GIT PHARMACOLOGY

BY
SAFIYA BORODO
(B.PHARM,MSc.)

Department of Pharmacology and Therapeutics

Bayero University, Kano
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 Acid Peptic Disease
• Peptic ulcer (gastric and duodenal)

• Hyperacidity

• Gastroesophageal reflux disease (GERD)

• Stress induced mucosal erosions

• Zollinger-Ellison syndrome induced by gastrin secreting

tumour.

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PEPTIC ULCER

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 Peptic Ulcer
• Imbalance between damaging effects of gastric acid, pepsin
and mucosal defence
• Types - duodenal and gastric
• Causes – multifactorial
– H. pylori infection (Gram –ve bacteria) (70%)
– NSAIDs (26%)
– Increased HCl secretion
– Inadequate mucosal defence
– Tumours (Zollinger-Ellison syndrome)

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G I T PHARMACOLOGY (ANTI ULCER)

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PATHOPHYSIOLOGY

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 Physiology of Gastric Acid Secretion
• The parietal cell contains receptors for gastrin, histamine
(H2), and acetylcholine (muscarinic, M3)
• When acetylcholine or gastrin bind to the parietal cell
receptors, it stimulates protein kinases
• Which stimulate acid secretion from a H+/K+ ATPase (the
proton pump) on the canalicular surface.
• In close proximity to the parietal cells are gut endocrine
cells called enterochromaffin-like (ECL) cells.
• ECL cells have receptors for gastrin and acetylcholine and
are the major source for histamine release.

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 Treatment Approach
 Drugs for reduction of acid secretions
– Proton pump inhibitors (PPI’s): Omeprazole, Lansoprazole, Rabeprazole,
Esomeprazole and Pantoprzole
– H2 receptor antagonists: Cimetidine , Ranitidine, Famotidine and
Nizatidine.
– Anticholinergics : Pirenzipine & Propantheline
 Drugs that neutralize acid secretions (Antacids):
Sodium bicarbonate, Calcium carbonate, Magnisium hydroxide &
Aluminium hydroxide
 Mucosal protective agents:
Prostaglandins, Sucralfate, Bismuth subsalicylate
 Anti-H.pylori agents :
Amoxycillin, Clarithromycin, Metronidazole Tinidazole, Tetracycline and
Bismuth citrate

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 Proton Pump Inhibitors (PPI)
• Omeprazole, Lansoprazole, Rabeprazole, Pantoprazole,
and Esomeprazole
• MOA-Inactive prodrugs requires acidic medium for activation
• Prodrug rapidly becomes protonated to reactive thiophilic
sulfonamide cation.
• The sulfonamide reacts with the sulphyhydryl group of H+/K+
ATPase, forms a covalent disulfide linkage, and irreversibly
inactivates the enzyme and thus inhibits acid secretion.
• PPI’s are the most effective supressors of gastric acid secretion.
Diminish daily production by over 95%. Widely used for their
efficacy and safety.

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 PPI’s
• Pharmacokinetics –
– Administered on an empty stomach to increase bioavailability
(oral, IV)
– Readily crosses lipid membranes into acidified compartments
– PPI’s have a short serum half-life and they have a long duration of
action.
• Interactions –
– Inhibit C-P450 = decrease in clearance of benzodiazepines,
phenytoin, warfarin
– Absorption of ketaconazole is reduced
– No interaction with antacids
• Side effects –
– Diarrhea, headache, abdominal pain, can cause hypochlorhydria
which may favor bacterial overgrowth (enteric infections)

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 Newer PPI’s
• Newer PPIs are developed either for their reversible
proton pump inhibitory activity or resistance to acid
degradation on oral administration

• Lansoprazole: inhibition is partly reversible

• Pantoprazole: more acid stable
• Rabeprazole and esomeprazole: better ulcer healers

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 Therapeutic Uses
• P.U, D.U

• GERD

• ZE Syndrome

• Ulcers refractive to H2 antagonists

• H pylori therapy

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 H2 Antagonist
• Cimetidine, Ranitidine, Famotidine, and Nizatidine
• MOA –
– H2 antagonists selectively and reversibly competes with
hisatamine for binding to the H2 receptor of parietal cell.
– Histamine released from ECL cells by gastrin or vagal stimulation is
blocked from binding to the H2 receptor of parietal cell.
– Direct stimulation of the parietal cell by gastrin or Ach results in
diminished acid secretion in the presence of H2-receptor blockade
• Pharmacokinetics – cimetidine
– Oral, IV Dose: 400 mg bd (breakfast and bedtime); not more than 2.4g
daily
– The serum half-lives from 1.1-4 hours

