Scribd
Upload
90 views5 pages

Cisapride Is Also Used When Nothing Else Works But Has Fatal Cardiac Arrhythmias Possible

Peptic ulcer disease is caused by an imbalance between acid and protective factors in the stomach and duodenum. Triple therapy using antibiotics, acid suppressants, and proton pump inhibitors is highly effective at eradicating Helicobacter pylori and healing ulcers. Gastroesophageal reflux disease is treated with lifestyle changes, antacids, and proton pump inhibitors to reduce gastric acid coming back up the esophagus. Metoclopramide and domperidone stimulate upper gastrointestinal motility while proton pump inhibitors and H2 receptor antagonists are used to treat nausea, vomiting, and various gastrointestinal disorders by reducing acid production.

Uploaded by

Kristin Douglas
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
90 views5 pages

Cisapride Is Also Used When Nothing Else Works But Has Fatal Cardiac Arrhythmias Possible

Peptic ulcer disease is caused by an imbalance between acid and protective factors in the stomach and duodenum. Triple therapy using antibiotics, acid suppressants, and proton pump inhibitors is highly effective at eradicating Helicobacter pylori and healing ulcers. Gastroesophageal reflux disease is treated with lifestyle changes, antacids, and proton pump inhibitors to reduce gastric acid coming back up the esophagus. Metoclopramide and domperidone stimulate upper gastrointestinal motility while proton pump inhibitors and H2 receptor antagonists are used to treat nausea, vomiting, and various gastrointestinal disorders by reducing acid production.

Uploaded by

Kristin Douglas
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
You are on page 1/ 5

AS 25/26 - GI Pharmacology I/II Pathophysiology and pharmacology of peptic ulcer disease.

Peptic ulcer disease is an imbalance of between acid+pepsin and mucus+bicarbonate to result in deterioration of the epithelial barrier. o Gastric Acid Secretion: ACh, gastrin, histamine, PgE - stim adenylate cyclase o Helicobacter pylori is the most common cause of gastric/duodenal ulcers

Basis and application of triple therapy, to include role of antimicrobial agents.


Two anti-biotics(microbial): amoxicillin and clarithromycin One acid suppressant: Proton pump inhibitor (H2 antagonist) Given for 1-2 weeks, results in 90% eradication, acid suppression continued

Pathophysiology and pharmacology of gastroesophageal reflux disease.


Gastric acid comes back up and erodes the oesophagus Lifestyle modification, antacids (symptomatic relief ), H2 (OTC), Proton pump inhibitors, metoclopramide and Domperidone

Stimulants of upper GIT motility


Metoclopramide , Domperidone - Stim. the upper GIT motility and gastric emptying and increases the LES tone, extrapyramidal side effects (Meto), increased prolactin secretion (Dom)

**Cisapride is also used when nothing else works but has fatal cardiac arrhythmias possible

Pathophysiology and pharmacology of nausea and vomiting (emesis).


Nausea frequently precedes the act of vomiting Stimuli for vomiting: GI irritation, motion sickness, intracranial pathology, pain, drug side effects, metabolic disturbance, hormonal, horrific sight or smell. Involves: the vomiting center (In medulla), chemoreceptive trigger zone (floor of 4th ventricle outside of blood-brain barrier) Regulating receptors: cholinergic (M), histaminergeric (H1), dopaminergic (D2), serotonergic (5-HT3), cannabinoid (CB1) **Preferred treatment of vomiting is removal of the source/drug/stimulus

Mechanism of action and adverse effects of proton pump inhibitors, histamine H2 antagonists, cytoprotective agents and antacids.
Proton Pump Inhibitors Omeprazole o Irreversibly blocks the H+/K+ ATPase (proton pump) o Inactive prodrug (protonated at acid pH to active derivative) o Side effects: Diarrhoea, flatulence, nausea o Treats: Peptic ulcer, gastroesophageal reflux, prophylaxis against ulcer development by NSAIDS (Single daily dose gives long-lasting inhibition) H2 Receptor Antagonist - Cimetidine and Ranitidine o Competitively block histamine-induced acid released by parietal cells. o Less acid suppression than PPI o Cimetidine - inhibits cytochrome P450 enzymes Drug interacts with phenytoin and warfarin (inactivates them) Antiandrogenic - gynaecomastia (swelling of breasts) Prolactin Confusion, drowsiness, headache, rash, diarrhoae o Ranitidine - little to no inhibition of cytochrome P450 enzymes and antiadrogenic activity and fewer side effects Cytoprotective Agents - Misoprostol, Sucralfate, Bismuth o Analogue of PgE1 (cytoprotective PG) o Side effects: Diarrhoea, uterine contraction, contraindicated in pregnancy o Sucralfate - binds to ulcer base (mucosal protecting action, stimulates PG and bicarbonate production) o Bismuth - binds to ulcer base (inhibits H. pylori), precipitates at acid pH to protect mucosa and stimulates PG and bicarbonate production. Antacids - AlOH, MgOH, NaHCO3 (used in combinations) o Weak bases acting to neutralize gastric acid o Symptom relief (not usually used in ulcer healing) o NaHCO3 - Can cause alkalosis (not intended for long-term use)

