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Transcript File - Sheffield Peer Teaching Society
Phase 2
Simon Berry + Mary Preston
The Peer Teaching Society is not liable for false or misleading information…
Aims
• To give a brief overview of the following 4 topics:
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Gasto-oesophageal refux disease (GORD)
Inflammatory Bowel Disease
Gastroenteritis
Coeliac Disease
• Apply the knowledge to practice exam questions
The Peer Teaching Society is not liable for false or misleading information…
Gastro-oesophageal Reflux
Disease (GORD)
Introduction
• A certain amount of gastro-oesophageal reflux of
acid is normal and there is a natural protective
mechanism
• If reflux is prolonged or excessive it may cause
breakdown of this protection with
– Inflammation of the oesophagus – oesophagitis
– Benign oesophageal stricture
– Barrett’s Oesophagus
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Pathophysiology
• Lower oesophageal sphincter in distal oesophagus is
in a state of tonic contraction and relaxes transiently
to allow passage of food bolus
• Oesophageal mucosal defence mechanisms: mucus
and unstirred water layer trap bicarbonate
• Bicarbonate buffers acid in cells and intracellular
spaces
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Epidemiology
• 2-3 male to 1 female
• Risk factors:
– Increased intra-abdominal pressure
– Inadequate lower oesophageal sphincter for anatomical reasons or factors
that reduce tone
– Smoking, alcohol, fat, coffee
– Pregnancy
– Obesity
– Big meals
– Systemic sclerosis
– Hiatus hernia
– Drugs eg tricyclic antidepressants, anticholinergics, nitrates and calciumchannel blockers
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Clinical presentation
• Heartburn
– Burning feeling
– Rising from stomach or lower chest up towards the neck
– Related to meals
– Lying down, stooping and straining
– Relieved by antacids
• Retrosternal discomfort
• Water brash – excessive salivation
• Odynophagia (pain on swallowing) – due to severe oesophagitis or
stricture
• Atypical symptoms: cough, chest pain, asthmatic symptoms
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Diagnostic tests
• Endoscopy
– Savary-Miller grading 1-5 or Los Angeles A to D
• FBC – to exclude significant anaemia
• Barium swallow – may show hiatus hernia
• Oesophageal pH monitoring
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Management
• Conservative management
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Reduce weight
Stop smoking
Reduce alcohol intake
Raise head of bed at night
Take small regular meals
Avoid hot drinks, alcohol, eating during three hours before bed
Avoid drugs that affect oesophageal motility or damage mucosa
Avoid citrus fruits, tomatoes, onions, spicy foods, soft drinks etc
The Peer Teaching Society is not liable for false or misleading information…
Management
• Pharmacological:
– Full dose Proton Pump Inhibitors (PPIs) for one month
– -ZOLE Eg omeprazaole, lanzoprazole, esomeprazole, pantoprazole etc
– If symptoms return after treatment, long-term acid suppression
– H.pylori eradication if evident on serology or urea breath test
• Refer to endoscopy if fails to respond to therapy or new emergent
symptoms
• Surgery is very late step
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Alternative pharmacological treatments
• Over the counter medicines
– Antacids eg aluminium hydroxide, magnesium carbonate,
magnesium trisilicate
– Alginates eg sodium alginate and alginic acid
• H2-receptor antagonists
– Eg cimetidine, famotidine, nizatidine, ranitidine
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RED FLAGS
• For upper GI cancer:
– Dysphagia - food sticking on swallowing, at any age.
– Dyspepsia at any age combined with one or more of the following 'alarm'
symptoms: Weight loss, Proven anaemia, Vomiting
– Dyspepsia in a patient aged 55 years or more with at least one of the following
'high-risk' features: Onset of dyspepsia <1 year previously, Continuous
symptoms since onset
– Dyspepsia combined with at least one of the following known 'risk factors':
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Family history of upper GI cancer in more than two first-degree relatives
Barrett's oesophagitis
Pernicious anaemia
Peptic ulcer surgery over 20 years previously
Known dysplasia, atrophic gastritis, intestinal metaplasia
Jaundice
Upper abdominal mass
The Peer Teaching Society is not liable for false or misleading information…
Inflammatory Bowel Disease
Introduction
• Group of inflammatory conditions of colon
and small intestine
• Can also affect and part of digestive tract e.g
mouth, oesophagus, anus
• Main 2 types are Crohn’s and Ulcerative colitis
Who gets it?
