Digestive (Y2 S2 W6) PDF
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University of Adelaide
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This document explains the different types of diarrhoea, their mechanisms, and associated diseases such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and Celiac disease. It also covers antibiotic-related diarrhoea.
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.1 Diarrhoea: causes & consequences 6 Explain the mechanisms behind the different types of diarrhoea: secretory, osmotic, inflammatory & altered motility. diarrhoea - 3 or more loose stools per day or more frequent stool passage than normal for the individual - acute diarrhoe...
.1 Diarrhoea: causes & consequences 6 Explain the mechanisms behind the different types of diarrhoea: secretory, osmotic, inflammatory & altered motility. diarrhoea - 3 or more loose stools per day or more frequent stool passage than normal for the individual - acute diarrhoea – lasts 14 days or less & is almost always caused by an infectious agent, typically a virus - persistent diarrhoea – lasts 15-30 days & generally is caused by an infectious agent - chronic diarrhoea – lasts >30 days secretory diarrhoea - watery diarrhoea independent of ingested substances - pathophysiology active secretion of H2O(with loss of K+ & bicarbonate)into the intestinal lumen via inhibition or activation of enzymes (e.g. ↑ cAMP activity) - causes neuroendocrine disorders e.g.: carcinoid syndrome, gastrinoma endocrine disorders e.g.: hyperthyroidism, Addison disease, diabetes foodborne infections e.g.: cholera, enterotoxigenic E. coli, viruses (e.g. norovirus, rotavirus, adenovirus) osmotic diarrhoea - watery diarrhoea related to ingestion of food or medication - pathophysiology poor absorption or excessive ingestion of hydrophilic substances (e.g. salts, sugars, laxatives) causes H2O to be drawn into the intestinal lumen - causes osmotic laxatives (e.g. magnesium citrate) carbohydrate malabsorption (e.g. lactose intolerance) inflammatory diarrhoea - pathophysiology damage to the intestinal mucosa may cause: cytokine-induced water hypersecretion impair absorption of osmotically active substances fat &/or disrupt water & electrolyte absorption mucus, blood & leukocytes present in the stool - causes IBD – ulcerative colitis (UC), Crohn’s disease colorectal cancer infections shigellosis (bacillary dysentery) nontyphoidal – salmonellosis (salmonella gastroenteritis) altered motility diarrhoea - pathophysiology ↑ bowel activity when the intestine contracts more frequently → rapid intestinal passage → ↓ the time available for H2O & electrolytes to be absorbed from the intestinal lumen → more fluid remains in the stool → diarrhoea - causes diarrhoea-predominant IBS (IBS-D) prokinetics(drugs that stimulate contractions alongGIT) escribe the key features & the mechanisms of intestinal diseases associated with diarrhoea. D irritable bowel syndrome (IBS) - altered bowel habits associated with abdominal pain, whereby the pain is influenced by defecation - can be diarrhoea predominant (IBS-D), constipation predominant (IBS-C) or mixed (IBS-M) - pathophysiology not fully understood but common findings are: altered GI motility (↑ frequency &/or irregularity of bowel contractions) visceral hypersensitivity/hyperalgesia ➔ possibly caused by hypersensitivity of the afferent nerves → GI process may cause pain altered permeability of GI mucosa psychosocial aspects - clinical features characterised by chronic abdominal pain & changes in bowel habits abdominal pain varies from patient to patient typically related to defecation –pain is often alleviatedby defecation altered bowel habits diarrhoea &/or constipation (may alternate or present with either as main symptom) other symptoms nausea, reflux, early satiety passing of mucus, abdominal bloating general somatic symptoms (e.g. pain or fatigue) disturbed sexual function ↑ urinary frequency & urgency in female – dysmenorrhea(pain shortly before or duringmenstruation) physical exam – normal inflammatory bowel disease (IBD) 1) Crohn's disease (CD) - can affect any part of the GIT (from mouth to colon) - characterised by ‘skip lesions’ – discrete areas of inflamed tissue interspersed with healthy tissue(hallmark of CD) - transmural inflammation– inflammation can penetratethe entire thickness of the bowel wall - often lead to thickening of the bowel wall (mural thickening) & fibrosis - can lead to formation of fistulae(abnormal connectionsbetween different parts of the intestine)or sinuses - smoking is a RF - pathophysiology inflammation is most likely caused by immune dysregulation dysregulation of IL-23-Th17 signalling → unrestrained Th17 cell function → inflammation → local tissue damage (edema, erosions/ulcers, necrosis) → obstruction, fibrotic scarring, stricture & strangulation of the bowel mutations in the nucleotide oligomerization binding domain 2 (NOD2) protein are likely involved in the development of CD - clinical features can manifest anywhere in the GIT but most commonly affects the terminal ileum & colon rectal involvement is uncommon chronic diarrhoea fever, weight loss, low-grade fever abdominal pain, typically in the RLQ palpable abdominal mass features of CD complications malabsorption (e.g. weight loss, anaemia, failure to thrive) enterocutaneous or perianal fistula, often associated with abscess formation perianal fistula & abscesses are often the 1st signs of CD lower GI bleeding (uncommon) 2) Ulcerative colitis (UC) - typically presents as a continuous & diffuse inflammation of the colon - inflammation always starts in the rectum & extends upwards into the colon - superficial inflammation– inflammation limited tomucosal & submucosal layers of the colon - no well-developed mural thickening - smoking is protective - pathophysiology dysregulation of the immune system upregulation of lymphatic cell activity (T cells, B cells, plasma cells) in bowel walls → enhanced immune reaction & cytotoxic effect on colonic epithelium → inflammation with local tissue damage (ulcerations, erosions, necrosis)in the submucosa& mucosa: ➔ autoantibodies (pANCA) against cells of the intestinal epithelium ➔ Th2 cell-mediated response pattern of involvement ascending inflammation begins in the rectum & spreads continuously proximally throughout the colon the rectum is always involved in UC - clinical features limited to the colon, rectal involvement is very common intestinal symptoms bloody diarrhoea faecal urgency abdominal pain tenesmus –distressing & persistent but ineffectualurge to empty the bladder or rectum extraintestinal symptoms fatigue osteoarthritis, ankylosing spondylitis, sacroiliitis uveitis, episcleritis primary sclerosing cholangitis (up to 90% of all patients with PSC will also have ulcerative colitis) ➔ chronic liver disease characterised by inflammation & scarring of the bile ducts Celiac disease - immunologically-mediated disease in genetically susceptible people caused by intolerance to gluten - pathology – mucosal inflammation & villous atrophy - autoimmune disease – strong genetic link to HLA antigens (HLA-DQ2 & HLA-DQ8) - pathophysiology consumption offood containing gluten → tissue transglutaminase( TG) is released → modifies gliadin from gluten proteins → pathogenic T cells react to & are activated by modified gliadin → mediate chronic intestinal inflammation → epithelial damage resulting in villous atrophy, crypt hyperplasia & loss of brush border → impaired absorption of nutrients in the small intestine (especially in the distal duodenum & proximal jejunum) → malabsorption symptoms - clinical features GI symptoms chronic or recurring diarrhoea steatorrhea –foul-smelling, bulky, oily, floatingstool caused by ↑ stool fat content flatulence, abdominal bloating & pain extraintestinal symptoms malabsorption symptoms ➔ fatigue ➔ weight loss ➔ vitamin deficiency ➔ iron-deficiency anaemia &/or other vitamin & mineral deficiencies ➔ osteoporosis ➔ hypocalcemia in children ➔ failure to thrive, growth failure ➔ delayed puberty ➔ secondary hyperparathyroidism neuropsychiatric