Gastrointestinal (2) Flashcards
Define coeliac disease
Systemic autoimmune inflammatory disease triggered by dietary gluten peptides found in wheat, rye, barley, and related grains.
Gluten intolerance which leads to villous atrophy and crypt hyperplasia cuasing chronic intestinal malabsorption.
Explain the aetiology of coeliac disease
Due to sensitivity to the GLIADIN component of gluten. Gliadins are resistant to proteases and persist in SI where they are deamidated by tTG. Exposure to gliadin triggers an immunological reaction in the small intestine leading to mucosal damage and loss of villi.
What are the risk factors of coeliac disease?
Family history of coeliac disease IgA deficiency T1DM Autoimmune thyroid disease Genetic susceptibility associated with HLA-B8, HLA-DR3 and HLA-DQW2 haplotype.
Describe the epidemiology of coeliac disease
Common in Irish
Prevalence around 1%
Women slightly more likely
Can be diagnosed at any age
1st peak period of presentation = infancy soon after the initial exposures to gluten
2nd peak period of presentation = fourth and fifth decades
What are the presenting symptoms of coeliac disease?
Diarrhoea Bloating Abdominal pain/discomfort/distension Steatorrhoea Fatigue Weight loss Failure to thrive Amenorrhoea
What are the signs on examination of coeliac disease?
Signs of anaemia: pallor
Signs of malnutrition: Short stature, Abdominal distension, Wasted buttocks in children
Signs of vitamin/mineral deficiencies: osteomalacia, easy bruising, aphthous ulcers
Dermatitis herpetiformis: Intense, itchy blisters
on elbows, knees or buttocks
What are the appropriate investigations for coeliac disease?
Blood: FBC (low Hb, iron and folate, microcytic) Albumin - low Calcium - low Phosphate - high
Serology:
IgG anti-gliadin antibodies, IgA and IgG anti-endomysial tranglutaminase antibodies can be diagnostic (IgA and IgG-tTG) IgA may give false negative
Stool: culture to exclude infection, faecal fat tests for steatorrhoea
D-xylose test: reduced urinary excretion after oral xylose indicates small bowel malabsorption
Endoscopy: allows direct visualisation of villous atrophy
in the small intestine (mucosa appears flat and smooth)
Biopsy: villous atrophy and crypt hyperplasia in the duodenum. Epithelium adopts a cuboidal appearance, inflammatory infiltrate of lymphocytes and plasma cells in the lamina propri.
What is the management for coeliac disease?
Avoid gluten
Vitamin and mineral (calcium, vit D, iron) supplements
Oral corticosteroids if avoidance of gluten does not subside disease
What are the possible complications of coeliac disease?
Osteoporosis/osteopenia
Dermatitis herpetiformis
Malignancy - lymphoma, small bowel and oesophageal cancer
Idiopathic recurrent acute/chronic pancreatitis
Pneumococcal infection
Iron, folate, B12 deficiency
Ulcerative jejunoileitis
What is the prognosis of coeliac disease?
Most patients have complete and lasting resolution of symptoms on a gluten-free diet alone. Symptoms usually resolve within a few weeks.
For those with persistent symptoms, most of these will be attributed to ongoing gluten exposure, lactose intolerance, and IBS.
Less than 1% can be expected to develop refractory coeliac disease.
Define colorectal carcinoma
Malignant adenocarcinoma of the large bowel
Distribution:
60% - rectum and sigmoid
30% - descending colon
10% - rest of colon
What are the risk factors for colorectal carcinoma?
Western diet (e.g. red meat, alcohol) Colorectal polyps Previous colorectal cancer Family history IBD Increasing age Familial adenomatous polyposis (FAP) – APC mutation, autosomal dominant Hereditary non-polyposis colorectal cancer (HNPCC or Lynch syndrome) – microsatellite instability, autosomal dominant Obesity
Summarise the epidemiology of colorectal carcinoma?
Third most common cancer in the Western world.
Highest incidence in Europe, North America and Australasia
Lowest incidence in Africa and Asia
Rare before 40 years old - average age of diagnosis is 60-65
What are the presenting symptoms of colorectal carcinoma?
