almost time for your next dose,
wait until then and take a regular dose. Do not take extra medicine to make up for a missed dose.
• Storage: Store the medicine in a closed container at room temperature, away from heat,
moisture, and direct light. Keep all medicine out of the reach of children. Never share your
medicine with anyone.

71. Prescribing PPIs-
The lowest effective dose of the cheapest drug for the shortest
possible time.
• PPIs are one of the most frequently prescribed classes of drugs in the world
becuase of –
1. High level of Efficacy
2. Low toxicity
3. Reduced cost
4. Lack of alternative therapy

72. Imidazopyridines-Tenatoprazole
• It is an Imidazopyridine PPIs, is a novel compound.
• Prolonged plasma life- 7hrs. Similar activity as other PPIs.
• It reduces the rate of metabolism, allowing longer plasma residence.
• Increased bioavailability.( crystal structure and hydrophobic in nature)

73. Acid pump antagonists(APAs)
• Potassium- competitive acid blockers (PCABs) are a third type of inhibitor
that blocks acid secretion by binding to the K+ active site.
• APAsprovide faster inhibition than PPIs, because they do not require acid
activation.
• Eg- Revaprazan- Ist APA(South Korea)

74. Anticholinergics
• Pirenzepine- it is a selective M1 anticholinergics (Europe)

75. Prostaglandin Analogue
• PGE2 and PGI2 are produced in the gastric mucosa and appear to serve a
protective role by inhibiting acid secretion and promoting mucus +HCO3-
secretion.
• in addition PGs inhibit gastrin production, increase mucosal blood flow and
probably have an ill-defined ‘cytoprotective’ action.
• Most important is ability to reinforce the mucus layer covering gastric and
duodenal mucosa which is buffered by HCO3- secreted into this layer by the
underlying epithelial cells.
• Natural PGs have very short t1/2.

76. Misoprostol( Methyl –PGE1 ester)
• It inhibits acid output dose dependently.
• Shorter duration of action (~3hr)
• Ulcer healing rates comparable to cimetidine have been obtained in 4-8 weeks. But
Misoprostol is poorer in relieving ulcer pain.
• Dose- 200µg QID.
• ADR- diarrhea, abdominal cramps, uterine bleeding, abortion, need multiple daily
dose.
• Use- prevention and treatment of NSAIDs associated GI injury and blood loss.

77. Antacids
• These are basic substances which neutralize gastric acid and raise pH of gastric
contents.
• Antacids do not decrease acid production , rather agents that raise the antral pH to
> 4 evoke reflex gastrin release more acid is secreted, especially patients
with hyperacidity and duodenal ulcer, “ acid rebound” occurs and gastric motility is
increased.
• The potency of an antacid is generally expressed in terms of its acid neutralizing
capacity.(ANC)
• Taken with meals antacids may act for at the most 2-3 hr.

79. SystemicAntacids- Sodium bicarbonate
• It is water soluble, acts instantaneously, but duration of action is short.it is potent
neutralizer.(1G- 12mEq HCl), pH may rise above 7.
• Demerits
Absorbed systemically, large doses will induce alkalosis.
Produce CO2 on stomach- distention, discomfort, belching, risk of ulcer
perforation
Acid rebound occurs, but is usually short lasting.
Increases Na+ load, may worsen edema and CHF
• Use- quick symptomatic relief, alkalinize urine and to treat Acidosis.
• Dose- 325mg – 2g

80. Non- systemic antacids
• These are insoluble and poorly absorbed basic compounds.
• React in stomach to form the corresponding chloride salt.The chloride salt
again reacts with the intestinal bicarbonate, no acid –base disturbance
occurs.

81. Magnesium hydroxide
• It has low water solubility.
• Its aq. Suspension( Milk of Magnesia) has low con. Of OH- ions and thus low
alkalinity.
• Rebound acidity is mild .
• Dose- Milk of Magnesia 0.4g/5ml suspension, 5 ml neutralizes 12mWq acid.

