Drugs for GI Diseases Outline PDF

**OUTLINE** I. **Drugs used in Acid Peptic Disease** II. **Drugs Stimulating Gastrointestinal Motility** III. **Laxatives** IV. **Antidiarrheal Agents** V. **Drugs used in the Treatment of Irritable Bowel Syndrome** VI. **Antiemetic Agents** VII. **Probiotics** VIII. **GI Drugs for Infecti...

**OUTLINE** I. **Drugs used in Acid Peptic Disease** II. **Drugs Stimulating Gastrointestinal Motility** III. **Laxatives** IV. **Antidiarrheal Agents** V. **Drugs used in the Treatment of Irritable Bowel Syndrome** VI. **Antiemetic Agents** VII. **Probiotics** VIII. **GI Drugs for Infectious Diseases** +-----------------------+-----------------------+-----------------------+ | **LEGEND** | | | +=======================+=======================+=======================+ | ⭐ | 🖊️ | 📖 | | | | | | Must | Lecture | Book | | | | | | Know | *\[lec\]* | *\[bk\]* | +-----------------------+-----------------------+-----------------------+ DRUGS USED IN ACID-PEPTIC DISEASE {#drugs-used-in-acid-peptic-disease.TransOutline} ================================= ACID PEPTIC DISEASE {#acid-peptic-disease.TransSubtopic1} ------------------- - 🖊️ *When talking about APC, we do not simply refer to a single kind of disease process. It compasses several different kinds* - Include the following: - Gastroesophageal reflux - Peptic Ulcer (Gastric and Duodenal) - Stress-related Mucosal Injury - 🖊️ *This is more of a consequence of what you usually see in patients who have a very high disease burden (e.g. severely septic and severe burns)* - *Thus, releasing several cytokine intermediates that will break down the mucosal barrier → injury in the GI wall* - **Aggressive Factors** - Acid, Pepsin, Bile - 🖊️ *Mucosal erosions/ulcerations from the aggressive factors* - **Defensive factors of the Gastrointestinal Mucosa** - Mucus and Bicarbonate Secretion - Prostaglandins - Blood Flow - Process of restitution and regeneration after-cellular injury - **Two classes of Drugs for treatment** - Agents that reduce intragastric acidity - Agents that promote mucosal defense - 🖊️ *Regardless of the cause, medications will still be the same* - ⭐ Over 90% of peptic ulcers are caused by infection of H. pylori or by use of NSAIDS - 🖊️ *H. pylori multiply: layer of the stomach lining and duodenum* - Urease → converts urea to ammonia thus protecting the bacteria from stomach acid - Multiple H. pylori → Gastritis and Gastric Ulcer - It also decreases the secretion of mucous and bicarbonate by eating through the gastric mucosa - NSAIDS causes ulcers by inhibiting cyclooxygenase 1 in the GI tract → ↓ prostaglandin secretion DRUGS THAT REDUCE INTRAGASTRIC ACIDITY {#drugs-that-reduce-intragastric-acidity.TransSub-subtopic2} -------------------------------------- - **Antacids (**🖊️**reduce intragastric acidity)** - H2 Receptor Antagonist - Proton Pump Inhibitor - **Mucosal Protective Agents (**🖊️**demulcents)** - Sucralfate PHYSIOLOGY OF ACID SECRETION {#physiology-of-acid-secretion.TransSubtopic1} ---------------------------- - **Gastric Acid** - Hydrochloric Acid (pH 1.5 -- 2) - 🖊️ *Plays a key role in the digestion of proteins by activating digestive enzymes → breaks down long chain amino acids* - After a meal, approx. 45 mEq/h of hydrochloric acid is secreted - Secreted by: Antrum parietal cell (through H+/K+-ATPase) - Stimulated by: - Histamine (H2) - **Gastrin (CCK-B)** secreted in the antrum - **Acetylcholine (muscarinic, M3)** 🖊️ neurotransmitter for rest-and-digest - 🖊️ *Acetylcholine is secreted by the vagal post-ganglionic neurons and gastrin which is released from the G cells in the antrum → bind to the parietal cells' receptors causing an increase in intracytosolic calcium → stimulates protein kinase thus stimulating secretion of acid from the H+/K+-ATPase pump to surface of the canaliculi of the GI mucosa* A diagram of blood vessels Description automatically generated **Figure 1. Physiology of Acid Secretion** *(Source: © Doc Abella)* - **Antral D Cells** - Stimulated to release somatostatin by: - Rise of intraluminal H+ concentration - CCK - 🖊️ *Very important mechanism that ↓ gastric acid secretion* - 🖊️ *Secreted at multiple regions