PCC2 - Gastrointestinal System

1. Responsibility of Responsible for the processing of food and water, extractthe GI system ? ing nutrients and getting rid of waste. 2. Describe gastric - Secreted by the stomach as part of the normal digestive juice ? process - Main constituents = HCl (gastric acid), mucin, pepsinogen and prorennin. 3. Why is gastric acid useful ? - It activates pepsinogen and prorennin - It kills bacteria and other unwanted organisms ingested with the food. 4. How does the stomach protect itself from gastric acid ? - Stomachs surface is covered by a protective layer of mucus - Mucus is alkaline and neutralises any HCl that comes close to the gastric lining. - Prevents self-digestion of the stomach by inhibiting pepsin that comes close to the lining - Cells of the gastric mucosa are replaced every 3 days = these cells are always at their functional peak. 5. Normal Mecha- - Parietal cells (also known as oxyntic cells) actively senism for gastric crete HCl into the lumen of the stomach = lowers pH to acid production around 2-3 - Luminal or apical membranes contain H+/K+ pumps (proton pumps) = pump H+ ions in the stomach lumen During initial cephalic phase: - Vagus nerve (cranial nerve X) releases ACh = stimulates M1-muscarinic receptors on parietal and paracrine cells During gastric phase: 1 / 22 - Food enters the stomach - Stimuli (e.g., protein / distension of stomach wall) trigger the release of the hormone gastrin from G cells. - Gastrin stimulates its receptors on parietal and paracrine cells - Stimulation of muscarinic + gastrin receptors on parietal cells = increase in intracellular concentration of free Ca2+ pumps which activate H+/K+ ATPase pumps - Accounts for approximately 20% of total gastric acid production. Stimulation of muscarinic and gastrin receptors on parietal cells: - Causes histamine to be released - Histamine stimulates H2-histamine receptors on parietal cells - This increases the intracellular concentration of cAMP = combination with muscarinic and gastrin receptor stimulation results in maximal gastric acid production. 6. What effect do - Cause the release of highly acidic gastric juice (even if substances such no food is present in the stomach) as caffeine and - Extra acidity risks irritating the stomach and duodenum. alcohol have on gastric juice production ? 7. What molecules - Acetylcholine control the pro- - Histamine ton pumps ? - Gastrin 8. Dyspepsia General term used to describe symptoms that take in problems such as: - Hyperacidity - Indigestion - Bloating - Heartburn These problems usually occur after eating and cause discomfort or pain in the lower chest or abdomen. E.g., if lower oesophageal sphincter does not properly 2 / 22 close, stomach contents can reflux back up into oesophagus = HCl can now affect the lining of the oesophagus, causing a burning sensation or 'heartburn'. 9. Treatment of dys- - use of Antacids pepsia - If severe + symptoms persist = a proton pump inhibitor or histamine H2-receptor agonist may be used. 10. Antacids - Bases that neutralize the gastric acid in the stomach's lumen = this raises pH and provide an effective treatment for many dyspepsias. - Provide symptomatic relief for oesophageal reflux and peptic ulcers - Reduction in gastric acid stimulates more gastrin release = causes more gastric acid to be produced. - Secondary rise in acid section is commonly referred to as 'acid rebound' 11. Types of antacids ? - Sodium bicarbonate = (sodium hydrogen carbonate) NaHCO3 - Magnesium hydroxide = Mg(OH)2 - Aluminium hydroxide = Al(OH)3 12. Sodium bicar- Water soluble bonate antacid ? - Rapid action 13. Disadvantages of sodium bicarbonate antacid ? - CO2 produced stimulates gastrin release = can produce an acid rebound effect - NaHCO3 can be absorbed by the intestine = frequent or large dose can cause systemic alkalosis - NaHCO3 is not recommended for patients on a sodium restricted diet = BNF recommends it should not be prescribed alone for the relief of dyspepsia. 