SlideShare a Scribd company logo
ACID SECRETION DISORDER DRUGS
& ANTI-EMETIC DRUGS
By BME III 2023-2023
Group 5
BME III SYSTEMS PHARMACOLOGY
Members
1. 21/U/24081/HTG Asiimwe Anne
2. 20/U/21960/HTG Kibirige John Paul
3. 21/U/24115/HTG Niwamanya Derrick
Presentation Outline
Part 1: Acid secretion disorder drugs
Physiology of acid secretion
Acid secretion disorders
Drugs used in acid secretion disorders
Part 2: Anti-Emetic Drugs
Physiology of emesis
Classes of anti-emetic drugs
ACID SECRETION DISORDER DRUGS
Part 1
Introduction: Physiology of Gastric Acid Secretion
Gastric acid secretion depends mainly on Gastrin, Histamine &
Acetylcholine (Ach)
Acetylcholine (ACh) is released by parasympathetic neurons. Gastrin is
secreted by G cells, and histamine is a paracrine substance released by
mast cells in the nearby lamina propria.
Acetylcholine and gastrin stimulate parietal cells to secrete more HCl in the
presence of histamine. In other words, histamine acts synergistically,
enhancing the effects of acetylcholine and gastrin.
Receptors for all three substances are present in the plasma membrane of
parietal cells.
 The histamine receptors on parietal cells are called H2 receptors.
 Acetylcholine (ACh) receptors are the muscarinic, M3
 Gastrin receptors are CCK-B receptors
• Acetylcholine & Gastrin
(food stimulated) bind to
parietal cell receptors [M3
& CCK-B, respectively],
increase cytosolic Ca2
+ &
stimulate acid secretion
from the H+/K+
ATPase(proton pump)
• Histamine (released from
enterochromaffin cells,
ECC) binds to H2 receptors
on parietal cells and
activate adenylyl cyclase
and increase cAMP which
stimulates protein kinases
and activate H+/K+ ATPase
pump leading to HCl
secretion
Physiology of
Gastric Acid Secretion
Introduction
https://youtu.be/W9nyXXh*htM?si=9jg7_byI223Vx-wt
Watch mechanism of HCL secretion by parietal cell on
YOUTUBE. (Click on the link)
Pathogenesis of Gastric acid disorders
Imbalance between defenses and aggressive factors results into gastric acid/stomach
disorders
• Defensive factors: These prevent the stomach and duodenum from self-digestion.
• Mucus Coats and lines the stomach and is the first line of defense
• Bicarbonate: secreted from endothelial cells
• Blood flow: good blood flow maintains mucosal integrity
• Prostaglandins: stimulate secretion of bicarbonate and mucus, promote blood
flow, suppress secretion of gastric acid
• Aggressive factors:
• Helicobacter pylori: inflammatory response and mucosal toxicity
• Gastric Acid: activates pepsin enzyme and injures mucosa
• Decreased blood flow: causes ↓ in mucus production and HCO3-
• NSAIDS: inhibit the production of prostaglandins
• Smoking: nicotine stimulates gastric acid production, reduces duodenal HCO3-
• Alcohol/Ethanol: causes erosive gastritis
• Caffeine: increases gastric acid secretion.
• These include:
• GERD (gastro-esophageal reflux disease)
• Acute Gastritis
• Peptic Ulcers (gastric and duodenal ulcers)
• Excessive gastric acid secretion.
• Stress-induced gastritis
• Zollinger-Ellison syndrome: Caused by a Gastrinoma, a
neuroendocrine tumor secreting gastrin hormone.
ACID SECRETION DISORDERS
DRUGS USED IN ACID SECRETION DISORDERS
Class/Subclass Mechanism of Action Example
Protein Pump inhibitors Inhibit action of H+/K+ pump
and thus inhibit synthesis of
gastric acid
Omeprazole, Lansoprazole,
pantoprazole
Histamine H2-receptor blockers Block the histamine receptors
and prevent binding of
histamine and thus cause
reduced acid secretion
Ranitidine, Cimetidine
Antiacids Neutralize acid and prevents
formation of pepsin.
Magnesium hydroxide
Magnesium trisilicate
Prostaglandin analogues Reduce gastric acid and
enhance mucosal resistance to
injury
Misoprostol
Mucosal barrier fortifiers
(cytoprotective agents)
Form a protective coat Sucralfate, Bismuth sulfate
H-Pylori eradication Regimens Combination of drugs for H-
pylori induced acid disorders to
eradicate the bacteria
Quadruple therapy
Tripple therapy
Antacids
• They were the first and mainstay of treatment for acid-peptic
disorders until the discovery of H2− receptor antagonists and
proton-pump inhibitors (PPIs).
• Examples
Sodium bicarbonate, Calcium carbonate, Magnesium salts
(hydroxide, carbonate, trisilicate), and Aluminum hydroxide
• MOA:
Their principal mechanism of action is reduction of intragastric
acidity.
Antacids are weak bases that react with gastric hydrochloric
acid to form a salt and water. Drug interaction
Therapeutic Actions:
Antacids have a number of actions which include:
Neutralizing gastric acid and thus relieving associated pain and nausea
Reducing delivery of acid into the duodenum following a meal
Inactivation of the proteolyticc enzyme pepsin by raising the gastric pH above 4–5.
Interactions:
Antacids should be taken approximately one hour before or after food, as this
maximizes the contact time with stomach acid and allows the antacid to coat the
stomach in the absence of food.
Antacids may affect the absorption of other medications by binding the drug (reducing
its absorption) or by increasing intragastric pH so that the drug’s dissolution or solubility
(especially weakly basic or acidic drugs) is altered. Therefore, antacids should not be
given within 2 hours of doses of tetracyclines, fluoroquinolones, itraconazole, and iron.
Antacids:
Sodium bicarbonate (eg, baking soda, Alka Seltzer)
• Reacts rapidly with hydrochloric acid (HCl) to produce carbon dioxide and
sodium chloride. Formation of carbon dioxide results in gastric distention and
belching.
• Unreacted alkali is readily absorbed, potentially causing metabolic alkalosis
when given in high doses or to patients with renal insufficiency.
• Sodium chloride absorption may exacerbate fluid retention in patients with
heart failure, hypertension, and renal insufficiency
Magnesium hydroxide or aluminum hydroxide Compounds:
• React slowly with HCl to form magnesium chloride or aluminum chloride and
water.
• Because no gas is generated, belching does not occur. Metabolic alkalosis is
also uncommon because of the efficiency of the neutralization reaction.
• Because unabsorbed magnesium salts may cause an osmotic diarrhea and
aluminum salts may cause constipation, these agents are commonly
administered together in proprietary formulations to minimize the impact on
Antacids: Examples
H2 receptor antagonists
Commonly used in the 1970s until the early 1990s, With the recognition of the
role of H pylori in ulcer disease and the advent of PPIs, the use of prescription
H2 blockers has declined markedly over time.
Examples:
• Cimetidine, Ranitidine, Famotidine, Nizatidine
Pharmacokinetics:
• All four agents are rapidly absorbed from the intestine.
• Cimetidine, ranitidine, and famotidine undergo first-pass hepatic
metabolism resulting in a bioavailability of approximately 50%. Nizatidine
has little first-pass metabolism.
• 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 secretion. Dose reduction is
required in patients with moderate to severe renal (and possibly severe
hepatic) insufficiency.
MOA
• The H2 antagonists exhibit competitive inhibition at the parietal cell.
• H2 receptor and suppress basal and meal-stimulated acid secretion.
• They are highly selective and do not affect H1 or H3 receptors
• They also reduce the volume of gastric secretion and the
concentration of pepsin.
Drug Interactions
• They interfere with several important hepatic cytochrome P450 drug
metabolism pathways, including those catalyzed by CYP1A2,
CYP2C9, CYP2D6, and CYP3A4.
• H2 antagonists compete with creatinine and certain drugs (eg,
procainamide) for renal tubular secretion. All of these agents except
famotidine inhibit gastric first-pass metabolism of ethanol, increased
bioavailability of ethanol could lead to increased blood ethanol levels.
H2 receptor antagonists
Side effects
• H2 antagonists are relatively safe drugs.
• In adults H2-receptor antagonists might mask symptoms of gastric cancer;
• 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 intravenous H2 antagonists
• Cimetidine inhibits binding of dihydrotestosterone to androgen receptors,
inhibits metabolism of estradiol, and increases serum prolactin levels.
When used long-term or in high doses, it may cause gynecomastia or
impotence in men and galactorrhea in women. These effects are specific to
cimetidine and do not occur with the other H2 antagonists
H2 receptor antagonists
Ranitidine
Available in
• Tablets: 75mg, 150mg, 300mg
• Injection solution: 25mg/ml
• Capsule 150mg, 300mg.
• Syrup 15mg/ml
Dosage (For GERD):
• Oral: 150mg 12hrly or 4-8mg/kg not beyond 300mg in children
• IV/IM: 50mg 6-8hrly, or 2-4mg/kg/day in divided doses.
MOA:
• Blocks H2 receptors of gastric parietal cells leading to inhibition of HCL secretion.
Bioavailability: 50%(PO), 90-100% (parenteral)
Protein bound: 10-19%
Metabolized in liver, does not inhibit liver enzymes
Excreted mainly in urine, half life is 2.5-3hours
Proton Pump Inhibitors (PPIs)
Since their introduction in the late 1980s, these efficacious acid inhibitory agents have
assumed the major role for the treatment of acid-peptic disorders. PPIs are now among the
most widely prescribed drugs worldwide due to their outstanding efficacy and safety
Examples:
Omeprazole, Lansoprazole, Pantoprazole, Rabeprazole, esomeprazole, Dex-lansoprazole
Pharmacokinetics
• PPIs are administered as inactive prodrugs.
• To protect the acid-labile prodrug from rapid destruction within the gastric lumen, oral
products are formulated for delayed release as acid-resistant, enteric-coated capsules or
tablets. After passing through the stomach into the alkaline intestinal lumen, the enteric
coatings dissolve and the prodrug is absorbed.
• For children or patients with dysphagia or enteral feeding tubes, capsule formulations (but
not tablets) may be opened and the microgranules mixed with apple or orange juice or
mixed with soft foods
MOA
• In contrast to H2 antagonists, PPIs inhibit both fasting and meal-stimulated
secretion because they block the final common pathway of acid secretion, the
proton pump. In standard doses, PPIs inhibit 90–98% of 24-hour acid secretion.
Side Effects
• PPIs are extremely safe.
• Diarrhea, headache, and abdominal pain are reported in 1–5% of patients
• Nutrition—Acid is important in releasing vitamin B12 from food. A minor
reduction in oral cyanocobalamin absorption occurs during proton pump
inhibition, potentially leading to subnormal B12 levels with prolonged therapy.