symptoms – peripheral neuropathies mild or asymptomatic cases are more common than the classic presentation of the disease - associated conditions autoimmune thyroid disease (e.g. Hashimoto thyroiditis, Graves), T1DM, IBS, IBD, RA, sarcoidosis - diagnosis blood tests IgA tissue transglutaminase antibody (tTG IgA)– initialtest ➔ ↑ tTG-IgA antibodies indicate a high likelihood of celiac disease ➔ if the patient has IgA deficiency, tTG-IgA levels may be falsely low in this case, it is important to check total serum IgA deamidated gliadin peptide (DGP) ➔ DGP IgG & DGP IgA testing ➔ ↑ DGP antibodies can indicate celiac disease upper GI endoscopy with small intestine biopsy(confirmatorytest) - treatment life-long gluten free diet abstain from products containing wheat, rye, barley, spelt iron & vitamin supplementation escribe the mechanisms underlying the development of antibiotic-related diarrhoea & explain the impact on D patient health. antibiotic-related diarrhoea - diarrhoea that occurs during or shortly after antibiotic use, most likely due to altered intestinal microbiota - several mechanisms: antibiotics disrupt gut microbiota → ↓ good bacteria → pathogenic organisms can overgrow & produce toxins → diarrhoea can occur due to transient loss of bacteria that normally absorb short-chain fatty acids - Clostridium difficile (C. difficile) infection is a severe form of antibiotic-related diarrhoea overgrowth of C. difficile can lead to antibiotic-associated colitis & cause inflammation most often in older individuals who are in hospitals & institutions can be treated with antibiotics or stool transplant impact - dehydration & electrolyte imbalance - nutritional deficiencies - potential complications with infections like C. difficile, there can be more serious complications such as pseudomembranous colitis escribe key considerations for the clinical management of chronic diarrhoea. D investigations - blood tests CBC –to evaluate for anaemia, leukocytosis & /orleukopenia CMP – assessment of laboratory findings in dehydration(e.g.electrolyte abnormalities, AKI) &/or liver disease CRP, ESR – inflammatory markers blood cultures – identify bacteremia - stool diagnostic studies stool culture – can be indicated if red flags in diarrhoea are present stool tests for CDI – if C. difficile infection is suspected stool osmotic gap equation used in patients with watery diarrhoea to differentiate between osmotic, secretory & functional diarrhoea calculation – 290 - [2 × (stoolsodium + stool potassium)] normal stool osmotic gap – 50–100 mmol/L management - start oral hydration (or IV fluids) & offer symptom relief - consider empiric or targeted therapy (e.g. antibiotics) based on clinical presentation & study results antibiotics should only be utilised for specific conditions - red flags in chronic diarrhoea hypoalbuminemia bloody stools symptoms that wake the patient up from sleep unintended weight loss family history of GI cancer symptoms onset after 50yo .2 Infections of the gastrointestinal tract 6 Describe the defence mechanisms against infection provided by the gastrointestinal tract. anatomical barriers - mucosal layers GIT is lined with a mucus layer that acts as a physical barrier to pathogens, preventing their invasion & adherence - tight junctions epithelial cells are connected by tight junctions that limit the permeability of the intestinal lining to pathogens & toxins chemical defences - gastric acid stomach secretes HCl, creating a acidic environment that can destroy many ingested pathogens microbial defences - normal flora (gut microbiota) GIT harbours a diverse community of beneficial microorganisms that compete with pathogenic bacteria for resources & space → can inhibit pathogen colonisation & growth immunological defences - innate immune response mucosal immunity gut-associated lymphoid tissue (GALT) ➔ provides localised immune responses to pathogens ➔ including production of secretory immunoglobulin A (slgA) – helps neutralise pathogens & prevent their adherence to epithelial cells phagocytic cells macrophages & dendritic cells in the mucosa can recognise & phagocytose pathogens - adaptive immune response GIT can mount a specific immune response through the activation of T & B lymphocytes, producing antibodies against specific pathogens Outline how various pathogens cause gastroenteritis and diarrhoea. gastroenteritis - broad term that refers to inflammation of the GIT, particularly the stomach & small intestine - can be caused by infections, food intolerances, toxins, medications, autoimmune diseases, not all of which are infectious infectious gastroenteritis - specifically gastroenteritis caused by pathogens such as viruses, bacteria or parasites - most commonly caused by viruses but can also be caused by bacteria, fungi, parasites utline the epidemiology, routes of infection & life cycles of common/important gastroenteritis-causing bacteria. O *discussed in previous LO* escherichia coli (E. coli) – leading cause of bacterial gastroenteritis pathogenic cycle 1) transmission from host or reservoir (environment) 2) colonisation - motility flagella aid in motility, helping pathogens to reach their target site (typically epithelial surface of mucosa) - adherence fimbriae (fine protein chains) are essential for attachment 3) proliferate within host once attached, the pathogen proliferate 4) transmission to new host or escape to reservoir the pathogen then leaves the current host, either to infect another host or return to the reservoir (environment), perpetuating the cycle utline the impact of hospital or community-acquiredClostridium difficileinfections. O clostridium difficile infections (CDI) - an infection caused by toxigenic clostridium difficile in the lower GIT - hospital-acquired confirmed CDI in an individual with documented inpatient care in a healthcare facility in the preceding 12 weeks more common in individuals aged > 65yo - community-acquired confirmed CDI in an individual withnodocumentedinpatient care in a healthcare facility in the preceding 12 weeks affected individuals are typically younger (~50 yo) Explain the linkage betweenHelicobacter pyloriinfections& peptic ulcers. - gastric ulcers H.pylori secretes urease → converts urea to ammonia → alkalinisation of acidic environment → survival of bacteria in gastric lumen bacterial colonisation & attachment to epithelial cells → release of cytotoxins → disruption of mucosal barrier & damage to underlying cells → weakens mucosal defence, allowing acid to penetrate & cause ulcers - duodenal ulcers in the stomach, H. pylori colonises the antrum(lowerpart of stomach), where it directly damages the D-cellsthat produce somatostatin H. pylori inhibits somatostatin secretion → ↑ gastrin secretion → stimulates parietal cells to ↑ H+ secretion(↑ gastric acidity)→ excess H+ delivery to duodenum → duodenalulcer Describe the epidemiology, routes of infection & life cycles of common/important gastroenteritis-causing viruses. 1) norovirus - most common viral cause of gastroenteritis - routes of transmission faecal-oral aerosol 2) rotavirus - leading cause of severe gastroenteritis in children < 5yo - routes of transmission primarily faecal-oral - intussusception was associated with natural rotavirus infection in 1 or 2 of several published studies intussusception a proximal part of the intestine (‘intussusceptum’) slides into a distal part of the intestine (‘intussuscipiens’) this telescoping (invagination) often blocks food or fluid from passing through also cuts off blood supply to the part of the intestine being affected 3) enteric adenovirus - young children are most commonly affected - routes of transmission primarily faecal-oral 4) astrovirus - primary affects children < 2yo & elderly patients - routes of transmission primarily faecal-oral xplain the basis of common investigative tests used to detect pathogens and diagnose gastrointestinal E infections. clinical diagnosis - perform a thorough history & physical examination - evaluate for risk factors for specific pathogens (e.g. recent hospitalisation, recent travel, contact with animals) - evaluate for clinical features of dehydration & hypovolemia - viral gastroenteritis may be asymptomatic or manifest with non-bloody watery diarrhoea & vomiting, which is accompanied by abdominal pain or cramps & fever investigative tests 1) faecal microscopy - used to identify parasites & their eggs, while bacterial culture is used to isolate & identify bacteria 2) cytotoxic assays - can detect toxins produced by some bacteria 3) PCR (polymerase chain reaction) - a molecular diagnostic technique that can detect the DNA of pathogens in stool samples with high sensitivity & specificity 4) histology - involves examining a biopsy of the gastrointestinal tract for signs of inflammation, damage or infection. 