Useful for BSC nursing students

1. Acid-Controlling Agents
 Syed tajamul
 BHCNMT

2. Acid-Related physiology
The stomach secretes:
 Hydrochloric acid (HCl)
 Bicarbonate
 Pepsinogen
 Intrinsic factor
 Mucus
 Prostaglandins
 K, Cl, Na

4. Glands of the Stomach
 Oxyntic(Gastric/ parietal) 80%
 Pyloric 20%
* The cells of the gastric gland are the largest
in number and of primary importance when
discussing acid control

5. Cells of the Gastric
Gland
 Mucoid cells
 Mucus-secreting cells (surface epithelial cells)
 Provide a protective mucous coat
 Protect against self-digestion by HCl
 Parietal cells
 Produce and secrete HCl
 Primary site of action for many acid-controller drugs
 Chief cells
 Secrete pepsinogen, a proenzyme
 Pepsinogen becomes pepsin when activated by
exposure to acid
 Pepsin breaks down proteins (proteolytic)

6. Classification of Drugs Acting
Against Gastric Acid
 1. Drugs which neutralises Gastric Acid( Antacids)
 Absorbable and non absorbable antacids
 2. Drugs which reduce Gastric Acid Secretion (anti
secretory agents)
 H2-Receptor Antagonists, PPIs, Anticholinergics. And PG
analogs
 3. Mucosal Protective Agents
 4. Ulcer Healing Agents
 5. Anti Helicobecter pylori agents

7. INDICATIONS
 Gastric oesophageal reflux
disease•
 Gastric and duodenal ulcers
 Acute/chronic gastritis and
gastroduodenitis
 Gastropathy secondary to non-
steroidal anti-inflammatorydrugs
(NSAIDs)
 Pain and dyspeptic syndromes
 Cholecystitis & Biliary dyskinesia
 Chronic pancreatitis
 Prevention of stress ulcers
 To affect the actions of other
drugs.

8. Antacids
 Antacids were developed based on hydroxides and car-
bonates of the group II and III metals, as well as the
bicarbonates of the alkali metals.
 All antacids contain at least one of the following
metals: aluminium, calcium, magnesium,
sodium,potassium, or bismuth.
 Antacids can be classified into two main classes,
namely absorbable( Sysytemic) and non-absorbable(
Non- systemic) antacids.

9. Absorbable antacids
 These are soluble, readily absorbable and capable of
producing systemic electrolyte abnormalities.
 They have brief duration of action and are Absorbed
into the systemic circulation.
 Raises pH up to 7.4
 On neutralising HCL produces salt+CO2+H2O
 CO2 results in gastric distension and can be
dangerous for ulcers.
 Unreacted alkali is readily absorbed and. Can raise pH
of blood(Systemic/ metaboic Alkalosis)
 Sudden rise of gastric pH and CO2 promotes gastric
release causes Rebound Acidity.

10. Non-absorbable
antacids
 These agents do not produce a metabolic
alkalosis.
 Accumulation of calcium (Ca2+), magnesium
(Mg2+) and aluminium (Al2+).
 Dangerous with use in renal insufficiency with
aluminium compounds being contraindicated
in renal insufficiency.

11. Absorbable antacids
 Sodium bicarbonate
 Calcium carbonate
 Magnesia(magnesium
oxide)
 Magnesium carbonate
 Bourget mixture( Sulphate,
Na, sodium sulphate)
 Rennies- CaCO3 & MgCO3
Non-Absorbable
antacids
 Aluminium Salt of
phosphoric acid
 Aluminium magnesium
 Aluminium magnesium
with other salts
 Magnesium salicylate
 Megnesium Hydroxide,
 Slimethicon ( Silicon
Polymer)
 Sodium Alignate (Aliginic
Acid)

12. Pharmacokinetics
 Antacids are used in the form of tablets and
suspensions in empty stomach.
 Therapeutic dose of 10-15ml or 1to 4 tablets
TID/QID before 1-2 hrs before meals
 Readily emptied into duodenum.
 Small Vd ( except Absorbable antacids), minimal
hepatic metabolism &excreted in faeces.
 Periodic monitoring of calcium and phosphorus
levels in patients on chronic therapy. Careful
dosing in those with hepatic and renal
impairment.