14. Magnesium hydroxide antacid - Insoluble in water - Rapidly reacts with HCl = forms magnesium chloride and water - Magnesium salts are poorly absorbed by the intestine = risk of causing alkalosis is low. 3 / 22 15. Magnesium trisil- - Insoluble icate antacid - Reacts slowly with gastric acid (Mg2O8Si3) 16. Disadvantage of Magnesium salts can produce a laxative effect = may Magnesium con- cause diarrhoea. taining antacids ? 17. Aluminium hy- - Not absorbed well from the intestine droxide antacids - Slow neutralises HCl over a period of hours + disadvantages - Causes constipation 18. Magnesium hydroxide + aluminium hydroxide antacid preparations - Both have opposing effects on gastrointestinal motility = so they are combined so these effects are cancelled out. 19. Alginates + antacids - They are combined together to increase mucus viscosity - This increases it adherence to the intestine's mucosa = supports the barrier forming nature of the mucus. 20. Difference between Mucous and Mucus ? Mucous = used in reference to moist membrane linings. Mucus = is the viscous fluid that is secreted by mucous membranes. 21. Peptic ulcer Damage to the gastric wall when pepsin and acid are present in abnormally high concentrations / occurs when the normal protective mechanism of the mucosa have been reduced. - Causes very noticeable burning pain high up in the abdomen = can be temporarily relieved with antacids. - They are chronic, recurrent and solitary formed of a round pit (1cm in diameter) + base of ulcer is surrounded by a rim of inflamed tissue. 4 / 22 - Blood loss from an ulcer is a common problem = chronically can cause anaemia. 22. Where do Peptic - Oesophagus = oesophageal ulcer (associated with gasulcers occur ? tric reflux) - Stomach = gastric ulcer - Small intestine 23. Peptic ulcer symptoms ? Patients may experience weight loss, nausea and vomiting. 24. What factors can - Alcohol consumption lead to Peptic ul- - Smoking cers ? - Long-term NSAID use - Chronic gastritis - Corticosteroid use - Psychological stress = e.g., Zollinger-Ellison syndrome is a condition in which high levels of gastrin causes excessive amounts of gastric acid to be produced. (excessive gastrin section may come from a pancreatic tumour). 25. Peptic ulcers treatments - Proton pump inhibitor or histamine H2-receptor antagonist - Some patients may receive treatment long term as they are likely to develop the ulcer again. 26. Stress ulcers - They are erosions (tend to be acute in nature and form superficial mucosal damage) - Multiple lesions may occur across the stomach mucosa & may be associated with something stressful e.g., acute alcohol abuse, acute gastritis, brain injury, extensive burns, major surgery or some other major illness or trauma. - Chronic NSAID and corticosteroid use may also cause stress ulcers. 27. Patients at high - Critically ill patients with severe burns, head injury or risk of develop- sepsis. ing stress ulcers - These patients can be given stress ulcer prophylaxis ? 5 / 22 = usually involves the use of a histamine H2-receptor antagonist or proton pump inhibitor. 28. Treatments for Ulcers: Histamine H2-Receptor Antagonists - The drugs (e.g., Cimetidine and Ranitidine) antagonise the H2-receptor on parietal cells - Gastric acid secretion is greatly reduced, but this does not completely remove it as ACh and gastrin will still be active - These drug relieve peptic ulcer pain and will help peptic ulcers to heal. 29. Treatment for ulcers: Proton Pump Inhibitors (PPIs) - PPI drugs e.g., Lansoprazole and Omeprazole = inactive when administered but activated in acid (very low pH) - Irreversibly inhibit H+/K+ ATPase pumps (proton pumps) on parietal cells - Causes almost no gastric acid to be produced - This greatly relieves the pain of peptic ulcers and helps them to heal. - Stomach will produce new H+/K+ ATPase pumps = PPIs need to be administered daily. 30. Describe Lansoprazole and Omeprazole ? - Pro-drugs = only activated at very low pH - Weak bases with pKa of 4.0 = free bases at blood pH (7.4) & are only ionised in strongly acidic environments where the pH is less than 4 (these conditions are only found in the secretory canaliculus of parietal cells where pH is 2 or less). 