GI Flashcards
GORD (Gastro-Oesophageal Disease) definition
• Abnormal reflux of gastric contents which causes mucosal damage, troublesome symtpoms and/or complications
how common is GORD (Gastro-Oesophageal Disease)
• 10-20% in the West with around ≈5% of adults affected
risk factors of GORD (Gastro-Oesophageal Disease) can be split into what
lifestyle and medical
lifestyle risk factors of GORD (Gastro-Oesophageal Disease)
- Obesity (esp abdominal) (raised intra-abdominal pressure)
- Smoking (faulty oesophageal sphincter)
- Alcohol
- Coffee
- Fatty food (faulty oesophageal sphincter – delay gastric emptying)
- Big meals (raised intra-abdominal pressure)
- Tight clothes (raised intra-abdominal pressure)
- Stress
medical risk factors of GORD (Gastro-Oesophageal Disease)
- Hiatus hernia
- Lower oesophageal sphincter hypotension
- Loss of oesophageal persitaltic function
- Gastric acid hypersecretion
- Dealyed gastric emptying
- Systemic sclerosis
- Pregnancy (raised intra-abdominal pressure, hormonal smooth muscle relaxation)
- Surgery for achalasia (failure of lower oesophageal sphincter to relax due to degeneration of the myenteric plexus)
- Pyloric stenosis (increased gastric contents volume – projectile vomiting)
- Drugs (tri-cyclic anti-depressants, anticholinergics, nitrates, alendronate, calcium-chanelle blockers, theophylline, benzodiazepenes)
normal physiology of GORD (Gastro-Oesophageal Disease)
- Some GOR is normal
- Lower oesophageal sphincter is tonically contracted and relaxes only to allow food to pass
- Intra-abdominal segment of oesophagus acts like a flap valve
- Mucosal rosette formed by folds of gastric mucosa and contraction of diaphragm
- Rapid clearance of oesophagus by 2° peristalsis, gravity and bicarbonate
symptoms / signs of GORD (Gastro-Oesophageal Disease)
- ‘Heartburn’ aka dyspepsia – burning; retrosternal; aggravated by bending, stooping or lying down (therefore worse at night) which ↑ acid exposure
- Regurgitation of food into the mouth - especially on lying flat or bending
- Belching, nausea and vomiting, abdominal/non-cardiac chest pain, globus sensation
- Related to meals, pain on drinking alcohol or hot liquids
- Relieved by antacids
- Waterbrash (excess salivation) and acid brash (acid or bile regurgitation)
- Odynophagia (pain on swallowing due to ? oesophagitis or ulceration)
- Extra-oesophageal symptoms: nocturnal asthma, chronic cough, laryngitis, sinusitis – due to aspiration of refluxed stomach contents
DDx of GORD (Gastro-Oesophageal Disease)
- Oesophagitis (corrosives, NSAIDs)
- Infection (CMV, herpes, Candida)
- Duodenal ulcer
- Gastric ulcers or cancers
- Non-ulcer dyspepsia
- Heart pain (crushing, gripping, radiates to left arm, worse with exercise, dyspnoea)
Investigations of GORD (Gastro-Oesophageal Disease)
• 1st LINE:
- PPI TRIAL: further tests are indicated if symptoms do not improve with therapeutic 8-week trial of a PPI or if patient has alarm symptoms
• RED FLAGS: upper abdo mass, dysphagia and aged over 55 with weight loss
• IF RED FLAGS PRESENT – DO THE FOLLOWING:
- Endoscopy and pH monitoring
• CONSIDER: oesophagogastroduodenoscopy (OGD), ambulatory pH monitoring, oesophageal manometry, barium swallow, oesophageal capsule endoscopy
Management of GORD (Gastro-Oesophageal Disease)
• ACUTE:
- 1st LINE: standard-dose PPI e.g. omeprazole 20mg orally once daily
- PLUS: lifestyle changes, weight loss, head of bed elevation, avoidance of late night eating
• ONGOING:
- 1ST LINE: continued standard-dose PPI
- 2nd LINE: surgery – reserved for those who have a good response to PPIs but do not wish to take long-term medical treatment
• INCOMPLETE RESPONSE TO PPI:
- 1ST LINE: high-dose PPI + futher testing – dosing is twice daily, before breakfast and dinner
- WITH NOCTURNAL COMPONENT: add a H2-anatognist
Complications of GORD (Gastro-Oesophageal Disease)
- Oesophageal ulcer, haemorrhage or perforation
- Oesophageal stricture
- Barrett’s oesophagus
- Adenocarcinoma of the oesophagus
Peptic Ulcer Disease (PUD) and Dyspepsia definition
- Peptic Ulcer = distinct breach in the mucosal lining of either the stomach (gastric ulcer) or duodenum (duodenal ukcer)
- Gastric ulcers commonly occur on the lesser curvature of the stomach elsewhere it is more likely to be malignancy
- Duodenal ulcers are most common on the duodenal cap/ampulla (first part of the duodenum) - where acidic chime from the stomach meets the mucosa before it has an opportunity to mix with the alkaline secretions of the SI
• Functional/Non-Ulcer Dyspepsia (Indigestion) = pain or discomfort in the upper abdomen with symptoms of reflux
how common is Peptic Ulcer Disease (PUD) and Dyspepsia
• Duodenal ulcers (DU) affect 10-15% of adults and are 4x more common than gastric ulcers
- Very common in elderly; ↓ rates in young but ↑ in females
- More prevalent in developing countries due to high H. pylori infection rates
- Can be present with damage via NSAIDs/ Zollinger-Ellison syndrome
biological causes for Peptic Ulcer Disease (PUD) and Dyspepsia
H. PYLORI:
• H. Pylori infection is the main cause of gastric ulcers (80%) and duodenal ulcers (95%)
• Causes inflammation of the mucosal lining of the stomach, depleting the layer of alkaline mucus and altering gastric acidity
• If H. Pylori is limited ot the upper part of the stomach, gastric acid secretion increases
• MECHANISM:
- H. Pylori impairs the function of cells which produce somatostatin, which normally limits the secretion of gastric acid by parietal cells
- This increases the risk of duodenal ulceration – but when H. Pylori in all parts of the stomach then gastric acid secretion decreases
risk factors for Peptic Ulcer Disease (PUD) and Dyspepsia
NSAIDs:
• Cause 20% of gastric ulcers and 5% duodenal ulcers
• Aspirin and NSAIDs inhibit prostaglandin synthesis, reducing the production of protective alkaline mucus and thereby increasing the risk of ulceration, particularly in the stomach
PATHOLOGY:
• Peptic ulcers are due to a break in the superficial epithelial cells penetrating down to the muscularis mucosa
• There’s a fibrous base and inflammatory reaction (erosions are just superficial breaks in the mucosa).