13. Mechanism of action
 Antacids act similar to when an acid reacts with a hydroxide; a salt and
water are produced as in the following equation: HCl (aq) + NaOH (aq)
→ NaCl (aq) + H2O
 Sodium bicarbonate: HCl (aq) + NaHCO3 (aq) → NaCl (aq) + H2O +
CO2.
 Calcium carbonate: HCl (aq) + CaCO3 (aq) → CaCI2 (aq) + H2O +
CO2.•
 Magnesium compounds: MgO + H2O → Mg (OH)2;
 HCl (aq) + Mg (OH)2 → MgCl2 + H2O
 The anionic group of Non Absorbable anti acids neutralises the
hydrogen ions (H+) in gastric acid. This releases their cationic group
which combine with HCO3- from the pancreas to form an insoluble
basic compound that is excreted in faeces.
 Non absorbable antacids absorb pepsin, stimulates production of.
Mucin, cell proliferation of cells and angiogenesis.

14. Drug Interactions
 Antacids that contain calcium, magnesium
and aluminium ions are chelators.
 They bind a great number of drugs such as
digitoxin, tetracycline, indomethacin, aspirin,
cimetidine, ranitidine, famotidine,
theophylline, etc.
 Antacids also reduce the bioavailability of
drugs like barbiturates, sulphonamides,
NSAIDs and penicillin.
 To avoid undesirable interactions, antacids
are usually used two hours before or after
taking any medication.

15. Contraindications
 Renal failure
 Cardiac failure
 Oedema
 Cirrhosis
 Low sodium diet
 Uraemia
 Upper GI bleed
 Hyperparathyroidism & Renal calculi

16. Adverse effects
 Altered acid base balance-metabolic alkalosis.
 Reduced gastric and intestinal emptying
 Tendency of constipation.
 Undesirable effects on pregnant woman, elderly and
persons with renal insufficiency
 Hyper magnesemia, renal calculus

17. 02
Drugs which reduce Gastric
Acid Secretion (antisecretory
agents)

18. I. H2-RECEPTOR ANTAGONISTS
 First introduced in 1970s
 Commonly referred as H2-blockers
 Until 1990s most commonly drug in the world
for peptic ulcer diseases, dyspepsia and in
combination with H-pylori drug therapy.
 AGENTS
 Cemitidine PO 150mg
 Ranitidine po/ I/v 150
 Fomitidine i/v 20 mg
 Nizatidine po 150mg

19. Pharmacokinetics
 Rapidly absorbed from intestines after oral
Administration
 Undergo first pass metabolism resulting in 50%
bioavailability
 The serum half-lives of the four agents range
from 1.1 to 4 hours
 H2 antagonists are cleared by a combination of
hepatic metabolism, glomerular filtration, and
renal tubular secre- tion
 In the elderly, there is a decline of up to 50% in
drug clearance as well as a significant reduction
in volume of distribution.

20. Pharmacodynamics
 H2 antagonists exhibit competitive inhibition at the
parietal cell H2 receptor and donot affect H1 and
H3 receptors.
 histamine released from ECL cells by gastrin, vagal
and Acetylecholine stimulation is blocked from
binding to the parietal cell H2 receptor
 effective at inhibiting nocturnal acid secretion
 the duration of acid inhibition is 6–10 hours
 inhibit 60–70% of total 24-hour acid secretion
 nocturnal and fasting intragastric pH is raised to 4–
5

21. Clinical Uses
 GERD- 50% healing
 Peptic Ulcer diseases-80-90% after 6-8 weeks
therapy
 Non ulcer dyspepsia- used OTC
 Prevention of Stress related gastritis
 ICU patients
 Combination therapy in H-pylori infection

22. Adverse Effects
 H2 antagonists are extremely safe drugs
 Adverse effects occur in less than 3% of
patients and include diarrhea, headache,
fatigue, myalgias, and constipation.
 Mental status changes (confusion,
hallucinations, agitation) may occur with
administration of Iv H2-blockers in elderly
ICU patients with renal and hepatic
dysfunctions
 Secreted in milk may affect infants