31. PPI drugs MOA (Lansoprazole and Omeprazole) - Drugs pass through the membrane as un-ionised lipophilic bases but once in the acidic environment they become protonated - Drug is unable to cross back over the membrane and therefore accumulate in the canaliculi = there is 1000 fold accumulation. - Protonation triggers an acid catalysed conversion = activates the drug - Once activated = they bind irreversibly to exposed cysteine residues of the proton pump (H+/K+ ATPase) and 'block' the pump, preventing further release of HCl 6 / 22 Drug is most active when parietal cells are secreting HCl and show little activity when in their resting state. 32. Issues associated with using Proton Pump Inhibitors ? - Headaches, Diarrhoea and Rashes may occur occasionally - Dizziness - Gynaecomastia - Impotence - Hyponatraemia - Hypomagnesia - They decrease gastric acidity = may increase the risk of gastrointestinal infections, including Clostridium difficile. - Omeprazole could interact with clopidogrel 33. Re-occurrence of Ulcers: Helicobacter pylori - Can cause inflammation of the stomach wall - Organism attaches to a sugar molecule on the surface of the cell walls in the stomach and uses the mucus layer (protects the stomach from acidic gastric juice) as its protection. 34. How does H.Pylori survive the harsh acidic conditions in the stomach ? - It is motile = uses its flagella to migrate through the alkaline gastric mucus so its protected. - Mostly settles in the antrum of the stomach which has no parietal cells - Produces urease = breaks down urea to produce ammonia and CO2. Ammonia will neutralise HCl in the area local to the H.pylori. 35. How does H.py- - Produces inflammatory toxins that weaken the gastric lori contribute to mucosal barrier ulcer formation ? - This means gastric acid and pepsin can come into direct contact with the stomach and cause damage. 36. How can H.pylori - Stool antigen test be detected ? - Laboratory-base serology (blood test) - [13C] urea breath test 37. How does the - A drink containing radiolabelled urea is consumed [13C] urea breath - if H.pylori is present then the urease it produces will test work? liberate 13CO2 7 / 22 - This can be detected on the breath - If no H.pylori is present then no 13CO2 will be detected. 38. What is Triple therapy treatment used for H.pylori ? - administration a proton pump inhibitor along with 2 antibiotics (e.g., amoxicillin, clarithromycin or metronidazole), initially for one week. 39. What test must be used to confirm eradication of H.pylori if needed ? [13C] urea breath test must be used because: - There is insufficient evidence for use of the stool antigen test - Blood test remains positive for H.pylori even if it has been eradicated. 40. Gastrointestinal Any bleeding that occurs in the gastrointestinal tract from bleeding the mouth to the rectum. 41. Upper gastroin- Occurs from the oesophagus to the duodenum (includes testinal bleeding the stomach as well). Causes = peptic ulcers, oesophageal varices and cancer (rare). 42. Lower gastroin- Occurs in the jejunum, ileum, colon rectum or anus. testinal bleeding Causes = Inflammatory bowel disease, haemorrhoids and cancer. 43. Acute gastroin- - It is a medical emergency testinal bleeding - Usually intravenous fluids are used to stabilise the patient. 44. Mucosal Protec- Drugs involved with forming a protective physical barrier tants over the surface of an ulcer, shielding it from harsh environment of the stomach lumen. Examples : - Alginates - Acid sucralfate - Bismuth chelate Acid sucralfate and Bismuth chelate must be given on 8 / 22 an empty stomach; otherwise they will instead react with dietary proteins and then will not function effectively. 45. Mucosal Protec- In acid sucralfate polymerizes to form a sticky gel that tants: Acid sustrongly coats ulcer craters. cralfate 46. Sucralfate - side - Constipation effects - Nausea - Vomiting - A dry mouths - Headache - Rashes 47. Mucosal Protec- Forms protective layer by having a high affinity for the tants: Bismuth exposed mucosal glycoproteins and necrotic tissue found chelate in ulcers. 