• Respiratory and enteric infections—Gastric acid is an important barrier to
colonization and infection of the stomach and intestine from ingested
bacteria. Increases in gastric bacterial concentrations are detected in
patients taking PPIs
• Potential problems due to increased serum gastrin—Gastrin levels are
regulated by intragastric acidity. Acid suppression alters normal feedback
Proton Pump Inhibitors (PPIs):
Omeprazole
Mechanism: Inhibits gastric acid secretion by blocking the hydrogen-potassium
adenosine triphosphatase enzyme system (the ‘proton pump’) of the gastric parietal cell.
Formulations available:
• Suspension: 2mg/ml
• Tablet: 20mg
• Capsule: 10mg, 20mg, 40mg
• Powder for injection: 40mg(4mg/ml)
Dosage: 20mg-40mg BD
Drug interactions
• Decreased gastric acidity may alter absorption of drugs for which intragastric
acidity affects drug bioavailability, e. g, ketoconazole, itraconazole, digoxin, and
atazanavir.
• All PPIs are metabolized by hepatic P450 cytochromes, including CYP2C19 and
CYP3A4.
• Clopidogrel and PPIs. Clopidogrel is a prodrug that requires activation by the
hepatic P450 CYP2C19 isoenzyme, which also is involved to varying degrees in
Prostaglandin analogues
• The human gastrointestinal mucosa synthesizes a number of
prostaglandins; Prostaglandins of the E and I series have a generally
homeostatic protective action in the gastrointestinal tract, and a
deficiency in endogenous production (after ingestion of a NSAID, for
example) may contribute to ulcer formation.
• Misoprostol, a methyl analog of PGE1 , has been approved for
gastrointestinal conditions.
• Misoprostol has both acid inhibitory and mucosal protective
properties. It is believed to stimulate mucus and bicarbonate
secretion and enhance mucosal blood flow.
• Misoprostol can reduce the incidence of NSAID-induced ulcers to
less than 3% and the incidence of ulcer complications by 50%. It is
approved for prevention of NSAID-induced ulcers in high-risk
Prostaglandin analogues: Misoprostol
• Available formulations:
• Tablets 100mcg, 200mcg
• Dosage: Given orally, 200mcg 6hrly with food
• However, misoprostol has never achieved widespread use
owing to its high adverse-effect profile and need for multiple
daily dosing.
• Unwanted effects include diarrhea and abdominal cramps;
uterine contractions can also occur, so the drug should not
be given during pregnancy as it may induce abortion
Mucosal barrier fortifiers (cytoprotective
agents)
The gastroduodenal mucosa has evolved a number of defense
mechanisms to protect itself against the noxious effects of acid and pepsin.
Both mucus and epithelial cell-cell tight junctions restrict back diffusion of
acid and pepsin. Epithelial bicarbonate secretion establishes a pH gradient
within the mucous layer
Sucralfate
• Is a salt of sucrose complexed to sulfated aluminum hydroxide. In water
or acidic solutions it forms a viscous, tenacious paste that binds
selectively to ulcers or erosions for up to 6 hours. Sucralfate has limited
solubility, breaking down into sucrose sulfate (strongly negatively
charged) and an aluminum salt.
MOA
• Forms ulcer-adherent complex. The negatively charged sucrose sulfate
binds to positively charged proteins in the base of ulcers or erosion,
forming a physical barrier that restricts further caustic damage and
Mucosal barrier fortifiers
(cytoprotective agents)
• Available in: Tabs (1g) suspension (100mg/ml)
• Dosage: 1g 6hrly and 12hrly for maintenance
Adverse Effects
• Because it is not absorbed, sucralfate is virtually devoid
of systemic adverse effects. Constipation occurs in 2%
of patients due to the aluminum salt.
• Because a small amount of aluminum is absorbed, it
should not be used for prolonged periods in patients
with renal insufficiency.
PUD Treatment: H-Pylori Eradication
Regimens
Regimen name Number of
Drugs
Drugs Used
Tripple therapy 3 PPI
Clarithromycin or
Levofloxacin
Amoxicillin or
metronidazole
Bismuth quadruple
therapy
4 PPI
Bismuth Compound
Tetracycline
Nitro-imidazoles
ANTI-EMETIC DRUGS
Part 2
Introduction
• These are drugs taken to prevent or treat nausea and vomiting.
• Vomiting or emesis is the abnormal emptying of stomach and upper
part of intestine through esophagus and mouth.
• Causes may include; Presence of irritating contents in GI tract,
Mechanical stimulation of pharynx, Pregnancy, Excess intake of
alcohol, Nauseating sight, odor or taste.
• Vomiting is always preceded by nausea;
• Nausea is unpleasant sensation which induces the desire for
vomiting. It is characterized by secretion of large amount of saliva
containing more amount of mucus.
Path way of emesis
•Chemoreceptor trigger zone, GIT,
hypothalamus stimulation
•Central vomiting center stimulation
(D2, ACH, NK serotonin 5-HT3,)
•Vomiting events (reverse peristalisis)
Classes of Anti-emetic drugs include;
• Serotonin 5-HT3 antagonists like ondansetron, granisetron,
delesetron.
• Neurokinin receptor antagonists like fosaprepitant.
• Dopamine antagonists like chloropromazine, metoclopramide.
• H1 anti histamines and anticholinergic drugs like diphenhydramine
and, dimenhydrinate.
1. SEROTONIN 5-HT3 ANTAGONISTS
Mechanism of action.
• Selective 5-HT 3 -receptor antagonists have potent antiemetic
properties that are mediated in part through central 5-HT 3 -receptor
blockade in the vomiting center and chemoreceptor trigger zone but
mainly through blockade of peripheral 5-HT 3 receptors on extrinsic
intestinal vagal nerve.
• The antiemetic action of these agents is restricted to emesis attributable
to vagal stimulation (e.g., postoperative) and chemotherapy.
•antagonists block serotonin both
peripherally on vagal nerve terminals in
the gastrointestinal Gastro-Intestinal
system and centrally in the chemoreceptor
trigger zone in the area postrema of the
fourth ventricle, resulting in powerful
antiemetic effects.
Examples of Serotonin 5-ht 3 antagonists
DRUG DRUG DESCRIPTION
Alosetron A 5-HT3 antagonist used to treat diarrhea-predominant IBS.
Tropisetron A 5HT-3 receptor antagonist used as an antiemetic in the treatment of chemotherapy-induced nausea
and vomiting.
Granisetron A 5HT3 antagonist used to treat nausea and vomiting in cancer therapy and postoperatively.
Ondansetron A serotonin 5-HT3 receptor antagonist used to prevent nausea and vomiting in cancer chemotherapy
and postoperatively.
Palonosetron A serotonin antagonist used in the prophylaxis or management of vomiting that results from
emetogenic chemotherapy, and for the management of postoperative nausea and vomiting.
Vortioxetine A serotonin modulating antidepressant indicated for the treatment of major depressive disorder
(MDD).
Mirtazapine A tetracyclic antidepressant used in the treatment of major depression and is used off-label as a drug
for insomnia and to increase appetite.
Dolasetron An antinauseant and antiemetic used in chemotherapy and postoperatively.
Esmirtazapine Investigated for use/treatment in insomnia and sleep disorders
2. NEUROKININ RECEPTOR
ANTAGONISTS.
Mechanism of action.
• They have antiemetic properties that are mediated
through central blockade in the area postrema.
• Aprepitant (an oral formulation) is a highly selective
NK 1 -receptor antagonist that crosses the blood-
brain barrier and occupies brain NK 1 receptors
blocking the vomiting centers.
• NK-1 receptor antagonists have antinausea and anti-
vomiting properties relayed through a central
blockade in the area postrema, nucleus tractus
solitarius, and visceral afferent nerves.
• NK-1 receptors mediate most of the central and peripheral effects
of substance P. Substance P is an excitatory neurotransmitter that
has a role in pain perception. It is among a class of neuropeptides
called neurokinins. Its receptor, NK-1, is a G protein-coupled
consisting of seven transmembrane helical elements.
• Therefore, NK-1 receptor antagonists can prevent both central and
peripheral stimulation of vomiting centers. NK-1 receptor
antagonists such as aprepitant (oral and IV formulations) are highly
selective NK-1 receptor antagonists which cross the blood-brain
barrier and occupy NK-1 receptors in the brain
Postrema Area
•a highly vascular paired structure in the
medulla oblongata in the brainstem.[1] It lies in
the caudal fourth ventricular floor, overlying the
inferior portion of vagal trigone while facing the
foramen of Magendie and rostral to the obex,
the inferior point of the floor of the fourth
ventricle.
Examples of Neurokinin receptor antagonists.
•aprepitant,
•rolapitant,
•casopitant,
•fosaprepitant,
•netupitant, and maropitant are effective to
treat postsurgical nausea and vomiting
and cancer chemotherapy-induced
nausea and vomiting
3. PHENOTHIAZINES AND
BUTYROPHENONES.
• Mechanism of action.
• The antiemetic properties of phenothiazines are mediated through
inhibition of dopamine and muscarinic receptors.
• Sedative properties are due to their antihistamine activity. The
agents most commonly used as antiemetics are prochlorperazine,
promethazine, Chlorpromazine and thiethylperazine.
• Antipsychotic butyrophenones also possess antiemetic properties
due to their central dopaminergic blockade.
Examples of Phenothiazines and
butyrophenones.
•Phenothiazines and butyrophenones are
the antipsychotic (neuroleptic) agents.
•Commonly used agents include;
chlorpromazine, prochlorperazine,
droperidol and haloperidol. Other unfamiliar
agents include fluphenazine, Pericyazine,
Pipothiazine and Trifluoperazine
Side effects of Anti-emetic drugs
•they all cause dose-dependent CNS
depression, tachycardia, hypotension and
anticholinergic effects.
•Chlorpromazine causes a coma in doses >
5 grams.
•Sedation
•Urinary retention is common
4. H 1 ANTIHISTAMINES & ANTICHOLINERGIC
DRUGS
• MOA; These drugs have weak antiemetic activity, although they are
particularly useful for the prevention or treatment of motion
sickness.eg cetirizine, levocetirizine, desloratadine, loratadine, and
fexofenadine.
• Atropine causes reversible blockade of muscarinic receptors; that is,
blockade by a small dose of atropine can be overcome by a larger
concentration of acetylcholine or equivalent muscarinic agonist.
• Anti cholinergic effects like dry mouth, sedation
References
1. Essentials of Medical Pharmacology_Seveth Edition, KD
Tripathi
2. Katzung & Trevor’s Pharmacology_ 10th Edition
3. Uganda Clinical guidelines 2022,.
4. Robert E. Stitzel and Joseph J. McPhillips () Modern
Pharmacology with Clinical Applications, 5th edition