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 H2 Antagonist
– Duration of action depends on the dose given
– Widely distributed inc. breast milk and placenta
– 30% metabolised by CYP450 system
– Potent enzyme inhibitor
– 70% renally excreted unchanged
– Dose reduction is required in patients with renal insufficiency
• Interaction :
– Antacids decrease their absorption, inhibits CYP P450 thus inhibits
metabolism of metronidazole, phenytoin, warfarin etc
– Cimetidine is rarely used now due to undesirable side effects and
interactions.

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 H2 Antagonist
• Side effects
– diarrhea, headache, fatigue, constipation, confusion,
hallucinations and agitation. Cimetidine produces reversible
gyanaecomastia.

• Ranitidine is 5-times more potent than cimetidine with minimal cyto

p450 inhibition, less permeability to cross BBB and placenta it also has
longer duration of action than cimetidine
• Oral bioavailability Famotidine (40%), Ranitidine (50%), cimetidine
(80%) and Nizatidine(>90%).
• Famotidine and nizatidine are more potent and have less side effects

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 Anticholinergics
• Pirenzepine and propantheline: relative specific M1
receptor antagonist on the enterochromaffin-like cells
• Given orally and is usually as effective as cimetidine in
healing gastric and duodenal ulcers
• It may produce unwanted side effects like blurring of
vision and dry mouth

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 Mucosal Protective Agents
• Sucralfate
• MOA - In acidic solutions it forms a viscous paste that binds selectively
to ulcers for up to 6 hours
• Negatively charged sucrose sulfate binds to positively charged proteins
in the base of ulcers
• Forming a physical barrier that restricts caustic damage
• Stimulates mucosal prostaglandin and bicarbonate secretion
• Should not be administered with PPIs, H2 receptor antagonist or
antacids
• Little systemic absorption
• Route: oral (tablet, liquid); Dose: 1g qds
• Side effects constipation, not used in renal insufficiency

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 Mucosal Protective Agents
• Prostaglandin analogs : Misoprostol
• MOA - stimulates mucus and bicarbonate secretion and enhance
mucosal blood flow.
• also binds to prostaglandin receptor on parietal cells
• reducing histamine-stimulated cAMP production, causing modest acid
inhibition
• used for prevention of NSAID-induced ulcers
• 800 mcg daily (in 2-4 divided doses), co-administered with NSAIDs
• Side effects: uterine contractions (CI in pregnancy), diarrhoea, nausea,
gynaecological disturbances (vaginal spotting, dysmenorrhoea)
• Contraindicated in pregnancy and women of childbearing age
• Used to induce labour

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 Mucosal Protective Agents
• Bismuth Salicylate
• MOA - Creates a protective layer against acid and pepsin.
• Has direct antimicrobial activity against H pylori.
• Also stimulate prostaglandin, mucus, and bicarbonate secretion.
• Binds enterotoxins hence used in preventing and treating
traveler's diarrhea.
• Oral (liquid, chewable tablet)
• Little systemic absorption
• Renally excreted (avoid in impaired renal function)
• Side effects – darkens tongue, teeth and stool (esp. liquid
formulation) contraindicated in impaired renal function

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 Antacids
• Basic substance that neutralize acid and raise PH
• Relieve symptoms of hyperacidity like- dyspepsia, heart
burn, ulcer pains etc
• Sodium bicarbonate + HCl → CO2 + NaCl.
• Formation of CO2 results in gastric distention and belching.
• Metabolic alkalosis in high doses due to alkali absorption.
• NaCl absorption may cause fluid retention in patients with
heart failure, hypertension, and renal insufficiency.