23. II. PROTON-PUMP INHIBITORS
(PPIs)
 Introduced in 1980
 Majorly used in Acid-peptic disorders
 Agents
 Omperazole 20-40mg
 Lansoparazole. 30-40mg
 Dexlansoperazole 30-60mg
 Pantaparzole 40mg
 Rabeparazole 20 mg

24. Pharmacokinetics
 PPIs are administered as inactive prodrugs and enteric coated capsules
 Also available in suspensions
 These are lipophilic weak bases, diffuse readily across lipid membranes
into acidified compartments of parietal cell canaiculus.
 Become rapidly protonated and rapidly undergoes to active form
 Biovailibilty is decreased 50% by food should be administered 1 hr
before meals
 Serum half life is about 1.5hrs
 Rapid first pass metabolism and negligible renal clearance
 PPI are activated near the site of action can be termed as ideal drugs

25. Pharmacodynamics
 PPIs inhibit both fasting and meal-stimulated secretion
because they block the final common pathway of acid
secretion, the proton pump
 undergoes a molecular conversion to the active form, a
reactive thiophilic sulfenamide cation, which forms a
covalent disulfide bond with the H+/K+- ATPase,
irreversibly inactivating the enzyme.

27. Indication
 GERD- most effective agents. For erosive reflux disease.
80—90% recovery within 6 months of use.
 Peptic ulcers-
 Prevention of re bleeding from peptic and gastric
ulcers within 3-5 days of twice daily.
 Non ulcer dyspepsia-
 Prevention of stress related mucosal bleeding
 Gastronoma and other hypersecretory disorder

28. Adverse Effects
 Generally considered to be safe but in some patients
about 1.5 % report diarrhoeas, pain and abdominal.
Discomfort.
 Decrease absorption of Vit. B12 with prolonged
therapy and food bound minerals like iron, Ca, and
Mg.
 Increased risk of respiratory and enteric infections and
aggregates symptoms of H-Pylori
 Drug interactions are rare coz of shorter half-life.
 Alter absorption of acidic drugs like ketoconazole,
digoxin, and atazanavir.

29. Anticholinergics
 Antimuscarinic agents used to block basal scretions(asking
phase)
 They deeply gastric emptying and relax lower oesophageal
spinster.
 Their use is discouraged, can exacerbate the symptoms of
GERD by allowing the acid mixed food into oesophagus.
 Produce side effects like blurred vision, dr mouth
constipation and urinary retention.
 Props the line, oxyphenonium, pirezepine and telezepine.

30. PROSTAGLANDIN ANALOGS
 gastrointestinal mucosa synthesizes a number of pros-
taglandins like PGE& PGF.
 Methylene analog Misoprostrol of PGE is approved for GI
conditions,
 it is rapidly absorbed and metabolized to a metabolically active
free acid.
 The serum half-life is less than 30 minutes; hence, it must be
administered 200 mic.g 3–4 times daily in NSAID induced
Gastritis.
 It is excreted in the urine
 Misoprostol has both acid inhibitory and mucosal protective
properties however unknown
 It has high adverse effect profile related to the function of PGs
in other organs.

31. MUCOSAL PROTECTIVE AGENTS
Sucralfate
 Sucralfate is a salt of sucrose complexed to sulfated
aluminum hydroxide.
 In water or acidic solutions it forms a viscous, tena- cious
paste that binds selectively to ulcers or erosions for up to 6
hours.
 Dietary as well as mucosal protiens also get absorbed over
this coat forming another layer to provide resistance.
 Evidences of stimulating PGE2 synthesis and HCO3
production

32. MUCOSAL PROTECTIVE
AGENTS
 Dosage of 1g QD
 Sucralfate has limited solubility, breaking down into sucrose
sulfate (strongly negatively charged) and an aluminum salt.
 Less than 3% of intact drug and aluminum is absorbed from the
intestinal tract; the remainder is excreted in the feces.
 Binds phosphate ions in intestines can result in
hypophosphatemia
 Sucralphates adsorb tetracyclines, flouroquinolones, H2
blockers, phenytoin and digoxin.
 Also used as glycerine pastes for stomatitis, burn dressing and
bed sores.