5) serology - measures the levels of antibodies in the blood against a particular pathogen, indicating a previous or ongoing infection utline the general principles of intestinal infection treatments and discuss newly emerging approaches. O bacterial infections - the treatment of bacterial infections of the intestine typically involves the use of antibiotics - however, not all bacterial infections require antibiotics & the use of antibiotics should be reserved for cases where bacterial infection is confirmed, strongly suspected &/or the infection is not self-limiting - the indiscriminate use of antibiotics can lead to the development of antibiotic-resistant strains of bacteria viral infections - the treatment of viral intestinal infections is primarily supportive, as there are currently no antiviral drugs available for routine use in the treatment of these infections - treatment typically focuses on relieving symptoms & preventing dehydration - antidiarrhoeal agents such as loperamide can help to reduce the frequency & severity of diarrhoea parasitic infections - the treatment of parasitic intestinal infections depends on the specific parasite involved - antiparasitic medications can be used to treat parasitic infections such as giardiasis & cryptosporidiosis emerging approaches probiotics - probiotics are live microorganisms that, when administered in adequate amounts, confer a health benefit on the host - probiotics have been shown to be effective in preventing & treating certain types of diarrhoea caused by infections Faecal Microbiota Transplant (FMT) - FMT involves the transfer of faecal matter from a healthy donor to a patient with a diseased gut microbiota - FMT has shown promising results in the treatment of recurrent Clostridium difficile infection & is being studied as a potential treatment for other types of intestinal infections Phage therapy - phage therapy involves the use of bacteriophages, which are viruses that infect & kill bacteria, to treat bacterial infections - phage therapy is still in the experimental stage & is not yet widely available .3 Disorders of the upper gastrointestinal tract 6 Outline the aetiology, pathogenesis, signs, symptoms, investigation & management of common &/or important oesophageal disorders: gastroesophageal reflux disease (GORD), achalasia, dysphagia & oesophageal carcinoma. gastroesophageal reflux disease (GORD) aetiology - smoking - stress - foods caffeine, alcohol, chocolate, fatty meals, spicy food, citrus food, tomato-based food, peppermint, carbonated drinks - medications beta-agonist, calcium channel blockers, anticholinergics - obesity - pregnancy - inadequate esophageal protective factors (e.g. saliva, peristalsis) - large meal, delayed gastric emptying pathogenesis 1) imbalance between intragastric & lower esophageal sphincter (LES) pressure - certain food & medications → abnormal LES relaxation → prolonged transient LES relaxation - HCl in the stomach can be pushed up by ↑ intra-abdominal pressure(e.g. exercise, obesity, pregnancy)or positional changes(lying down)→ reflux occurs 2) ↑ frequency of transient LES - large meal, delayed gastric emptying → gas build up in the stomach, ↑ pressure on the cardia → pressure receptors indirectly stimulate the vagus nerve → vagus nerve stimulates LES relaxation → prolonged transient LES relaxation → HCl in the stomach pushed up into the oesophagus 3) hiatal hernia(portion of the stomach protrudes abovethe diaphragm) - hernia → LES misaligned with the level of diaphragmatic contraction → LES seal has ↓ structural support → prolonged transient LES relaxation → HCl in the stomach pushed up into the oesophagus 4) impaired esophageal acid clearance - normally, acid reflux is neutralised by salivary bicarbonate & evacuated back to the stomach via esophageal peristalsis. - clearance can be disrupted by↓salivation (e.g.,due to smoking) &/or↓peristalsis (e.g. due to inflammation) - GORD damages mucosa → inflammation → erosion signs & symptoms - typical symptoms retrosternal/epigastric burning pain (heartburn) acid regurgitation → chronic cough (esp. at night), asthma, hoarse voice dysphagia, odynophagia water brash – excessive salivation triggered by reflux of stomach acid - aggravating factors lying down shortly after meals certain foods, medications, beverages investigation - diagnosis is based on clinical presentation - endoscopy - esophageal pH monitoring management - pharmacology antacids – neutralise acid proton pump inhibitors (PPIs) – 8 weeks, once daily, 30-60 mins before a meal H2 receptor antagonists – ↓ acid production - lifestyle changes weight loss in patients with obesity ↓ or avoid triggers – e.g. smoking, alcohol, caffeine, medications that may worsen symptoms - complications of GORD – strictures (scarring that narrows the lumen), Barrett’s oesophagus (discussed in next few page) red flag symptoms of GORD - dysphagia, odynophagia - bleeding (haematemesis, melaena) - anaemia - weight loss - presence of >1 risk factor for Barrett oesophagus complications of GORD 1) esophageal stricture - narrowing of the oesophagus caused by damage & subsequent scarring (fibrosis formation) of the esophageal lining 2) Barrett’s oesophagus - intestinal metaplasia (transformation of the epithelium) of the esophageal mucosa due to chronic reflux esophagitis - stratified squamous epithelium changes to simple columnar epithelium with goblet cells - a precancerous condition that requires close surveillance 3) erosive esophagitis - a form of esophagitis characterised by visible damage or erosion in the esophageal lining 4) reflux esophagitis - inflammation of the oesophagus specifically caused by the backflow of stomach contents, particularly acid distal oesophageal spasm - abnormal, uncoordinated contractions of the oesophagus, specifically in the distal (lower) portion - gold standard for diagnosis – esophageal manometry jackhammer (nutcracker) oesophagus - characterised by excessive, high-amplitude/high-pressure peristaltic contractions, contractions are coordinated - diagnostic tool of choice – HRM eosinophilic oesophagitis - chronic, immune-mediated inflammatory disease of the oesophagus characterised by eosinophil infiltration in the esophageal mucosa - gold standard for diagnosis – upper endoscopy with biopsy achalasia - failure of the LES to relax due to degeneration of inhibitory neurons in the myenteric plexus that are responsible for releasing nitric oxide (NO) & vasoactive intestinal peptide (VIP), which facilitate smooth muscle relaxation - chief complaint – dysphagia to both solids & liquids aetiology - primary achalasia (most common) unknown cause - secondary achalasia (pseudoachalasia) esophageal cancer stomach cancer or other extraesophageal cancer chagas disease – an infectious disease sarcoidosis amyloidosis pathogenesis - swallowing is controlled through excitatory (ACh, substance P) & inhibitory (NO, VIP) neurohormonal substances - atrophy of inhibitory neurons in the myenteric plexus → lack of inhibitory neurotransmitters (e.g. NO, VIP) → inappropriate contraction of smooth muscle in distal oesophagus & inability to relax LES &→ loss of peristalsis in distal oesophagus & lack of LES relaxation → esophageal dilation proximal to LES signs & symptoms - dysphagia to solids & liquids progressive dysphagia – difficulty swallowing food & eventually followed by difficulty swallowing liquids paradoxical