More Related Content

Similar to Group 5_ Year 3 Pharmacology 2023.pptx

Peptic ulcer.pptx
Peptic ulcer.pptxPeptic ulcer.pptx
Peptic ulcer.pptx
sapnabohra2
 
Gastrointestinal Drugs N.pptx
Gastrointestinal Drugs N.pptxGastrointestinal Drugs N.pptx
Gastrointestinal Drugs N.pptx
syed bari
 
Peptic ulcer
Peptic ulcer Peptic ulcer
Peptic ulcer
aakriti garg
 
Drugs to treat digestive disorders in ruminants
Drugs to treat digestive disorders in ruminantsDrugs to treat digestive disorders in ruminants
Drugs to treat digestive disorders in ruminants
nandinisharma4848
 
GIT 7.pptx
GIT 7.pptxGIT 7.pptx
GIT 7.pptx
Imtiyaz60
 
Pharmacology powerpoint git drugs
Pharmacology powerpoint  git drugsPharmacology powerpoint  git drugs
Pharmacology powerpoint git drugs
Fred Ecaldre
 
Anti ulcer drugs classification
Anti ulcer drugs classificationAnti ulcer drugs classification
Anti ulcer drugs classification
Zulcaif Ahmad
 
Gastrointestinal drugs - Pharmacology
Gastrointestinal  drugs - PharmacologyGastrointestinal  drugs - Pharmacology
Gastrointestinal drugs - Pharmacology
Areej Abu Hanieh
 
Anti ulcer drug Pharmacology
Anti ulcer drug PharmacologyAnti ulcer drug Pharmacology
Anti ulcer drug Pharmacology
ManashDas26
 
Antiulcer drugs Advance Pharmacology .pptx
Antiulcer drugs Advance Pharmacology .pptxAntiulcer drugs Advance Pharmacology .pptx
Antiulcer drugs Advance Pharmacology .pptx
Rohit chaurpagar
 
Drugs Acting on GastroIntestinal System.ppt
Drugs Acting on GastroIntestinal System.pptDrugs Acting on GastroIntestinal System.ppt
Drugs Acting on GastroIntestinal System.ppt
Haftom Gebregergs Hailu
 
GIT drugs Ch 2.pptx
GIT drugs Ch 2.pptxGIT drugs Ch 2.pptx
GIT drugs Ch 2.pptx
SolimanAbuDalfa
 
Drugs affecting GI function.pptppppptgtť
Drugs affecting GI function.pptppppptgtťDrugs affecting GI function.pptppppptgtť
Drugs affecting GI function.pptppppptgtť
peculiarmichaels2
 
NurseReview.Org - Antacids And Controllers Updates (pharmacology for advanced...
NurseReview.Org - Antacids And Controllers Updates (pharmacology for advanced...NurseReview.Org - Antacids And Controllers Updates (pharmacology for advanced...
NurseReview.Org - Antacids And Controllers Updates (pharmacology for advanced...
jben501
 
Drugs for Peptic Ulcer
Drugs for Peptic UlcerDrugs for Peptic Ulcer
Drugs for Peptic Ulcer
Dr Vinay Gupta
 
Antacids and controlling agents
Antacids  and  controlling agentsAntacids  and  controlling agents
Antacids and controlling agents
raj kumar
 
Laxatives and antidiarrhoelas moa uses adr
Laxatives and antidiarrhoelas moa uses adrLaxatives and antidiarrhoelas moa uses adr
Laxatives and antidiarrhoelas moa uses adr
vijiarumugamvsvs
 
Drugs acting on the gastro-intestinal tract
Drugs acting on the gastro-intestinal tractDrugs acting on the gastro-intestinal tract
Drugs acting on the gastro-intestinal tract
Elton Nyengo
 