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 Antacids
• Calcium carbonate + HCl → CO2 + CaCl2.
• Belching and metabolic alkalosis.
• NaHCO3 or CaCO3 with calcium-containing dairy products can lead
to hypercalcemia, renal insufficiency, (milk-alkali syndrome).
• Magnesium hydroxide or aluminum hydroxide + HCl → MgCl2
or AlCl3+ H20.
• Belching does not occur. Metabolic alkalosis is also uncommon.
• Osmotic diarrhea with magnesium salts, aluminum salts may
cause constipation
• To be taken with caution in renal insufficiency

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 H.Pylori
• A gram negative bacillus with a spiral shape which helps it
burrow through mucosal lining
• H.Pylori weakens the protective mucosal layer of the
stomach and duodenum
• Thus allowing acid to get to the sensitive layer, both acid
and bacteria irritate the lining causing sore or ulcer
• It produces “urease” which catalyses the hydrolysis of urea
to ammonia, this neutralizes gastric acid to create a neutral
protective cloud over bacteria and disrupt integrity of
gastric mucosa

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 H.Pylori
• Produces :Cytotoxin Associated Gene A (CAG-A) and
Vaculizing Cytotoxin A (VAC-A) (toxins)
• CAG-A distrupts the tight junctions of the stomach cells
allowing HCl to leak into the cells.
• H.pylori infection is associated with over 90% of D.U and
80% G.U, chronic active gastritis, gastric adenocarcinoma

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 Eradication of H.Pylori
Triple Therapy
• Lansoprazole 30 mg BD or ranitidine 300 mg OD or bismuth
subcitrate 120 mg QID
Plus
• Any 2 of (i) Amoxycillin 500 mg TDS, (ii) Clarithromycin 500 mg
BD and (iii) Metronidazole 400 mg QID/tinidazole 500 mg BD.

Quadruple therapy
• Omeprazole 40 mg BD + Tetracyclin hydrochloride 500 mg QID +
Bismuth subcitrate 120 mg QID + Metronidazole 500 mg TDS

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 Eradication of H.Pylori
• Quadruple therapy is proven to be more superior triple
than therapy
• PPIs have weak antibacterial effects against H. pylori
• Bismuth salts increase mucosal defence
• 1 week vs 2 weeks

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 NSAID’s Associated Ulcers
• Common in chronic usage and the elderly
• NSAIDs - Cause superficial erosions and hemorrhages
• Reduce mucosa prostaglandin production
• Cox-2 selective inhibitors have shown lower likelihood
of ulcer formation compared to non selective NSAIDs
• Risk factors- elderly, C.V prophylaxis with low dose
aspirin, concurrent oral corticosteroids or
anticoagulants and history of prior ulcer
• Risk can be reduced by prophylaxis with a P.P.I or
misoprostol

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Treatment of NSAID’s Associated Ulcers
A. Withdraw precipitating NSAID if possible then give H 2
antagonist or P.P.I or misoprostol x 1month
B. If replacement of analgesic or anti-inflammatory
therapy is required :
– i. Paracetamol in standard doses + A
– ii. Lowest acceptable dose of Ibuprofen (safest
gastrointestinally of the NSAIDs) + P.P.I
– iii. Replacement of NSAID used by a COX-2 selective
inhibitor (Rofecoxib, celecoxib)

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ANTISPASMODIC DRUGS
(SPASMOLYTICS)

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 Antispasmodic Drugs (Spasmolytics)
• Symptomatic treatment of acute and chronic diseases
accompanied by GIT smooth muscles spasm
• Relax spasms of the stomach, intestine or urinary bladder
• Classification
– Neurotropic spasmolytics – parasympatholytics
– Musculotropic spasmolytics -papaverine like, calcium
channel blockers
– Nonspecific spasmolytics - (nitrates, local anesthetics)

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 Neurotropic Spasmolytics
a) Non-selective (general muscarinic receptor blockade – GI,
bronchial, urogenital)
• atropine , scopolamine ,butylscopolamine , hyoscine
butylbromide (Buscopan) ,dicyclomine , hyoscyamine
b) Selective - specific muscarinic M1 receptor blockade
• pirenzepine
• Indications
• Smooth muscle spasm in stomach and intestine
• Renal colic
• Bladder spasm

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 Neurotropic Spasmolytics
• Adverse effects
– Dry mouth, flushing, nausea, vomiting, tachycardia,
urinary retention, dizziness, sedation, blurred vision
– increased intraocullar pressure (glaucoma)
– accomodation disorders- midriasis

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 Musculotropic Spasmolytics
a) Papaverine-like drugs Papaverine, mebeverine
• Direct smooth muscle relaxation
• papaverine – opium alkaloid without analgesic effect and
euphoria, has vasodilation effect
• indication: irritable bowel, billiary colic
b) Calcium channel blockers (pinaverin)
• selective inhibition of calcium channel
• indication: irritable bowel, biliary colic
Adverse effects: paralytic ileus and toxic megacolon

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EMETICS AND ANTIEMETICS

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 EMESIS
• Vomiting or emesis is a protective mechanism which leads
to expulsion of substances from the upper gastrointestinal
tract (GIT)
• Symptom not a disease
• Can cause discomfort and dehydration
• Can be life saving, physiological response to the ingested
toxic substances
• Usually managed with fluid and electrolyte replacement
and antiemetic drugs

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 Causes of Emesis
1. Infectious &non infectious GI disorders
2. Motion sickness
3. Morning sickness
4. Labyrinthitis (vertigo)
5. Drug induced (cytotoxics)
6. Radiotherapy
7. Emergence from general anaesthesia
8. Migraine
9. Acute pain& repulsive sights.