33.  Colloidal Bismuth subcitrate and Bismuth Subsalicylate
 In acidic medium colloidal bismuth subcitrate forms acid resistance
coating over ulcer base
 Stimulates PGE2, Mucus and HCO3 secretion
 Dislodges H. Pylori from the surfaces of gastric mucosa, produces anti
microbial effect against Hpylori
 Dosage 120mg QD
 Heals peptic Ulcer 4-8 weeks
 Has an excellent safety profile
 Causes blackening of stools and darkening tongue
 Prolonged use may lead to bismuth toxicity( Osteodystrophy and
encephalopathy.
 Used as one the agents in Hpylori treatment
MUCOSAL PROTECTIVE
AGENTS

34. Ulcer Healing Agents
 Carbenoxolone sodium
 It is Glycyrretinic acid derivative with a steroid like structure
 Derived from licorice plant
 Produces mineralocorticoid like effects
 Electrolyte imbalance Na and water retention, hypertension
and hypokalemia and its use has become outdated
 Also used in topical creams as Carbosan gel for treatment of
lip sores and mouth ulcers.

35. Anti Helicobacter pylori agents
 about 90% of duodenal ulcers, 65% of gastric ulcers and 50% of non
ulcer dyspepsia are H-pylori positive
 Increases the risk of adenocarcinemo and non-Hodgkin lymphoma
 Bacteria is able to survive high acidic medium by its. Ability to produce
urease, which hydrolyses urea into ammonia
 Ammonia neutralises gastric HCL to create protectective cloud over
bacteria.
 Ammonia disturbs normal negative feedback mechanisms leads to
more acid secretion
 H-pylori also produces proteolytic enzymes such as proteases and
lipases leads to further damage to mucus membrane.
 Can be detected by urea. Breath

36. Treatment for H. pylori

38. DRUGS STIMULATING
GASTROINTESTINAL MOTILITY
(Pro-kinetics)
 Drugs that can selectively stimulate gut motor
function are (prokinetic agents). They are
 Agents that increase lower esophageal sphincter
pressures-useful for GERD.
 Drugs that improve gastric emptying - gastroparesis
and postsurgical gastric emp- tying delay.
 Agents that stimulate the small intestine - beneficial
for postoperative ileus or chronic intestinal pseudo-
obstruction.
 agents that enhance colonic transit - useful in the
treatment of constipation
 limited number of agents in this group are available
for clinical use

40. AGENTS
 Cholinomimetic agonists stimulate
muscarinic M3 receptors on muscle cells. -
Bethanechol suede to treat GERD and
gastroparesis, seldom used due to
cholinergic effect.
 Neostigmine- used to treatment of acute
bowel distension ( acute acute colonic
pseudo-obstruction or Ogilvie’s
syndrome).
 Administration of 2 mg results in prompt
colonic evacuation of flatus and feces in
the majority of patients.
 Cholinergic effects include excessive
salivation, nausea, vomiting, diarrhea, and
bradycardia.

41. METOCLOPRAMIDE &
DOMPERIDONE
 Mechanism of action
 are dopamine D2-receptor antagonists.
 activation of dopa- mine receptors inhibits
cholinergic smooth muscle stimulation;
blockade of this effect is believed to be the
primary prokinetic mechanism of action of
these agents
 also block dopamine D2 receptors in the
chemoreceptor trigger zone of the medulla
(area postrema), resulting in potent
antinausea and antiemetic action.

42. Pharmacokinetics
 METOCHLOPRAMIDE:
(Raglan): 5-10mg PO;
10mg i/V
 Absorption: rapid and
complete
 Bio availability ; 70%
 Metabolism : Liver
 T1/2: 4-6hrs
 Excretion: urine
 DOMPERIDONE: 10-20mg
PO and 10mg IM
 Absorption: rapid
 Bioavailability: 77%
 Metabolism: Liver
 T1/2; 1-2hrs
 Excretion : urine and feces

