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GI Drugs

Drugs used to treat GI Diseases

Which conditions require lower acid secretion? GERD / Peptic ulcer disease/Stress-related Mucosal Injury
What is Barret's Esophagus? serious complication of GERD. It's the Scarring of the Esophagus which causes high incidences of Cancer
What are some causes of Stress related mucosal injury? Shock/Decreased blood flow to the gut/ Poor Cardiac output
What are some protective factors for Gastric mucosa? Mucus, Bicarbonate, Prostaglandins, Blood flow, Restitution (repair)
Why are prostaglandins protective to the gastric mucosa? Stimulate production of bicarbonate, production of mucus, increase blood flow to the gut. Upregulate these protective factors.
What class of drugs inhibit prostaglandins? NSAIDS and Aspirin
What are some damaging factors to the Gastric Mucosa? Acid secretion, Pepsin, NSAIDs, H.Pylori, Smoking, Ischemia, Bile Acids, Alcohol
What is Pepsin? protein digestive enzyme that is in the intestine and in high concentrations can dissolve the proteins in the gut. If it refluxes into the esophagus/stomach it can stop digestive proteins
What cells are responsible for producing Stomach Acid? Parietal Cells
How does H. Pylori survive? the bacteria produces an enzyme (UREASE) that converts UREA in the gut as a waste product into Ammonia, increase the pH of the stomach --> For it's survival
Proton Pump pump called H+/Hydrogen/K+ ATPase. Takes protons and pumps them into the stomach contents to lower pH of the gut.
Why does the proton pump require ATP? because it pumps protons against the Gradient
How many types of receptors can activate the Proton Pump to decrease pH? H2 / M3 / CCK
H2 Receptors Histamine receptors activate the proton pump
M3 Receptors Muscarinic receptors activate parasympathetic system (rest/digest) to increase acid secretion. Muscarinic receptors active Parasympathetic involved in digestion.
CCK These receptors are activated by Gastrin. When the stomach detects an increase of pH, the G cells release gastrin. The gastrin bind to receptor and turns on the Proton Pump
Types of Antacids Sodium Bicarbonate (Alka-Seltzer) / Calcium Carbonate (Tums) / Magnesium Hydroxide / Aluminum Hydroxide
Antacids May affect absorption of drug from gut by affecting solubility or pH. It can Chelate molecules in the intestines making drugs more or less absorb. Do not give within 2hrs. of tetracyclines, fluroquinolones, itraconazole, iron
H2 Antagonists competitive inhibitors of PARIETAL Cell H2 receptors.
Which H2 Antagonist does not undergo 1st pass metabolism? Nizatadine
Which H2 antagonist can affect CYP activity? Affects CYP3A4, 1A2/ 2C9/ 2D6 and cause drugs intearactions Cimetidine/ 1st drug on the market
Name a few H2 Antagonist? Cimetidine, Ranitidine, Famotidine, Nizatidine
What is the mechanism of action of PPI's? Irreversible inhibitors of parietal cell proton pumps. Inhibits ATPase needed for active transport. Drug blocks the ATPase which prevents the pump from splitting the ATP (no energy for proton pump to work)
How are PPI's administered? Given as Prodrugs. Activated at low pH. Undergo conversion in the low pH of the stomach which allow it to covelently bond to the proton pump
What disease are PPI used to treat? GERD / PUD (H. Pylori, NSAID) / Stress ulcers. 90% healing of PUD in 6-8 weeks
How does omePRAZOLE work? Sulfer bound to O2 enter the stomach, the O2 leaves and sulfer is exposed. The loss of O2 occurs only @ low pH. When sulfer is exposed, the drug covalently binds with ATPase in the pump. It blocks the ATP = Blocks the proton pump
What is the triple therapy to heal H. Pylori Ulcers? PPI (BID) -PRAZOLE / Clarithromycin / Amoxicillin or Metronidazole
Which one is the #1 cause of Ulcers? H. Pylori
Which is the #2 cause of Ulcers? NSAIDS
What are the two newer PPI's with better bio-availability? Esomeprazole / Dexlansoprazole
What is the biggest concern of chronic increases in gastric pH? increased gastrin secretions/ Gaastrinoma's in rats/ Increased bacterial colonization / Absorption of vit. can be affected
What is does it not matter that PPI has a short 1/2 life? They have 24 hrs inhibition of proton pump. Circulation drug level is not important
Name a Mucosal Protectant? Sucralfate
Sucrafate Sucrose (barrier) + Sulfated aluminum Hydroxide (base). Antacid bound to polymer. Viscous past that binds selectively to ulcers or erosions up to 6 hrs.
What is one drawback of Sucrafate? May bind positively charged drugs in the GIT (Phenytoin/Digoxin/Warfarin/Thyroxine)
Name a prostaglanin analog? Misoprostol
How are Prostaglandins protective in the GIT? Increase muscus secretion, bicarbonate secretion, blood flow, acid secretion
Which drugs do NSAIDS inhibit? Prostaglandins Analogs
What are the Side Effects of Misoprostol? Diarrhea / Cramping/ Uterine Contractions. Prostaglandins affect motility& Peristalsis. Prokinetic effect.
