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Summary

The on-demand teaching session by Kazi Mahathir revolves around Gastroesophageal Reflux Disease (GORD). This session will delve into the pathophysiology of GORD and provide an in-depth understanding of the mechanism of action for drugs used to treat it. It examines side-effects and contraindications of GORD medications and the function and location of the drugs used. The session also allows for the exploration of the pathogenesis of various forms of gastritis, the role of proton pump inhibitors and their associated risks. Participant engagement is encouraged with multiple-choice questions throughout. This rigorous academic exploration will be vital for medical professionals seeking to expand their knowledge or specialize in Gastroenterology.

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Learning objectives

  1. By the end of this teaching session, participants will be able to describe the pathophysiology of Gastroesophageal Reflux Disease (GORD).
  2. Participants will demonstrate an understanding of the mechanism of action of various drugs used to manage and treat GORD.
  3. Participants will be able to identify potential side effects and contraindications associated with the pharmacological treatment of GORD.
  4. Participants will acquire the knowledge to explain the function and structure of the gastrointestinal tract relevant to GORD as well as the true characteristics and causes of erosive and haemorrhagic gastritis.
  5. Participants will develop the ability to connect the theoretical aspects of GORD with clinical practice situations, recognizing symptomatology and developing appropriate therapeutic plans for patients.
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(03% Name: Kazi Mahathir Email: kazi.mahathir21@imperial.ac.uk0#+&$5*7&4▯ • Pathophysiology of GORD • Mechanism of action of the drugs used to treat GORD • Side effects +/- contraindications of GORD5IF▯TUPNBDI▯▯ • Functions: • Breaks food into smaller particles (acid & pepsin) • Hsteady rate into duodenumn controlled • Kills parasites & certain bacteria • Cardia & Pyloric Region: Mucus only • Body & Fundus: Mucus, HCl, pepsinogen • Antrum: Gastrin(BTUSJUJT▯▯ • Erosive & haemorrhagic gastritis • Numerous causes • Acute ulcer – gastric bleeding & perforation • Nonerosive, chronic active gastritis • Antrum • Helicobacter pylori - Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14/7 • Atrophic (fundal gland) gastritis • Fundus • Autoantibodies vs parts & products of parietal cells • Parietal cells atrophy • ↓acid & IF secretion • Reactive gastritis 1SFTFOUBUJPO▯PG▯(03%▯ GORD may just be an occasional nuisance for some people. But for others, GORD can be a severe, lifelong problem. Symptoms of GORD can include: • Heartburn (an uncomfortable burning sensation in the chest that often occurs after eating) • Acid reflux (where stomach acid comes back up into your mouth and causes an unpleasant, sour taste) • Oesophagitis (a sore, inflamed oesophagus) • Bad breath • Bloating and belching • Feeling or being sick • Pain when swallowing and/or difficulty swallowing • Sore throat / hoarse voice • Persistent cough / wheezing, which may be worse at night • Tooth decay (external link opens in a new window / tab)and gum disease6MDFS▯▯SFHVMBUJPO▯PG▯HBTUSJO▯ • Stimulation • Neural • parasympathetic fibresransmitter of vagal • Endocrine • Gastrin (G cells of antrum) • Paracrine • Histamine (ECL cells & mast cells of gastric wall). • Inhibition • Endocrine • Secretin (small intestine) • Paracrine • Somatostatin (SIH) • Paracrine & autocrine • PGs (E & I ), TGF-α & adenosine 2 26MDFS▯▯NVDPTBM▯QSPUFDUJPO▯▯6MDFS▯▯GPSNBUJPO▯/4"*%4▯ • selective i.e. also inhibits COX1)is non- • endings (analgesia)eral nociceptive nerve • (PG). PGs do not directly cause painns themselves, but they sensitise peripheral nociceptors mediators (bradykinin and histamine) which causes pain. NSAIDs inhibit COX. • Indirect effect on pain – PGs mediate reduce inflammationence NSAIDs will1SPUPO▯QVNQ▯JOIJCJUPST▯ • ‘Target’ – H /K -ATPase (‘proton pump’) • ‘Location’ – Parietal cell (secretory membrane) • ‘Effect’ – Reduced acid production from parietal cells. • NSAIDs leave stomach wall exposed to the effect of acid, which is causing pain. PPIs reduce the acid production.)JTUBNJOF▯BOUBHPOJTUT▯ • Target – Histamine H2 receptor • Location – Cell surface of the parietal cell • Effect – ↓ acid production from parietal cell. Histamine receptors ↑ acid production via +AM+ dependent activation of H /K ATPase. The stomach wall exposed to acid à symptoms pain. ↓ acid production, ↓ corrosive nature of environment.