Anti Ulcer drugs pharmacology and classification
Anti Ulcer drugs pharmacology and classificationAnti Ulcer drugs pharmacology and classification
Anti Ulcer drugs pharmacology and classification
Imtiyaz60
 
Paptic ulcer.pptx
Paptic ulcer.pptxPaptic ulcer.pptx
Paptic ulcer.pptx
Rahul B S
 

Similar to Group 5_ Year 3 Pharmacology 2023.pptx (20)

Peptic ulcer.pptx
Peptic ulcer.pptxPeptic ulcer.pptx
Peptic ulcer.pptx
 
Gastrointestinal Drugs N.pptx
Gastrointestinal Drugs N.pptxGastrointestinal Drugs N.pptx
Gastrointestinal Drugs N.pptx
 
Peptic ulcer
Peptic ulcer Peptic ulcer
Peptic ulcer
 
Drugs to treat digestive disorders in ruminants
Drugs to treat digestive disorders in ruminantsDrugs to treat digestive disorders in ruminants
Drugs to treat digestive disorders in ruminants
 
GIT 7.pptx
GIT 7.pptxGIT 7.pptx
GIT 7.pptx
 
Pharmacology powerpoint git drugs
Pharmacology powerpoint  git drugsPharmacology powerpoint  git drugs
Pharmacology powerpoint git drugs
 
Anti ulcer drugs classification
Anti ulcer drugs classificationAnti ulcer drugs classification
Anti ulcer drugs classification
 
Gastrointestinal drugs - Pharmacology
Gastrointestinal  drugs - PharmacologyGastrointestinal  drugs - Pharmacology
Gastrointestinal drugs - Pharmacology
 
Anti ulcer drug Pharmacology
Anti ulcer drug PharmacologyAnti ulcer drug Pharmacology
Anti ulcer drug Pharmacology
 
Antiulcer drugs Advance Pharmacology .pptx
Antiulcer drugs Advance Pharmacology .pptxAntiulcer drugs Advance Pharmacology .pptx
Antiulcer drugs Advance Pharmacology .pptx
 
Drugs Acting on GastroIntestinal System.ppt
Drugs Acting on GastroIntestinal System.pptDrugs Acting on GastroIntestinal System.ppt
Drugs Acting on GastroIntestinal System.ppt
 
GIT drugs Ch 2.pptx
GIT drugs Ch 2.pptxGIT drugs Ch 2.pptx
GIT drugs Ch 2.pptx
 
Drugs affecting GI function.pptppppptgtť
Drugs affecting GI function.pptppppptgtťDrugs affecting GI function.pptppppptgtť
Drugs affecting GI function.pptppppptgtť
 
NurseReview.Org - Antacids And Controllers Updates (pharmacology for advanced...
NurseReview.Org - Antacids And Controllers Updates (pharmacology for advanced...NurseReview.Org - Antacids And Controllers Updates (pharmacology for advanced...
NurseReview.Org - Antacids And Controllers Updates (pharmacology for advanced...
 
Drugs for Peptic Ulcer
Drugs for Peptic UlcerDrugs for Peptic Ulcer
Drugs for Peptic Ulcer
 
Antacids and controlling agents
Antacids  and  controlling agentsAntacids  and  controlling agents
Antacids and controlling agents
 
Laxatives and antidiarrhoelas moa uses adr
Laxatives and antidiarrhoelas moa uses adrLaxatives and antidiarrhoelas moa uses adr
Laxatives and antidiarrhoelas moa uses adr
 
Drugs acting on the gastro-intestinal tract
Drugs acting on the gastro-intestinal tractDrugs acting on the gastro-intestinal tract
Drugs acting on the gastro-intestinal tract
 
Anti Ulcer drugs pharmacology and classification
Anti Ulcer drugs pharmacology and classificationAnti Ulcer drugs pharmacology and classification
Anti Ulcer drugs pharmacology and classification
 
Paptic ulcer.pptx
Paptic ulcer.pptxPaptic ulcer.pptx
Paptic ulcer.pptx
 

More from ssuser504dda

Palliative care presentation slide4.pptx
Palliative care presentation slide4.pptxPalliative care presentation slide4.pptx
Palliative care presentation slide4.pptx
ssuser504dda
 
Palliative class presentation slid3.pptx
Palliative class presentation slid3.pptxPalliative class presentation slid3.pptx
Palliative class presentation slid3.pptx
ssuser504dda
 
Palliative care presentation slide2.pptx
Palliative care presentation slide2.pptxPalliative care presentation slide2.pptx
Palliative care presentation slide2.pptx
ssuser504dda
 
Palliative care presentation slides.pptx
Palliative care presentation slides.pptxPalliative care presentation slides.pptx
Palliative care presentation slides.pptx
ssuser504dda
 
Development studies - presentation .pptx
Development studies - presentation .pptxDevelopment studies - presentation .pptx
Development studies - presentation .pptx
ssuser504dda
 
Group Reproductice health Coursework.ppt
Group Reproductice health Coursework.pptGroup Reproductice health Coursework.ppt
Group Reproductice health Coursework.ppt
ssuser504dda
 
Mortality Audit presentation - slid.pptx
Mortality Audit presentation - slid.pptxMortality Audit presentation - slid.pptx
Mortality Audit presentation - slid.pptx
ssuser504dda
 
Examinating the Resipiratory System.pptx
Examinating the Resipiratory System.pptxExaminating the Resipiratory System.pptx
Examinating the Resipiratory System.pptx
ssuser504dda
 
crush-injury-and-crush-syndrome-191.pptx
crush-injury-and-crush-syndrome-191.pptxcrush-injury-and-crush-syndrome-191.pptx
crush-injury-and-crush-syndrome-191.pptx
ssuser504dda
 
Male Reproductive System ......... .pptx
Male Reproductive System ......... .pptxMale Reproductive System ......... .pptx
Male Reproductive System ......... .pptx
ssuser504dda
 
Antenatal Care -REPRODUCTIVE HEALTH.pptx
Antenatal Care -REPRODUCTIVE HEALTH.pptxAntenatal Care -REPRODUCTIVE HEALTH.pptx
Antenatal Care -REPRODUCTIVE HEALTH.pptx
ssuser504dda
 
Student Academic - PLACEMENT REPORT.pptx
Student Academic - PLACEMENT REPORT.pptxStudent Academic - PLACEMENT REPORT.pptx
Student Academic - PLACEMENT REPORT.pptx
ssuser504dda
 
Intravenous Urography lecture detai.pptx
Intravenous Urography lecture detai.pptxIntravenous Urography lecture detai.pptx
Intravenous Urography lecture detai.pptx
ssuser504dda
 
IVU contrasted studies - lecture....pptx
IVU contrasted studies - lecture....pptxIVU contrasted studies - lecture....pptx
IVU contrasted studies - lecture....pptx
ssuser504dda
 
Cranial nerves - esson presentation.pptx
Cranial nerves - esson presentation.pptxCranial nerves - esson presentation.pptx
Cranial nerves - esson presentation.pptx
ssuser504dda
 
HEPATITIS IN Children a case study.pptx
HEPATITIS IN Children  a case study.pptxHEPATITIS IN Children  a case study.pptx
HEPATITIS IN Children a case study.pptx
ssuser504dda
 
children. palliative care.pptx
children.     palliative       care.pptxchildren.     palliative       care.pptx
children. palliative care.pptx
ssuser504dda
 
PALLIATIVE CARE (GROUP2) BME3 2023.pptx
PALLIATIVE CARE (GROUP2)  BME3 2023.pptxPALLIATIVE CARE (GROUP2)  BME3 2023.pptx
PALLIATIVE CARE (GROUP2) BME3 2023.pptx
ssuser504dda
 
Group pharmacology uuuuu. .pptx
Group pharmacology   uuuuu.        .pptxGroup pharmacology   uuuuu.        .pptx
Group pharmacology uuuuu. .pptx
ssuser504dda
 
STEP Session 10b. - Networking.ppt
STEP Session 10b.       - Networking.pptSTEP Session 10b.       - Networking.ppt
STEP Session 10b. - Networking.ppt
ssuser504dda
 

More from ssuser504dda (20)

Palliative care presentation slide4.pptx
Palliative care presentation slide4.pptxPalliative care presentation slide4.pptx
Palliative care presentation slide4.pptx
 
Palliative class presentation slid3.pptx
Palliative class presentation slid3.pptxPalliative class presentation slid3.pptx
Palliative class presentation slid3.pptx
 