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 EMETICS
• Emetics are drugs used to evoke vomiting when a toxic
substance has been swallowed
1. Direct acting (apomorphine)
• Dopaminergic agonist on CTZ in the medulla.
2. Reflex acting (copper sulphate, strong salt solution, strong
coffee)
Cause gastric irritation which causes reflex emesis
3. Both : Ipecacuanha (contains emetine)
Also used as cough expectorant
Used in decreasing absorption of poison in poisoned
patients
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 Contraindications of emetics
 Corrosive (alkali, acid) poisoning (danger of perforation)
 CNS stimulant (precipitation of convulsion)
 Kerosene (petroleum) poisoning (aspiration pneumonia)
 Unconscious patients (danger of aspiration due to absence
of laryngeal reflex)

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 Anti emetics

• Drugs that control vomiting that help alleviate discomfort

and help control electrolyte balance
• Most are given parenterally, as the patient may vomit the
medication before it can be absorbed through the GI tract

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 Classification
1. Anticholinergics – Hyoscine, dicyclomine
2. H1 antihistaminics – Promethazine, cyclizine, meclizine,
cinnarizine, diphenhydramin, doxylamine
3. Neuroleptics – Phenothiazines- chlopromazine,
prochloperazine
Butyrophenones- haloperidol
4. Prokinetics – Metoclopramide, domperidone,
5. 5-HT3 antagonists- Ondansetron, granisetron,
palonosetron
6. Miscellaneous- Cannabinoids (nabilone), Dexamethasone,
benzodiazepines (lorazepam) cisapride

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 Anticholinergics
Hyoscine
• Muscarinic receptor antagonists
• Blocks the cholinergic pathway from vestibular apparatus
to vomiting centre.
• Most effective for motion sickness and used for prophylaxis
(Admin ½ - 1 h b4 travelling) and treatment
• Side effects :Drowsiness, dryness of mouth, blurring of
vision and retention of urine

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 H1 antihistaminics
• Have central antihistaminic, antichorlinergic and sedative
properties
• Effective in vomiting due to motion sickness, Meniere’s
disease, pregnancy, uremia and postoperative emesis.
 Promethazine HCl (Phenergan)
 Promethazine theoclate (Avomine, 25 mg Tab.)
• Cyclizine and meclizine are long acting

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 H1 Antihistamine
• Cinnarazine (anti-vertigo) has in addition to H1-blocking
property also inhibits influx of calcium from endolymph
into the vestibular sensory cells which mediates
labyrinthine reflexes
• S/E : Sedation, dizziness, dry mouth e.t.c
• Meclizine – less common due to sedation
• Doxylamine can be used in morning sickness (vomiting
during the first trimester of pregnancy, due to the effect of
increased oestrogen level on CTZ).

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 Neuroleptics
Chlopromazine, haloperidol
• Antipsychotic agents
• Act by blocking D2 receptors in the CTZ
• Antiemetic dose is much lower than antipsychotic doses
• Chlorpromazine 20-30% of antipsychotic dosage

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 Neuroleptics
Uses
 Chemotherapy induced vomiting
 Post-anaesthesia
 Malignancy and radiation
 Hyperemesis gravidarum

S/E
 Sedation
 Anticholinergic SE
 Extrapyramidal SE (Rx- benzhexol, benztropine)

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 Prokinetics
Metoclopramide, domperidone
MOA
 Block D2 receptors in the CTZ
 Stimulate cholinergic activity in the gut, increasing gut motility.
 Promote gastroduodenal peristalsis and speed gastric emptying
(Prokinetic)
 Antagonize peripheral 5HT3 receptors in the intestines

Pharmacokinetics
• It is rapidly absorbed orally, enters brain, crosses placenta and is
secreted in milk.
• It hastens absorption of many drugs like aspirin and diazepam