Left-Sided Colon and Rectum:
Change in bowel habit
Rectal bleeding (blood or mucus mixed with the stools)
Tenesmus (due to a space-occupying tumour in the rectum)
Right-Sided Colon:
Presents later Anaemia symptoms (lethargy) Weight loss Non-specific malaise Lower abdominal pain (rare) Blood covering stool or streaked
20% of tumours will present as an EMERGENCY with pain and distension due to:
Large bowel obstruction
Haemorrhage or peritonitis due to perforation
What are the signs on examination of colorectal carcinoma?
Anaemia
Abdominal mass
Low-lying rectal tumours may be palpable on DRE
If metastatic: Hepatomegaly, Ascites (shifting dullness)
What are the appropriate investigations for colorectal carcinoma?
Bloods:
FBC - anaemia
LFTs
Tumour markers - CEA
DRE
Stools:
Faecal Occult Blood Test - screening test
Endoscopy: Sigmoidoscopy or Colonoscopy and biopsy
Double-Contrast Barium Enema
Contrast CT - For staging (Duke’s staging)
Define Crohn’s disease
A chronic relapsing and remitting granulomatous systemic disease involving transmural inflammation of any part of the gastrointestinal tract.
Describe some of the difference between Crohn’s Disease and Ulcerative Colitis
Depth - Crohn’s is transmural inflammation whereas UC only affects the mucosa
Location - CD can affect anywhere in the GI tract from mouth to anus but is usually terminal ileum and ascending colon, UC affects rectum extending proximally
CD is often patchy with skip lesions but UC is continuous inflammation
CD has pathognomonic granulomas (swellings,
macrophages, giant cells), thickened bowel wall with strictures, fistulae and abscesses, aphthous ulcers
UC has red, inflamed, friable mucosa, crypt ulcers and pseudopolyps
What are the risk factors of Crohn’s Disease?
Unknown aetiology but relation between genetic and environmental factors
Genetic factors: Family history CARD15 HLA-B27 Increased serum p-ANCA
Environmental factors: Smoking OCP NSAIDs High sugar and fat intake Chronic stress and depression Intestinal dysbiosis Infectious agents Dietary deficiencies Age 15-40 or 60-80
Describe the epidemiology of Crohn’s Disease
Peak age of onset is 15-40 years and a smaller peak at 60-80 years. Equally prevalent among men and women. More common in white people. Higher prevalence among smokers. UK prevalence: 50-80/100,000
What are the presenting symptoms of Crohn’s Disease?
Crampy abdominal pain (due to inflammation, fibrosis or bowel obstruction)
Diarrhoea (may be bloody or steatorrhoea)
Fever, malaise, weight loss
Symptoms of complications
Sometimes right iliac fossa pain due to inflammation of terminal ileum
What are the signs on examination of Crohn’s Disease?
Weight loss
Clubbing
Signs of anaemia
Abdominal tenderness
Aphthous ulcers in mouth
Perianal lesions - skin tags, fistulae and abscesses
Uveitis, erythema nodosum, pyoderma gangrenosum
What are the appropriate investigations for Crohn’s Disease?
Bloods: FBC - Low Hb, high WCC and platelets Raised ESR/CRP Low albumin Deranged LFTs (associated liver disease) Iron studies - may show iron deficiency Serum B12 and folate - may be low due to malabsorption
Stool:
MC&S – exclude infectious colitis
Faecal calprotectin – indicates migration of neutrophils to intestinal mucosa i.e. inflammation; distinguishes IBD from IBS and assesses disease severity
AXR – dilated bowel loops indicates ileus, exclude toxic megacolon
Erect CXR - abdominal perforation
OGD or colonoscopy Monitor disease severity/progression Cobblestone mucosa Fistulae/abscesses Granulomas
Small bowel barium follow-through:
Deep ulceration
Fibrosis/strictures (string sign of Kantor: part of intestine looks like a piece of string, showing incomplete filling of intestinal lumen)
Cobblestone mucosa
CT/MRI - skip lesions, bowel wall thickening, surrounding inflammation, abscess, fistulae
What is the management for Crohn’s Disease?