Palliative care presentation slide2.pptx
Palliative care presentation slide2.pptxPalliative care presentation slide2.pptx
Palliative care presentation slide2.pptx
 
Palliative care presentation slides.pptx
Palliative care presentation slides.pptxPalliative care presentation slides.pptx
Palliative care presentation slides.pptx
 
Development studies - presentation .pptx
Development studies - presentation .pptxDevelopment studies - presentation .pptx
Development studies - presentation .pptx
 
Group Reproductice health Coursework.ppt
Group Reproductice health Coursework.pptGroup Reproductice health Coursework.ppt
Group Reproductice health Coursework.ppt
 
Mortality Audit presentation - slid.pptx
Mortality Audit presentation - slid.pptxMortality Audit presentation - slid.pptx
Mortality Audit presentation - slid.pptx
 
Examinating the Resipiratory System.pptx
Examinating the Resipiratory System.pptxExaminating the Resipiratory System.pptx
Examinating the Resipiratory System.pptx
 
crush-injury-and-crush-syndrome-191.pptx
crush-injury-and-crush-syndrome-191.pptxcrush-injury-and-crush-syndrome-191.pptx
crush-injury-and-crush-syndrome-191.pptx
 
Male Reproductive System ......... .pptx
Male Reproductive System ......... .pptxMale Reproductive System ......... .pptx
Male Reproductive System ......... .pptx
 
Antenatal Care -REPRODUCTIVE HEALTH.pptx
Antenatal Care -REPRODUCTIVE HEALTH.pptxAntenatal Care -REPRODUCTIVE HEALTH.pptx
Antenatal Care -REPRODUCTIVE HEALTH.pptx
 
Student Academic - PLACEMENT REPORT.pptx
Student Academic - PLACEMENT REPORT.pptxStudent Academic - PLACEMENT REPORT.pptx
Student Academic - PLACEMENT REPORT.pptx
 
Intravenous Urography lecture detai.pptx
Intravenous Urography lecture detai.pptxIntravenous Urography lecture detai.pptx
Intravenous Urography lecture detai.pptx
 
IVU contrasted studies - lecture....pptx
IVU contrasted studies - lecture....pptxIVU contrasted studies - lecture....pptx
IVU contrasted studies - lecture....pptx
 
Cranial nerves - esson presentation.pptx
Cranial nerves - esson presentation.pptxCranial nerves - esson presentation.pptx
Cranial nerves - esson presentation.pptx
 
HEPATITIS IN Children a case study.pptx
HEPATITIS IN Children  a case study.pptxHEPATITIS IN Children  a case study.pptx
HEPATITIS IN Children a case study.pptx
 
children. palliative care.pptx
children.     palliative       care.pptxchildren.     palliative       care.pptx
children. palliative care.pptx
 
PALLIATIVE CARE (GROUP2) BME3 2023.pptx
PALLIATIVE CARE (GROUP2)  BME3 2023.pptxPALLIATIVE CARE (GROUP2)  BME3 2023.pptx
PALLIATIVE CARE (GROUP2) BME3 2023.pptx
 
Group pharmacology uuuuu. .pptx
Group pharmacology   uuuuu.        .pptxGroup pharmacology   uuuuu.        .pptx
Group pharmacology uuuuu. .pptx
 
STEP Session 10b. - Networking.ppt
STEP Session 10b.       - Networking.pptSTEP Session 10b.       - Networking.ppt
STEP Session 10b. - Networking.ppt
 

Recently uploaded

Microbiology & Parasitology Exercises Parts of the Microscope
Microbiology & Parasitology Exercises Parts of the MicroscopeMicrobiology & Parasitology Exercises Parts of the Microscope
Microbiology & Parasitology Exercises Parts of the Microscope
ThaShee2
 
Call Girls in Kolkata 💯Call Us 🔝 7374876321 🔝 💃 Top Class Call Girl Servic...
Call Girls in Kolkata   💯Call Us 🔝 7374876321 🔝 💃  Top Class Call Girl Servic...Call Girls in Kolkata   💯Call Us 🔝 7374876321 🔝 💃  Top Class Call Girl Servic...
Call Girls in Kolkata 💯Call Us 🔝 7374876321 🔝 💃 Top Class Call Girl Servic...
daljeetsingh9909
 
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
shruti jagirdar
 
13. PROM premature rupture of membranes
13.  PROM premature rupture of membranes13.  PROM premature rupture of membranes
13. PROM premature rupture of membranes
TigistuMelak
 
biomechanics of running. Dr.dhwani.pptx
biomechanics of running.   Dr.dhwani.pptxbiomechanics of running.   Dr.dhwani.pptx
biomechanics of running. Dr.dhwani.pptx
Dr. Dhwani kawedia
 
Cervical Disc Arthroplasty ORSI 2024.pptx
Cervical Disc Arthroplasty ORSI 2024.pptxCervical Disc Arthroplasty ORSI 2024.pptx
Cervical Disc Arthroplasty ORSI 2024.pptx
LEFLOT Jean-Louis
 
Mechanical injuries(ICS) due to sharp force.ppt
Mechanical injuries(ICS) due to sharp force.pptMechanical injuries(ICS) due to sharp force.ppt
Mechanical injuries(ICS) due to sharp force.ppt
SatrajitRoy5
 
Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)
Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)
Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)
MuskanShingari
 
2nd-generation Antihistaminic Part I.pptx
2nd-generation Antihistaminic Part I.pptx2nd-generation Antihistaminic Part I.pptx
2nd-generation Antihistaminic Part I.pptx
Madhumita Dixit
 
Breast cancer: Post menopausal endocrine therapy
Breast cancer: Post menopausal endocrine therapyBreast cancer: Post menopausal endocrine therapy
Breast cancer: Post menopausal endocrine therapy
Dr. Sumit KUMAR
 
Call Girl Pune 7339748667 Vip Call Girls Pune
Call Girl Pune 7339748667 Vip Call Girls PuneCall Girl Pune 7339748667 Vip Call Girls Pune
Call Girl Pune 7339748667 Vip Call Girls Pune
Mobile Problem
 
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
MuskanShingari
 
Tele Optometry (kunj'sppt) / Basics of tele optometry.
Tele Optometry (kunj'sppt) / Basics of tele optometry.Tele Optometry (kunj'sppt) / Basics of tele optometry.
Tele Optometry (kunj'sppt) / Basics of tele optometry.
Kunj Vihari
 
Call Girls Electronic City 🥰 Bangalore Call Girl No Advance Book Now
Call Girls Electronic City 🥰 Bangalore Call Girl No Advance Book NowCall Girls Electronic City 🥰 Bangalore Call Girl No Advance Book Now
Call Girls Electronic City 🥰 Bangalore Call Girl No Advance Book Now
saftyhealth48
 
Call Girls Goa (india) +91-7426014248 Goa Call Girls
Call Girls Goa (india) +91-7426014248 Goa Call GirlsCall Girls Goa (india) +91-7426014248 Goa Call Girls
Call Girls Goa (india) +91-7426014248 Goa Call Girls
sagarvarma453
 
PGx Analysis in VarSeq: A User’s Perspective
PGx Analysis in VarSeq: A User’s PerspectivePGx Analysis in VarSeq: A User’s Perspective
PGx Analysis in VarSeq: A User’s Perspective
Golden Helix
 
Demystifying Fallopian Tube Blockage- Grading the Differences and Implication...
Demystifying Fallopian Tube Blockage- Grading the Differences and Implication...Demystifying Fallopian Tube Blockage- Grading the Differences and Implication...
Demystifying Fallopian Tube Blockage- Grading the Differences and Implication...
FFragrant
 
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdf
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdfOsvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdf
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdf
Osvaldo Bernardo Muchanga
 
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...
Donc Test
 
Call Girls Kolkata 💯Call Us 🔝 7374876321 🔝 💃 Top Class Call Girl Service A...
Call Girls Kolkata   💯Call Us 🔝 7374876321 🔝 💃  Top Class Call Girl Service A...Call Girls Kolkata   💯Call Us 🔝 7374876321 🔝 💃  Top Class Call Girl Service A...
Call Girls Kolkata 💯Call Us 🔝 7374876321 🔝 💃 Top Class Call Girl Service A...
daljeetsingh9909
 

Recently uploaded (20)

Microbiology & Parasitology Exercises Parts of the Microscope
Microbiology & Parasitology Exercises Parts of the MicroscopeMicrobiology & Parasitology Exercises Parts of the Microscope
Microbiology & Parasitology Exercises Parts of the Microscope
 
Call Girls in Kolkata 💯Call Us 🔝 7374876321 🔝 💃 Top Class Call Girl Servic...
Call Girls in Kolkata   💯Call Us 🔝 7374876321 🔝 💃  Top Class Call Girl Servic...Call Girls in Kolkata   💯Call Us 🔝 7374876321 🔝 💃  Top Class Call Girl Servic...
Call Girls in Kolkata 💯Call Us 🔝 7374876321 🔝 💃 Top Class Call Girl Servic...
 