dysphagia – difficulty swallowing liquids while solids are easily swallowed achalasia typically manifests with progressive dysphagia while esophageal obstruction manifests with dysphagia to solids only - regurgitation - retrosternal pain & cramps - weight loss investigation - esophageal manometry(confirmatory test) findings: peristalsis is absent of uncoordinated in the lower ⅔ of the oesophagus incomplete or absent LES relaxation high LES resting pressure no evidence of mechanical obstruction - upper GI endoscopy &/or esophageal barium swallow upper GI endoscopy to rule out pseudoachalasia usually normal esophageal barium swallow serial x-rays of the chest are taken while a patient swallows liquid barium (a contrast medium) barium coats the walls of the oesophagus & can be used to identify anatomical defects in the oesophagus findings suggestive of achalasia: ➔ bird-beak sign – dilation of proximal oesophagus with stenosis of the gastroesophageal junction ➔ delayed barium emptying or barium retention management - patients with a low surgical risk 1) pneumatic dilation endoscope-guided graded dilation of the LES that tears the surrounding muscle fibres with the help of a balloon 2) LES myotomy (Heller myotomy) a surgical procedure where the LES is incised longitudinally to re-enable passage of food/liquid to stomach - patients with a high surgical risk 1) botulinum toxin injection in the LES 2) if unsuccessful – nitrates or calcium channel blockers dysphagia aetiology - oropharyngeal dysphagia stroke Parkinson’s disease Guillain-Barre syndrome brain tumour Myasthenia Gravis progressive muscular dystrophies - esophageal dysphagia achalasia GORD esophageal hypermotility disorders intraluminal disorders – impacted foreign object or food bolus esophagitis (e.g. infectious esophagitis, secondary to GORD, eosinophilic esophagitis) esophageal cancer signs & symptoms - oropharyngeal dysphagia difficulty initiating swallowing process ↓ cough reflex malnutrition &/or anorexia drooling choking sensation early in the swallowing process - esophageal dysphagia impaired passage of solids & liquids through the oesophagus towards the stomach symptoms occur seconds after swallowing predominantly experienced retrosternally (ie. sensation of food getting stuck within the oesophagus) halitosis – may be a sign of obstruction - structural dysphagia dysphagia due to a mechanical or anatomical obstruction dysphagia predominantly with solid food - motility-related dysphagia dysphagia due to a neurological or muscular defect dysphagia predominantly with liquids - dysphagia predominantly with solid food should raise suspicion for an underlying structural disorder, including malignancy - dysphagia predominantly with liquids is suggestive of an esophageal motility disorder investigation - oropharyngeal dysphagia preferred test – modified barium swallow – functional evaluation of swallowing nasopharyngolaryngoscopy – structural assessment of nasopharynx pharyngoesophageal high-resolution manometry – identify patients who can benefit from a myotomy - esophageal dysphagia preferred test – upper GI endoscopy – direct visualisation of mucosal lesions & abnormalities esophageal barium swallow High-resolution esophageal manometry – gold standard for diagnosing esophageal motility disorders management - oropharyngeal dysphagia tailored to each patient, focusing on symptom control, minimise aspiration risk & ensure adequate nutrition swallowing rehabilitation – postural techniques (e.g. eating upright, chin tuck), exercise & retrain tongue, jaw, neck optimise nutrition – diet modifications (e.g. thickening of liquids, pureeing solid food) management of underlying cause - esophageal dysphagia depends on the underlying cause esophageal carcinoma - 2 types: adenocarcinoma – mostly located in the lower 3rd of the oesophagus squamous cell carcinoma (SCC) – mostly located in the upper ⅔ of the oesophagus aetiology - adenocarcinoma smoking obesity GORD Barrett esophagus - squamous cell carcinoma (SCC) alcohol smoking diet low in fruits & vegetables hot beverages caustic strictures HPV achalasia diet rich in nitrosamines pathogenesis - signs & symptoms - early stages – often asymptomatic - advanced stages progressive structural dysphagia (from solids to liquids) with possible odynophagia retrosternal chest or back pain unintentional weight loss dyspepsia signs of anaemia signs of upper GI bleeding – hematemesis, melena investigation - upper GI endoscopy + biopsy – best initial & confirmatory tests - staging investigations CT chest & abdomen with IV contrast transesophageal endoscopic ultrasound with fine-needle aspiration biopsy management - surgical resection endoscopic submucosal resection for mucosal lesions subtotal or total esophagectomy - chemoradiotherapy neoadjuvant chemoradiotherapy utline the aetiology, pathogenesis, signs, symptoms, investigation & management of common &/or important O gastric conditions: peptic ulcers & gastric carcinoma. peptic ulcers - presence of 1 or more ulcerative lesions in the stomach or duodenum - caused by a breach in the mucosa of the stomach & duodenum that is produced by the action of gastric secretions - usually affects the distal stomach (lesser curvature, antrum) & proximal duodenum aetiology - Helicobacter pylori (H. pylori) –gram-negative, helical,microaerophilic, flagellated bacteria - chronic NSAID use - H. pylori or NSAID use alone do not typically cause ulcer formation but often there are additional risk factors present: diet shared risk factors for PUD, GORD & gastritis– smoking,heavy alcohol use, glucocorticoids, caffeine psychological factors (e.g. stress, anxiety) pathogenesis - H. pylori gastric ulcers H. pylori secretes urease → converts urea to ammonia → alkalisation of acidic environment → survival of bacteria in gastric lumen → bacteria colonise & attach to epithelial cells → release of cytotoxins → disruption of the mucosal barrier & damage to underlying cells duodenal ulcers H. pylori inhibits somatostatin secretion → ↑ gastrin secretion → ↑ H+ secretion → excess H+ delivery to the duodenum → inhibit duodenal bicarbonate secretion → acidification & insufficient neutralisation of duodenal contents - NSAIDs inhibits COX-1 enzymes → ↓ production of prostaglandin → erosion of gastric mucosa ↓ mucosal blood flow inhibit mucosal cell proliferation - acid hypersecretion acid hypersecretion & ↑ gastrin secretion → ↑ H+ secretion & parietal cell mass → delivery of excess acid to duodenum signs & symptoms - abdominal pain – can be acute or chronic commonly located in epigastrium often described as ‘gnawing’ or ‘burning’, pain worse at night nausea &/or vomiting, belching bloating investigation - CBC, electrolytes, LFTs, lipase, coags, troponin + blood tests for H. pylori antibodies - faecal occult blood test - urea breath test - upper GI endoscopy – to confirm the diagnosis management - non-pharmacological – e.g. avoid NSAIDs, restrict alcohol, caffeine, smoking, avoid stress - H. pylori-positive – triple therapy – 1 PPI + 2 antibiotics (e.g. PPI + amoxicillin & clarithromycin) - acid suppression medications & antacids - cytoprotective agents (GI mucosal protection) – e.g. sucralfate, misoprostol outcomes of chronic peptic ulcers 1) healing - overcomes damaging stimulus & defect fills with fibrous scar + recovered mucosa 2) bleeding - penetrates blood vessels - small, occult bleeding – asymptomatic or iron-deficiency anaemia - large, occult bleeding – may get massive life-threatening haemorrhage 3) perforation - gastric acid → extensive damage & ulcer extends transmurally → can lead to pancreatitis or peritonitis → septicaemia - ulcer extends through full thickness of the wall 4) obstruction - during healing of the ulcer, scarring can lead to obstruction (esp. if located in pylorus) gastric carcinoma aetiology - diet rich in nitrates &/or salts - obesity, alcohol, smoking - H. pylori infection - nicotine use - Epstein-Barr virus - gastric conditions (e.g. gastric ulcers, GORD, partial gastrectomy) - positive family history - blood type A signs & symptoms - early stages – often