Acute Exacerbation:
Fluid resuscitation
IV/oral corticosteroids
5-ASA analogues (e.g. mesalazine and olsalazine)
Analgesia
Parenteral nutrition may be necessary
Monitor markers of disease activity e.g. fluid balance, ESR, CRP, platelets, Hb
Long-Term:
Steroids - for acute exacerbations
5-ASA analogues - decreases the frequency of relapses (useful for mild to moderate disease)
Immunosuppression: using steroid-sparing agents (e.g. azathioprine, 6-mercaptopurine, methotrexate) reduces the frequency of relapses
Anti-TNF agents: (e.g. infliximab and adalimumab) - very effective at inducing and maintaining remission. Usually reserved for refractory Crohn’s.
General Advice:
Stop smoking
Dietician referral (low fibre diet necessary if there are stricture present)
Surgery indicated if:
Medical treatment fails
Failure to thrive in children in the presence of complications
Involves resection of affected bowel and stoma formation
What are the possible complications of Crohn’s Disease?
Anaemia
GI: Abscess Haemorrhage Obstruction Strictures Perforation Fistulae (between bowel, bladder, vagina) Perianal fistulae and abscesses GI cancer Malabsorption Toxic megacolon
Extraintestinal Features: Uveitis Episcleritis Gallstones Kidney stones Arthropathy Sacroiliitis Ankylosing spondylitis Erythema nodosum Pyoderma gangrenosum Amyloidosis Primary sclerosing cholangitis
What is the prognosis of Crohn’s Disease?
CD is a chronic disease with variable frequency of relapses and multiple possible complications.
Intermittent exacerbations followed by periods of remission, with 10% to 20% of patients experiencing a prolonged remission after the initial presentation.
2/3 of CD patients will require surgery
CD has lower life expectancy
Define Diverticular Disease
Diverticular disease = diverticulosis associated with complications.
Diverticulosis = the presence of diverticulae outpouchings (herniation of the mucosa and submucosa through the muscular layer of the large bowel wall).
Diverticulitis = acute inflammation of a diverticulum or diverticula
What is the aetiology/risk factors of diverticular disease?
Low-fibre diet leads to loss of stool bulk. Leads to generation of high colonic intraluminal pressures to propel the stool out. Leads to the herniation of the mucosa and submucosa through the muscularis
Inspissated food or faecal matter can cause diverticular obstruction -> bacterial overgrowth, toxin production and mucosal injury -> diverticulitis
Most commonly found in sigmoid and descending colon. NOT in rectum.
Risk factors: Low dietary fibre (Western diet) Age >50 y Decreased physical activity Obesity Increased red meat consumption Tobacco smoking Excessive alcohol and caffeine intake Steroids NSAIDs
Summarise the epidemiology of diverticular disease
Prevalence is difficult to determine because most patients are asymptomatic but VERY COMMON.
Prevalence increases with age - affects 50% to 66% of over 80 year olds.
Right-sided diverticular disease is more common in Asia.
No overall sex difference in prevalence of diverticular disease.
What are the presenting symptoms of Diverticular Disease?
Often asymptomatic Left lower quadrant pain Diarrhoea PR bleeding Bloating Constipation
If diverticulitis - LIF and lower abdo pain and fevero
If diverticular fistulation - causing pneumaturia (see bubbles in urine), faecaluria and recurrent UTI
What are the signs on physical examination of Diverticular Disease?
Guarding and tenderness in LLQ
Pelvic tenderness on DRE
Signs of generalised peritonitis if a diverticulum has perforated
What are the appropriate investigations for Diverticular Disease?
Bloods:
FBC - raised WCC if acute diverticulitis, raised CRP
Abdo CT - thickening of bowel wall, mass, abscess, streaky mesenteric fat, gas in the bladder in cases of fistula.
Abdo USS - if CT unavailable
Abdo X-ray - pneumoperitoneum, ileus, soft tissue densities, free air in bowel perforation if acute diverticulitis
CXR - if suspect perforation
Barium Contrast enema - saw-tooth appearance of lumen. Used to confirm acute diverticulitis diagnosis following resolving of symptoms - do not use in acute setting as risk of perforation.