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
 
13. PROM premature rupture of membranes
13.  PROM premature rupture of membranes13.  PROM premature rupture of membranes
13. PROM premature rupture of membranes
 
biomechanics of running. Dr.dhwani.pptx
biomechanics of running.   Dr.dhwani.pptxbiomechanics of running.   Dr.dhwani.pptx
biomechanics of running. Dr.dhwani.pptx
 
Cervical Disc Arthroplasty ORSI 2024.pptx
Cervical Disc Arthroplasty ORSI 2024.pptxCervical Disc Arthroplasty ORSI 2024.pptx
Cervical Disc Arthroplasty ORSI 2024.pptx
 
Mechanical injuries(ICS) due to sharp force.ppt
Mechanical injuries(ICS) due to sharp force.pptMechanical injuries(ICS) due to sharp force.ppt
Mechanical injuries(ICS) due to sharp force.ppt
 
Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)
Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)
Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)
 
2nd-generation Antihistaminic Part I.pptx
2nd-generation Antihistaminic Part I.pptx2nd-generation Antihistaminic Part I.pptx
2nd-generation Antihistaminic Part I.pptx
 
Breast cancer: Post menopausal endocrine therapy
Breast cancer: Post menopausal endocrine therapyBreast cancer: Post menopausal endocrine therapy
Breast cancer: Post menopausal endocrine therapy
 
Call Girl Pune 7339748667 Vip Call Girls Pune
Call Girl Pune 7339748667 Vip Call Girls PuneCall Girl Pune 7339748667 Vip Call Girls Pune
Call Girl Pune 7339748667 Vip Call Girls Pune
 
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
 
Tele Optometry (kunj'sppt) / Basics of tele optometry.
Tele Optometry (kunj'sppt) / Basics of tele optometry.Tele Optometry (kunj'sppt) / Basics of tele optometry.
Tele Optometry (kunj'sppt) / Basics of tele optometry.
 
Call Girls Electronic City 🥰 Bangalore Call Girl No Advance Book Now
Call Girls Electronic City 🥰 Bangalore Call Girl No Advance Book NowCall Girls Electronic City 🥰 Bangalore Call Girl No Advance Book Now
Call Girls Electronic City 🥰 Bangalore Call Girl No Advance Book Now
 
Call Girls Goa (india) +91-7426014248 Goa Call Girls
Call Girls Goa (india) +91-7426014248 Goa Call GirlsCall Girls Goa (india) +91-7426014248 Goa Call Girls
Call Girls Goa (india) +91-7426014248 Goa Call Girls
 
PGx Analysis in VarSeq: A User’s Perspective
PGx Analysis in VarSeq: A User’s PerspectivePGx Analysis in VarSeq: A User’s Perspective
PGx Analysis in VarSeq: A User’s Perspective
 
Demystifying Fallopian Tube Blockage- Grading the Differences and Implication...
Demystifying Fallopian Tube Blockage- Grading the Differences and Implication...Demystifying Fallopian Tube Blockage- Grading the Differences and Implication...
Demystifying Fallopian Tube Blockage- Grading the Differences and Implication...
 
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdf
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdfOsvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdf
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdf
 
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...
 
Call Girls Kolkata 💯Call Us 🔝 7374876321 🔝 💃 Top Class Call Girl Service A...
Call Girls Kolkata   💯Call Us 🔝 7374876321 🔝 💃  Top Class Call Girl Service A...Call Girls Kolkata   💯Call Us 🔝 7374876321 🔝 💃  Top Class Call Girl Service A...
Call Girls Kolkata 💯Call Us 🔝 7374876321 🔝 💃 Top Class Call Girl Service A...
 