48. Bismuth chelate - can blacken teeth, tongue and faeces - side effects - can cause nausea and vomiting 49. Mucosal Protec- - Stable analogue of Prostaglandin E1 tants: Misopros- - Have a protective GI action tol - Acts on parietal cells to reduce gastric acid production - It also increases protective mucus secretion 50. Misoprostol side effects - Diarrhoea - Abdominal cramps - Can induce uterine contractions = should not be used during pregnancy. 51. Bristol stool chart Clinical aid that classifies faeces (or stools) into 7 groups based on their appearance. Appearance of the stool = shows how long the stool has spent in the bowel. - Type 1 = spent the longest time in the bowel - Type 7 = spent the shortest time in the bowel 52. Type 1 and 2 stools 9 / 22 What type of stools indicate constipation ? 53. What type of Type 5 to 7 stools stools indicate diarrhoea and urgency ? 54. Constipation A condition in which: - bowel evacuations occur infrequently or - when the faeces becomes hard and small or - where the act of defection causes difficulty or pain. If it develops in a person of previously regular bowel habits = may be a symptom of intestinal disease. 55. Symptoms that can be used to identify constipation ? 2 or more have continued for at least 12 weeks: - Infrequent passage of stools, which is considered to be less than 3 per week - Straining more than 25% of the time during defecation - Passage of hard stool - Feelings of incomplete bowl evacuation - Sensation of anorectal blockage 56. Causes of constipation: Common reasons - Poor diet = low fibre - Pregnancy 57. Causes of constipation: Drug induced - Antimuscarinics - Calcium channel blockers - Opiates 58. Causes of con- - Anal fissure stipation: GI tract - Colonic carcinoma problems - Intestinal obstruction - Irritable bowel syndrome - Rectal prolapse 10 / 22 59. Causes of constipation: Metabolic and Endocrine disorders - Diabetes mellitus - Hypothyroidism - Porphyria 60. Causes of con- - Parkinson's disease stipation: Neuro- - Spinal cord lesions logical causes 61. Bulk forming lax- e.g., Bran, Ispaghula husk atives - all contain polysaccharides like cellulose - cellulose is indigestible and remains in the lumen of the intestine MOA: - bulks out intestinal contents = stimulates mucosal stretch receptor to induce peristaltic movements. 62. Osmotic laxatives e.g., Epsom salts (MgSO4), lactulose, macrogols MOA: - bulk out intestinal contents with water - water is retained in the bowel by an osmotic effect Helps to soften stools - Patients must be adequately hydrated 63. Stimulant laxatives e.g., Senna, bisacodyl MOA: - stimulate/irritate the mucosa and myenteric plexus to produce intestinal movements. 64. Side effects associated with stimulant laxatives ? - Cause intestinal cramps - Prolonged use may actually damage to the intestine 65. Faecal soften- e.g., Arachis (peanut) oil, liquid paraffin ers (lubricants) - MOA: Laxatives - soften and may lubricate faeces = promoting bowel evacuation. 11 / 22 66. Side effects associated with Faecal softeners ? - Prolonged use is not recommended as it can interfere with the absorption of fat soluble vitamins (Vitamin A,D,E and K) - May also cause paraffinomas (cancers) 67. Diarrhoea Frequent bowel evacuations 68. Causes of diarrhoea ? - Intestinal inflammation: Colitis, Crohn's Disease - Loose blood-stained stools = suggest an inflammatory cause - Malabsorption of intestinal contents: Lactose intolerance, anxiety etc. - Loss of appetite, weight loss, and the production of unpleasant/offensive and pale stools that float suggest steatorrhea (presence of excess fat in the faeces) - Intestinal infections = Bacterial (E.coli, Vibrio cholera, Salmonella spp), Viral (Rotavirus), Fungal (Histoplasmosis), Parasitic (amoebic dysentery). Sudden onset of abdominal cramps + fever and diarrhoea = suggests an infection. 