Colonoscopy or sigmoidoscopy - if unclear or supsect bowel cancer
Angiogram if profuse bleeding
What is the management plan for Diverticular Disease?
Asymptomatic:
Soluble high-fibre diet (20-30 g/day) and increase fluids
Probiotics and anti-inflammatories??
GI Bleed:
IV rehydration and antibiotics
Blood transfusion if necessary
Angiography and embolisation or surgery if severe
Diverticulitis:
IV antibiotics
IV fluid rehydration
Bowel rest
Abscesses may be drained by radiologically sited drains
Surgery:
Necessary in patients with recurrent attacks or complications (e.g. perforation and peritonitis)
Open surgery:
Hartmann’s procedure (proctosigmoidectomy leaving a stoma)
One-stage resection and anastomosis (risk of leak) with or without defunctioning stoma
Laparoscopic drainage, peritoneal lavage and drain placement can be effectively
What are the possible complications of Diverticular Disease?
Diverticulitis Pericolic abscess Perforation Faecal peritonitis Colonic obstruction Fistulae - Bladder: causes pneumaturia, faecaluria, recurrent UTI - Small intestine - Vagina Haemorrhage Strictures
What is the prognosis of Diverticular Disease?
Most patients with uncomplicated diverticulitis recover following medical treatment and do not require surgical intervention.
Diverticular disease recurs in one third of patients following response to medical treatment, mostly within 5 years.
Following surgical treatment, approximately one fourth of all patients continue to remain symptomatic.
10-25% have one or more episode of diverticulitis
Define Irritable Bowel Syndrome
Chronic condition characterised by abdominal pain and bowel dysfunction with no underlying structural abnormalities – diagnosis of exclusion
What is the aetiology/risk factors of IBS?
No specific aetiological cause (mucosa is normal)
Disorder of GI motility with a potential inflammatory/immune basis often triggered by stress
Risk factors: Female Age <50 years GI infection Previous physical or sexual abuse Stress
What is the epidemiology of IBS?
Affects 10-15% of adults
The prevalence is higher in women than men
Rare for onset of symptoms after 50 years
What are the presenting symptoms of IBS?
Abdominal discomfort
Altered bowel habits associated with pain
Bloating
Passage of mucus with stool
Cramping pain relieved following defecation
What are the signs on physical examination of IBS?
Nil signs of note - a normal abdominal exam
What are the appropriate investigations for IBS?
Bloods:
FBC - if low Hb or high WCC suggests not IBS
Anti-endomysial antibodies - if positive, coeliac
Anti-tTG antibodies - if positive, coeliac
Stool studies - WBCs or parasites in stool suggests not IBS
Abdo X-ray - check for obstruction
Flexible sigmoidoscopy and colonoscopy - if abnormal mucosa, suggests IBD
Serum CRP - if more than 0.5mg/L then IBD more likely
Faecal calprotectin - if high more likely IBD
What is the management of IBS?
Lifestyle and dietary modifications - decrease caffeine, lactose and fructose, add fibre, probiotics Laxatives If painful, add antispasmodics SSRIs if constipated CBT or hypnotherapy If having diarrhoea, antidiarrhoeals
What are the possible complications of IBS?
Damage to family and work relationships
Diverticulosis
What is the prognosis of IBS?
Normal life expectancy and no long-term complications.
The symptoms recur for much of adulthood, particularly at times of stress, emotional difficulty or dietary indiscretions.
Define biliary colic
Pain resulting from obstruction of the gallbladder, cystic duct or common bile duct, usually by a stone.
It is usually felt in the upper abdomen (in the midline or to the right) but can also be poorly localised due to its visceral nature.
What is the aetiology/risk factors of biliary colic?
Occurs due to contractions of the biliary tree in attempt to relieve an obstruction due to a stone.