82. Magnesium trisilicate
• Low solubility and reactivity. About 5% of administered Mg is absorbed
systemically- If renal function inadequate
• All Mg salts have a laxative action. Soluble Mg salts are used as Osmotic
purgatives.
• 1 g can react with 10 mEq acid, but in clinical use only about 1 mEq is
neutralized.

83. Aluminium hydroxide gel
• It is a bland, weak, and slowly reacting antacid. On keeping it slowly polymerizes to
variable extents into still less reactive forms.
• Thus ANC of a preparation gradually declines on storage.
• 5 ml of its suspension may neutralize just 1 mEq HCl.
• The Al3+ ions relax smooth muscle, thus it delays gastric emptying – constipation-
due to its smooth muscle relaxation and mucosal astringent action.
• Alu. Hydrox. Binds phosphate in the intestine and prevents its absorption-
hypophosphatemia occurs on regular use. This may
Cause Osteomalacia
Be used therapeutically in hyperposphatemia and phosphate stones.
• Small amountAl3+ that is absorbed is excreted by kidney- no renal failure---
aluminium toxicity can occur- encephalopathy, osteoporosis.
• ALUDROX-0.84g tab, 0.6g/10ml susp.

84. Magaldrate
• It is a hydrated complex of hydroxy magnesium aluminate that initially
reacts rapidly with acid and releases Alum. hydro.Which then reacts more
slowly.
• The freshly released alum. Hydro. Is in the unpolymerized more reactive
form. Its ANC is estimated to be 28mEq HCL/g.
• Stacid- 400mg tab, 400mg/5ml susp., ULGEL

85. Calcium carbonate
• It is a potent and rapidly acting acid neutralizer. (1g- 20mEq HCl)
• It liberatesCO2 in the stomach at a slower rate than NaHCO3, it can cause
distension and discomfort.
• The Ca2+ ions are partly absorbed.
•Demerits
Acid rebound occurs.
Milk alkali syndrome- headache, anorexia, weakness, abdominal
discomfort, abnormal ca deposits and renal stones due to concurrent
hypercalcemia and alkalosis.

86. Antacid combinations
• Fast (Mag.hydro) and Slow (Alum. hydro.)
• Acting components yield prompt as well as sustainable effect.
• Mg. salts are laxative, while Alum salts are constipating.- bowel movement
may be least affected.
• Gastric emptying is least effected.
• Dose of individual components is reduced. Systemic toxicity is reduced.

89. Drug interactions
• By raising gastric pH and forming complexes, the non-absorbable antacids
decrease the absorption of many drugs, especially tetracyclines, iron salts,
fluoroquinolones, ketoconazole, H2 blockers, diazepam, phenothiazines,
indomethacin, phenytoin, isoniazid, ethambutol and nitrofurantoin.
• Increased stomach pH
• Increased urinary pH
• Uses
Only for intercurrent pain relief and acidity. Continue to be used for non-ulcer
dyspepsia and minor episodes of heartburn., GERD

90. Patient counseling
• Allergies and preexisting conditions that may restrict use of antacids-fluid
imbalance, renal diseases, pregnancy, lactation,CHF, GI obstruction
• Use with caution with other medications due to the many drug interactions.
• Antacids may cause premature dissolving of enteric –coated medications, resulting
in stomach upset.
• Be sure that chewable tablets are chewed thoroughly, and liquids forms are shaken
well before giving.
• Administer with at least 8 ounces of water to enhance the absorption.( except for
the rapid dissolve form).
• Caffeine, alcohol, spicy foods, and black pepper may aggravate the underlying GI
condition.
• Monitor for side effects
• Monitor for therapeutic response

91. Ulcer protectives
•Sucralfate-it is a basic aluminium salt of sulfated sucrose
• Sucralfate polymerizes at pH< 4 by cross linking of molecules, assuming a sticky
gel like consistency.
• It preferentially and strongly adheres to ulcer base especially duodenal ulcer. It
precipitates surface proteins at ulcer base and acts as a physical barrier preventing
acid, pepsin and bile from coming in contact with ulcer base.
• Sucralfate has no acid neutralizing action, but delays gastric emptying.
• Augmented gastric mucosal PG synthesis may supplement physical protective
action of sucralfate.
• It is considered to be superior in patients who continue to smoke.