69. Diarrhoea: Intestinal infections - Secretions are stimulated = producing symptoms of diarrhoea to flush out the problem causing microbes and stop their population size from constantly increasing the gut. - More fluid and electrolytes are secreted and lost than those absorbed - Begins to cause problems of dehydration and electrolyte imbalance + nutrients not absorbed effectively. 70. Antidiarrhoeal treatments: Oral Rehydration therapy (ORT) - Oral solutions of electrolytes and glucose are administered to overcome the losses that occur in diarrhoea - water in ORT follows absorbed Na+ ions and glucose by osmosis - WHO has strongly promotes use of ORT = simple, cheap 12 / 22 and highly effective - ORT is so effective that IV rehydration can be reserved for those cases that require it. 71. Antimotility treatment: Loperamide - Hybrid molecule, methadone-like structure functionalised with 4-phenylpiperidine - Lipophilic, Slowly absorbed, Prone to metabolism = selectively agonises the opioid receptors in the GI tract - Cannot cross the blood brain barrier and has few central actions = less likely to cause problems of dependence. 72. Loperamide MOA - Selectively agonises opioid receptors in the GI tract - After stimulation of myenteric neuronal mu (u)-opioid receptors in the intestine = K+ ion channels open - Cell is hyperpolarised = inhibits the release of neurotransmitters like ACh - Bowl motility is reduced. 73. Antimotility treatment: Adsorbents Kaolin - Fine, pure form of natural clay (China clay, hydrated aluminium silicate) used to treat symptoms of diarrhoea - Orally administered as a fine suspension on its own or - as a mixture with other drugs like morphine. 74. Adsorbents MOA Either: - absorb microbes or their toxins - coat and protect the intestinal mucosa - simply absorb the excessive fluid present in the bowel that causes the diarrhoeal symptoms 75. Antimotility treatment: Antibiotics Tetracycline = useful in treating cholera and bacillary dysentery 13 / 22 Ciprofloxacin = used in cases of travellers' diarrhoea (most common cause is E.coli) 76. Lipase inhibitors e.g., Orlistat - used to produce a modest weight loss in combination with a low-calorie diet. 77. Lipase inhibitors - Lipases normally digest dietary lipids into fatty acids and - orlistat MOA glycerol - Orlistat irreversibly inhibits gastric and pancreatic lipases - Fat can't be digested effectively = reduced lipid absorption and reduces calorific intake. 78. Side effects: Orli- - Increase in faecal excretion of fat = leads to abdominal stat bloating and cramps - Flatus with discharge - Oily spotting - Faecal incontinence 79. Nausea Unpleasant feeling of wanting of vomit. 80. Vomiting Expulsion of gastric contents 81. Causes of nau- - Constipation sea and vomiting - Anxiety and fear - Metabolic causes - Pain - Post chemotherapy - Infections - Drugs - Motion sickness - Gastric stasis - Intestinal obstruction - Raised intracranial pressure 82. Predisposing factors to nausea and vomiting - Female - Non-smoker - Opioids during surgery - Age 14 / 22 - Migraine - Type of surgery - Anaesthesia - Eating too early post-op or delayed gastric emptying - Hypotension, hypoxaemia - Obesity - Drugs - Previous N&V experienced during pregnancy 83. Stimuli that can - Highly disturbing, stressful, emotional sights and situatrigger nausea tions and vomiting ? - Unpleasant odours - Drug induced (alcohol, anaesthetics, cytotoxic, opioids, etc.) - Migraines - Motion sickness - Pregnancy 84. Where is vomit- Emesis (vomiting) - co-ordinated by the area in the lateral ing co-ordinated reticular formation of the medulla = called the vomiting ? centre. 85. Chemoreceptor trigger zone (CTZ) - Located close by vomiting centre - Communicates with the vomiting centre + able to detect chemical stimuli - Monitors the chemical composition of the blood - Receives information from the eyes and vestibular system of the inner ears = disharmony of inputs can result in motion sickness for some individuals. 86. Receptors that can stimulate the vomit centre and CTZ - Dopamine - ACh - Histamine - 5-hydroxytriptamine - Opioid - Substance P 87. Limbic cortex - Vomiting centre also receives information from here = signals from here may be involved with the nausea triggered by unpleasant sights and smells. 