Risk factors of gallstones: Fair (Caucasian) Fat Fertile Forty Female
Family history, Obesity, Drugs e.g. OCP, octreotide, Pregnancy, terminal ileum disease
Pigment gallstones – calcium bilirubinate
• Chronic haemolytic anaemia
• Cirrhosis
• Cystic fibrosis
• Ileal disease
• Bile duct strictures
Summarise the epidemiology of gallstones and biliary colic
10-15% of adults in the Western World will develop gallstones
In more than 80% of people, gallstones are generally symptomatic
What are the presenting symptoms of gallstones and biliary colic?
Crampy RUQ pain
Nausea and vomiting
Pain may radiate to the right scapula
The pain does NOT fluctuate and has a tendency to persist
Individuals may present with pain following ingestion of a fatty meal
What are the signs on physical examination of gallstones and biliary colic?
RUQ or epigastric tenderness
What are appropriate investigations for gallstones and biliary colic?
Bloods:
FBC - elevated WCC suggests inflammation due to complication
LFTs - if stone blocking CBD, high ALP and bilirubin
Serum lipase and amylase - if elevated, may be pancreatitis
Ultrasound - Look for dilatation of the CBD, thickened gallbladder, may be able to see stones
Urinalysis, CXR and ECG to exclude other causes (e.g. basal pneumonia, inferior MI)
ERCP - useful diagnostically and therapeutically
CT - may be useful if other forms of imaging have been insufficient
What is the management of gallstones and biliary colic?
If asymptomatic gallstones, OBSERVATION
If symptomatic:
Analgesia
IV fluids
NBM
Surgical:
Laparoscopic cholecystectomy
ERCP can also be used to help remove stones or stent a blocked bile duct
What are the possible complications of biliary colic?
ERCP-associated pancreatitis
Cholecystitis
Ascending cholangitis
Acute biliary pancreatitis
Complications due to cholecystectomy:
Injury to the bile duct
Fat intolerance - due to inability to secrete a large amount of bile into the intestine because the patient no longer has a gallbladder
Post-cholecystectomy syndrome - presence of abdominal symptoms (e.g. dyspepsia, nausea/vomiting, RUQ pain) after the removal of the gallbladder
What is the prognosis of gallstones/biliary colic?
Good prognosis with appropriate treatment
Define gastric cancer
A neoplasm that can develop in any portion of the stomach and may spread to the lymph nodes and other organs. Most tumours are adenocarcinomas.
Other histological types include lymphoma, leiomyosarcoma, neuroendocrine tumours, and squamous cell carcinomas.
What is the aetiology/risk factors of gastric cancer?
The aetiology is unknown - linked to environment and genetics
Risk Factors: Smoked and processed foods Smoking Alcohol Helicobacter pylori infection Atrophic gastritis Pernicious anaemia Partial gastrectomy Gastric polyp Male sex
Summarise the epidemiology of gastric cancer
Higher incidence in East Asia, Eastern Europe, and South America - highest in JAPAN More common in men COMMON cause of cancer death worldwide 6th most common cancer in the UK Usual age of presentation: > 50 yr
What are the presenting symptoms of gastric cancer?
Often asymptomatic in early stages
Abdominal pain/epigastric discomfort FLAWS Nausea Dysphagia Haematemesis Lower GI bleeding eg meleana Early satiety Anorexia Symptoms of metastases e.g. ascites, jaundice Symptoms of anaemia - fatigue
What are the signs on physical examination of gastric cancer?
Epigastric mass Abdominal tenderness Ascites Signs of anaemia Lymphadenopathy Virchow's Node (aka Troisier's sign) Sister Mary Joseph's Nodule (metastatic node on the umbilicus) Krukenberg's Tumour (ovarian metastases)
Metastases
• Ascites
• Jaundice
• Hepatomegaly
What are the appropriate investigations for gastric cancer?
Bloods - FBC (check for anaemia), LFTs
Upper GI endoscopy with biopsy
Once diagnosed: CT/MRI for staging Endoscopic USS to assess depth of gastric invasion and lymph node involvement - determine T and N stages CT abdo and pelvis - check for mets CXR - check for mets CT chest - check for mets
Define GORD
Symptoms or complications resulting from the reflux of gastric contents into the oesophagus, oral cavity or lung
Explain the aetiology of GORD
Reduced Lower oesophageal sphincter tone
Prolonged oesophageal acid clearance
Delayed gastric emptying
What are the risk factors of GORD?
