Pharmacology exam

• GI tract


  Accessory organs: Tongue, Salivary glands, pancreas, liver, gallbladder
• Ingestion


  The taking of food into the body
• Digestion


  Mechanical and chemical breakdown of food
• Peristalsis


  Propulsion of food along the GI tract
• Absorption


  Movement of nutrients and other substances from the alimentary canal into the blood circulation
• G cells


  Secrete GASTRIN
• Chief cells


  Secrete PEPSINOGEN
• Parietal cells


  Secrete GASTRIC ACID (HCI) and intrinsic factor
• ECL Cells


  Secrete HISTAMINE
• Proton Pump


  Secretes HYDROGEN IONS, which combine with CHLORIDE IONS in the gastric lumen to form gastric acids
• Acid production in the GI tract

  Stimulated by gastrin, ACh and histamine
• Peptic ulcer: in stomach or duodenum
• Gastric Ulcer: in stomach
• Duodenal Ulcer: in duodenum
• Causes of peptic ulcers

  Associated with H. Pylori bacteria, NSAID
• Symptoms of peptic ulcers

  • Asymptomatic
  • Epigastric pain
  • Dyspepsia
  • Bloating/abdominal fullness
  • Loss of appetite
  • Nausea
  • Vomiting (may be with blood- hematemesis)
  • Weight loss
  • Blood in stool (Melena)
• Treatment of peptic ulcers

  • Stop NSAID or aspirin if possible
  • PPI Therapy: 4-8 weeks depending on site of ulcer
  • H. Pylori-positive ulcers: helicobacter pylori eradication
• Gastroesophageal reflux disease (GERD)


  Excessive reflux of gastric content into the esophagus, oropharynx or lungs
• Symptoms of GERD


  • Heartburn
  • Regurgitation
  • Dry cough
• Complications of GERD


  • Inflammation
  • Ulcer
  • Bleeding
  • Cancer
• Non-pharmacological treatments for GERD

  • Reduce weight if BMI is greater than 30 kg/m^2 or recently gained weight
  • Stop smoking
  • Elevate the head of the bed by 10-20 cm if nocturnal reflux symptoms are present
• Pharmacological treatments for GERD

  • PPIs (OTC and Rx)
  • H2 antagonists (OTC and Rx)
  • Antacids (prn relief)
• PPIs


  Superiors to h2RAs for reduction of symptoms and healing of esophagitis
• PPI treatment for GERD

  Treat for 4-8 weeks: if response, stop therapy: if PARTIAL response at 4-8 weeks (confirm compliance 30 min before breakfast or evening meal if primarily nocturnal GERD): try BID for 4-8 weeks if nocturnal symptoms: if NO response (consider specialist referral
• Trade names of PPIs


  • esomeprazole- NEXIUM
  • Lansoprazole- PREVACID
  • omeprazole- LOSEC
  • pantoprazole sodium- PANTOLOC
  • Pantoprazole magnesium- TECTA
  • rabeprazole- PARIET
  • dexlansoprazole- DEXILANT
• Mechanism of action of PPIs

  Irreversibly bind and inhibit the proton pump of parietal cells, reduction of H+ secretion, reduced acid production, acid suppression lasts for 24-48 hrs
• Adverse effects of PPIs

  • Generally well tolerated
  • Risk with long term use: enteric infections, fractures, pneumonia, depletion of magnesium (paresthesia, seizures, arrhythmia), chronic kidney disease, vitamin b12 deficiency
• Drug interactions of PPIs

  • May decrease absorption of atazanavir, digoxin, iron salts, ketoconazole, cefuroxime
  • Impact on CYP P450* decreases clearance of drugs including - benzodiazepines, warfarin, phenytoin
  • Lowers anti platelet effect of clopidogrel (PLAVIX)- used for prevention of heart attack/stroke
• Trade names of H2 receptor antagonists

  • cimetidine (TAGAMET)
  • famotidine (PEPCID)
  • nizatidine (AXID)
  • ranitidine (ZANTAC)
• Mechanism of action of H2 receptor antagonists

  Completely inhibit H2 receptors - reduced secretion of acid and pepsin
• Adverse effects of H2 receptor antagonists

  • Diarrhea
  • Constipation
  • Headache
  • Fatigue
  • Confusion (most likely in elderly and those with poor renal function)
  • Cardiac effects
  • Rash
• Trade names of antacids

  • sodium bicarbonate (Alka- seltzer, Bromo- seltzer)
  • calcium carbonate (TUMS)
  • aluminium hydroxide (GAVISCON)
  • magnesium salts- carbonate/hydroxide and trisilicate salt
• Mechanism of action of antacids

  Neutralize acid already present in stomach, Don't reduce acid production
• Adverse effects of antacids

  • Flatulence, belching, abdominal distention (sodium bicarbonate)
  • Constipation (calcium carbonate)
  • Diarrhea (magnesium salts)
• Drug interactions of antacids

  • Decrease absorption of: fluoroquinolones and tetracycline antibiotics, digoxin, iron, levotyroxine
• Sucralfate


  Stimulates mucus, bicarbonate and prostaglandin secretion, reacts with HCl and forms a paste (buffer), binds and forms protective barrier on damaged mucosal surface/ulcer crater, does not affect secretion of gastric acid
• Indications for sucralfate


  Peptic ulcers and GERD
• Contraindications for sucralfate


  Hypersensitivity, renal failure, swallowing difficulty, pregnancy and lactation
• Treatment for H. Pylori

  • Triple therapy: PPI + Clarithromycin + amoxicillin
• Nausea


  Unpleasant sensation of the imminent need to vomit, may or may not lead to vomit