15 / 22 - Consists of complex neuronal networks involved with expressing instincts and moods (e.g., fear, pleasure, rage). 88. Nucleus solitar- - Found in the medulla oblongata ius - Involved with the gag reflex - Vomiting centre also receives information from here 89. Spinal cord - Involved with nausea due to physical injury - Vomiting centre also receives information from here 90. How does vomit- - Reversal of peristalsis in the upper (proximal) part of ing occur ? the small intestine = intestinal contents and bile enter into stomach - Closure of the glottis - Breath is held - Oesophagus and gastric sphincter relax - Contraction of abdominal muscle to eject the stomach contents 91. Disorders asso- Low intestinal obstruction or gastrocolic fistula between 2 ciated with vom- hollow organs (in this case stomach and colon). iting: Feculent vomiting 92. Disorders associated with vomiting: Haematemesis Blood in vomit that appears like coffee grounds. 93. Disorders asso- Upper intestinal obstruction or the outlet of gastric conciated with vom- tents. iting: Large volume vomiting with or without projectile vomiting 94. Disorders associated with Common in pregnancy, some metabolic disorders and alcohol dependency. 16 / 22 vomiting: Motion sickness 95. Disorders asFrequently a psychogenic (origin in mind) symptom. sociated with vomiting: Nausea with small amounts of stomach regurgitation with no other abdominal symptoms 96. Antiemetic drugs - Should be administered before the emetic stimulus starts - Useful in reducing the severity of nausea and vomiting caused by other drug therapies e.g., cancer chemotherapy 97. Antiemetic e.g., Hyoscine (scopolamine) drugs: - directly antagonises muscarinic receptors on the vomitAntimuscarinics ing centre - Used to prevent motion sickness 98. Antiemetic drugs: H1-Histamine receptor antagonists e.g., Cyclizine (cinnarizine and promethazine) - antagonise H1 receptors on the vomiting centre - useful in treating conditions such as, motion sickness, vestibular disorders e.g., Meniere's disease and severe morning sickness in pregnancy. - not effective against CTZ stimuli 99. Antiemetic drugs: Dopamine D2 receptor antagonists Antipsychotics phenothiazines e.g., prochlorperazine - block dopamine D2 receptors on CTZ + antagonise muscarinic and histamine receptors - effectively used to treat nausea and vomiting due to cancer therapies, opioids and anaesthetics. e.g., Metoclopramide: - acts directly on the CTZ, treats sickness caused by radiation, cytotoxics and uraemia 17 / 22 - acts on the GI tract = increases motility, so it can also be used to treat gastro-oesophageal reflux - Can pass through the blood-brain barrier = can cause some centrally mediated side effects. - Domperidone is similar to metoclopramide and often used to try and prevent nausea and vomiting in cytotoxic therapy = does not cross the blood-brain barrier and causes less sedation and extrapyramidal effects. These drugs are not effective for motion sickness 100. Antiemetic drugs: 5-hydroxytryptamine (5-HT3) receptor antagonists e.g., Ondansetron - acts directly on the 5-HT3 receptors of the CTZ as well as 5-HT3 receptors that occur in places like the intestine. - useful in treating sickness caused by cytotoxic drugs, postoperative vomiting and radiation sickness. - 90% of the body's total amount of 5-HT3 is held in the GI tract, some cytotoxics and radiotherapy can cause the intestinal release of 5-HT = triggers nausea and vomiting - So antagonising internal receptors may help to reduce symptoms 101. Side effects of 5-HT3 receptor antagonists ? Gastrointestinal upsets 102. Antiemetic drugs: Cannabinoids e.g., Nabilone - reduce vomiting caused by stimulants of the CTZ - used to reduce cytotoxic induced vomiting in cases where other antiemetics have failed. 103. 