43. Adverse Effects
 Restlessness,
 Drowsiness,
 insomnia,
 anxiety, and
 Agitation occur in 10–20% of patients,
especially the elderly.
 Extrapyramidal effects (dystonias,
akathisia, parkinsonian features)
 Elevated prolactin levels (caused by
both metoclopramide and
domperidone) can cause galactorrhea,
gynecomastia, impotence, and
menstrual disorders

44. MACROLIDES-
Erythromycin
 Macrolide antibiotics such as erythromycin
directly stimulate motilin receptors on
gastrointestinal smooth muscle and promote
the onset of a migrating motor complex.
 Intravenous erythromycin (3 mg/kg) is
beneficial in some patients with
gastroparesis; however, tolerance rapidly
develops.
 It may be used in patients with acute upper
gastrointestinal hemorrhage to promote
gastric emptying of blood before endoscopy.

45. Antacids: Nursing Implications
Be sure that chewable tablets are chewed
thoroughly, and liquid forms are shaken
well before giving
Administer with at least 8 ounces of
water to enhance absorption (except for
the “rapid dissolve” forms)
Caffeine, alcohol, harsh spices, and black
pepper may aggravate the underlying GI
condition

46. Antacids: Nursing Implications
 Monitor for side effects
 Nausea, vomiting, abdominal pain, diarrhea
 With calcium-containing products: constipation, acid rebound
 Monitor for therapeutic response
 Notify heath care provider if symptoms are not relieved

47. H2 Antagonists:
Nursing Implications
 Assess for allergies and impaired renal or liver function
 Use with caution in patients who are confused, disoriented,
or elderly (higher incidence of CNS side effects)
 Take 1 hour before or after antacids
 For intravenous doses, follow administration guidelines

48. Proton Pump Inhibitors:
Nursing Implications
 Assess for allergies and history of liver
disease
 pantoprazole (Protonix) is the only proton
pump inhibitor available for parenteral
administration, and can be used for patients
who are unable to take oral medications
 May increase serum levels of diazepam,
phenytoin, and cause increased chance for
bleeding with warfarin

49. Proton Pump Inhibitors:
Nursing Implications
Instruct the patient taking omeprazole (Prilosec):
It should be taken before meals
The capsule should be swallowed whole,
not crushed, opened, or chewed
It may be given with antacids
Emphasize that the treatment will be
short term

50. Laxatives and Purgatives
 Constipation: it is the delayed passage of feces through
the intestines.
 Dyschezia: it is the derangement of defaecation process
due to pain r/t haemorrhoids and fissures, presence of
dehydrated faecal matter and sudden sensation of a
habitual use of purgative.
 Laxative: to loose the hardened faecal matter
 Purgatives: provide more watery evacuation of. Stools
 Purgatives in smaller doses can work as laxatives and.
Viceversa.

52. Indications
 To treat constipation
 To treat undue straining in
cases like hernia,
hemmorhoids, CV diseases
and bleeding from surgical
sites.
 Before and after anorectal
surgery and endoscopy
 For post operative bed ridden
patients
 Preoperatively and diagnostic
procedures

53. Bulk-Forming
Laxatives
 High fiber, hydrophilic, indidigestible
vegitable fibre
 Absorbs water to increase bulk
 Distends bowel to initiate reflex bowel
activity
 Effect- 1-3 days
 Examples:
 Wheat bran (bran powder or husk)
 Psyllium husk (Metamucil)
 Catrboxy methylcellulose
(Citrucel)
 Polycarbophil-synthetic fiber
(FiberCon)

54. Indications and Side effects
Use
Acute and chronic
constipation
Irritable bowel
syndrome
Diverticulosis
Acute and chronic
constipation
 Increased bloating and
flats
 Fluid overload

55. Lubricant and Surfactant
Purgatives (Emollients)
 Stool softeners and lubricants
 Promote more water and fat in the stools
 Lubricate the fecal material and intestinal
walls
 Examples:
 Liquid Paraffin 15-30ml/ day 1-3 days
 docusate salts PO 100-400mg &enema
 Glycerine Suppository
 Lubricants: mineral oil

56. Indications & Side Effects
Softening of fecal
impaction;
facilitation of BMs in
anorectal conditions
 Long-term use can impair
absorption of fat-soluble
vitamins (A, D, E, K
 Cramps, abdominal pain