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 Prokinetics

• Side effects
• Sedation, dizziness, diarrhea and extrapyramidal side effects (muscle
dystonia).
• On long term use it can cause parkinsonism, prolactin release (galactorrhoea
and gynaecomastia)
• Uses
• Antiemetic
– Drug of choice in vomiting due to migraine
• Dyspepsia
• Hiccup
• Gastroesophageal reflux disease (GERD)

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 5HT3 Antagonists
• Ondansetron, Granisetron
• MOA
– Block serotonin receptors (5HT3) peripherally in the GIT and centrally in the medulla
(CTZ )
• Used in cytotoxic drug-induced vomiting
• Given half an hour before chemotherapeutic infusion as slow i.v.
injection.
• Headache, dizziness and constipation
 Ondansetron (oral and I.V )
 Granisetron (oral, I.V and transdermal patch )

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 Preferable Choices
1. Motion sickness- Hyoscine, antihistamines

2. Drug induced, radiotherapy & postoperative

- Neuroleptics, ondansetron, metoclopramide (I.V)(except intestinal
operation or obstruction)

3. Prevention of chemotherapy-induced nausea and vomiting - Same as 2,

lorazepam, olanzepam, dexamethasone

4. Migraine- Metoclopramide

5. Pregnancy- Promethazine, cyclizine, meclizine, doxylamine, severe

cases phenothiazines

6. Motion sickness, vestibular disorder (meniere’s disease)- Cinnarizine 49

DIARRHEA

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 Diarrhea
• Passage of watery stools at least 3x in 24hr
• A symptom
• Leads to severe dehydration and electrolyte lose

• Mechanism
 Excessive secretion of water and electrolytes into the
lumen
 Increased osmotic load in the intestine (presence of non
absorbable solutes)
 Increased motility of the intestine (rapid transit

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 Causes of diaerrhea
• Acute diarrhea
 infectious agents (enterotoxigenic E. coli Vibrio
cholera, Campylobacter, Shigella and Salmonella)
 toxin ingestion
 medications (broad spectrum antibiotics,
metoclopramide, quinidine , etc)
• Rota virus (common cause of diarrhea in children)

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 Antidiarrheal therapy
• Dehydration is the most common cause of death
• Correction of fluid depletion, shock and acidosis are of
central importance to all forms of acute diarrhea
• Treatment of diarrhea therefore, consists of
 Correction of dehydration by oral rehydration therapy
 Maintenance of adequate nutrition
 Drug therapy which can be either specific against the
microbials or non-specific antidiarrhoeal agents

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 Treatment
1. Treat underlying cause

2. Replace fluid & electrolyte lose

3. Zinc therapy in children

4. Antidiarrheal drugs (symptomatic)

5. Antibacterial drugs (if evidence of infection)

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 Fluid and electrolyte replacement
• Oral Rehydration Therapy (ORT)
• With glucose-electrolyte solution
• Replaces water and electrolyte lost
• Oral Rehydration Salts (ORS) contain standard
concentrations of Na+, K+, Cl-, citrate and glucose
• Glucose may be replaced with other substrates e.g. glycine
or rice powder
• IV therapy may be needed in severe cases
• Especially important in children

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 Antimotility Drugs
Loperamide (Imodium®) diphenoxylate (Lomotil)
• Opioid agonists which do not cross BBB
• Stimulate mu- and delta-receptors in the small and large
intestines
• Activation of mu-receptors decreases peristaltic
movements
• Activation of delta receptors contributes to their
antisecretory effects
• Increase tone of anal sphincter and reduce central
awareness for defecation

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 Loperamide
• Quickly absorbed orally
• 40 to 50 times more potent than morphine as an anti-motility
agent
• Poor CNS penetration and no abuse liability with longer duration
of action.
• Increases the transit time, anal tone and has got antisecretory
property
• t½ (11 hours)
• 4 mg should be given initially followed by 2 mg after each
subsequent stool with a maximum total dose of 16 mg/day
• Overdose may result in CNS depression (especially in children)
and paralytic ileus

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 Specific infections
• Cholera- TCN, Cotrimoxazole
• Salmonella infections-
-Typhoid fever- Cipro, ceftriaxone,amoxycilliin,
cotrimoxazole,
• Shigellosis – Cotrimox, TCN,CPL ,Amp
• Amoebiasis / giardiasis - Metronidazole
• Travellers diarr. – Cotrimox, cipro
• Rota virus (self limiting)- Rehydration +
symptomatic treatment