92. • Dose – the ulcer healing dose of sucralfate is 1G taken 1 hr before the 3
major meals and the bed time for 4-8weeks.
• Antacids should not be taken with sucralfate because its polymerization is
dependent on acid pH.
• ADR- Constipation -2% patients
Induces hypophosphatemia
Dry mouth and nausea are infrequent.

93. USES
• Healing of both duodenal and gastric ulcers.
• Bile reflux, gastritis and prophylaxis of stress ulcers.
• Topical formulation of sucralfate PESIGUARD LIGHT GEL is available for
application on burns, bedsores, diabetic/radiation ulcers, Excoriated skin
etc. as a protective.

94. Interactions
• Sucralfate adsorbs many drugs and interferes with the absorption of
tetracyclines, fluoroquinolones, cimetidine, phenytoin and digoxin.
• Antacids given concurrently reduce the efficacy of sucralfate.

95. Colloidal bismuth subcitrate (CBS:
Tripotassium diciratobismuthate)
• It is a colloidal bismuth compound, water soluble but precipitates at pH<5.
• Increased secretion of mucus and bicarbonate through stimulation of
mucosal PGE2 production.
• CBS and mucus form a glycoprotein-Bicomplex which coats the ulcer and
acts as a diffusion barrier to HCl.
• Detaches H.pylori from the surface of mucosa and directly kill this organism
involved in causation of ulcers and relapses.

96. USES
• Gastritis and nonulcer dyspepsia associated with H. pylori are also improved
• Dose – 120mg taken 1 hr before 3 major meals and at bedtime for 4-8
weeks.
• Milk and antacids should not be taken concomitantly.

97. Most of the ingested CBS passes in the faeces.
Small amounts absorbed are excreted in urine.
• Side effects- diarrhea, headache, dizziness
• Prolonged use has the potential to cause osteodystrophy and
encephalopathy due to bismuth toxicity.
• Blackening of tongue, dentures and stools
• Presently used occasionally in Anti H.pylori treatment.

98. Anti- Helicobacter pylori drugs.
• H. Pylori is a gram negative bacillus uniquely adapted to survival in the
hostile environment of stomach.
• It attaches the surface epithelium beneath the mucus, has high urease
activity.
• It produces ammonia which maintains a neutral environment around the
bacteria and promotes back diffusion of H+ ions.

99. Diagnosing H.Pylori
• H. Pylori diagnosed through
Blood
Breath test
Stool
Tissue test
This Photo by Unknown Author is licensed under CC BY-SA-NC

100. H. Pylori EradicationTherapy
• Triple therapy
Proton pump inhibitor(BD)
2 Antibiotics
Metronidazole + Clarithromycin(500mg BD)
Clarithromycin+ Amoxicillin( 1G+500mg BD)
• QuadrupoleTherapy( A 4 drug regimen)
PPI+Tetracycline+ CBS+ Metronidazole

101. Failed Eradication
• If the initial treatment fails to eradicate HP, second line empiric treatment should
Use antibiotics that were not included in the initial regimen
Include antibiotics that do not have resistance problems
Use a drug that has a topical effect(CBS) and
Be extended to 14 days
Thus if a PPI- amoxicillin- clarithromycin regimen fails, therapy should be
instituted with a PPI, Bismuth subsalicylate, metronidazole and tetracycline for 14
days.

103. Carminatives- an agent that prevent or relieves flatulence
in GI tract.
 These are mixtures of essential oils and herbal spices.
 Used to treat digestive disorders.it is used to digest CH,
fats, proteins, and to treat dyspepsia, flatulence and colic
pain.
 They help to increase gastric emptying and mildly
irritating to the gastric mucosa, so that peristalsis
increased.Thereby relieving cramping and expelling gas.

104. Surgical procedures
Antrectomy Vagotomy Pyloroplasty