RISK FACTORS:
DUODENAL ULCERS:
• H. pylori, Drugs e.g. NSAIDs, steroids, SSRIs, increased gastric acid secretion, Increased gastric emptying, Blood group O, Smoking
GASTRIC ULCERS:
• H. pylori, Smoking, NSAIDs, Reflux of duodenal contents, delayed gastric emptying, stress
symptoms of Peptic Ulcer Disease (PUD) and Dyspepsia
- Often asymptomatic – more commonly associated with bleeding; common in Taiwan
- Burning epigastric pain – relieved by eating/worse with hunger/at night in duodenal ulcers – due to un-neutralised acid from stomach in duodenum
- Epigastric pain – worse after meals in gastric ulcers – due to pressure of food on stomach wall
- Pain worse with specific foods
- Nausea, bloating, fullness after meals, reflux symptoms
- Back pain – suggest penetrating posterior ulcer
ALARM SYMPTOMS – if dyspepsia + >55y or ALARM Sx then send for endoscopy
• Anaemia – suggests bleeding
• Loss of weight – suggests malignancy
• Anorexia – suggests malignancy
• Recent onset/progressive symptoms
• Malaena/haematemesis – suggests bleeding
• Swallowing difficulty – suggests malignancy
signs of Peptic Ulcer Disease (PUD) and Dyspepsia
• Tender Epigastrium
DDx of Peptic Ulcer Disease (PUD) and Dyspepsia
- Gastritis
- GORD – reflux Sx without pain
- Gastric malignancy – red flag Sx; epigastric mass
- Pancreatitis
- Cholecystitis/gallstones – right upper quadrant pain; Murphy’s sign; radiates to shoulder
- Hepatitis – right upper quadrant pain; no reflux Sx
- IBD – diorrhoea; unassociated with food
- IBS – diorrhoea/constipation; generalised abdominal pain; associated with specific foods
- AAA – pulsatile abdominal mass
- MI – central crushing chest pain; limb/jaw weakness; acute
Investigations of Peptic Ulcer Disease (PUD) and Dyspepsia
• 1st LINE:
- H. pylori urea breath test or stool antigen test – ordered in pts aged <55 even in the presence of alarm symptoms, PPI will interfere with this test so stop 2 wks prior
- Upper GI endoscopy – ordered in pts with dyspeptic symptoms is aged >60 (>55 with associated weight loss), stop PPI 2 wks prior
- FBC – ordered only if pt seems clinically anaemic or has evidence of GI bleeding
• CONSIDER:
- Fasting serum gastrin level – ordered if there are multiple duodenal ulcers (especiall postbulbar) or in pts with ulcers and diarrhoea, patient must fast and PPI stopped
management of Peptic Ulcer Disease (PUD) and Dyspepsia
• If on NSAID – STOP or STOP FOR AS LONG AS POSSIBLE to let the ulcer heal and then reduce the dose
• ACUTE:
- ACTIVE BLEEDING ULCER: 1st LINE - endoscopy +/- blood transfusion, + PPI, 2nd LINE: surgery or embolization via interventional radiology
- NO ACTIVE BLEEDING – H. PLYORI –ve: 1st LINE – treat underlying cause and give PPI, 2nd LINE: H2 antagonist
- NO ACTIVE BLEEDING – H. PYLORI +ve: 1st LINE – H. pylori eradication therapy, 2nd LINE: alternative regimen, 3rd LINE: acid suppression therapy
• ONGOING:
- FREQUENT RECURRENCES, LARGE OR REFRACTORY ULCERS: 1st LINE - acid suppression therapy – GIVE PPI
prognosis of Peptic Ulcer Disease (PUD) and Dyspepsia
- Excellent if underlying cause is treated.