57. OSMOTIC
LAXATIVES
 Increase fecal water content
 Result: bowel distention, increased
peristalsis, and evacuation
 Examples:
 polyethylene glycol (GoLYTELY) 300-
500ml/day
 sorbitol (increases fluid movement into
intestine)
 glycerin
 lactulose (Chronulac) 10-15ml Bd/td

58. OSMOTIC LAXATIVES
 Purgatives
 NONABSORBABLE SUGARS AND SALTS
 Increase osmotic pressure within the intestinal tract, causing more water to enter the
intestines
 Result: bowel distention, increased peristalsis, and evacuation
 Saline laxative examples:
 magnesium sulfate (Epsom salts)
 magnesium hydroxide (MOM)
 magnesium citrate
 sodium phosphate (Fleet Phospho-Soda, Fleet enema)
 When taking these purgatives, it is very important that patients maintain adequate
hydration by taking increased oral liquids to compensate for fecal fluid loss.

59. Indications & Side Effects
Chronic constipation
Diagnostic and surgical
preps
Constipation
 Hyperosmotic
 Abdominal bloating
 Rectal irritation
 Saline
 Magnesium toxicity
(with renal
insufficiency)
 Cramping
 Diarrhea
 Increased thirst
 Dehydration

60. STIMULANT/ IRRITANT
PURGATIVES (CATHARTICS)
 Stimulant laxatives (cathartics) -poorly understood
mechanisms.
 These include direct stimulation of the enteric nervous
system and colonic electrolyte and fluid
secretion.Increases peristalsis via intestinal nerve
stimulation
 Examples:
 castor oil (Granulex) 15-25ml in morning effects
within 3hrs( seldom used)
 Phenolphathaline 60-130mg and Biscodyl 5-
10mg & (suppository)
 Senna 12-25 mg bed time (Senokot)
 cascara
 Sodium picosulfate 5-10mg at bed time

61. Anthraquinone
Derivatives
 Plant derivatives
 Poorly absorbed after hydrolysis in the colon
 Produce bowel movements after 6-12 hrs
given orally and 2hrs after given rectally.
 Agents:
 Aloe, senna and cascara
 Can. Produce brown pigmentation of colon
known as meanosis coil.

62. Indications & Side Effects
Chronic constipation
Fecal impaction
Neurological deficit and
bed ridden patients
 Stimulant
Nutrient
malabsorption
Skin rashes
Gastric irritation
Rectal irritation
Colonic atony and
dilation

63. Miscellaneous
Laxatives
 Lubiprostone 24mcg po : chloride
secretion activator, increases chloride rich
fluid in small intestines, increases motility
and shortens transit time
 Tegaserod 6mg PO BD : 5HT4 receptor
stimulation used to treat IBS with
constipation in women less than 65yrs old
of age.
 methylnaltrexone bromide and
alvimopan: approved for the treatment of
opioid-induced constipation in patients
receiving palliative care for advanced
illness who have had inadequate response
to other agents. It is administered as a
subcutaneous injection (0.15 mg/ kg)
every 2 days.

64. Laxatives: Nursing Implications
Obtain a thorough history of presenting
symptoms, elimination patterns, and
allergies
Assess fluid and electrolytes before
initiating therapy
Patients should not take a laxative or
cathartic if they are experiencing nausea,
vomiting, and/or abdominal pain

65. Laxatives: Nursing Implications
 A healthy, high-fiber diet and increased
fluid intake should be encouraged as an
alternative to laxative use
 Long-term use of laxatives often results in
decreased bowel tone and may lead to
dependency
 All laxative tablets should be swallowed
whole, not crushed or chewed, especially
if enteric coated

66. Laxatives: Nursing Implications
 Patients should take all laxative tablets with 6 to 8 ounces of
water
 Patients should take bulk-forming laxatives as directed by
the manufacturer with at least 240 mL (8 ounces) of water

67. Laxatives: Nursing Implications
 Bisacodyl and cascara sagrada should be given with water
due to interactions with milk, antacids, and H2 blockers
 Patients should contact their provider if they experience
severe abdominal pain, muscle weakness, cramps, and/ or
dizziness, which may indicate fluid or electrolyte loss
 Monitor for therapeutic effect