GI Motility is controlled by which system? Enteric Nervous system (Sympathetic NS and Parasympathetic NS)
Which neurotransmitters are involved in Peristalsis? ACh / Dopamine / Serotonin
How do Serotonin receptors regulate GI motility? Alters the rate at which acetylcholine receptors in the stomach fire. Has two types = 5HT3 / 5HT4
What is an example of a Cholinomimetic agent? Bethanchol
What is a Cholinomimetic agent? mimic Acetylcholine.
Drug Bethanchol Cholinomimetics - seldom used due to multiple cholinergic side effects. Activates Parasympathetic system. Increases acid secretion.
Metoclopramide Dopamine (D2) receptor antagonist Significant CNS effect – restlessness, drowsiness, “extra-pyramidal” symptoms. Increases motility
Erythromycin IV 3 mg/kg. Macrolide agent that increases motility. Stimulate GI “motilin" receptors but rapid tolerance
Tegaserod Serotonin receptor (5HT4) partial agonist. For Chronic constipation in IBS-C. Serious cardiovascular side effects due to interaction with other serotonin receptor subtype and K+ channels (QT prolongation). Removed from market, special request only….
psyllium, methycellulose Bulk Forming – indigestible colloids that absorb water to distend colon & promote peristalsis. Distends the wall of the intestine and stimulates peristalsis
Magnesium hydroxide, magnesium citrate Osmotic laxative. Hypermagensemia with renal disease
Sorbitol, lactulose Osmotic laxative. Non-absorbable sugars that may be metabolized but gut bacteria – flatus, bloating, cramps
senna, bisacodyl Stimulant. Stimulate enteric nervous system, increase peristalsis, fluid secretion
Loperamide does not cross BBB. Opioid Agonists. Constipation is a significant side effect of opioid therapy. No CNS addiction.
Diphenoxylate crosses BBB, + atropine to prevent abuse. Opioid Agonists. Constipation is a significant side effect of opioid therapy.
Alosetron Serotonin receptor (5HT3) antagonists. Approved for IBS with diarrhea ONLY! May cause significant constipation. Can cause ischemic colitis!!! and paralyze the bowel. Agent that decreases motility
Emesis Complex process that involves a Central Chemo-Receptor Trigger zone in the mid-brainstem as well Serotonin, Dopamine and Muscarinic receptors….
Antiemetics Nausea and vomiting that requires treatment most frequently occurs in patients undergoing chemotherapy and/or radiation therapy. Also – motion sickness.
Ondansetron, Dolasetron, Granisetron -SETRON Serotonin (5HT3 ) Receptor Antagonists.Oral or i.v., 4-9 hr half-life. Uses:1. CINV – iv injection 30 minutes before chemotherapy. Combination therapy with Corticosteroids and NK1 receptor antagonist. 2. Post-operative, Post-radiation therapy
Palonosetron 40 hr half-life i.v., high affinity. Serotonin (5HT3 ) Receptor Antagonists. CINV
What are the mainstay drugs for CINV? Serotonin (5HT3 ) Receptor Antagonists (- Setron).
Which cardiovascular side effect does Serotonin (5HT3) have? All -Setron drugs can prolong QT interval. Most pronounced with DolaSETRON
Dexamethasone Corticosteroid drug. Exhibit antiemetic properties. Enhance the efficacy of 5-HT3 receptor (-Setron) antagonists for CINV.
Prochlorperazine, Chlorpromazine Antagonize Dopamine, Histamine and Cholinegic receptors at the chemoreceptor trigger zone. Not as effective as metoclopramide & ondansetron for CINV. Antihistaminic & Anitcholinergic make them good for motion sickness.
What side effects do Phenothiazines have? Very Sedating, pronounced anticholinergic effects. (Prochlorperazine, Chlorpromazine)
Diphenhydramine Anticholinergic and Antihitaminergic properties. (Antihistamines)
Meclizine Minimal anticholiergic actions = less sedation (Antihistamines)
Scopolamine Potent antimuscarinic actions = very sedating Best tolerated by transdermal patch form motion sickness. (Antihistamines)
Aprepitant (Emend) A highly selective oral substance P neurokinin 1 (NK1) receptor antagonist. Prevention of CINV in combination with standard antiemetic regimens (5HT3 antagonist plus a corticosteroid).
Goal standard of CINV therapy? Neurokinin receptor antagonist (NK1), -Setron and corticosteroid
Fosaprepitant i.v. drug converted to aprepitant within 30 minutes
What is the effect of Triple therapy for CINV? 94% Prevention of acute emesis in groups receiving (5HT3 antagonist, dexamethasone and NK1 receptor antagonist)
Dronabinol Naturally-occurring cannabinoid – CB1 receptors in brain Useful for treating nausea in cancer patients who do not respond to other agents. Used as an appetite stimulant in AIDS patients.