* Recurrence rate post H. pylori eradication is 10-20%.
complications of Peptic Ulcer Disease (PUD) and Dyspepsia
- Haemorrhage – acute upper GI bleed
- Perforation of peptic ulcer – surgery required ↓ frequency; DUs perforate > GUs, usually into peritoneal cavity
- Malignancy - distal gastric adenocarcinoma is H pylori associated; also, 70% of pts with gastric B cell lymphoma have H. pylori infection
- Gastric outflow obstruction - obstruction may be prepyloric, pyloric or duodenal; obstruction occurs due to active ulcer with surrounding oedema or because an ulcer has healed and scarred area; main symptom is projectile vomiting large volume
causes of Acute Upper GI Bleed
- Peptic ulceration - commonest cause (50%)
- Oesophageal varices (10-20%)
- Oesophagitis/Gastritis (5-10%)
- Mallory-Weiss syndrome/tear (5-10%) - haematemesis from a tear in the mucosa of the oesophagus, brought on by prolonged vomiting; linear mucosal tear at the oesophagogastric junction and produced by sudden ↑ in intra-abdo pressure: after bout of coughing or retching; most bleeds are minor and stop spontaneously
- Oesophageal/gastric cancer (uncommon)
- Swallowed blood from nosebleed
- Bleeding after Percutaneous Coronary Inetrvention (PCI)
risk factors Acute Upper GI Bleed
- Alcohol abuse
- Chronic liver disease - bleeding associated with liver disease is often from varices
- NSAID use - can produce ulcers and anticoagulation = bigger bleed)
- H. Pylori
- Oral steroid use
- Anticoagulant use
- Evidence of co-morbidity (HF, IHD, renal disease, malignant disease)
symptoms of Acute Upper GI Bleed
- Haematemesis – coffee-ground vomit indicates less severe
- Malaena – offensive, black tarry stool; always indicates a significant bleed
- Fresh red bleeding PR = massive upper GI bleed
- Faintness/dizziness - shock
- Collapse +/- cardiac arrest
- Dark blood and clots w/o shock: lower GI bleed
- Acute massive upper GI bleeding may present with rectal bleeding almost always in association with shock
signs of Acute Upper GI Bleed
- Cold/clammy and sweating – peripherally shut down
- Capillary refill <2 sec – peripherally shut down
- Hypotensive/decreased JVP
- Postural drop
- Sudden tachycardia
- Weak pulse
- Rapid breathing
- Decreased or no urine output
- Signs of shock – confusion or lack of alertness
DDx of Acute Upper GI Bleed
• Lower GI bleed – fresh blood PR
Investigations of Acute Upper GI Bleed
- Upper GI: FBC, LFTs, U&E’s, clotting screen and ‘group and save’
- Both: IV fluids whilst examination and history are undertaken, Rockall risk score – assess risk of rebleeding or death, abdo exam +/- PR, Glasgow-Blatchford bleeding score (GBS) – assess need for intervention e.g. endoscopy, transfusion
Management of Acute Upper GI Bleed
• Determine site of bleeding through history (vomiting preceding the haematemesis suggests Mallory-Weiss tear)
• Establish IV access i.e. cannula (central line if brisk bleed)
• Give IV fluids
• Give blood transfusion/colloid if necessary, indications are:
- SHOCK – cold nose, pallor, systolic BP <100mmHg, >100 b.p.m
- HAEMOGLOBIN - <10g/dL in patients with recent or active bleeding
• Give oxygen
PRE-ENDOSCOPY:
• Stop aspirin, NSAIDs and warfarin and INR reversed
• PPIs given to high risk patients who cannot have an endoscopy immediately
• Abx given to pateitns with suspected variceal haemorrhage
• 85% of bleeding stops on its accord but if not then suggest surgery for thermal therapy
Prognosis of Acute Upper GI Bleed
• Mortality remained same for past years at 5-12% due to ↑ elderly with co-morbidities
how common is Acute Lower GI Bleed
• Massive bleeds are rare and usually due to diverticular disease or ischaemic colitis; small bleeds = haemorrhoids or anal fissures
causes of Acute Lower GI Bleed
- Peptic ulceration - commonest cause (50%)
- Oesophageal varices (10-20%)
- Oesophagitis/Gastritis (5-10%)
- Mallory-Weiss syndrome/tear (5-10%) - haematemesis from a tear in the mucosa of the oesophagus, brought on by prolonged vomiting; linear mucosal tear at the oesophagogastric junction and produced by sudden ↑ in intra-abdo pressure: after bout of coughing or retching; most bleeds are minor and stop spontaneously
- Oesophageal/gastric cancer (uncommon)
- Swallowed blood from nosebleed
- Bleeding after Percutaneous Coronary Inetrvention (PCI)
risk factors of Acute Lower GI Bleed
- Alcohol abuse
- Chronic liver disease - bleeding associated with liver disease is often from varices
- NSAID use - can produce ulcers and anticoagulation = bigger bleed)
- H. Pylori
- Oral steroid use
- Anticoagulant use
- Evidence of co-morbidity (HF, IHD, renal disease, malignant disease)
symptoms of Acute Lower GI Bleed
- Fresh blood PR, brisk bleeding – medical emergency
- Mixed blood and stool – bleeding proximal to sigmoid colon
- Blood around stool – more distal bleed
- Blood on toilet paper/in pan – anal bleeding e.g. haemorrhoids/anal fissure
signs of Acute Lower GI Bleed
- Cold/clammy and sweating – peripherally shut down
- Capillary refill <2 sec – peripherally shut down
- Hypotensive/decreased JVP
- Postural drop
- Sudden tachycardia
- Weak pulse
- Rapid breathing
- Decreased or no urine output
- Signs of shock – confusion or lack of alertness
Investigations of Acute Lower GI Bleed
- Lower GI: proctoscopy to look for anorectal disease (e.g. Piles), sigmoidoscopy or colonoscopy for IBD, polyps, colon cancer, diverticula disease, ischaemic colitis, vascular esions, angiography for vascular abnormality (e.g. angiodysplasia)
- If patient is <45 y/o and isolated bleeding, DRE and flexibile sigmioidoscopy only required as probability of a significant proximal lesion is very low unless a strong Fx of CRC at young age