Family history of GORD Older Age Obesity Pregnancy Hiatus hernia Systemic sclerosis Drugs e.g. nitrates, tricyclics, NSAIDS Smoking Alcohol Stress Asthma Intake of specific foods (such as coffee, mints, citrus fruits, or fats)
Summarise the epidemiology of GORD
Affects 10-30% of people in developed world
All age groups affected
What are the presenting symptoms of GORD?
Heart burn (worse on lying down, bending over, after drinking alcohol or eating large meals) Epigastric burning discomfort Acid regurgitation (waterbrash) Dysphagia due to peptic stricture Cough (vagal stimulation and aspiration) Pain is relieved by antacids Early satiety
What are the signs on physical examination of GORD?
Epigastric tenderness
Wheeze on chest auscultation
Dysphonia
Asthma due to aspiration
What are the appropriate investigations for GORD?
Often a CLINICAL diagnosis
PPI trial - if after 8 week trial no improvement, further tests
OGD/Upper GI endoscopy, biopsy and cytological brushings - may show oesophagitis or Barrett’s oesophagus and can exclude malignancy
Ambulatory pH monitoring - pH less than 4 more than 4% of time is abnormal. pH probe in lower oesophagus determines the temporal relationship between symptoms and pH.
Oesophageal manometry
Barium Swallow can detect:
Hiatus hernia, Peptic stricture, Extrinsic compression of the oesophagus
CXR: This is NOT specific for GORD. Can lead to the incidental finding of a hiatus hernia (gastric bubble behind the cardiac shadow)
What is the management of GORD?
Stanard-dose PPI and lifestyle changes (weight loss, avoid late eating, elevate head of bed, avoid provoking factors, stop smoking)
2nd line = anti-reflux surgery for those who are responsive but do not adhere
If irresponsive to PPI: strong dose PPI and H2 antagonist
Endoscopy: Annual endoscopic surveillance
Nissen Fundoplication: Fundus of the stomach is wrapped around the lower oesophagus - helps reduce the risk of hiatus hernia and reduce reflux.
What are the possible complications of GORD?
Oesophageal ulceration, haemorrhage or perforation
Peptic stricture
Anaemia
Barrett’s oesophagus
Oesophageal adenocarcinoma
Associated with asthma and chronic laryngitis
What is the prognosis of GORD?
50% respond to lifestyle measures alone
In patients that require drug therapy, withdrawal is often associated with relapse
20% of patients undergoing endoscopy for GORD have Barrett’s oesophagus
Define gastroenteritis
Acute inflammation of the GI tract typically resulting from bacterial toxins or viral infections.
Incubation period typically lasts 16-24h.
What is the aetiology of gastroenteritis?
Transmission may occur due to eating improperly prepared foods, drinking contaminated water or through close contact with an infected individual.
Viral: Rotavirus Adenovirus Norovirus Astrovirus Calcivirus Norwalk virus Small round structures viruses
Bacterial: Campylobacter jejuni (chicken) Escherichia coli Salmonella (eggs, poultry) Shigella Vibrio cholerae Listeria Yersinia enterocolitica
Protozoal:
Entamoeba histolytica
Cryptosporidium parvum
Giardia lamblia
Toxins from: Staphylococcus aureus Clostridium botulinum Clostridium perfringens Bacillus cereus Mushrooms Heavy metals Seafood
Commonly contaminated foods: Improperly cooked meat Old rice Eggs and poultry Milk and cheeses Canned food
Parasitic
Giardia – Eastern Europe/Russia
Entamoeba – tropical regions
Non-infectious
• Drugs e.g. NSAIDs
• Food e.g. (lactose intolerance, coeliac disease)
• Crohn’s disease
What are the risk factors for gastroenteritis?
Young
Old
Travellers
Summarise the epidemiology of gastroenteritis
In the UK, around 20% of the UK population will have an infectious intestinal disease each year
COMMON
Serious cause of morbidity and mortality in the developing world
Viral gastroenteritis is a common cause of D&V in children
Bacteria is the most common cause of gastroenteritis in adults
What are the presenting symptoms of gastroenteritis?