Group 5_ Year 3 Pharmacology 2023.pptx

  • 1. ACID SECRETION DISORDER DRUGS & ANTI-EMETIC DRUGS By BME III 2023-2023 Group 5 BME III SYSTEMS PHARMACOLOGY Members 1. 21/U/24081/HTG Asiimwe Anne 2. 20/U/21960/HTG Kibirige John Paul 3. 21/U/24115/HTG Niwamanya Derrick
  • 2. Presentation Outline Part 1: Acid secretion disorder drugs Physiology of acid secretion Acid secretion disorders Drugs used in acid secretion disorders Part 2: Anti-Emetic Drugs Physiology of emesis Classes of anti-emetic drugs
  • 3. ACID SECRETION DISORDER DRUGS Part 1 Introduction: Physiology of Gastric Acid Secretion Gastric acid secretion depends mainly on Gastrin, Histamine & Acetylcholine (Ach) Acetylcholine (ACh) is released by parasympathetic neurons. Gastrin is secreted by G cells, and histamine is a paracrine substance released by mast cells in the nearby lamina propria. Acetylcholine and gastrin stimulate parietal cells to secrete more HCl in the presence of histamine. In other words, histamine acts synergistically, enhancing the effects of acetylcholine and gastrin. Receptors for all three substances are present in the plasma membrane of parietal cells.  The histamine receptors on parietal cells are called H2 receptors.  Acetylcholine (ACh) receptors are the muscarinic, M3  Gastrin receptors are CCK-B receptors
  • 4. • Acetylcholine & Gastrin (food stimulated) bind to parietal cell receptors [M3 & CCK-B, respectively], increase cytosolic Ca2 + & stimulate acid secretion from the H+/K+ ATPase(proton pump) • Histamine (released from enterochromaffin cells, ECC) binds to H2 receptors on parietal cells and activate adenylyl cyclase and increase cAMP which stimulates protein kinases and activate H+/K+ ATPase pump leading to HCl secretion Physiology of Gastric Acid Secretion Introduction
  • 5. https://youtu.be/W9nyXXh*htM?si=9jg7_byI223Vx-wt Watch mechanism of HCL secretion by parietal cell on YOUTUBE. (Click on the link)
  • 6. Pathogenesis of Gastric acid disorders Imbalance between defenses and aggressive factors results into gastric acid/stomach disorders • Defensive factors: These prevent the stomach and duodenum from self-digestion. • Mucus Coats and lines the stomach and is the first line of defense • Bicarbonate: secreted from endothelial cells • Blood flow: good blood flow maintains mucosal integrity • Prostaglandins: stimulate secretion of bicarbonate and mucus, promote blood flow, suppress secretion of gastric acid • Aggressive factors: • Helicobacter pylori: inflammatory response and mucosal toxicity • Gastric Acid: activates pepsin enzyme and injures mucosa • Decreased blood flow: causes ↓ in mucus production and HCO3- • NSAIDS: inhibit the production of prostaglandins • Smoking: nicotine stimulates gastric acid production, reduces duodenal HCO3- • Alcohol/Ethanol: causes erosive gastritis • Caffeine: increases gastric acid secretion.
  • 7. • These include: • GERD (gastro-esophageal reflux disease) • Acute Gastritis • Peptic Ulcers (gastric and duodenal ulcers) • Excessive gastric acid secretion. • Stress-induced gastritis • Zollinger-Ellison syndrome: Caused by a Gastrinoma, a neuroendocrine tumor secreting gastrin hormone. ACID SECRETION DISORDERS
  • 8. DRUGS USED IN ACID SECRETION DISORDERS Class/Subclass Mechanism of Action Example Protein Pump inhibitors Inhibit action of H+/K+ pump and thus inhibit synthesis of gastric acid Omeprazole, Lansoprazole, pantoprazole Histamine H2-receptor blockers Block the histamine receptors and prevent binding of histamine and thus cause reduced acid secretion Ranitidine, Cimetidine Antiacids Neutralize acid and prevents formation of pepsin. Magnesium hydroxide Magnesium trisilicate Prostaglandin analogues Reduce gastric acid and enhance mucosal resistance to injury Misoprostol Mucosal barrier fortifiers (cytoprotective agents) Form a protective coat Sucralfate, Bismuth sulfate H-Pylori eradication Regimens Combination of drugs for H- pylori induced acid disorders to eradicate the bacteria Quadruple therapy Tripple therapy
  • 9. Antacids • They were the first and mainstay of treatment for acid-peptic disorders until the discovery of H2− receptor antagonists and proton-pump inhibitors (PPIs). • Examples Sodium bicarbonate, Calcium carbonate, Magnesium salts (hydroxide, carbonate, trisilicate), and Aluminum hydroxide • MOA: Their principal mechanism of action is reduction of intragastric acidity. Antacids are weak bases that react with gastric hydrochloric acid to form a salt and water. Drug interaction
  • 10. Therapeutic Actions: Antacids have a number of actions which include: Neutralizing gastric acid and thus relieving associated pain and nausea Reducing delivery of acid into the duodenum following a meal Inactivation of the proteolyticc enzyme pepsin by raising the gastric pH above 4–5. Interactions: Antacids should be taken approximately one hour before or after food, as this maximizes the contact time with stomach acid and allows the antacid to coat the stomach in the absence of food. Antacids may affect the absorption of other medications by binding the drug (reducing its absorption) or by increasing intragastric pH so that the drug’s dissolution or solubility (especially weakly basic or acidic drugs) is altered. Therefore, antacids should not be given within 2 hours of doses of tetracyclines, fluoroquinolones, itraconazole, and iron. Antacids:
  • 11. Sodium bicarbonate (eg, baking soda, Alka Seltzer) • Reacts rapidly with hydrochloric acid (HCl) to produce carbon dioxide and sodium chloride. Formation of carbon dioxide results in gastric distention and belching. • Unreacted alkali is readily absorbed, potentially causing metabolic alkalosis when given in high doses or to patients with renal insufficiency. • Sodium chloride absorption may exacerbate fluid retention in patients with heart failure, hypertension, and renal insufficiency Magnesium hydroxide or aluminum hydroxide Compounds: • React slowly with HCl to form magnesium chloride or aluminum chloride and water. • Because no gas is generated, belching does not occur. Metabolic alkalosis is also uncommon because of the efficiency of the neutralization reaction. • Because unabsorbed magnesium salts may cause an osmotic diarrhea and aluminum salts may cause constipation, these agents are commonly administered together in proprietary formulations to minimize the impact on Antacids: Examples
  • 12. H2 receptor antagonists Commonly used in the 1970s until the early 1990s, With the recognition of the role of H pylori in ulcer disease and the advent of PPIs, the use of prescription H2 blockers has declined markedly over time. Examples: • Cimetidine, Ranitidine, Famotidine, Nizatidine Pharmacokinetics: • All four agents are rapidly absorbed from the intestine. • Cimetidine, ranitidine, and famotidine undergo first-pass hepatic metabolism resulting in a bioavailability of approximately 50%. Nizatidine has little first-pass metabolism. • 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 secretion. Dose reduction is required in patients with moderate to severe renal (and possibly severe hepatic) insufficiency.
  • 13. MOA • The H2 antagonists exhibit competitive inhibition at the parietal cell. • H2 receptor and suppress basal and meal-stimulated acid secretion. • They are highly selective and do not affect H1 or H3 receptors • They also reduce the volume of gastric secretion and the concentration of pepsin. Drug Interactions • They interfere with several important hepatic cytochrome P450 drug metabolism pathways, including those catalyzed by CYP1A2, CYP2C9, CYP2D6, and CYP3A4. • H2 antagonists compete with creatinine and certain drugs (eg, procainamide) for renal tubular secretion. All of these agents except famotidine inhibit gastric first-pass metabolism of ethanol, increased bioavailability of ethanol could lead to increased blood ethanol levels. H2 receptor antagonists
  • 14. Side effects • H2 antagonists are relatively safe drugs. • In adults H2-receptor antagonists might mask symptoms of gastric cancer; • 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 intravenous H2 antagonists • Cimetidine inhibits binding of dihydrotestosterone to androgen receptors, inhibits metabolism of estradiol, and increases serum prolactin levels. When used long-term or in high doses, it may cause gynecomastia or impotence in men and galactorrhea in women. These effects are specific to cimetidine and do not occur with the other H2 antagonists H2 receptor antagonists
  • 15. Ranitidine Available in • Tablets: 75mg, 150mg, 300mg • Injection solution: 25mg/ml • Capsule 150mg, 300mg. • Syrup 15mg/ml Dosage (For GERD): • Oral: 150mg 12hrly or 4-8mg/kg not beyond 300mg in children • IV/IM: 50mg 6-8hrly, or 2-4mg/kg/day in divided doses. MOA: • Blocks H2 receptors of gastric parietal cells leading to inhibition of HCL secretion. Bioavailability: 50%(PO), 90-100% (parenteral) Protein bound: 10-19% Metabolized in liver, does not inhibit liver enzymes Excreted mainly in urine, half life is 2.5-3hours
  • 16. Proton Pump Inhibitors (PPIs) Since their introduction in the late 1980s, these efficacious acid inhibitory agents have assumed the major role for the treatment of acid-peptic disorders. PPIs are now among the most widely prescribed drugs worldwide due to their outstanding efficacy and safety Examples: Omeprazole, Lansoprazole, Pantoprazole, Rabeprazole, esomeprazole, Dex-lansoprazole Pharmacokinetics • PPIs are administered as inactive prodrugs. • To protect the acid-labile prodrug from rapid destruction within the gastric lumen, oral products are formulated for delayed release as acid-resistant, enteric-coated capsules or tablets. After passing through the stomach into the alkaline intestinal lumen, the enteric coatings dissolve and the prodrug is absorbed. • For children or patients with dysphagia or enteral feeding tubes, capsule formulations (but not tablets) may be opened and the microgranules mixed with apple or orange juice or mixed with soft foods
  • 17. MOA • In contrast to H2 antagonists, PPIs inhibit both fasting and meal-stimulated secretion because they block the final common pathway of acid secretion, the proton pump. In standard doses, PPIs inhibit 90–98% of 24-hour acid secretion. Side Effects • PPIs are extremely safe. • Diarrhea, headache, and abdominal pain are reported in 1–5% of patients • Nutrition—Acid is important in releasing vitamin B12 from food. A minor reduction in oral cyanocobalamin absorption occurs during proton pump inhibition, potentially leading to subnormal B12 levels with prolonged therapy. • Respiratory and enteric infections—Gastric acid is an important barrier to colonization and infection of the stomach and intestine from ingested bacteria. Increases in gastric bacterial concentrations are detected in patients taking PPIs • Potential problems due to increased serum gastrin—Gastrin levels are regulated by intragastric acidity. Acid suppression alters normal feedback Proton Pump Inhibitors (PPIs):