Management of Acute Lower GI Bleed
- Most acute lower GI bleeds start and stop spontaneously
- If they don’t stop and patient is haemodynamically unstable then follow immediate steps as for acute upper GI bleed
- Surgery is rarely required
DDx of Acute Lower GI Bleed
• Upper GI bleed – haematemesis, melaena
Crohn’s Disease (Inflammatory Bowel Disease) definition
- Chronic inflammatory disease characterized by transmural granulomatous inflammation affecting any part of the gut from mouth to anus (especially terminal ileum in approx. 70%)
- Unlike UC, there is unaffected bowel between areas of active disease
how common is Crohn’s Disease (Inflammatory Bowel Disease)
- 10-20/100 000, typically presents 20-40yrs of age
- World-Wide distribution but more in northern Europe, UK and North America
- Increased likelihood in Hispanic, Asians, Jewish races
- Equal distribution between males and females
- Common in smokers
causes of Crohn’s Disease (Inflammatory Bowel Disease)
- Genetic Susceptibility: genetic association is strong in CD, familial aggregation of the disease, concordance rates are higher in monozygotic (58%) than dizygotic (4%), CARD15(NOD2) gene on chromosome 16 confer susceptibility
- Environment: smoking is associated with a two-fold increased risk, stress and depression may precipitate relapses in IBD, altered enteric microflora, appendicectomy may result in more aggressive, NSAIDs, oral contraception
- Host Immune Response: IBD results from a defective mucosal immune system producing an abnormal response to luminal antigens such as bacteria which enter the intestine via a leaky epithelium, E. coli, more anaerobic bacteria, disrupted toll like receptor signalling
risk factors Crohn’s Disease (Inflammatory Bowel Disease)
Genes, Smoking Stress Depression Appendectomy NSAIDs Oral Contraceptives Fx
pathology of Crohn’s Disease (Inflammatory Bowel Disease)
- Affects: all GI tract – especially terminal ileum and ascending colon, rectum involved in 50% of cases, lesions are patchy (unaffected areas between areas of disease)
- Macroscopic: small bowel thickened, deep ulcers and fissures in mucosa, cobblestone appearance, fistulae and abscesses in colon, aphthoid ulceration is an early features
- Microscopic: granulomas present in 50-60% non-caseating epithelioid cell aggregates with Langhans’ giant cells
- Inflammation: transmural/deep
- Strictures: common
- Crypt Abscesses: uncommon
- Goblet Cells: present
symptoms of Crohn’s Disease (Inflammatory Bowel Disease)
• SYMPTOMS DEPEND ON THE REGIONS OF INVOLVED BOWEL
- Commonest site is ileocecal (40% of patients)
- Small Bowel = pain, weight loss, steatorrhoea
- Terminal Ileal Disease = acute abdomen with right iliac fossa pain mimicking appendicitis (uncommon)
- Colonic Disease = diarrhoea, bleeding and pain related to defecation
- Perianal Disease = anal tags, fissures, fistulae an abscess formation, full thickness of wall is inflamed
- Extra Intestinal Manifestations = iritis, arthritis, erythema nodosum and pyoderma gagrenosum
signs of Crohn’s Disease (Inflammatory Bowel Disease)
- Mouth Ulcers
- Signs of systemic illness – anorexia, fatigue, malaise, fever and clubbing
- Anal or peri-anal skin tag fistula or abscess
- Abdominal pain and tenderness – with tenderness or a mass in lower right quadrant
- Aphthous ulcers
- Joint arthritis
- Conjunctivitis/uveitis
- Pyoderma gangrenosum
- Fatty liver
- Malnutrition
DDx of Crohn’s Disease (Inflammatory Bowel Disease)
- Infective colitis – systemic Sx; following travel/infection risk
- IBS – diagnosis of exclusion; alternating diarrhoea and constipation; related to certain foods
- Coeliac disease – malnutrition; related to certain foods
- Diverticulitis – affects elderly
- Endometriosis
- Intestinal ischaemia
Investigations of Crohn’s Disease (Inflammatory Bowel Disease)
- 1st LINE:
- FBC – thrombocytosis is a useful marker of active inflammation, leucocytosis associated with acute or chronic inflammation, abscess or corticosteroid treatment, anaemia can be due to chronic inflammation
- IRON STUDIES – serum iron, serum ferritin, total iron binding capacity, transferrin saturation
- SERUM VIT B12 AND SERUM FOLATE
- CMP – comprehensive metabolic panel
- CRP AND ESR
- STOOL TESTING
- YERSINIA ENTERCOLITICA SEROLOGY – pathogen which causes an acute ileitis, should be negative in crohns
- ABDO X-RAY, CT ABDO, MRI ABDO/PELVIS
- COLONOSCOPY – shows disease extent, allows for biopsy, first line investigation for diagnosis
• RECTAL BIOPSY – diagnosis usually made from this, can differentitate between UC and CD
management of Crohn’s Disease (Inflammatory Bowel Disease)
- Lifestyle – smoking cessation, nutrition
- Screening – screen for CRC, ensure the risk of osteoporosis is managed
- Pain – manage with analgesics, paracetamol preferred
- Corticosteroids – topical preferred to systemic, only used for induction of remission
- Immunosupressant’s – azathioprine, merceptopurine and methotrexate OR cyto-line modulating drugs such as infliximab and adalimumab
- Treatment is not always needed in mild Crohn’s (18% entered remission with a placebo)
treatment - biological gents of Crohn’s Disease (Inflammatory Bowel Disease)
INDUCTION OF REMISSION:
• Glucocorticoids useful in moderate-severe attacks of CD (oral prednisolone 30-60mg/day)
• Enteral nutrition; efficacy independent of nutritional status; low fat diets best
• Infliximab: anti-TNF-α monoclonal Ab induces remission in corticosteroid/immunosuppressive resistant pts and helps maintain it; infusion reactions may occur via host Ab against infliximab Ab.