Ulcerative colitis
• Equal in men and
women
• Less common in
smokers
• Peaks 15-25 ad 60-80
Crohn’s
• More commone in
women
• More common in
smokers
• Peaks 15-30 and 60-80
What are the symptoms?
UC
• Bloody diarrhoea
• Abdo pain, urgency,
tenesmus
• Can be just in the
rectum(proctitis)constipation and rectal
bleeding
• Systemic symptoms-joints,
eyes, malaise, fever, weight
loss
Crohn’s
• Bloody diarrhoea, abdo
pain, weight loss
• Systemic symptomsmouth/skin/eyes/joints/peri
anal ulcers/fissures
• Malaise, anorexia, fever
Anything to see on examination?
UC
• Abdo:Pain, tenderness,
palpable masses
• Tachcardia, hypotension,
febrile (severe)
• If pain and distension ?toxic
megacolon
Crohn’s
• Signs of weight loss,
anaemia, dehydration
• Hypotension, tachcardia,
dehydration
• Abdo tenderness and
distension
• Anal and perianal lesions
• Mouth ulcers
Extraintestinal bits and pieces
• Joint diseases: type 1 (pauci-articular) and type 2
(polyarticular)
• Type 1: acute, self-limiting (<10 weeks) and occur with IBD
relapses
• Type 2: Arthropathy lasts longer (months to years),
independent of IBD activity, usually associated with uveitis
• Eyes: uveitis, episcleritis, conjunctivitis
• Skin: erythema nodosum, pyoderma gangrenosum
• Liver: sclerosing cholangitis
• Nephrolithiasis in Crohn’s (oxalate stones in patients with
small bowel disease or after resection)
• Clubbing
Histopathology
UC
• Restricted to the colon
and rectum
• Only affects mucosa
• Backwash ileitis
• Crypt abscesses
Crohn’s
• Can affect any part of
the gastrointestinal
tract (skip lesions)
• Affects full thickness of
bowel wall (transmural
lesions)
• Granulomas
• Cobblestone mucosadeep fissured ulcers
How do I investigate?
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Colonoscopy
Biopsy histology
Stool samples for gastroenteritis
Bloods
Abdo imaging-for toxic megacolon/perforation
How do I treat it? – Crohn’s
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If mild – smoking cessation
Mesalazine – for mild/moderate active Crohn’s
Corticosteroids – to induce remission
Symptomatic rx – eg loperamide, bile acid sequestrants, antispasmodics
Immunomodulators eg azathioprine, mercaptopurine
or methotrexate
• Cytokine modulators (TNF-α) eg infliximab
• Surgery
How do I treat it? – UC
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Aminosalicylate eg Mesalazine (5-ASA)
Corticosteroids – relapses of UC, NOT maintenance
Thiopurines eg azathioprine
Ciclosporin
Infliximab
Surgery – 30%, colectomy is curative
Complications
• ↑incidence of bowel cancer
• Toxic megacolon
• Pouchitis
Gastroenteritis
Introduction
• Most common form of acute gastrointestinal
infection
• Combinations of nausea, vomiting, diarrhoea
and abdominal pain
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Epidemiology + Aetiology
• 20% UK population develop infectious intestinal
disease each year
• Viral causes: norovirus, rotavirus, adenovirus
• Bacterial: Campylobacter spp, E. coli O157,
Salmonella spp. Shigella Spp. O toxins from Staph.