68. ANTIDIARRHOEAL
AGENTS

69. INTRODUCTION
 Diarrhoea is condition characterised by the frequent passage of
loose, watery stools due to them disruption in the normal
functioning of the digestive system, particularly in the absorption
and secretion of water and electrolytes in the intestines.
 CAUSES
 Increased fluid secretion- due to toxins , drugs and infections.
 Impaired water absorption
 Altered intestinal motility- abnormally increased intestinal motility.
 Inflation and the infections.
 Malabsorption- celiac disease, lactoses intolerance
 Osmotic diarrhoea- due to poorly absorbed sugars and artificial
sweeteners.

70. ANTIDIARRHOEAL AGENTS
CLASSIFICATION
1. ANTIMOTILITY AND
ANTISECRETORY AGENTS
2.ADSORBENTS
3. ORT

71. ANTIMOTILITY AND
ANTISECRETORY AGENTS
Pharmacokinetics
 1. Opioid agonists agents
 Loperamide 2-4mg PO
 Diphenoxylate 2.5mg PO
 Difenoxin 2mg PO
 (LOMITIL, LOMOFEN )
 Racecadotril 100-300mg PO
 Well absorbed
 Peak plasma time 4-5hrs
 Half life 7-19 hrs
 Extensive first pass metabolism, <1%
bioavailabiity
 About 90% drugs are eliminated through
stools.
Pharmacodynamics
 Stimulate peripheral (mu) and
(delta)opioid receptors in small
and larger intestines;
 (Mu) opioid receptors
decreases intestinal motility
 (Delta) opioid receptors
decreases intestinal secretion
 Suppression of both activities
facilitates water absorption.

72. SIDE EFFECTS
 Dry mouth,
 Abdominal discomfort
 Constipation, gas
 Dizziness and Headache
 Vomiting
 Should be. Avoided in bacterial diarrhoea with high fever,
blood in stools and lactating mothers, andchildren below the
age of 2yrs

73. ANTIMOTILITY AND
ANTISECRETORY AGENTS
Anticholinergics
 Hyoscyamine 0.15-0.25 mg PO, and
dicyclomine 5,10,15 20mg PO
 Inhibit the mucarinic recptors of
acetylcholine in smooth muscles,
secretory glands and CNS
 Decreases bowel motitlity which
increases fluid absorption in intestines
 Used in combination with other
antidiarrheal drugs and as
antispasmodic- renal colic, biliary colic
infant colic, spastic bladder.
Alfa-2 Adrenergic
Receptor Agonists
 Clonidine 0.1mg PO
 Stimulating a-2 receptors in the
vast motor center in the brain
stem and enterocytes inhibits
the release of acetylecholine in
neuromuscular junction.
 Decreases the colonic and
rectal tone of smooth muscles
of intestines and inhibits
secreton
 Allows the water absorption.

74. 2. Adsorbent agents
 Kaolin- Hydrated
magnesium aluminium
silicate
 Pectin - indigestible
carbohydrate from apple
 Activated Charcoal
 Available in liquid
formaltions
 adsorbs bacteria, toxins
and fluid
 Increases the consistency
of fecal matter.
 Bismuth Subsalicylate
524mg(30-60ml)
 Bismuth binds to
enterotoxins. And provides
protective coating over
inflamed gastric mucosa;
 Subsalicylate inhibits the
synthesis of Pgsnad
prevents chlorine section
 Reduces fluid liquidity and
frequency.
 Causes blackening of stools
and dark tongue

75. 3. Probiotics
 Lactobacillus Sporogens
 Lactase

76. 4. Non pharmacological
Measures
Glucose based ORS
 ORT
 NaCL 3.5g
 KCl 1.5g
 Sodium Citrate 2.9g
 Glucose 20g
 Water 1L
 Total o solarium
311mmol/L
Cereal basedORT
 Precooked Rice 10.15gm
 NaCl 0.95g
 Sodium Citrate 0.20g
 Potassium Citrate 0.44g
 Water 200ml
 Others
 I/V fluids, NS, RL, DNS