MAINTENANCE OF REMISSION:
• Azathioprine, 6-mercaptopurine, methotrexate, mycophenolate mofetil; rate of relapse on discontinuation of drugs is ~70%!
SURGERY:
• ~80% patients will require surgery at some point of their disease but should be avoided if possible as recurrence in 15%/year is inevitable
• Panproctocolectomy and end-ileostomy (remove rectum, colon and attach ileum to skin surface of stomach) may be needed => ileostomy is lifelong and has its own problems
prognosis of Crohn’s Disease (Inflammatory Bowel Disease)
- Prognosis is poorer if steroids required at diagnosis, early presentation, perianal or structuring disease, weight loss >5kg.
- Relapses and remissions are unpredictable and vary. Many will have lots of relapses at beginning.
complications of Crohn’s Disease (Inflammatory Bowel Disease)
- Strictures
- Fistulae
- Perforation
- Haemorrhage
- Colorectal cancer
- Toxic megacolon
- Anaemia – iron or B12/folate
- Osteoporosis- due to steroid therapy
- Renal disease – due to obstruction of right ureter by ileocaecal disease
Ulcerative Colitis (Inflammatory Bowel Disease) definition
- Relapsing and remitting inflammatory disorder of the colonic mucosa
- May affect just the rectum (proctitis, as in around 30%) or extent to involve part of the colon (left sided colitis, in 40%) or the entire colon (pancolitis, in 30%)
- Never spreads proximal to the ileocaecal valve (except for backwash ileitis)
how common is Ulcerative Colitis (Inflammatory Bowel Disease)
- World-Wide distribution but more in northern Europe, UK and North America
- Increased likelihood in Hispanic, Asians, Jewish races
- Equal distribution between males and females
- Common in smokers
causes of Ulcerative Colitis (Inflammatory Bowel Disease)
- Genetic Susceptibility: genetic association is stronger in CD than UC, familial aggregation of the disease
- Environment: smoking halves the risk of UC, stress and depression may precipitate relapses in IBD, altered enteric microflora, appendicectomy may result in more aggressive, NSAIDs, oral contraception
- Host Immune Response: IBD results from a defective mucosal immune system producing an abnormal response to luminal antigens such as bacteria which enter the intestine via a leaky epithelium, E. coli, more anaerobic bacteria, disrupted toll like receptor signalling
risk factors for Ulcerative Colitis (Inflammatory Bowel Disease)
• Genes, Smokng, Stress, Depression, Appendectomy, NSAIDs, Oral Contraceptives and Fx
pathology of Ulcerative Colitis (Inflammatory Bowel Disease)
- Affects: rectum is always involved, colon, appendix, and terminal ileum (in backwash ileitis), continuous rather than patchy
- Macroscopic: mucosa is reddened, inflamed and bleeds easily, ulcers may be present if severe with adjacent mucosa appearing as inflammatory polyps
- Microscopic: mainly mucosal, with inflammatory cells in lamina propria, no granulomas
- Inflammation: superficial
- Strictures: uncommon
- Crypt Abscesses: common
- Goblet Cells: depletion
symptoms of Ulcerative Colitis (Inflammatory Bowel Disease)
- Diarrhoea – often containing blood and mucus, may be persistent, relapses, remissions or severe fulminant colitis
- Faecal Urgency with Nocturnal Defecation
- Tenesmus – persistent, painful urge to pass stool even when rectum is empty
- Abdominal Pain – particularly in the lower left quadrant
- Pre-Defecation Pain – relieved upon passage of stool
signs of Ulcerative Colitis (Inflammatory Bowel Disease)
- Extra-intestinal Manifestations – uveitis, irits, inflammatory arthritis, erythema nodosum, pyoferma gangrenosum, fatty liver, mouth ulcers
- Weight Loss – faltering growth in children, anorexia, malnutrition
- Signs of Systemic Illness – fatigue, malaise, fever and clubbing
DDx of Ulcerative Colitis (Inflammatory Bowel Disease)
- Infective colitis – systemic Sx; following travel/infection risk
- IBS – diagnosis of exclusion; alternating diarrhoea and constipation; related to certain foods
- Coeliac disease – malnutrition; related to certain foods
- Diverticulitis – affects elderly
- Endometriosis
- Intestinal ischaemia
investigations of Ulcerative Colitis (Inflammatory Bowel Disease)
• 1st LINE:
- STOOL STUDIES: faecal calprotectin – elevated when there is bowel inflammation
- FBC: may show leucocytosis, thrombocytosis and anaemia
- CMP – LFTs
- ESR AND CRP
- PLAIN ABDO RADIOGRAPH
- FLEXIBLE SIGMOIDOSCOPY
- COLONOSCOPY – indicated in patients with UC who are not responding well to treatment in order to rule out infections
- BIOPSIES
treatment of of Ulcerative Colitis (Inflammatory Bowel Disease)
DRUGS:
- Aminosalicylate/mesalazine; released in terminal ileum when right pH; mechanism unknown but induce remission in mild-moderate and maintain remission in all forms of disease
- If moderate-severe flare ups in the past 3 years, consider starting azathioprine
SURGERY:
- May be life-saving, curative and eliminates cancer risk; subtotal colectomy with end-ileostomy is common procedure
management of Ulcerative Colitis (Inflammatory Bowel Disease)
- Lifestyle – smoking cessation, nutrition
- Screening – screen for CRC, ensure the risk of osteoporosis is managed
- Pain – manage with analgesics, paracetamol preferred
- Corticosteroids – topical preferred to systemic, only used for induction of remission
- Immunosupressant’s – azathioprine, merceptopurine and methotrexate OR cyto-line modulating drugs such as infliximab and adalimumab
- Treatment is not always needed in mild Crohn’s (18% entered remission with a placebo)
Prognosis and Complications
Prognosis is poorer if steroids required at diagnosis, early presentation, perianal or structuring disease, weight loss >5kg.
