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WEEK 2:
Pharmacology of the upper GI tract:
| Question | Answer |
|---|---|
| dyspepsia | upper gut pain or burning that feels like indigestion (bad digestion) affecting the upper GIT for 4 weeks or more |
| symptoms of dyspepsia | getting full quickly, excessive fullness, bloating, reflux and nausea |
| 60% of those having endoscopy have | functional dyspepsia or non ulcer dyspepsia (NUD) |
| 20% of those having endoscopy have | oesophagitis |
| 13% of those having endoscopy have | gastric/duodenal ulcers (PUD) |
| 1.4% of those having endoscopy have | Barrett's oesophagus |
| 3% of those having endoscopy have | gastric cancer |
| in younger patients with good clinical hx can diagnose what | GORD or NUD without scoping |
| GORD | gastro-oesophageal reflux disease |
| effect of hiatus hernia on GORD | worsen/ contribute to GORD |
| GORD can lead to | Barrett's oesophagus |
| explain why some babies have GORD | reflux is very common in infants, 40% |
| what can worsen GORD | hiatus hernia or drug induced reflux |
| complications of GORD include | stricture, ulceration and Barrett's oesophagus |
| GORD is characterised by | clinical condition from episodes of reflux of acid and pepsin into the oesophagus from the stomach |
| what can contribute to GORD | transient lower oesophageal sphincter relaxations and reduced tone, hiatus hernia and abnormal oesophageal acid clearance |
| two thirds of patients with GORD have | normal mucosa on scoping |
| symptoms of GORD | unpleasant sour taste, bad breath, bloating and belching, pain of swallowing/ difficulty swallowing, feeling sick, tooth decay and gum damage, and cough (silent GORD) |
| 80% of hiatus hernias are | sliding (junction between oesophagus and stomach moves upwards through diaphragm so stomach moves into chest) |
| when is medical treatment given to babies with GORD | if distressed behaviour, gagging, choking, faltering growth, chronic cough, single case of pneumonia |
| babies with GORD are treated by | being bottle fed more frequent in smaller feeds with thickened formula such as Carobel or Enfamil AR |
| babies with GORD should be | breast fed then feeding assessment then add in alginate trial (!-2 weeks Gaviscon Infant Sachets Max 6 in 24 hours) |
| alginate trial for babies with GORD | 1-2 weeks Gaviscon Infant Sachets Max 6 in 24 hours |
| Barrett's oesophagus | normal flat squamous cells in lower oesophagus replaced by columnar (normally found in intestines) becoming premalignant for adenocarcinoma |
| effect of PPIs in Barrett's oesophagus | do not cause regression |
| what is observed in Barrett's oesophagus | low grade dysplasia (mildly abnormal cells) monitor 2-3 yearly endoscopy |
| risk factors for GORD | obesity increased pressure on stomach, pregnancy changes in hormones, things relaxing oesophageal sphincter (alcohol, smoking, caffeine, chocolate), fatty foods, citrus fruits, gastroparesis (longer to remove acid), medications |
| medications which are risk factors for GORD (5) | NSAIDs, iron, antimuscarinics (anti-SLUD), progesterone, and bisphosphonates |
| things which relax oesophageal sphincter (4) | alcohol, smoking, caffeine and chocolate |
| causes of peptic ulceration | H pylori, drugs (NSAIDs, SSRIs, steroids, antiplatelets, iron), smoking, alcohol, stress, and blood group O |
| drugs which cause peptic ulceration | NSAIDs, SSRIs, steroids, antiplatelets, and iron |
| signs and symptoms of gastric/ duodenal ulcers | epigastric pain, night pain woken up by dull ulcer pain in DU and GU patients, heartburn/acid reflux, episodes of nausea, and in more serious cases vomiting of blood (haematemesis) |
| why do individuals with duodenal ulcers experience epigastric pain before a meal | excess acid produced by hunger stimulation passes into duodenum |
| epigastric pain experienced in those with gastric ulcers after eating food | dull aching pain |
| epigastric pain in those with duodenal ulcers are relieved by | food/antacids |
| what should be done for those who are suspected to have peptic ulcer disease (post endoscopy) | stop any NSAIDs being taken and test for H. pylori |
| what should happen if individual positive for H. pylori and no NSAIDs | use eradication therapy followed by endoscopy and test for H. pylori 6-8 weeks after treatment |
| what should happen if individual negative for H. pylori | give full dose PPI or H2RA for 4-8 weeks and once healed give low dose treatment as required with annual review to discuss symptoms |
| alarming symptoms | dysphagia, progressive unintentional weight loss, haematemesis, melaena, dyspepsia or reflux, anaemia, chronic gastrointestinal bleed, epigastric mass/suspicious barium meal, >55 with >4-6wk recent onset reflux, worsening reflux with Barrett's oesophagus |
| haematemesis meaning | vomiting blood |
| melaena | black tarry stool |
| Zollinger-Ellison syndrome | rare syndrome where cells in pancreas release gastrin leading to severe gastric acid production and severe ulcer disease where extrapancreatic gastrinomas (which release gastrin) can occur in wall of duodenum usually |
| what is needed for extrapancreatic gastrinomas | surgery and higher doses of PPIs long term |
| what increases acid secretion (3) | gastrin, histamine via H2 receptors, and acetylcholine via M receptors - M3 on parietal cells |
| what decreases acid secretion (2) | prostaglandins E2 and I2, and cytoprotective by bicarbonate and mucous release |
| gastrin is released from where | G cells in antrum of stomach during food ingestion |
| gastrin combines with | cholecystokinin-2 receptors (CCK2) to release intracellular calcium in acid producing parietal cells |
| main form of action of making stomach acid | CCK2 receptor on enterochromafin- like cells (ECL) with release of histamine which activates cAMP and acid production |