18 / 22 Side effects of - Drowsiness Cannabinoids ? - Hypotension - Psychotic effects (loss of contact with reality) 104. Antiemetic drugs: Substance P e.g., Aprepitant - a neurokinin-1 receptor antagonist - blocks the actions of substance P on the CTZ 105. Antiemetic e.g., dexamethasone drugs: - used in vomiting associated with cancer chemotherapy Glucocorticoids - often used in combination with other drugs such as 5-HT3 or a neurokinin-1 receptor antagonist. 106. Irritable Bowel Long-term condition affecting the gastrointestinal tract. Syndrome (IBS) - related to increased sensitivity of the gut and involve problems digesting food. 107. Symptoms of IBS - Abdominal pain and cramping - Change in bowel habits (Constipation, Diarrhoea or both) - Bloating - Flatulence - Feeling of incomplete evacuation of the bowel - Passing mucus from the rectum - Urgent need to pass a stool 108. 19 / 22 IBS - epidemiolo- - Common condition gy - Affects 1 in 5 people at some point - Usual age of onset is between 20 and 30 yrs old - Women are 2x as likely as men to be affected 109. Common IBS triggers - Alcohol - Caffeine containing drinks - Fatty or fried food Patients can be encouraged to keep a food diary to identify if they have any triggers, which they can then avoid. 110. IBS treatment: Laxatives - Used to treat constipation associated with IBS - Macrogols are the preferred osmotic laxative to be used as lactulose can cause bloating - Stimulant laxatives are not recommended for frequent use in IBS 111. IBS treatment: Diarrhoea Can be treated with loperamide 112. IBS treate.g., hyoscine butylbromide, alverine citrate, mebeverine ment: Antispas- and peppermint oil modic drugs - can be used to relieve pain associated with stomach cramping. 113. How is IBS treated in patients with severe symptoms where the usual treatment methods are not effective ? - A tricyclic antidepressant can be used in an attempt to relieve abdominal pain or discomfort 114. What are the 2 main forms of IBS ? - Crohn's disease = affects any part of the gastrointestinal tract - A selective serotonin reuptake inhibitor may then be considered if a patient does not respond to a tricyclic antidepressant. (both are unlicensed indications) 20 / 22 - Ulcerative colitis = only affects the large bowel Both are chronic relapsing conditions 115. Crohn's disease - Diarrhoea symptoms - Abdominal pain - Weight loss - Malaise - Lethargy - Anorexia - Nausea - Vomiting - Low-grade fever 116. Ulcerative colitis - Diarrhoea with blood and mucus symptoms - Lower abdominal discomfort - Malaise - Lethargy - Anorexia - Weight loss - Aphthous ulcers 117. Ulcerative coli- 10-20/100,000 population per year tis incidence per year 118. Crohn's disease 5-10/100,000 population per year incidence per year 119. Crohn's disease - Inflammation is typically transmural (affects the full thickness of the bowel) and can be discontinuous (or patchy) can be classified by: - its location = terminal ileal, colonic, ileocolic or upper gastrointestinal - its patterns = inflammatory, fistulating or stricturing. - most common location for it too occur = at the end on ileum and start of large intestine (ileocaecal disease). 120. - can be controlled with anti-diarrhoeas e.g., loperamide 21 / 22 Management strategies for Crohn's Disease: Diarrhoeal symptoms 121. Management strategies for Crohn's Disease: Glucocorticoids - anti-inflammatory treatment = using oral prednisolone to induce remission - Oral slow release budesonide = has a high hepatic first pass metabolism, so is less likely to supress the adrenal glands and cause systemic side effects 122. Ulcerative colitis - affects the rectum and colon only - continuous and superficial (non-transmural) 123. Ulcerative coli- - Affects the Rectal mucosa tis sub classification: Proctitis 124. Ulcerative coli- - Affects the rectum and sigmoid colon tis sub classification: Proctosigmoiditis 125. Ulcerative coli- - Affects the rectum, sigmoid colon and descending colon, tis sub classifi- up to the splenic flexure. cation: Left sided colitis 126. Ulcerative coli- - Disease extending from the rectum up past the splenic tis sub clasflexure. sification: Pancolitis/ extensive colitis 22 / 22