• Relapses and remissions are unpredictable and vary. Many will have lots of relapses at beginning.
complications: • Strictures • Fistulae • Perforation • Haemorrhage • Colorectal cancer • Toxic megacolon • Anaemia – iron or B12/folate • Osteoporosis- due to steroid therapy • Renal disease – due to obstruction of right ureter by ileocaecal disease
Irritable Bowel Syndrome (IBS) Definition
• IBS is a functional bowel disorder – means that symptoms occur in the absence of any demonstrable abnormalities in the digestion and absorption of nutrients, fluid and electrolytes and no structural abnormality can be identified in the GI tract
• Denotes a group of abdominal symptoms for which no cause can be found
• It can be classified as:
- IBS-D – diarrhoea predominated
- IBS-C – constipation predominated
- IBS-A – alternating stool pattern
- Pain-predominant IBS
- IBS-PI – post-infective
• Co-exists with chronic fatigue syndrome, fibromyalgia, temporomandibular joint dysfunction
how common is Irritable Bowel Syndrome (IBS)
- Prevalence 10-20%
- Most common functional gastrointestinal disorder (FGID)
- Up to 1 in 5 patientss report symptoms suggestive of IBS – only 50% of which will consult doctors and up to 30% of these will be referred to hospital
who does Irritable Bowel Syndrome (IBS) affect
- 20-30 years of age most common
- Twice a scommon in F vs M due to higher anxiety and depression in women - gut more sensitive; women more focussed on internal events; food and eating have more psychological significance; pelvic region carries more significance (defecation, urination, sexuality AND pregnancy, childbirth, menstruation); women more likely to seek medical attention anyway.
biological causes of Irritable Bowel Syndrome (IBS)
• The cause is unknown but it is thought to be due to biopsychosocial interactions that may interact to cause dysregulation of brain-gut function
risk factors of Irritable Bowel Syndrome (IBS)
- Affective disorders: depression, (hypochondrial) anxiety
- Psychological stress and trauma, life events
- GI infection
- Ax therapy
- Sexual, physical, verbal abuse
- Pelvic surgery
- Eating disorders
- Female!
- Severity and duration of diarrhoea
symptoms of Irritable Bowel Syndrome (IBS)
• Abdominal Pain – described as crampy, relieved by defecation or the passage of wind
• Altered Bowel Habit – sensation of incomplete evacuation (tenesmus), abdominal bloating and distention are common symptoms
• Morning Rush – urgent need to defecate in the morning and several times through breakfast
• Subtypes can be identified corrding to the predominant stool pattern
- IBS-D – diarrhoea predominated
- IBS-C – constipation predominated
- IBS-A – alternating stool pattern
- Pain-predominant IBS
- IBS-PI – post-infective
• Psychological Problems - anxiety, depression
• Extra-intestinal Symptoms - headache, asthma, backache, lethargy, dyspareunia, urinary frequency and urgency, dysmenorrhoea
• Signs may be few and non-specific e.g. tenderness
symptoms / signs of Irritable Bowel Syndrome (IBS)
- IBD – no constipation; aphthous ulcers; blood/mucous in stools
- Coeliac disease
- Gastroenteritis – acute; no constipation; could be infective trigger for IBS
- Colorectal carcinoma – older presentation; red flag symptoms
Investigations of Irritable Bowel Syndrome (IBS)
• No investigations to confirm – rectal biopsy shpuld be taken (if frequency of defecation is a feature) to exclude IBD
• 1st LINE:
- FBC – if anaemic or FBC count is raised, other diagnoses should be considered
- STOOL STUDIES – performed if the patient has diarrhoea
- ANTI-ENDOMYSIAL ANTIBODIES – may be ordered if the patient has a diarrhoea component and/or weight loss and coeliac disease is suspected
- ANTI-tTG Abs – may be ordered if the patient has a diarrhoea component and/or weight loss
- PLAIN ABDO X-RAY
- FLEXIBLE SIGMOIDOSCOPY
- COLONOSCOPY – should be performed if the patient is >50 years or has a FX of a firstdegree relative with a colon neoplasm <60yrs but is not nexessary in younger pts
• Manning and Rome II criteria to help establish a diagnosis
management of Irritable Bowel Syndrome (IBS)
Referral:
• If diagnosis unsure
• If changing symptoms in ‘known IBS’
• To surgeon if rectal mucosal prolapse
• To dietician if food intolerance
• To psycho/hypno-therapist if stress of depression or refactory symptoms
• To gynaecologist If cyclical pain, dyspareuinia, dysmennorhoea as endometriosis can mimic IBS
• To dermatologist if co-existing atopy
• To pain clinic if chronic pain overlap syndromes (fibromyalgia, chronic fatigue, chronic pelvic pain)
treatment - biological
Irritable Bowel Syndrome (IBS)
NUTRITION:
• Explore dietary triggers
• High fibre diet and fibre supplements for constipation – refer to dietician and prescribe ISPAGHULA HUSK
DRUGS:
• Antidiarrhoeal drugs for bowel frequency – loperamide, codeine, co-phenotrope
• Smooth muscle relaxants for pain - mebeverine hydrochloride, dicycloverine hydrochloride, peppermint oil
• Antidepressants - clomipramine in functional diarrhoea, TCAs (amitriptyline) in IBS-D, SSRIs (paroxetine) in IBS-C
prognosis of Irritable Bowel Syndrome (IBS)
- In 50% Sx go or improve after 1 year.