asymptomatic, nausea, loss of appetite - late stages – general signs weight loss - signs of gastric outlet obstruction dysphagia abdominal pain early satiety vomiting - signs of upper GI bleeding hematemesis, melena - signs of metastatic disease hepatomegaly ascites left supraclavicular adenopathy (Virchow node) investigation - bloods - diagnostic confirmation – upper GI endoscopy + biopsy - evaluate for lymph node involvement & metastatic disease CT abdomen, pelvic, thorax management - localised, resectable disease surgical or endoscopic resection margin-free resection is the only potentially curative therapy total gastrectomy ➔ complete resection of the stomach ➔ GI continuity is reestablished with Roux-en-Y esophagojejunostomy subtotal gastrectomy ➔ resection of the body & pylorus of the stomach .4 Disorders of the lower gastrointestinal tract 6 Describe the mechanisms underpinning intestinal inflammation. - disruption of intestinal epithelial barrier, leading to: ↑ permeability → allows pathogens to cross into the underlying tissue dysbiosis disruption to the microbiome, resulting in an imbalance in the microbiota imbalance in the gut microbiota can lead to an overgrowth of pathogenic bacteria & ↓ in beneficial microbes - immune cell activation infiltration of immune cells mucosal immune response ➔ activation of dendritic cells & macrophages in the intestinal mucosa → recruitment of T cells, B cells & other immune cells → exacerbate inflammation immune cells produce pro-inflammatory cytokines → amplify inflammation & recruit more immune cells - oxidative stress arises from an imbalance between the production of ROS & the body’s ability to eliminate them high ROS can damage cellular structure → tissue injury & inflammation Outline the autoimmune processes relevant to digestive disorders. - celiac disease*discussed in previous LO* - IBD*discussed in previous & next LO* escribe the main symptoms and signs of irritable bowel syndrome & the differentiating features to inflammatory D bowel disease & food allergies. irritable bowel syndrome - chronic condition affecting mainly the large intestine - functional disorder of the GIT - no active organic inflammation - clinical features characterised by abdominal pain & changes in bowel habits abdominal pain ➔ typically related to defecation pain is often alleviated by defecation but in a subgroup of patients, the pain may ↑ or remain unchanged altered bowel habits ➔ diarrhoea &/or constipation may alternate between both or present with either as main symptom patients may describe urgency or straining during defecation other GI symptoms ➔ nausea, reflux, early satiety ➔ passing of mucus ➔ abdominal bloating physical examination – normal inflammatory bowel disease ulcerative colitis Crohn’s disease bloody diarrhoea with mucus low-grade fever faecal urgency(sudden & strong urge to defecate) weight loss abdominal pain fatigue tenesmus(distressing & persistent but ineffectualurge to chronic diarrhoea empty bladder or rectum) abdominal pain(typically in RLQ) palpable abdominal mass in RLQ(most commonly terminalileum) differences - affects rectum & colon(inflammation is continuous, - most commonly affects the terminal ileum & colo, but can starting from rectum & ascending upwards) involve any part of the GIT(from mouth to anus) - inflammation is typically limited to the mucosal & - inflammation can penetrate deeper through the intestinal submucosal layer of the intestinal wall wall(transmural) - diffuse lesions - characterised by ‘skip lesions’ - strictures – rare - can lead to complications such as strictures, fistulas - rectal involvement - always - rectal involvement – sometimes food allergies - hypersensitivity reactions to allergens contained in food - clinical features skin (most common) – urticaria (hives), atopic dermatitis (eczema) respiratory – rhinitis(inflammation of the nasalmucosa), often with sneezing GIT – nausea, vomiting, abdominal pain, diarrhoea cardiovascular – hypotension, tachycardia Outline the use of laboratory markers/serology to assist the diagnosis of malabsorption disorders. - blood tests CBC – check for infection (↑ WBC), anaemia inflammatory markers (ESR, CRP) LFTs – screen for liver & bile duct issues EUC – electrolyte loss due to diarrhoea vitamin B12 – may be low if small intestine not absorbing due to Crohn’s disease - biomarkers antibody tests perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) ➔ significant in ulcerative colitis anti-saccharomyces cerevisiae antibodies (ASCA) ➔ more commonly associated with Crohn’s disease but both is not specific enough to differentiate between ulcerative colitis & Crohn’s disease neutrophil-derived proteins in stools faecal calprotectin ➔ protein released from activated neutrophils ➔ ↑ levels indicate intestinal inflammation & may help predict relapse in patients with IBD ➔ often used to differentiate between IBD & IBS lactoferrin ➔ protein found in neutrophils ➔ ↑ levels suggest active inflammation in the intestines xplain the mechanisms & risk factors underlying diverticular disease & diverticulitis. E diverticulosis - the presence of diverticula(tiny bulging pouches)in the colon - risk factors diet (low fibre, rich in fat & red meat) obesity low physical activity smoking ↑ age - mechanism ↑ intraluminal pressure from straining to pass stool weakness of the intestinal wall - most common site for diverticula formation – sigmoid colon - usually asymptomatic - may manifest with abdominal discomfort - most common presentation of complicated diverticular disease is acute diverticulitis diverticulitis - inflammation of 1 or more diverticula - mechanisms: 1) chronic inflammation & ↑ intraluminal pressure → erosion of diverticula wall → inflammation & bacterial translocation 2) rarely– inspissated(thickened or hardened)stoolbecomes trapped in the diverticulum, rubbing the mucosa of the diverticulum → inflammation & localised ischaemia bacteria may breach the mucosa - clinical features low-grade fever LLQ pain – sigmoid colon most commonly affected possibly tender, palpable mass change in bowel habits (constipation in ~50% of cases, diarrhoea in ~25-35% of cases) - diagnosis CBC – leukocytosis CT abdomen & pelvis with IV contrast preferred initial imaging modality for suspected diverticulitis supportive findings ➔ colonic outpouching ➔ bowel wall thickening avoid colonoscopy during the acute phase of diverticulitis because of the risk of perforation!! recommended 6-8 weeks after the resolution of acute episode to assess the extent of diverticulitis & rule out colorectal cancer suspect acute diverticulitis in adult patients with LLQ pain, fever & leukocytosis the diagnosis is typically confirmed with imaging - treatment will need admission nil orally analgesia IV fluids IV antibiotics consider broad-spectrum antibiotics in selective patient groups recommended on a selective bases (not routinely) as it is thought to be more of a inflammatory than infectious disease complications of diverticulitis - perforation usually due to the rupture of a inflamed diverticulum perforation into the abdominal cavity causes either purulent or faecal peritonitis with associated shock treatment – fluid resuscitation, IV fluids, IV antibiotics, surgery 1 of the most common causes of death from benign disease - abscess presentation similar to acute diverticulitis occurs because a diverticulum has perforated & walled off locally treatment – IV antibiotics, radiological drainage, resection - obstruction(rare) can be either small bowel obstruction (extrinsic compression from an inflammatory mass) or large bowel obstruction (narrowing of lumen through progressive stricturing) large bowel obstruction will often require surgery with resection - fistula abnormal tract connecting 2 epithelial lined cavities most commonly colovesical – clinical features include recurrent UTIs & pneumaturia(passage of air in urine) colovaginal – clinical features include discharge PV(per vagina, through the vagina) treatment – surgery colovesical fistula – abnormal connection between the colon & urinary bladder colovaginal fistula – abnormal