Sulfasalazine mechanism of action 1st drug of choice with patient’s that have IBD. Contain 5-aminosalicylic Acid (5-ASA). Acts topically in the gut. Inhibit the production of inflammatory mediators, but not prostaglandins. Used to induce and maintain remission in IBD
Why does Sulfasalazine have different formulations? Numerous formulations designed to act at various points in the GI tract
Pentasa 5-ASA delayed release capsule that works in IBD in the Jejunum, Illeum, Proximal, Distal Colon and Rectum
Asacol, Lialda 5-ASA that works in IBD in the Ileum, proximal, Distal Colon and Rectum
Sulfasalazine Target area 5-ASA that works in IBD in the proximal, Distal Colon and Rectum
Balsalazide 5-ASA that works in IBD in the proximal, Distal Colon and Rectum just like Sulfasalazine
Rowasa 5-ASA enema that works in IBD in the distal colon and Rectum
Canasa 5-ASA suppository that works in IBD in Rectum
What is the adverse effect of Sulfasalazine? Sulfapyridine metabolite is absorbed systemically and can cause:Nausea, GI upset, Arthralgia, myalgia and Bone marrow suppression. Genetically “slow acetylators” of sulfapyridine have worse S/E.
High doses of aminosalicylates and subtle renal tubule injury?
Hydocortisone enemas Glucocorticoid used for IBD. 15-30% absorption. Potent anti-inflammatory and immune suppressing actions. Moderate to severe active IBD. Not for maintaining remission
Budesonide Glucocorticoid. Potent synthetic prednisolone analog. Oral controlled release for Crohn’s disease. 10% absorption - Poor absorption - Works topically.
Budesonide & Hydocortisone enemas Glucocorticoids used for IBD. Limit use 1-2 weeks to minimize systemic side effects!
Azathioprine, 6-Mercaptopurine (6-MP) Azathioprine is converted to 6-MP after absorption. Both are immunosuppressive. Used for the induction and maintenance of remission in Crohn’s and UC. 50-60% remission after 3-6 months. 80% maintain remission.
Which drugs can be used to reduce or eliminate steroid use for IBD? Azathioprine, 6-Mercaptopurine (6-MP)
What are the Adverse effects of Azathioprine, 6-Mercaptopurine (6-MP)? Nausea, vomiting, Bone marrow suppression, Hepatotoxicity Routine Blood counts and LFT’s in all patients! Be aware of TPMT Pharmacogenomic variation!! High activity, intermediate activity, low activity
Which enzyme metabolizes Azathioprine? TPMT - Thiopurine Methyltransferase
Methotrexate Antiproliferative at high doses, immunosuppressive at lower doses. Used to induce and maintain remission in Crohn’s disease. 15-25 mg s.c. weekly.
At high doses what are the Adverse effects of Methotrexate? Bone marrow suppression / Alopecia / Mucositis / Hepatic injury
What can help prevent adverse effect of Methotrexate? Folate supplementation can help prevent this
Anti-TNF Agents and monoclonal antibody drugs approved for IBD? Infliximab / Adalimumab / Certolizumab
Tumor necrosis factor released by T-cells appears to play an important role in the inflammation associated with IBD
What are - MABs used for in IBD? Acute and chronic treatment of moderate to severe IBD.
Which anti-TNF is given IV infusion for induction (initial therapy)? Infliximab
Which anti-TNF drugs are given S.C. every 2 weeks for maintenance? Adalimumab / Certolizumab
What is a major limiting factor with anti-TNF agents? Development of Autoantibodies (3-10% of patients). Limits drug effectiveness!
What are the adverse effects of anti-TNF agents? Powerful Immune suppressants.Bacterial sepsis,TB, URTI’s Fungal infections. Reactivation of hepatitis B. TB test before starting therapy.
What are some acute infusion reactions that anti-TNF drugs can cause? Fever, headache, chest pain, dizziness. Use Prophylactic acetaminophen, diphenhydramine Lymphoma risk? Increased potential risk
What risk is involved with the usage of - Mabs? Increased potential risk for developing Lymphoma
What is the connection between bleeding esophageal varices & hepatic encephalopathy in patients with liver disease? Blood goes into the gut and is metabolized by bacteria. Bacteria generates ammonia. Protein in blood is converted to Ammonia! (Normally metabolized by healthy liver to urea)
Hepatic Encephalopathy Tremor, impaired alertness, confusion, coma, convulsions
Somatostain & Octreotide Used i.v. to reduce portal blood flow and variceal pressure Mechanism is uncertain
Propranolol, Nadolol Non-Selective Beta-Blockers. Reduce cardiac output (beta-1 blockade). Block splanchnic vasoconstriciton (beta-2 blockade). Can help dilate and with congestion
Lactulose Used for hepatic encephalopathy. Osmotic laxative.
What does Lactulose do to the pH of the colon? Lowers the pH of the colon. Ammonia has + charges and is a base. If we acidify the gut, ammonia will be have more charged. It will be absorbed less.
Created by: 10621624