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 Zinc Therapy
• Zinc reduces the duration and severity of acute diarrhoea and the
likelihood of a prolonged episode
• WHO/United Nations Children's Fund (UNICEF) recommend that all
under-five children be treated with zinc (20 mg/day if age is 6-59
months and 10 mg/day if age is less than six months) for 10-14 days
• Zinc treatment is inexpensive, safe, and easy.
• Zinc treatment shortens the diarrhoea episode, reduces the risk of
episode being persistent, and reduces the risk of future diarrhoea or
pneumonia.
• Zinc treatment reduces overall mortality

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 Probiotics

– Probiotics seed the GI tract with beneficial bacteria; use

is based on the theory that some forms of diarrhea are
caused by disruption of the normal bacterial flora of the
GI tract
– Must be refrigerated to maintain the viability of the
bacteria
– Examples:
• Plain yogurt with active cultures
• Variety of trade-name products

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LAXATIVES

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 Constipation
 Difficulty in emptying the bowels, usually associated with
hardened faeces
Medically
 Fewer than three stools per week
• Severe – less than one stool per week
• Symptoms
• Decreased frequency
• Difficulty in the initiation and passage of stool
• Incomplete evacuation
• Formation of firm and small amount of feaces.

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 Constipation
• Causes
• Lack of dietary fibres
• Poor hydration
• Lack of exercise
• Certain drugs (opioids)
• Certain systemic illnesses
• Inappropriate bowel habit

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 Treatment of Constipation

1. General Measures :
1. Adequate fluid intake.
2. High fiber contents in diet.
3. Regular exercise
4. Regulation of bowel habit.
5. Avoid drugs causing constipation.

2. Drugs (laxatives, purgatives, cathartics):

Drugs that hasten the transit of food through the
intestine by several methods

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 Laxatives

– A laxative loosens the bowel contents and encourages

evacuation of stool
– Laxatives help animals evacuate without excessive
straining; treat chronic constipation from non-dietary
causes and movable intestinal blockages; and evacuate
the GI tract before surgery, radiography, or diagnostic
procedures
– Purgatives are harsh laxatives
– Cathartics are harsher purgatives;

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 Types of laxatives
• Osmotic laxatives
• Stimulants
• Bulk forming
• Emolients

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 Osmotic Laxatives
• Pull water into the colon and increase water content in the
feces, thereby increasing bulk and stimulating peristalsis
• S.E They may cause electrolyte imbalances if absorbed
systemically
• Examples include: lactulose, sodium phosphate with
sodium biphosphate, magnesium sulfate, magnesium
hydroxide

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 Stimulant Laxatives

• Increase peristalsis by chemically irritating sensory nerve

endings in the intestinal mucosa
• Many are absorbed systemically and cause a variety of side
effects
• Examples include bisacodyl, phenolphthalein, and castor
oil

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 Bulk-forming Laxatives

• Substances that absorb water into the intestine, increase

fecal bulk, and stimulate peristalsis, resulting in large, soft
stool production (which tends to look normal)
• Are not systemically absorbed, so side effects are rare
• Examples include psyllium hydrophilic mucilloid,
polycarbophil,and bran

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 Emollients
• Can be stool softeners (reduce stool surface tension and
reduce water absorption through the colon),
• Lubricants (facilitate the passage of fecal material,
increasing water retention in stool), or
• Feacal wetting agents (detergent-like drugs that permit
easier penetration and mixing of fats and fluid with the
fecal mass)
• Examples include docusate sodium, docusate calcium,
docusate potassium, liquid paraffin and petroleum
products

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 Uses of Laxatives
• Functional constipation
• Spastic and atonic conditions
• Bed ridden and postoperative patients to avoid straining
at stools
• Preparation of bowel before surgery
• Food and drug poisoning
• Worm infestations

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 Contraindications of Laxatives
• Patients of undiagnosed abdominal pain and vomiting
• Secondary constipation due to stricture or obstruction in
bowel
• Malignancies
 Long-term use of laxatives often results in decreased bowel
tone and may lead to dependency.
• Encourage
 A healthy, high-fiber diet
 Increased fluid intake

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 Preferred Choice
• Soft formed stool (1-3 days)- bulk softeners, lubricant
• Semi liquid stool (6-8hr) – bisacodyl, senna other irritants
• Watery stool– castor oil (1-3hr), lactulose (24-48hr)

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