in the GI tract, particularly the pyloric antrum, duodenum, and islet of Langerhans* - Binding somatostatin to receptors on adjacent astral G cells inhibits further gastrin release - 🖊️ *There is a hormonal release and membrane release at the cells of the stomach* - 🖊️*D cells (stomach) inhibit the G cells by releasing somatostatin*  **Figure 2. Feedback regulation of Gastric Acid Secretion by release of Somatostatin** *(Source: © Doc Abella)* ANTACIDS {#antacids.TransSubtopic1} -------- - 🖊️Non-Prescription medications - 🖊️Increases intragastric pH = may have drug interactions - Weak Bases: ⭐ Reduces/**Neutralizes** intragastric acidity - 1 dose of 156 mEq is given 1 hour after a meal - 2 Hours of Gastric Acid Neutralization - [Antacid + Gastric HCl = Salt and H2O] - 🖊️ Rate of dissolution and water solubility can affect or influence the effect of antacids. - Examples **(SCAM)** - **S**odium Bicarbonate **(RAPID ACTION)** - **C**alcium carbonate - **A**luminum Hydroxide - **M**agnesium Hydroxide - 🖊️ Bali yung products nila nasa name na - **Hydro**xide = Water - **Carbon**ate = Carbon Dioxide SODIUM BICARBONATE (BAKING SODA / ALKASELTZER) {#sodium-bicarbonate-baking-soda-alkaseltzer.TransSub-subtopic2} ---------------------------------------------- - ⭐ Reacts RAPIDLY with HCl to produce: - **Carbon Dioxide** - **Sodium Chloride** - Adverse Effects - Belching and Metabolic Alkalosis - Gastric Distension (due to CO2) - Spilling gastric contents to LES *→* erode the muscle *→* decrease sphincter strength - Fluid Retention (🖊️ *kasi nga NaCl yung product niya*) - 🖊️*Careful sa pagbigay sa mga HTN or HF* - 🖊️ *Might worsen condition* CALCIUM CARBONATE (TUMS) {#calcium-carbonate-tums.TransSub-subtopic2} ------------------------ - ⭐Reacts SLOWLY with HCl to produce: - **Carbon Dioxide** - Calcium Chloride (CaCl2) - Adverse Effects - Belching and Metabolic Alkalosis - Hypercalcemia - Renal Insufficiency - **Milk-Alkali Syndrome:** 🖊️**Triad: Hypercalcemia, Acute Kidney Injury, and Metabolic Alkalosis** ALUMINUM HYDROXIDE {#aluminum-hydroxide.TransSub-subtopic2} ------------------ - In combination with MgOH - Reacts SLOWLY with HCl to produce - Aluminum Chloride: Al ions: ↓ peristalsis *→* constipations - H20 - **Adverse Effects**: Constipation MAGNESIUM HYDROXIDE {#magnesium-hydroxide.TransSub-subtopic2} ------------------- - In combination with AlOH - Reacts SLOWLY with HCl to produce - Magnesium Chloride **(Laxative Salt)** - **🖊️Hindi ma-absorb ng tiyan + Salt nature (attracts water) = increased water in lumen or osmotic diarrhea** - H20 - **Adverse Effects**: Osmotic Diarrhea #### IMPORTANT TO REMEMBER FOR MgOH + AlOH {#important-to-remember-for-mgoh-aloh.TransSub-subtopic3} - 🖊️ *MgOH and AlOH both cancel each other\'s side effects kaya pinagcocombine silang dalawa* - 🖊️ *No Gas by-product = No Belching* - Both are excreted in the **kidneys (CI: Renal Insufficiency)** - Affects absorption of other drugs (🖊️ *Should not be given within 2 hours after being given these antacid*) - Tetracyclines - Fluoroquinolones - Itraconazole - Iron H2 RECEPTOR ANTAGONISTS {#h2-receptor-antagonists.TransSubtopic1} ----------------------- - PIONEER medications for acid INHIBITION - CIMETIDINE: 🖊️Prototype - Ranitidine: 🖊️Commonly used in clinical practice - Famotidine: 🖊️Minimal drug-drug interaction - **Nizatidine** PHARMACOKINETICS {#pharmacokinetics.TransSub-subtopic2} ---------------- - Rapidly absorbed from the intestine - Undergoes extensive first pass effect - - - **Half Life**: 1-4 Hours - **Metabolism:** - - - CLINICAL USES {#clinical-uses.TransSub-subtopic2} ------------- - Gastroesophageal reflux disease (GERD) - - Peptic Ulcer disease - - - - Non-Ulcer Dyspepsia - Prevention of bleeding from stress-related gastritis - Constipation +-----------------------------------+-----------------------------------+ | **Table 1. Adverse Effects of H2 | | | Receptor Blockers** | | +===================================+===================================+ | Crosses Placenta and Secreted in | Mental status changes | | Breast Milk | | | | (Cimetidine) | +-----------------------------------+-----------------------------------+ | Diarrhea (\