- More than 50% will continue to have Sx after 5 years.
- <5% worsen.
Infective gastroenteritis
- Infection of the stomach and intestinal tract that involves some sort of combination of diarrhoea, vomiting and abdominal pain and cramping
- It is also referred to as infectious diarrhoea, gastro, stomach bug and stomach virus
how common is infective gastroenteritis
- Most common form of acute GI infection, causing diarrhoea +/- vomiting
- Especially in developing world; 2.25 million still die/year despite oral rehydration programmes
- Less common and less likely to cause death in Western world
- Major cause of morbidity in elderly though
- Travellers to developing countries, homosexual men, infants in day care facilities are also at risk
causes of infective gastroenteritis
- Viral - common cause of D+V in young children; rarely seen in adults unless an outbreak in hospital; norovirus is the most common
- Bacterial - most common cause of significant adult gastroenteritis; can cause watery diarrhoea or dysentery (severe and mixed with blood and mucous)
- Parasitic – protozoa; most commonly giardia lamblia; also entamoeba histolytica cryptosporidium
MECHANISMS – cannot distinguish bacterial/viral based on clinical evidence alone
- Mucosal Adherence – most bacteria must adhere to specific receptors in the gut mucosa e.g. pili, fimbriae, may be the prelde to invasion or toxin production though EPEC causes diarrhoea just by binding
- Mucosal Invasion – penetration of intestinal mucosa e.g. shigella, EIEC, campylobacter, entrty helped by ‘invasins’ which disrupt the cell’s cytoskeleton, destruction of cells causes the symptoms of dysentery: low volume bloody diarrhoea and abdominal pain
- Toxin Production – enterotoxins: bacteria bind to intestinal epithelium, induce excessive fluid secretion into bowel lumen causing watery diarrhoea w/o damage to cell (so no blood) e.g. cholera, ETEC, cytotoxins: damage intestinal mucosa and vascular endothelium sometimes too
TYPES OF BACTERIAL/VIRAL INFECTION CAUSES:
- Salmonella: commensals in bowels of livestock (esp poultry) and in oviducts of chickens (which is why eggs can be infected); produce enterotoxins and invade mucosa
- Campylobacter (jejuni): bowel commensal of livestock; worldwide; childhood gastroenteritis; undercooked meat
- Shigella: (S. dysenteriae, S sonnei, S flexneri); spread by poor hygiene
- ETEC: enterotoxins; common in developing countries so cause of travellers’ diarrhoea
- EHEC (usually O157: H7 serotype): also known as verotoxin producing E coli (VTEC); associated with cattle; outbreaks (Scotland, Japan) associated with contaminated food; secretes Shiga-like toxin 1 affecting vascular endothelial cells in gut and kidney; after some days pts may develop thrombotic thrombocytopenic prupura or haemolytic uraemic syndrome; treatment is supportive
- Bacillus cereus: 2 toxins; one produces watery diarrhoea, the other is preformed in food and causes severe vomiting (‘fried rice poisoning’)
- Staph A: some strains produce heat stable (enterotoxin B); due to poor food hygiene; as toxin is preformed in contaminated food onset of symptoms is rapid
- C diff: causes Abx-associated diarrhoea, colitis and pseudomembranous colitis; G+ve, anaerobic, spore-forming bacillus; found in normal bowel flora of 3-5% of pop and up to 20% of hospital pts; produces 2 toxins: toxin A (enterotoxin), toxin B (cytotoxic = bloody diarrhoea); all Abx but esp with quinolones (ciprofloxacin); begin with 2-30 days of starting Abx; symptoms mild diarrhoea to watery haemorrhagic colitis and abdo pain; colonic mucosa inflamed and ulcerated and can be covered by an adherent membrane-like material (psurodmembranous colitis); can lead to death; detect toxins A or B in stools by ELISA; metronidazole 400mg TDS or vancomycin 125mg QDS; isolation of pts!, need CT/X-ray to exclude toxic megacolon
risk factors for infective gastroenteritis
- Poor personal hygiene
- Lack of sanitation
- Immunocompromisation
- Achlorydhia (when acid production in stomach is absent or low)
- Increased age or very young
- Poorly/un-cooked food
- Food left at room temperature for too long
- Insufficient reheating of food – even if reheating kills all bacteria enterotoxins are not destroyed
symptoms/ signs of infective gastroenteritis
- Diarrhoea – watery or mixed with blood/mucous (dysentery) – blood means more likely bacterial
- Vomiting
- Abdominal pain/cramps
- Fever – usually viral infections
- Fatigue – usually viral infections
- Headache – usually viral infections
- Muscle pain – usually viral infections
signs
• Usually none apart from maybe abdo tenderness or pyrexia.