*TTVFT▯XJUI▯VTJOH▯UIFTF▯ NFEJDBUJPOT▯▯ • NSAIDs leave stomach wall exposed to the effect of acid, which causes pain: • PPIs reduce the acid production to treat this. • Proton pump inhibitors are known to increase the risk of fracture: • This is even more likely if the patient has osteoporosis. • The mechanism of action is unclear, although absorption of calcium salts is pH PPIs might be responsible for a reduction in absorption and decrease in calcium available for bone.)PX▯UP▯DPNCBU▯JTTVFT▯PG▯11*T▯BOE▯ PTUFPQPSPTJT▯▯4#"▯▯▯ Q1: Which of the following do NSAIDs act upon? A. Cyclo-oxygenase B. Prostaglandin C. Arachidonic acid D. Thromboxane A2 E. Procrystalline4#"▯▯▯▯"OTXFS▯ Q1: Which of the following do NSAIDs act upon? A. Cyclo-oxygenase B. Prostaglandin C. Arachidonic acid D. Thromboxane A2 E. Procrystalline4#"▯▯▯ Q2: Lansoprazole and omeprazole are what class of drugs? A. NSAIDS B. Paracetamol C. Proton pump inhibitors D. H2 receptor E. Dopamine agonist4#"▯▯▯▯"OTXFS▯ Q2: Lansoprazole and omeprazole are what class of drugs? A. NSAIDS B. Paracetamol C. Proton pump inhibitors D. H2 receptor E. Dopamine agonist4#"▯▯▯▯"OTXFS▯ Q2: Lansoprazole and omeprazole are what class of drugs? A. NSAIDS B. Paracetamol C. Proton pump inhibitors D. H2 receptor E. Dopamine agonist4#"▯▯▯▯ Q3: What is the standard length of time for PPI therapy? A. 3 months B. 1-2 months C. 1 year D. 11 months E. 3 weeks4#"▯▯▯▯"OTXFS▯ Q3: What is the standard length of time for PPI therapy? A. 3 months B. 1-2 months C. 1 year D. 11 months E. 3 weeks4#"▯▯▯ Q4: Which location do proton pump inhibitors act on? A. Enterochromaffin cells B. Parietal cell C. Crypts D. Serosa E. Epithelium4#"▯▯▯▯"OTXFS▯ Q4: Which location do proton pump inhibitors act on? A. Enterochromaffin cells B. Parietal cell C. Crypts D. Serosa E. Epithelium4#"▯▯▯ Q5: What is an example of a histamine receptor antagonist? A. Acetaminophen B. Lanzoprazole C. Diclofenac D. Rantidine E. Naproxen4#"▯▯▯▯"OTXFS▯ Q5: What is an example of a histamine receptor antagonist? A. Acetaminophen B. Lanzoprazole C. Diclofenac D. Rantidine E. Naproxen4#"▯▯▯ Q6: What can proton pump inhibitors increase the risk of? A. Allergies B. Lethargy C. Diabetes D. Pregnancy E. Fracture risk4#"▯▯▯▯"OTXFS▯ Q6: What can proton pump inhibitors increase the risk of? A. Allergies B. Lethargy C. Diabetes D. Pregnancy E. Fracture risk4#"▯▯▯ Q7: If an individual has osteoporosis, what is the first line treatment for peptic ulcer disease? A. Omeprazole B. Metformin C. Rantidine D. Prostaglandin E. Paracetamol4#"▯▯▯▯"OTXFS▯ Q7: If an individual has osteoporosis, what is the first line treatment for peptic ulcer disease? A. Omeprazole B. Metformin C. Rantidine D. Prostaglandin E. Paracetamol4#"▯▯▯▯ Q8: Which of the following is a symptom in GORD? A. Chest burning sensation B. Haematemsis C. Left lower quadrant pain D. Pain in neck E. Paresthesia4#"▯▯▯▯"OTXFS▯ Q8: Which of the following is a symptom in GORD? A. Chest burning sensation B. Haematemsis C. Left lower quadrant pain D. Pain in neck E. Paresthesia4#"▯▯▯▯ Q9: Which of these is a painkiller ? A. Aripiprazole B. Simvastatin C. Amitriptyline D. Acetaminophen E. Propranolol4#"▯▯▯▯"OTXFS▯▯ Q9: Which of these is a painkiller? A. Aripiprazole B. Simvastatin C. Amitriptyline D. Acetaminophen E. Propranolol4#"▯▯▯▯▯▯▯ Q10: What is the first line treatment for an H.pylori infection? A. Antibiotics B. PPI C. Metronidazole D. Acetylcholine E. Triple therapy4#"▯▯▯▯▯▯"OTXFS▯▯ Q10: What is the first line treatment for an H.pylori infection? A. Antibiotics B. PPI C. Metronidazole D. Acetylcholine E. Triple therapy4#"▯▯▯▯ Q11. Which part of the stomach is responsible for releasing mucus, hydrochloric acid, and pepsinogen? A. Cardia B. Pyloric region C. Fundus D. Antrum E. Body4#"▯▯▯▯▯▯"OTXFS▯▯ Q11. Which part of the stomach is responsible for releasing mucus, hydrochloric acid, and pepsinogen? A. Cardia B. Pyloric region C. Fundus D. Antrum E. Body 4#"▯▯▯▯▯▯▯ Q12: Which neurotransmitter