Nausea and vomiting Diarrhoea (bloody or watery) Abdominal pain Malaise Sudden onset nausea, vomiting, anorexia Fever Dysentery (CHESS – Campylobacter, Haemorrhagic E. coli, Entamoeba histolytica, Salmonella, Shigella) Bloating, foul smelling eructation/flatus (Giardia)
Time of Onset:
Toxins = early (1-24 hours)
Bacterial/viral/protozoal = 12+ hours
Pay attention to the other effects of toxins:
Botulinum causes paralysis
Mushrooms can cause fits, renal or liver failure
What are the signs on physical examination of gastroenteritis?
History: recent travel, antibiotic use, recent food intake (how the food was cooked, sourced and whether anyone else is ill)
Diffuse abdominal tenderness
Abdominal distension
Bowel sounds are often INCREASED
In SEVERE gastroenteritis: pyrexia, dehydration (increased cap refill, reduced skin turgor), hypotension and peripheral shutdown
What are appropriate investigations for gastroenteritis?
Usually clinical diagnosis
Bloods:
FBC, blood culture (identify bacteraemia), U&Es (dehydration)
Stool: faecal microscopy and analysis for toxins
AXR or ultrasound: exclude other causes of abdominal pain (e.g. bowel perforation)
Sigmoidoscopy: usually unnecessary unless IBD needs to be excluded
What is the management of gastroenteritis?
Bed rest - mostly self-limiting so go away with time
Fluid and electrolyte replacement with oral rehydration solution (contains glucose and salt)
IV rehydration may be necessary in those with
severe vomiting
Antibiotics IF severe; infective agent has been identified; <3 months or >50 years old; immunosuppressed; internal
prostheses
If botulism is present (due to Clostridium botulinum) treat with IM botulinum antitoxin and manage in ITU
What are the possible complications of gastroenteritis?
Dehydration
Electrolyte imbalance
Prerenal failure (due to dehydration)
Secondary lactose intolerance (particularly in infants)
Sepsis and shock
Haemolytic uraemic syndrome (associated with toxins from E. coli O157)
Guillain-Barre Syndrome may occur weeks after recovery from Campylobacter gastroenteritis
Respiratory muscle weakness or paralysis due to botulism
What is the prognosis of gastroenteritis?
Good prognosis as usually self-limiting
If volume depletion and electrolyte disturbances are not recognised and managed, can cause serious morbidity and mortality.
Usually no long-term consequences following recovery
Define infectious colitis
Inflammation of the colon due to an infectious agent
What is the aetiology of infectious colitis?
Bacteria
Clostridium difficile – enterotoxin A + cytotoxin B
Shigella
Campylobacter
Salmonella
Yersinia enterolytica
E.coli (enteroinvasive and enteroaggregative)
Viruses
Rotavirus
CMV
Parasites
Entamoeba histolytica
What are the risk factors of infectious colitis?
Lack of sanitation Drinking contaminated water Antibiotic use - clindamycin, ampicillin and broad-spectrum cephalosporins IBD Serious acute illness GI procedures Age
Summarise the epidemiology of infectious colitis
Very common
Western countries: bacterial infection is most common
Developing countries: parasitic infection is much more common
What are the presenting symptoms of infectious colitis?
Diarrhoea Blood and mucus in the stools Lower abdominal pain/cramps Malaise Low-grade fever Rectal bleeding Tenesmus
What are the signs on physical examination of infectious colitis?
Fever
Localized or generalized abdominal tenderness
Rebound tenderness
What are the appropriate investigations for infectious colitis?
Diagnosis is largely CLINICAL
Stool culture may be used to identify the causative organism
Define gastrointestinal perforation
Perforation of the wall of the GI tract with spillage of
bowel contents
What are the risk factors for gastrointestinal perforation?