DDx of infective gastroenteritis
- IBD – chronic; aphthous ulcers; no vomiting
- IBS – chronic; no vomiting; constipation
- Coeliac disease – chronic; no vomiting
- Colorectal cancer – elderly; red flag Sx
- UTI – urinary Sx
- Chest infections in elderly – resp Sx
- Malaria
Investigations for infective gastroenteritis
e.g. to confirm diagnosis, exclude physical causes etc
• 1st LINE:
- STOOL CULTURE: positive for causative bacteria
- STOOL MICROSCOPY: presence of RBCs and neutrophils
management of infective gastroenteritis
• 1ST LINE: Adequate hydration
- ADJUNCT: antimotolity agents such as loperamide other than those with bloody diarrhoea or fever
• Antibiotic therapy is not usually given as the illness is self-limiting
- Abx are actively avoided in patients with suspected ENTEROHAEMORRHAGIC E.COLI INFECTION
- Only given in immunocompromised, pregnant women and those with symptoms lasting over a week
- May increase the risk of HUS (haemolytic uraemic syndrome)
• Empirical Abx therapy = ciprofloxacin and metronidazole given to patients with severe symptoms or bloody diarrhoea, pending the results of the stool sample
treatment of infective gastroenteritis
- Oral rehydration solutions (ORS)
- Abx if systemically unwell, elderly, immunocompromised
- For severe symptoms (but not dysentery) give antiemetics (prochlorperazine) and antidiarrhoeals (codeine or loperamide)
- Shigella, Campylobacter and Salmonella: ciprofloxacin 500mg/12hrs PO
- Cholera: tetracycline reduces transmission
- Food poisoning is a notifiable disease in the UK
prognosis of infective gastroenteritis
- Usually a self-limiting disease with spontaneous recovery.
- In children, acute gastroenteritis has a ↑ mortality due to dehydration; death and serious morbidity are less common but can still occur esp in developing countries and elderly.
complications of infective gastroenteritis
- Dehydration
- IBS
- Haemolytic uraemic syndrome – rare; usually affects young children and elderly
acute pancreatitis definition
- This is acute inflammation of the pancreas, releasing exocrine enzymes that cause autodigestion of the organ
- There may be involvement of local tissues and distant organs - this is not to be confused with chronic pancreatitis
how common is acute pancreatitis
- UK incidence = 150-420 cases per million and rising.
* There is significant geographical variation - much higher in Scandinavia and USA
biological causes/ risk factors of acute pancreatitis
I GET SMASHED - gallstones and alcohol account for majority of cases
- Idiopathic
- Gallstones - account for majority of cases; block the bile duct causing back pressure in the main pancreatic duct and increased cytosolic calcium
- Ethanol/alcohol - account for majority of cases; seems to be reason for geographic variation in prevalence; changes calcium homeostasisi in pancreatic acinar cells
- Trauma – blunt trauma
- Steroids
- Mumps (Coxsackie B)
- Autoimmune (+ tumour)
- Scorpion stings
- Hyperlipidaemia/hypercalcaemia
- ERCP (post-endoscopic retrograde cholangiopancreatography)
- Drugs - azathioprine, diuretics, oestrogens, corticosteroids, didanosine
symptoms of acute pancreatitis
- Epigastric/central abdominal pain – gradual or sudden severe (tpical)
- Radiates to back
- May be relieved by sitting forward/foetal position and worsens with movement
- Vomiting
- May be generalised with peritonism if peritonitis is suspected
signs of acute pancreatitis
- Abdominal tenderness - varies from mild tenderness in the upper abdomen to generalised peritonitis, rebound tenderness, and guarding in more severe attacks.
- Abdominal distention - common in attacks of acute pancreatitis. Caused by a leakage of fluid into the retroperitoneum in an effort to dilute pancreatic enzymes, causing abdominal contents to be pushed forward.
- A bluish discoloration - around the umbilicus (Cullen’s sign); or the flank (Grey-Turners sign) is sometimes associated with haemorrhagic pancreatitis (a late, serious complication) caused by blood vessel autodigestion and retroperitoneal haemorrhage, suggest necrotising pancreatitis
DDx for acute pancreatitis
- Any acute abdomen pain
* Ruptured/dissecting AAA – unzipping pain; hypotension; shock
Investigations for acute pancreatitis
1st LINE:
- SERUM AMYLASE: sensitive, 3x than upper limit of normal when measured within 24hrs of onset of pain, raised amylase may also be caused by cholecysits, mesenteric infarction, GI perforation, renal failure (as it is excreted renally), amylase will fall back to normal within 3-5 days so late presentation may result in false –ve diagnosis
- SERUM LIPASE: more sensitive, preferred to amylase, increased
- CRP – assess disease severity and prognosis
- OTHER BASELINE LEVELS – FBC, U&E’s, glucose, LFT, Plasma Ca, ABG
- CXR – mandatory to exclude gastroduodenal perforation which increases serum amylase, may also see gllastones or pancreatic calcification
- ABDO USS – screening test to identify biliary (gallstone) cause, distal bile duct obstruction difficult to detect but there will be dilated intrahepatic ducts, stones in GB cannot be used to diagnose gallstone-related pancreatitis
- CONTRAST-ENHANCED SPIRAL CT – essential in all except mild attacks of pancreatitis, do it after 72hrs to assess extent of pancreatic necrosis and prognosis info and complications
- MRI – assess degree of pancreatic damage and identifies gallstones in biliary tree
- ERCP – treatment measure to remove bile duct stones in gallstone-related pancreatitis
• Majority of cases of pancreatitis are mild, but 25% run into complications haemodynamic instability and multiple organ failure, early clinical assessment is not sensitive enough to predict severity
MODIFIED GLASGOW CRITERIA – FOR PREDICTING SEVERITY OF PRANCREATITIS:
• Have been validated for prancreatitis caused by gallstones and alcohol
• Within 48hrs
• Could also do RANSON’S CRITERIA for ALCOHOL INDUCED PANCREATITIS – only valid after 24hr
ACUTE PHYSIOLOGY AND CHRONIC HEALTH EVALUATION II (APACHE II) SCORE:
• Used to predict severity in a number of diseases and is adjusted for age and other chronic health problems
• Very sensitive even within first 24hrs for presentation