| acetylcholine (ACh) neurons stimulate | acid secretion directly via M3 receptors on parietal cell and histamine containing ECL cells |
| in antrum (pyloric mucosa), ACh neurons stimulate | gastrin secretion directly |
| H2 receptors on gastric parietal cells coupled to adenylate cyclase which stimulates | protein kinase and proton pump |
| H1 allergies associated with | allergies |
| effect of Cimetidine/ Tagamet (H2 antagonists) | inhibits cytochrome P450 and raises levels of drugs such as warfarin, carbamazepine and phenytoin |
| replacement for Cimetidine/ Tagamet (H2 antagonists) | Ranitidine (Zantac) |
| H2 antagonists are superseded by | PPIs |
| PPIs act via | irreversible inhibition of the proton pump and is activated by acidic pH and enters body and passes to parietal cells. pKa means activated at low pH which localises action |
| examples of PPIs (5) | lansoprazole, omeprazole, pantoprazole, rabeprazole and esomprazole |
| when are PPIs taken | before food (except pantoprazole) |
| features of PPIs | very effective in lifestyle maintenance, off patent (commercial use is expired), gastro-protection with NSAIDs and DAPT, available OTF |
| issues with long term PPI prescribing | regularly review whether person still needs them and whether they can use the lowest effective dose |
| risk in C.diff infection patients who received frequent PPIs | more than doubled risk |
| highest risk of those taking PPIs | highest risk in elderly and with broad spectrum antibiotics |
| misoprostol (cytotec) | synthetic prostaglandin E1 via direct stimulation of prostaglandin E1 receptors on parietal cells |
| misoprostol (cytotec) inhibits | formation of cAMP production in parietal cells and reduces gastric acid secretion and increases mucus and bicarbonate secretion and thickening of stomach mucosa and stimulating uterine contractions (so used in abortions) |
| misoprostol vs PPI | more adverse events with misoprostol |
| non NSAID induced peptic ulcers are usually associated with | H. pylori (spiral gram negative bacterium) |
| H. pylori is associated with what % of ulcers | 95% duodenal ulcers and 70% gastric ulcers |
| mode of transmission of H. pylori | acquired by oral (faecal) transmission |
| infection of H. pylori associated with | overcrowding during childhood |
| if infected with H. pylori when young then more likely to develop what | gastritis |
| what does H. pylori do | damages gastric epithelial cells to convert urea into ammonia using urease and releases proteases and phospholipases which results in gastritis and release of gastrin by G cells (making more parietal cells and increased acid production) |
| additive effect of H. pylori if individual taking | NSAIDs |
| gold standard tests for H. pylori (3) | stool antigen test or 13C urea breath test or endoscopy with biopsy |
| when is serology tests used for H. pylori | only if locally validated |
| requirements for testing for H. pylori | patients should not have used a PPI for at least 14 days before testing and if taking abx or bismuth then 2 weeks treatment free should elapse before testing |
| treatment for H. pylori | triple therapy usually for one week comprising of high dose PPI clarithromycin and either amoxicillin or metronidazole |
| standard triple therapy includes | PPI (omeprazole), clarithromycin, and amoxicillin all taken twice daily for 7-14 days |
| what do you do if ulcer large or complicated or perforation | continue PPI for at least another 3 weeks |
| treatment of H. pylori eradicates H. pylori in how many cases | 85% |
| rafting agents form | viscous cohesive gel in contact with gastric fluids (saliva) forming a continuous layer (raft) forming a barrier |
| antacids | raise pH by neutralising stomach acid |
| example of antacid | sodium bicarbonate |
| why do antacids have both magnesium hydroxide and aluminium hydroxide | magnesium causes diarrhoea and aluminium causes constipation so them together cancel the effects |
| how does sodium bicarbonate in antacids neutralise the stomach acids | HCO₃ ̄ + H⁺ -> CO₂ + H₂O |
| how does magnesium hydroxide in antacids neutralise stomach acids | Mg(OH)₂ + 2HCl -> MgCl₂ + 2H₂O |
| how are NSAIDs and steroids linked with peptic ulceration due to | inhibition of gastro-protective prostaglandins |
| dyspeptic symptoms occur in | 60% of patients taking NSAIDs and risk hospitalisation with GI complications of NSAIDs (between 1/50 and 1/150 patient years) |
| greatest risk is with | potent NSAIDs |
| lowest risk is with | ibuprofen |
| how should dosage of NSAIDs be given | at lowest effective dose and shortest duration of treatment should be used |
| patients taking NSAIDs have | four fold increase of ulcer complications over a year |
| when should NSAID prescribing be reviewed especially | in those at higher risk of GI, renal and CV morbidity and mortality (older patients) |
| PPI should also be considered for anyone receiving | NSAID who is at high risk of GI side effects including those over 65 years or using them long term |
| first line options if NSAID clinically necessary | consider low dose ibuprofen (1200mg/day or less) or naproxen (1000mg/day or less) |
| PPI should routinely be co-prescribed with NSAID (including coxibs) for who | osteoarthritis, rheumatoid arthritis, and anyone 45 years of age and older with chronic low back pain |
| drugs which increase risk of bleeding | antiplatelets and SSRIs |
| effect of nicorandil in GI patients | its an anti-anginal drug that can cause GI ulceration in some patients |
| effect of corticosteroids in GI patients | can contribute to GI complications especially when combined with NSAIDs |
| why is a PPI given alongside NSAID | protects stomach/ upper GIT by reducing acid |
| why should co-prescribing omeprazole/ esomeprazole with clopidogrel be avoided | omeprazole and esomeprazole inhibits CYP2C19 (needed to convert clopidogrel into its active form) |
Created by:
22tango
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