Mechanism of action and adverse effects of muscarinic anticholinergics, histamine H1 antagonists, dopamine D2 antagonists, serotonin 5-HT3 antagonists and cannabinoids.
Anticholinergics Muscarinic Antagonists Hyoscine o Motion sickness (Short duration) o Little antiemetic effect in other situations o Side effects: Anticholinergic side effects Antihistamines H1 Antagonists - Cyclizine o Motion sickness o Little antiemetic effect in other situations o Side effects: Sedation Dopamine receptor antagonists (D2) o Decrease vomiting caused by drugs (Chemotherapy) o Phenothiazines (Ex: prochlorperazine), Butyrophenones (Ex: haloperidol) o Side effects: Extrapyramidal, increased prolactin secretion Serotonin receptor antagonists (5-HT3) Ondansetron o Decrease vomiting caused by drugs (especially chemotherapy) o Side effects: constipation, headache Cannabinoids THC analogues acting on CB receptor Nabilone o Decrease vomiting due to drugs stimulating CTZ (chem-receptive trigger zone) o Side effects: drowsiness, psychological effects (incl. psychosis) o Steroids can be used as a refractory emesis.

Pathophysiology and pharmacology of inflammatory bowel disease.


Crohns Disease o Transmural inflammation of the lower GIT, panenteric (mouth to anus) o Diarrhoea with bleeding not common and TNF- (proinflamm cytokine) involved Ulcerative colitis o Mucosal/Sub-mucosal inflammation of rectum (always), colon (variable) o Diarrhoea with bleeding

Mechanism of action and adverse effects of aminosalicylates, corticosteroids, immunosuppressive agents, antimicrobials and TNFa inhibitors.
5-Aminosalicylates Sulfasalazine [Mesalamine] o Inhibit leukotriene/prostaglandin formation o Adverse effects: GIT disturbance, hypersensitivity reactions Corticosteroids - Hydrocortisone, prednisolone (topical), Budesonide (low bioavail.) o Inhibit of cytokine production to induce remission Immunosuppressive Agents Azathioprine [Mercaptopurine] o Purine analogues which inhibit nucleic acid synthesis Antimicrobials - Metronidazole o Interrupt bacterial role in inflammatory process TNF- inhibitors - Infliximab o Antibodies to inflammatory effects of TNF- in the gut for refractory Crohns

Pathophysiology and pharmacology of constipation and laxatives.


Laxatives promote defaecation, three main properties are characteristic: o 1. Retain water and electrolytes in lumen via hydrophilic/osmotic properties o 2. Decreasing mucosal absorption of water and electrolytes o 3. Increasing intestinal motility

Mechanism of action and adverse effects of dietary fibre/bulk-forming laxatives, osmotic laxatives and contact/stimulant laxatives.
Dietary Fibre/ Bulk-forming laxatives o Increasing stool mass via component polysaccharides (transit over 1-7 days) o Bran; methylcellylose; ispaghula o Adverse effects: Drug absorption, intestinal/oesophageal obstruction, +water Osmotic Laxatives MgSO4, MgOH, NaPO4, Lactulose o Engaged in bowel and hold water in lumen via osmotic properties o Increased transit over 1-3 hours o Adverse effects: Little absorbed but care in children and w/ renal impairment Contact/Stimulant Laxatives o Direct stimulation of myenteric plexus/mucosa o Decreased permeability of mucosal surface o Increased transit over 6-8 hours

Pathophysiology and pharmacology of diarrhoea and antidiarrhoea agents.


Three main approaches 1. Maintain fluid and electrolyte balance o Oral rehydration, use NaCl+Glucose for infant diarrhoea 2. Use of anti-infective agents o Little role in simple gastroenteritis, antimicrobial very common 3. Use of constipating agents o May be indicative of intestinal pathology (Crohns/ UC)

Mechanism of action and adverse effects of oral rehydration/electrolyte balance, anti-infective agents, absorbent agents and opioid derivatives.
Constipating Agents Absorbent compounds o Absorb fluids and toxins Opiates o Muscle tone and propulsive movements o Sensory stimulation for defaecation reflex Opiate derivatives without CNS effects and dependence of morphine o Diphenoxylate and Loperamide

You might also like