  • 18. Omeprazole Mechanism: Inhibits gastric acid secretion by blocking the hydrogen-potassium adenosine triphosphatase enzyme system (the ‘proton pump’) of the gastric parietal cell. Formulations available: • Suspension: 2mg/ml • Tablet: 20mg • Capsule: 10mg, 20mg, 40mg • Powder for injection: 40mg(4mg/ml) Dosage: 20mg-40mg BD Drug interactions • Decreased gastric acidity may alter absorption of drugs for which intragastric acidity affects drug bioavailability, e. g, ketoconazole, itraconazole, digoxin, and atazanavir. • All PPIs are metabolized by hepatic P450 cytochromes, including CYP2C19 and CYP3A4. • Clopidogrel and PPIs. Clopidogrel is a prodrug that requires activation by the hepatic P450 CYP2C19 isoenzyme, which also is involved to varying degrees in
  • 19. Prostaglandin analogues • The human gastrointestinal mucosa synthesizes a number of prostaglandins; Prostaglandins of the E and I series have a generally homeostatic protective action in the gastrointestinal tract, and a deficiency in endogenous production (after ingestion of a NSAID, for example) may contribute to ulcer formation. • Misoprostol, a methyl analog of PGE1 , has been approved for gastrointestinal conditions. • Misoprostol has both acid inhibitory and mucosal protective properties. It is believed to stimulate mucus and bicarbonate secretion and enhance mucosal blood flow. • Misoprostol can reduce the incidence of NSAID-induced ulcers to less than 3% and the incidence of ulcer complications by 50%. It is approved for prevention of NSAID-induced ulcers in high-risk
  • 20. Prostaglandin analogues: Misoprostol • Available formulations: • Tablets 100mcg, 200mcg • Dosage: Given orally, 200mcg 6hrly with food • However, misoprostol has never achieved widespread use owing to its high adverse-effect profile and need for multiple daily dosing. • Unwanted effects include diarrhea and abdominal cramps; uterine contractions can also occur, so the drug should not be given during pregnancy as it may induce abortion
  • 21. Mucosal barrier fortifiers (cytoprotective agents) The gastroduodenal mucosa has evolved a number of defense mechanisms to protect itself against the noxious effects of acid and pepsin. Both mucus and epithelial cell-cell tight junctions restrict back diffusion of acid and pepsin. Epithelial bicarbonate secretion establishes a pH gradient within the mucous layer Sucralfate • Is a salt of sucrose complexed to sulfated aluminum hydroxide. In water or acidic solutions it forms a viscous, tenacious paste that binds selectively to ulcers or erosions for up to 6 hours. Sucralfate has limited solubility, breaking down into sucrose sulfate (strongly negatively charged) and an aluminum salt. MOA • Forms ulcer-adherent complex. The negatively charged sucrose sulfate binds to positively charged proteins in the base of ulcers or erosion, forming a physical barrier that restricts further caustic damage and
  • 22. Mucosal barrier fortifiers (cytoprotective agents) • Available in: Tabs (1g) suspension (100mg/ml) • Dosage: 1g 6hrly and 12hrly for maintenance Adverse Effects • Because it is not absorbed, sucralfate is virtually devoid of systemic adverse effects. Constipation occurs in 2% of patients due to the aluminum salt. • Because a small amount of aluminum is absorbed, it should not be used for prolonged periods in patients with renal insufficiency.
  • 23. PUD Treatment: H-Pylori Eradication Regimens Regimen name Number of Drugs Drugs Used Tripple therapy 3 PPI Clarithromycin or Levofloxacin Amoxicillin or metronidazole Bismuth quadruple therapy 4 PPI Bismuth Compound Tetracycline Nitro-imidazoles
  • 24. ANTI-EMETIC DRUGS Part 2 Introduction • These are drugs taken to prevent or treat nausea and vomiting. • Vomiting or emesis is the abnormal emptying of stomach and upper part of intestine through esophagus and mouth. • Causes may include; Presence of irritating contents in GI tract, Mechanical stimulation of pharynx, Pregnancy, Excess intake of alcohol, Nauseating sight, odor or taste. • Vomiting is always preceded by nausea; • Nausea is unpleasant sensation which induces the desire for vomiting. It is characterized by secretion of large amount of saliva containing more amount of mucus.
  • 25. Path way of emesis •Chemoreceptor trigger zone, GIT, hypothalamus stimulation •Central vomiting center stimulation (D2, ACH, NK serotonin 5-HT3,) •Vomiting events (reverse peristalisis)
  • 26.
  • 27. Classes of Anti-emetic drugs include; • Serotonin 5-HT3 antagonists like ondansetron, granisetron, delesetron. • Neurokinin receptor antagonists like fosaprepitant. • Dopamine antagonists like chloropromazine, metoclopramide. • H1 anti histamines and anticholinergic drugs like diphenhydramine and, dimenhydrinate.
  • 28. 1. SEROTONIN 5-HT3 ANTAGONISTS Mechanism of action. • Selective 5-HT 3 -receptor antagonists have potent antiemetic properties that are mediated in part through central 5-HT 3 -receptor blockade in the vomiting center and chemoreceptor trigger zone but mainly through blockade of peripheral 5-HT 3 receptors on extrinsic intestinal vagal nerve. • The antiemetic action of these agents is restricted to emesis attributable to vagal stimulation (e.g., postoperative) and chemotherapy.
  • 29. •antagonists block serotonin both peripherally on vagal nerve terminals in the gastrointestinal Gastro-Intestinal system and centrally in the chemoreceptor trigger zone in the area postrema of the fourth ventricle, resulting in powerful antiemetic effects.
  • 30. Examples of Serotonin 5-ht 3 antagonists DRUG DRUG DESCRIPTION Alosetron A 5-HT3 antagonist used to treat diarrhea-predominant IBS. Tropisetron A 5HT-3 receptor antagonist used as an antiemetic in the treatment of chemotherapy-induced nausea and vomiting. Granisetron A 5HT3 antagonist used to treat nausea and vomiting in cancer therapy and postoperatively. Ondansetron A serotonin 5-HT3 receptor antagonist used to prevent nausea and vomiting in cancer chemotherapy and postoperatively. Palonosetron A serotonin antagonist used in the prophylaxis or management of vomiting that results from emetogenic chemotherapy, and for the management of postoperative nausea and vomiting. Vortioxetine A serotonin modulating antidepressant indicated for the treatment of major depressive disorder (MDD). Mirtazapine A tetracyclic antidepressant used in the treatment of major depression and is used off-label as a drug for insomnia and to increase appetite. Dolasetron An antinauseant and antiemetic used in chemotherapy and postoperatively. Esmirtazapine Investigated for use/treatment in insomnia and sleep disorders
  • 31. 2. NEUROKININ RECEPTOR ANTAGONISTS. Mechanism of action. • They have antiemetic properties that are mediated through central blockade in the area postrema. • Aprepitant (an oral formulation) is a highly selective NK 1 -receptor antagonist that crosses the blood- brain barrier and occupies brain NK 1 receptors blocking the vomiting centers. • NK-1 receptor antagonists have antinausea and anti- vomiting properties relayed through a central blockade in the area postrema, nucleus tractus solitarius, and visceral afferent nerves.
  • 32. • NK-1 receptors mediate most of the central and peripheral effects of substance P. Substance P is an excitatory neurotransmitter that has a role in pain perception. It is among a class of neuropeptides called neurokinins. Its receptor, NK-1, is a G protein-coupled consisting of seven transmembrane helical elements. • Therefore, NK-1 receptor antagonists can prevent both central and peripheral stimulation of vomiting centers. NK-1 receptor antagonists such as aprepitant (oral and IV formulations) are highly selective NK-1 receptor antagonists which cross the blood-brain barrier and occupy NK-1 receptors in the brain
  • 33. Postrema Area •a highly vascular paired structure in the medulla oblongata in the brainstem.[1] It lies in the caudal fourth ventricular floor, overlying the inferior portion of vagal trigone while facing the foramen of Magendie and rostral to the obex, the inferior point of the floor of the fourth ventricle.
  • 34. Examples of Neurokinin receptor antagonists. •aprepitant, •rolapitant, •casopitant, •fosaprepitant, •netupitant, and maropitant are effective to treat postsurgical nausea and vomiting and cancer chemotherapy-induced nausea and vomiting
  • 35. 3. PHENOTHIAZINES AND BUTYROPHENONES. • Mechanism of action. • The antiemetic properties of phenothiazines are mediated through inhibition of dopamine and muscarinic receptors. • Sedative properties are due to their antihistamine activity. The agents most commonly used as antiemetics are prochlorperazine, promethazine, Chlorpromazine and thiethylperazine. • Antipsychotic butyrophenones also possess antiemetic properties due to their central dopaminergic blockade.
  • 36. Examples of Phenothiazines and butyrophenones. •Phenothiazines and butyrophenones are the antipsychotic (neuroleptic) agents. •Commonly used agents include; chlorpromazine, prochlorperazine, droperidol and haloperidol. Other unfamiliar agents include fluphenazine, Pericyazine, Pipothiazine and Trifluoperazine
  • 37. Side effects of Anti-emetic drugs •they all cause dose-dependent CNS depression, tachycardia, hypotension and anticholinergic effects. •Chlorpromazine causes a coma in doses > 5 grams. •Sedation •Urinary retention is common
  • 38. 4. H 1 ANTIHISTAMINES & ANTICHOLINERGIC DRUGS • MOA; These drugs have weak antiemetic activity, although they are particularly useful for the prevention or treatment of motion sickness.eg cetirizine, levocetirizine, desloratadine, loratadine, and fexofenadine. • Atropine causes reversible blockade of muscarinic receptors; that is, blockade by a small dose of atropine can be overcome by a larger concentration of acetylcholine or equivalent muscarinic agonist. • Anti cholinergic effects like dry mouth, sedation
  • 39. References 1. Essentials of Medical Pharmacology_Seveth Edition, KD Tripathi 2. Katzung & Trevor’s Pharmacology_ 10th Edition 3. Uganda Clinical guidelines 2022,. 4. Robert E. Stitzel and Joseph J. McPhillips () Modern Pharmacology with Clinical Applications, 5th edition