connection between the colon & vagina Explain the aetiology & natural history of appendicitis & provide mechanisms for symptoms & signs. - aetiology caused by obstruction of the appendiceal lumen due to: lymphoid tissue hyperplasia (60% of cases) – most common cause in children & young adults appendiceal fecalith(hardened stool)& faecal stasis tumour (uncommon) - natural history obstructed appendiceal lumen, resulting in: stasis of mucosal secretion → bacterial multiplication & local inflammation → transmural spread of infection → clinical features seen appendix distension & spasms → ↑ intraluminal pressure → obstruction of veins → edema of appendiceal walls → obstruction of capillaries → ischemia → gangrenous appendicitis(necrosis of the tissue in the appendix) if appendix is not surgically removed → inflammation can spread to the serosa → perforation of colon wall, causing peritonitis (inflammation of peritoneum) - mechanisms for signs & symptoms migrating abdominal pain initial diffuse periumbilical pain – caused by irritation of visceral peritoneum (pain is referred to T8-T10) localises to RLQ within ~12-24 hrs – caused by irritation of parietal peritoneum non-specific symptoms nausea anorexia vomiting clinical signs of appendicitis McBurney point tenderness (RLQ tenderness) ➔ McBurney point – junction of the lateral 3rd & medial ⅔ of a line drawn from the right anterior superior iliac spine to the umbilicus RLQ guarding &/or rigidity rebound tenderness (Blumberg sign) – esp. in the RLQ Rovsing sign – RLQ pain elicited on deep palpation of the LLQ Psoas sign – can be performed in 2 ways: ➔ flexing right hip with stretched leg against resistance ➔ passive extension of the right hip when the patient is positioned on their left side obturator sign – RLQ pain on passive internal rotation of the right hip with the hip & knee flexed - diagnosis lab studies CBC – mild leukocytosis with left shift(↑ immatureneutrophils) CRP – elevated urinalysis – typically normal in appendicitis urine/serum hCG test hCG – a hormone produced by the placenta after implantation β-hCG subunit is measured to detect pregnancy perform in all women of reproductive age to rule out pregnancy (including ectopic pregnancy) imaging CT abdomen – most accurate initial imaging modality for appendicitis ➔ distended appendix abdomen ultrasound ➔ distended appendix ➔ Target sign – concentric rings of hypo- & hyperechogenicity in the axial/transverse section of appendix - treatment bowel rest(NPO – nothing should be taken by mouth) IV fluids IV antibiotics IV analgesics operative management appendectomy(surgical removal of appendix)– within24hrs of diagnosis is the current standard of care utline the non-surgical & surgical approaches used to treat infected & inflamed digestive organs. O *discussed in LO 5 & 6* .5 Treatment of inflammatory bowel disorders 6 Describe the basis for the treatments of inflammatory bowel diseases & newly emerging therapeutic approaches. conventional therapies in IBD - 5-ASA (aminosalicylic acid) e.g. sulfasalazine, mesalazine(not routinely recommended),olsalazine, balsalazide used in mild to moderate UC not useful in Crohn’s disease - corticosteroids used to ↓ remission oral prednisolone effective but associated with many side effects (e.g. weight gain, infections, diabetes, osteoporosis) budesonide gut-selective glucocorticoid with fewer systemic side effects IV methylprednisolone - thiopurines e.g. azathioprine, mercaptopurine immunosuppressive agents – suppresses immune system systemically ↑ risk of infections (particularly viral) small absolute ↑ risk of malignancy (particularly lymphoma, non-melanoma skin cancer) advanced therapies in IBD - used when conventional therapies are ineffective or not well-tolerated - biologics live drugs (derived from living organisms) – typically produced using rodent cell lines monoclonal antibodies (‘mab’) – bind to specific protein target involved in the inflammation large molecules – need to be given parenterally (IV or subcutaneously) e.g. anti-TNF agents, anti-integrin agents, anti-IL-12/23 agents - small molecules small in size so can be absorbed by the GIT nomenclature (‘nib’)(end with the suffix ‘nib’) interfere with specific immune interaction anti-TNFs - e.g. infliximab, adalimumab, golimumab - MOA:binds & neutralises soluble & membrane boundTNF-⍺ - given intravenous &/or subcutaneously anti-intergrin - e.g. vedolizumab (anti-integrin ⍺4ꞵ7) - blocks lymphocytes from entering intestine (lamina propria) - ↓ immune cells from entering into the gut → ↓ inflammation - no systemic immunosuppression (but ↑ risk of infections) - IV or subcutaneous available anti-IL-12/23 agent - e.g. ustekinumab (‘stelara’) - inhibits cytokine (IL-23) of the Th-17 pathway - beneficial in both Crohn’s disease & UC - single IV induction dose - side effects – systemic immunosuppression JAK-inhibitors - e.g. tofacitinib, upadacitinib - blocks the activity of janus kinases → prevent transmission of signals to the cell nucleus → ↓ inflammatory cascade - small molecule – administered orally in the form of tablets - licensed for UC - ↑ risk of complications ↑ LDL, malignancy, major adverse cardiovascular events & risk of venous thromboembolism (VTE) sphingosine-1 P receptor blockers - e.g. ozanimod - MOA: blocks S1P receptor on the surface of lymphocytes → prevents lymphocyte from leaving the lymphoid tissue → ↓ number of lymphocytes circulating in the bloodstream & migrating to sites of inflammation → ↓ inflammation treatment for IBD - Crohn’s disease induction phase used to manage acute flares agents that have a rapid onset of action (e.g. corticosteroids, biologics) are used maintenance phase used to maintain remission, typically in patients with moderate or severe CD & those at high risk of progression of CD biologics & immunomodulators are the principal agents of maintenance therapy commonly used medications corticosteroids –primary used to induce remission biologics –increasingly used as a primary agent toinduce remission immunomodulators –primary used to maintain remission ➔ e.g. thiopurine analogs (e.g. azathioprine, mercaptopurine) 5-ASA (aminosalicylic acid) - ulcerative colitis .6 Motility disorders of the gastrointestinal tract 6 Explain the pathophysiological mechanisms underlying common &/or important motility disorders of the gastrointestinal tract. GORD & achalasia *discussed in 6.3* gastroparesis - characterised by delayed gastric emptying that is not associated with mechanical obstruction - risk factors – poor glycemic control (e.g. sustained hyperglycemia) & obesity - damage to: vagus nerve (major nerve supply to the stomach) nerves within the stomach wall interstitial cells of Cajal (pacemaker cells) muscle layer of stomach - pathophysiology sustained hypertension → neuronal damage → impaired neural control of gastric function (e.g. interstitial cells of Cajal dysfunction, abnormal myenteric neurotransmission, smooth muscle dysfunction) → ↓ antral contractions, pyloric spasms & abnormal antroduodenal contractions → delayed gastric emptying constipation - infrequent or difficult bowel movements - normal transit constipation symptoms of constipation despite normal colonic transit time - slow transit constipation constipation with slow colonic transit time pathophysiology impaired response to meals & colonic stimulants ↓ function or number of ICCs - dyssynergic defecation (pelvic floor dyssynergia) difficulty evacuating stool once it reaches the rectum pathophysiology puborectalis muscle & external anal sphincter fail to relax → narrowed anorectal angle & ↑ pressure of anal canal → evacuation of faeces is less effective - causes sphincter damage or dysfunction – obstetric, surgery, diabetes, SCI, systemic sclerosis ↓ rectal compliance – prostate radiotherapy ↓ rectal sensation – diabetes, SCI altered stool consistency external factors (e.g. lack of exercise, inadequate fluid & fibre intake) – primary constipation internal factors (e.g. changes to colon or rectum) – secondary constipation - pathophysiology altered stool consistency → slow passage of stool → prolonged