is a postganglionic transmitter of vagal parasympathetic fibers, stimulating the release of gastrin? A. Serotonin B. Acetylcholine C. Dopamine D. Norepinephrine E. Histamine 4#"▯▯▯▯▯"OTXFS▯▯ Q12: Which neurotransmitter is a postganglionic transmitter of vagal parasympathetic fibers, stimulating the release of gastrin? A. Serotonin B. Acetylcholine C. Dopamine D. Norepinephrine E. Histamine4#"▯▯▯▯▯▯▯ Q13. What is the primary effect of NSAIDs on pain perception? A. Direct stimulation of nociceptive nerve endings B. Inhibition of COX2 enzyme C. Increased production of prostaglandins D. Sensitization of peripheral nociceptors E. Reduction of inflammation4#"▯▯▯▯▯"OTXFS▯▯ Q13. What is the primary effect of NSAIDs on pain perception? A. Direct stimulation of nociceptive nerve endings B. Inhibition of COX2 enzyme C. Increased production of prostaglandins D. Sensitization of peripheral nociceptors E. Reduction of inflammation4#"▯▯▯▯▯▯▯ Q14: What is the location of the target enzyme for proton pump inhibitors (PPIs)? A. Parietal cell (secretory membrane) B. Small intestine C. Antrum D. Cardia E. Fundus4#"▯▯▯▯▯"OTXFS▯▯▯ Q14: What is the location of the target enzyme for proton pump inhibitors (PPIs)? A. Parietal cell (secretory membrane) B. Small intestine C. Antrum D. Cardia E. Fundus4#"▯▯▯▯▯▯▯ Q15: Which substance reduces acid production from parietal cells and is the target of proton pump inhibitors? A. Histamine B. Somatostatin C. Prostaglandins D. H+/K+-ATPase E. Gastrin4#"▯▯▯▯▯▯▯ Q15: Which substance reduces acid production from parietal cells and is the target of proton pump inhibitors? A. Histamine B. Somatostatin C. Prostaglandins D. H+/K+-ATPase E. Gastrin4#"▯▯▯▯▯▯▯ Q16: What is the primary function of the pyloric region of the stomach? A. Absorption B. Storage C. Mucus secretion D. Mechanical breakdown E. Gastrin production4#"▯▯▯▯▯"OTXFS▯▯▯ Q16: What is the primary function of the pyloric region of the stomach? A. Absorption B. Storage C. Mucus secretion D. Mechanical breakdown E. Gastrin production4#"▯▯▯▯▯▯▯ Q17: Which neurotransmitter stimulates the release of gastric acid in response to neural stimulation? A. Histamine B. Serotonin C. Dopamine D. Norepinephrine E. Acetylcholine4#"▯▯▯▯▯"OTXFS▯ Q17: Which neurotransmitter stimulates the release of gastric acid in response to neural stimulation? A. Histamine B. Serotonin C. Dopamine D. Norepinephrine E. Acetylcholine4#"▯▯▯▯▯▯▯ Q18: What can chronic GORD lead to if left untreated? A. Respiratory infections B. Ovarian cancer C. Liver cirrhosis D. Kidney stones E. Esophageal stricture4#"▯▯▯▯▯"OTXFS▯▯ Q18: What can chronic GORD lead to if left untreated? A. Respiratory infections B. Ovarian cancer C. Liver cirrhosis D. Kidney stones E. Esophageal stricture4#"▯▯▯▯▯▯▯ Q19: What is the role of prostaglandins in the stomach? A. Increase acid production B. Inhibit COX2 enzyme C. Sensitize peripheral nociceptors D. Reduce inflammation E. Stimulate mucus production4#"▯▯▯▯▯"OTXFS▯ Q19: What is the role of prostaglandins in the stomach? A. Increase acid production B. Inhibit COX2 enzyme C. Sensitize peripheral nociceptors D. Reduce inflammation E. Stimulate mucus production4#"▯▯▯▯▯▯▯ Q20: Which hormone stimulates the release of gastric acid from parietal cells in the stomach? A. Insulin B. Gastrin C. Leptin D. Cortisol E. Thyroid hormone4#"▯▯▯▯▯"OTXFS▯ Q20: Which hormone stimulates the release of gastric acid from parietal cells in the stomach? A. Insulin B. Gastrin C. Leptin D. Cortisol E. Thyroid hormone46.."3:▯ Proton pump inhibitors : NSAIDS: • ‘Target’ – H /K -ATPase (‘proton pump’) • ‘Target’ – COX 2 enzyme (naproxen is non-selective i.e. also inhibits COX1) • ‘Location’ – Parietal cell (secretory membrane) • ‘Location’ – Peripheral nociceptive nerve endings • ‘Effect’ – Reduced acid production from parietal (analgesia) cells • ‘Effect’ – COX produces prostaglandins (PG). PGs do not peripheral nociceptors mediators (bradykinin andse histamine) which causes pain. NSAIDs inhibit COX Histamine receptor antagonists : Pain killer : • Target – Histamine H2 receptor • Location – Cell surface of the parietal cell • Effect – ↓ acid production from parietal cell. • Acetaminophen is an example of a pain killer5)"/,▯:06▯ Please fill in the Feedback form! Name: Kazi Mahathir Email: kazi.mahathir21@imperial.ac.uk QR code