Large Bowel: Diverticulitis Colorectal cancer Appendicitis Others: volvulus, ulcerative colitis (toxic megacolon)
Gastroduodenal:
Perforated duodenal or gastric ulcer
NSAIDs
Others: gastric cancer
Small Bowel (RARE):
Trauma
Infection (e.g. TB)
Crohn’s disease
Oesophagus:
Boerhaave’s perforation - rupture of the oesophagus following forceful vomiting
GI malignancy, IBD, Ingestion of corrosives e.g. batteries, Surgery/investigations e.g. ERCP
Summarise the epidemiology of gastrointestinal perforation
Duodenal ulcers are 2-3 times more likely to perforate than peptic ulcers
10-15% of patients with acute diverticulitis develop perforations
What are the presenting symptoms of gastrointestinal perforation?
Peritonitic severe abdominal pain originating at site of perforation Nausea and Vomiting Fever Pain worse on movement Pain becomes generalised
What are the signs on physical examination of gastrointestinal perforation?
Very UNWELL
Signs of shock - tachycardia, hypotensive
Pyrexia
Pallor
Dehydration
Signs of peritonitis (guarding, rigidity, rebound tenderness, absent bowel sounds)
Loss of liver dullness (due to overlying gas)
Lying still
What are the appropriate investigations for gastrointestinal perforation?
Bloods
FBC, U&E, LFTs
Amylase - will be raised with perforation
Erect CXR - air under the diaphragm
AXR - Shows abnormal gas shadowing
Gastrograffin Swallow - for suspected oesophageal perforations
What is the management for gastrointestinal perforation?
Resuscitation:
Correct fluid and electrolytes
IV antibiotics (with anaerobic cover)
Surgical Large Bowel: Identify site of perforation Peritoneal lavage Resection of perforated section (usually as part of a Hartmann's procedure)
Gastroduodenal:
Laparotomy
Peritoneal lavage
Perforation is closed with an omental patch
Gastric ulcers are biopsied and if positive, H. pylori eradication
Oesophageal:
Pleural lavage
Repair of ruptured oesophagus
What are the possible complications of gastrointestinal perforation?
Peritonitis
Oesophagus - mediastinitis, shock, overwhelming sepsis and death
What is the prognosis of gastrointestinal perforation?
Gastric ulcers have higher morbidity and mortality than duodenal ulcers
POOR prognosis for perforated gastric carcinomas
Define haemochromatosis
An autosomal recessive disease of iron metabolism in which increased intestinal absorption of iron and iron release from macrophages causes accumulation of iron in tissues, which may lead to organ damage.
What is the aetiology/risk factors of haemochromatosis?
Autosomal recessive
Caused be a mutation in the HFE gene on chromosome 6
Most common mutations are C282Y (60-90%) and H63D (3-7%)
The genetic penetrance of haemochromatosis is complex - not everyone who is homozygous will develop the clinical disease
Risk factors: Male (women present late due to protective menstrual loss) Middle age (40-50 years) White ancestry Family history High dietary iron intake
Summarise the epidemiology of haemochromatosis
Very rare
Most common in Northern Europeans
What are the presenting symptoms and signs on examination of haemochromatosis?
Often ASYMPTOMATIC until the late stages of the disease
EARLY symptoms are vague: Fatigue Weakness Arthropathy Erectile dysfunction Heart problems
LATE symptoms: Diabetes mellitus Skin pigmentation: Bronzed skin Signs of chronic liver disease: Hepatomegaly Impotence (inability to get an erection) Amenorrhoea Hypogonadism Cirrhosis Cardiac - arrhythmias and cardiomyopathy Signs of congestive heart failure Neurological and psychiatric problems
What are appropriate investigations for haemochromatosis?
Serum transferrin saturation - first test to become abnormal, >45%
Serum ferritin - raised in inflammation, alcoholism, chronic viral hepatitis, non-alcoholic fatty liver disease, and dysmetabolic syndrome
Tests to exclude other causes of high ferritin:
CRP - inflammation
Chronic alcohol consumption
ALT - liver necrosis
LFTs
Other investigations for abnormal liver function (e.g. hepatitis serology)
Genetic testing
Liver biopsy (rarely required) - raised iron content
In late disease: High fasting blood glucose Echo ECG Testosterone, LH, FSH