absorption of water by the bowel → dry, hard stool → painful defecation → sensation of incomplete & irregular bowel emptying → constipation ineffective peristalsis → difficult passage of stool regardless of stool consistency → sensation of incomplete & irregular bowel emptying ecognise the signs & symptoms of common &/or important motility disorders of the gastrointestinal tract. R GORD & achalasia *discussed in 6.3* gastroparesis - common symptoms nausea &/or vomiting bloating upper abdominal pain loss of appetite early satiety - examination findings: abdominal distension epigastric tenderness succussion splash splashing sound created by the movement of gastric contents occurs immediately after a meal if present after ≥ 3 hours of fasting, suggests gastric outlet obstruction constipation - inability to defecate for days or weeks - distended, tympanitic abdomen (produced a drum-like sound upon percussion) – indicating presence of gas - tenesmus – distressing & persistent but ineffectual urge to empty to rectum or bladder - digital rectal exam – hard, impacted stools distending the rectum xplain the basis & rationale for motility disorder investigations, including nuclear medicine transit studies and E manometry. measuring gut motility - pressure – manometry anorectal manometry resting & squeeze pressures (internal & external anal sphincter) rectal sensation response to rectal distension - wall movements – ultrasound, MRI - flow of contents – barium, scintigraphy(measuresgastric emptying) nuclear medicine transit studies 1) gastric emptying study - measures the time it takes for food to leave the stomach & enter the small intestine - commonly used to diagnose gastroparesis the patient consumes a meal containing a small amount of radiotracer sequential imaging captures the movement of the meal through the stomach over several hoursdelayed emptying suggests gastroparesis or other gastric motility disorders 2) small bowel & colonic transit study - assess the time it takes for material to move through the small intestine and colon. - help diagnose conditions such as small bowel dysmotility or slow-transit constipation - procedure after ingesting a meal or capsule containing radiotracers, images are taken at specific intervals to track the movement of contents through the intestines delays in transit times can indicate motility disorders specific to the small bowel or colon. manometry 1) high-resolution esophageal manometry (HRM) - indications – normal upper endoscopy & barium swallow in a patient with dysphagia - gold standard for diagnosing esophageal motility disorders - often used to diagnose conditions such as achalasia, diffuse esophageal spasm & GORD - procedure a thin, pressure-sensitive tube is passed through the nose & into the oesophagus the patient is asked to swallow & the device measures the pressure generated by muscle contractions & the relaxation of the LES 2) antroduodenal manometry - evaluates motility in the stomach & upper part of the small intestine - used to assess condition such as gastroparesis & intestinal pseudo-obstruction - procedure a catheter is placed through the nose into the stomach & small intestine the pressures generated by peristaltic contractions are recorded over several hours, especially after meals, to assess how effectively the stomach & small intestine move contents 3) anorectal manometry - used to measure the pressures & function of the rectum & anal sphincter muscles - helps evaluate the function of these muscles & the nerves controlling them, which is essential for maintaining continence & coordinating defecation endoanal ultrasound - particularly useful in assessing the anal sphincter muscles - commonly used to evaluate patients with faecal incontinence, particularly to detect defects or damage to the internal or external anal sphincters - measures: resting pressure the tone of the internal anal sphincter squeeze pressure the strength of the external anal sphincter during voluntary contraction rectoanal Inhibitory Reflex (RAIR) checks the reflexive relaxation of the internal anal sphincter in response to rectal distention sensation & compliance assesses rectal sensation & compliance(how the rectumstretches in response to pressure) scintigraphy - gastric emptying scintigraphy to evaluate the rate at which food leaves the stomach & enters the small intestine gold standard test for diagnosing gastroparesis - colon transit scintigraphy to assess colonic transit time in patients with chronic constipation, helping to differentiate between slow-transit constipation & normal-transit constipation - esophageal transit scintigraphy to evaluate the function of the oesophagus in conditions such as achalasia & esophageal motility disorders utline the non-surgical & surgical treatments of motility disorders. O GORD & achalasia *discussed in 6.3* gastroparesis - non-pharmacological initiate dietary modifications high-calorie liquids can be included to achieve nutrient intake carbonated drinks should be avoided, as they can worsen symptoms if possible, prescribe alternatives for patients taking medications associated with delayed gastric emptying (e.g. GLP-1 agonists, anticholinergics, opioids, tricyclics, pramlintide) - pharmacological prokinetics used to improve symptoms & gastric emptying 1st-line – metoclopramide alternatives – motilin agonists (e.g. erythromycin, azithromycin), 5-HT4 agonists (e.g. prucalopride) antiemetics improve symptoms (nausea, vomiting) but does not improve gastric emptying e.g. 5-HT3 antagonists (e.g. ondansetron), NK1 receptors antagonists (e.g. aprepitant) constipation - 1st-line (non-pharmacological measures) high-fibre diet ↑ fluid intake exercise use a step stool while on the toilet to raise the legs & straighten the colon - 2nd-line begin with osmotic laxative (e.g. polyethylene glycol, lactulose) if symptoms persist, add a short course of a stimulant laxative (e.g. bisacodyl, sodium, picosulfate) .7 Obstruction of the gastrointestinal tract 6 Understand the pathology & pathophysiology (local & systemic) of bowel obstruction, including of ischaemia & infection. - a bowel obstruction can be mechanical or functional mechanical bowel obstruction interruption of normal passage through the bowel due to a structural barrier (e.g. adhesions, tumour, hernias) functional (paralytic ileus) temporary functional impairment of peristalsis in the absence of a mechanical obstruction causes of mechanical small bowel obstruction - within the lumen intussusception(where a part of the intestine telescopesinto an adjacent segment, causing a blockage) gallstone (‘gallstone ileus’) foreign body bezoars(undigested material that can accumulate inthe digestive tract) - within the intestinal wall tumour (primary or secondary)– 2nd most common cause stricture (IBD, ischaemia) haematoma - outside the bowel adhesions– 1st most common cause hernia– 3rd most common cause volvulus –loop of intestine twists around itself& the mesentery (tissue that attaches intestine to abdominal wall) causes of large bowel obstruction - within the lumen foreign bodies impacted stool - relating to the wall colorectal cancer diverticular disease volvulus (sigmoid, caecum) stricture –, ischemia, IBD, TB Hirschsprung’s disease - external to the wall hernia adhesions (less common than for SBO) pathophysiology - bowel obstruction →stasis of luminal contents & gasproximal to the obstruction → ↑ intraluminal pressure, which leads to: gaseous abdominal distention → sequestration of fluids within the distended bowel loops(third spacing)→ dehydration & hypovolemia vomiting → loss of fluid & Na+, K+, H+ & Cl- → hypokalemia, metabolic alkalosis & hypovolemia compression of intestinal veins & lymphatics → bowel wall edema → compression of intestinal arterioles & capillaries → bowel ischemia, which leads to: ↑ bowel wall permeability → translocation of intestinal microbes to the peritoneal cavity → sepsis necrosis & perforation of the bowel wall → peritonitis anaerobic metabolism & lysis of ischemic cells → accumulation of lactic acid & release of intracellular K+ → metabolic acidosis & hyperkalemia - third-spacing – abnormal accumulation of fluid in spaces where it is not normally present or is minimal - sepsis – bacteria from the intestines escape into the surrounding abdominal cavity (peritoneum) → severe infection (sepsis) - peritonitis – inflammation of the abdominal lining caused by spilling of intestinal contents into abdomen from perforation - when cells don’t get enough O2, they switch to anaerobic metabolism → produces lactic acid - death of ischemic cells releases K+ into the bloodstream → hyperkalemia Outline the signs, symptoms, investigations, and management of small bowel obstructions. - small bowel obstruction – obstruction at the level of the duodenum, jejunum or ileum - 1 of the most common surgical emergencies clinical signs associated with bowel obstruction clinical feature small bowel obstruction large bowel obstruction onset more rapid onset, with symptoms developing often has a more gradual onset within hours to days symptoms often presents more acutely with symptoms long-standing symptoms such as abdominal such as nausea, vomiting, cramping abdominal bloating, intermittent cramping & gradual ↓ in pain, inability to pass gas or stool bowel movements are more common abdominal pain cramp, colicky, periumbilical colicky or constant(pain may be gradually progressive or acute & severe) - less pain as compared to SBO vomiting &/or nausea early onset slow, late onset larger volume of vomitus than in LBO initially bilious bilious progresses to faecal vomiting vomiting of bile presence of faeces in vomitus characterised by the presence of a bitter-tasting greenish-yellow fluid in the - less vomiting as compared to SBO vomit constipation or obstipation late onset in proximal SBO early onset in distal LBO abdominal distention typically less severe than in LBO early & significant abdominal distention examination findings dehydration & possible hypovolemia (hypotension, dry mucous membranes) diffuse abdominal tenderness tympanic percussion(due to gaseous distention ofthe bowel) ↑ high-pitched bowel sounds (early) or the absence of any bowel sounds (late) collapsed, empty rectum on digital rectal exam(completebowel obstruction)or impacted faeces - obstipation(complete inability to pass stool or gas)indicates complete bowel obstruction investigations - laboratory studies routine studies – CBC, BMP, serum lactate, CRP findings: in patients with recurrent vomiting ➔ hypochloremic hypokalemic metabolic alkalosis metabolic alkalosis characterised by low levels of Cl- & K+ in the blood, with ↑ blood pH due to ↑ bicarbonate ➔ hyponatremia bowel ischaemia ➔ leukocytosis, hyperkalemia, ↑ serum lactate & metabolic acidosis (ischaemia → metabolic acidosis) - initial imaging modality stable patients – CT abdomen & pelvis with IV contrast(gold standard) unstable patients – abdominal series x-ray or abdominal ultrasound, along with urgent surgical consultation abdominal ultrasound may be preferred over abdominal x-ray management - ABCDE approach - initial management IV fluid resuscitation electrolyte repletion as needed insert a nasogastric tube in patients with recurrent vomiting &/or significant abdominal distention parenteral analgesia (e.g. NSAIDs, opioids) – given through IV - treatment interventional management surgery – for complicated bowel obstruction (e.g. signs of ischaemia, perforation, clinical deterioration) if bowel obstruction is caused by faecal impaction → stool evacuation non-operative management bowel rest (NPO) –term used to indicate that nothing (e.g. medications, food) should be taken by mouth Outline the signs, symptoms, investigations, and management of large bowel obstructions. - large bowel obstruction – obstruction at the level of the cecum, colon or rectum - *signs & symptoms discussed in previous LO* investigations - blood tests – CBC, BMP, serum lactate, CRP - radiology x-ray CT - sigmoidoscopy/colonoscopy sigmoidoscopy – allows doctor to examine the inside of the colon & rectum difference between sigmoidoscopy & colonoscopy sigmoidoscopy – examines only the lower part of the colon, specifically the rectum & sigmoid colon colonoscopy – examines the entire colon management - ABCDE approach - initial management IV fluid resuscitation electrolyte repletion as needed insert a nasogastric tube in patients with recurrent vomiting &/or significant abdominal distention parenteral analgesia (e.g. NSAIDs, opioids) – given through IV - treatment laparotomy involves a large incision through the abdominal wall to gain access to the abdominal cavity able to directly visualise & address the cause of the obstruction resection of the pathology to remove the obstructing lesions (e.g. tumour, volvulus, diverticula) temporary stoma in acute setting where it may not be able to rejoin the bowel, temporary stoma is needed - functional LBO can be resolved with decompression colonoscopy or regular enemas decompression colonoscopy ➔ used to relieve pressure & ↓ distension in the colon ➔ often in cases of Ogilvie’s syndrome regular enemas ➔ involve introducing liquid into the rectum & lower colon to stimulate bowel movements & relieve constipation - colectomy involves removing a portion or all of the colon partial colectomy (hemicolectomy) – left & right hemicolectomy subtotal colectomy total colectomy – removing the entire colon proctocolectomy – removing the entire colon & rectum - colostomy involves bringing 1 end of the colon out through an opening (stoma) in the abdominal wall the stoma allows stool to exit the body into a colostomy bag, bypassing the rectum & anus cardinal signs of mechanical bowel obstruction regardless of the underlying aetiology - abdominal pain - vomiting - constipation - abdominal distention - ↓ bowel sounds post-operative ileus (common complication following abdominal surgery) - characterised by a temporary cessation of normal bowel movement - results in the bowel’s inability to properly contract & move contents through the GIT - exacerbated by medications (e.g. opiates) or metabolic disturbances (e.g. hypokalemia) acute colonic pseudo-obstruction (Ogilvie’s syndrome) - characterised by acute dilation of the colon without any physical obstruction - differentiate from toxic megacolon a condition associated with severe colitis, often due to infections such as Clostridium difficile or IBD characterised by inflamed, distended colon unlike toxic megacolon, Ogilvie’s syndrome is not caused by an inflammatory process but rather by a functional impairment of colonic motility chronic intestinal pseudo-obstruction - characterised by persistent dilation of the small &/or large intestine without any mechanical obstruction - results from a functional impairment in bowel motility due to underlying neuropathic, myopathic or other systemic causes - types: neuropathic – e.g. abnormalities in the END, damage to enteric nerves myopathic – e.g. smooth muscle dysfunction ICC loss or dysfunction - associated with CT disorders (e.g. SLE, scleroderma), neurologic disorders (e.g. diabetes, PD), paraneoplastic, mitochondrial disorders red flags in acute or persistent diarrhoea - symptoms of inflammatory diarrhoea (dysentery) systemic symptoms (e.g. fever,hypotension severe dehydration bloody stools severe abdominal pain - patient characteristics that suggest ↑ risk of severe disease chronic illness or immunocompromise age > 65yo recent antibiotic use - >48 hours duration without improvement red flags in chronic diarrhoea - hypoalbuminemia - bloody stools - symptoms wake the patient from sleep - unintended weight loss - family history of GI cancer - symptom onset after 50 years of age diagnostic for diarrhoea - acute diarrhoea testing is not required in the majority of cases indications for testing include the presence of red flags in diarrhoea & risk factors for specific aetiologies - persistent diarrhoea testing is usually limited to stool studies for infectious gastroenteritis - chronic diarrhoea testing is initially broad with advanced follow-up testing as indicated repeat stool testing for infectious gastroenteritis .8 Imaging the abdomen 6 *refer to abdomen imaging document*