Aureus, Bacillus cereus or Clostridium perfringens
• Parasitic pathogens: Crytosporidium spp. Entamoeba
histolytica (amoebiasis) or Giardia lamblia
The Peer Teaching Society is not liable for false or misleading information…
Pathophysiology
• Mechanisms:
– Mucosal adherence -> secretory diarrhoea
– Mucosal invasion - > dysentery = low-volume bloody
diarrhoea with abdominal pain
– Toxin production
• Two broad syndromes
– Watery diarrhoea – usually due to enterotoxins or
adherence
– Dysentery – due to mucosal invasion
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Organisms
• Need to learn a little about these
(microbiology time!)
• Dysentery: Shigella, Enterohaemorrhagic E.coli
(EHEC), ?Salmonella, C.difficile
• Watery diarrhoea: Bacillus, Campylobacter
jejuni, Vibrio cholerae, Yersiniosis, Staph
Aureus
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Risk Factors
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Poor personal hygiene and lack of sanitation
Compromised immune system eg AIDS
Achlorhydria increases risk
Poorly cooked food, cooked food left too long at
room temperature or from uncooked food eg
shellfish
• Reheating
The Peer Teaching Society is not liable for false or misleading information…
Presentation
• Incubation periods:
– Viruses: a day
– Bacillary dysentery: few hours to 4 days
– Parasites: 7-10 days
• Epidemics usually caused by a rotavirus or norovirus ‘winter
vomiting’
• Bloody diarrhoea:
– ?Bacterial infection: E.coli O157, or after return from exotic location,
E.histiolytica. Also, salmonella spp
• Pyrexia in adults suggests invasive organism
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Assessment
• DEHYDRATION
– Mild: anorexia, nausea, light-headedness, postural hypotension
– Moderate: apathy, tiredness, dizziness, muscle cramps, dry tongue,
sunken eyes, reduced skin eleasticity, postural hypotension,
tachycardia, oliguria
– Severe: profound apathy, weakness, confusion, shock, tachycardia,
systolic BP < 90mmHg, oliguria or anuria
• Also abdominal exam
• Check temperature, blood pressure, pulse rate, and
respiratory rate
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Investigations
• Stool investigations
– Microscopy (including ova, cysts and parasites), culture
and sensitivity. If:
• Blood and/or mucus in stool
• Patient is immunocompromised
• Patient has recently been abroad to anywhere other than western Europe, North
America, Australia or New Zealand
• Diarrhoea has not improved by day 7
• Uncertainty about diagnosis
– Unwell patients may need blood tests eg FBC, U+Es
The Peer Teaching Society is not liable for false or misleading information…
Management
• NOTIFICATION: dysentery and food poisoning are notifiable
• Admission to hospital? – if vomiting and unable to retain oral
fluids, or there are features of shock or severe dehyation
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Encourage as much fluid intake and eating as possible
Prevent spread of infection eg wash hands thoroughly
Avoid work until 48h diarrhoea and vomiting-free
In developing countries, oral rehydration solution (ORS)
The Peer Teaching Society is not liable for false or misleading information…
Prevention
• Cook meat properly. Wash vegetables and salads before
eating
• Separate uncooked meats from cooked and ready-to-eat food
• Wash chopping boards, knives and other utensils in hot soapy
water immediately after handling any raw meet
• Wash hands after going to toilet or handling pets before
eating, drinking or cooking
The Peer Teaching Society is not liable for false or misleading information…
Coeliac Disease
What is it?
• Immune-mediated, inflammatory systemic
disorder provoked by gluten (gliadin) and
related prolamines.
• Gluten is a protein found in wheat, rye and
barley.
Pathology
• Villous atrophy
• Crypt hyperplasia
Who gets it?
• Associated with HLA DQ2 and DQ8
• 1% people in the UK
• Rare in Central Africa and Asia
What are the symptoms?
• Tiredness/SOB (anaemia)
• Nonspecific-abdo discomfort, arthralgia,
malaise
• Smelly pale poo (Diarrhoea, steatorrhoea,
malabsorption)
• Weight loss
• Mouth ulcers, angular stomatitis
Systemic features
• Fractures-due to low absorption Ca/Vit D
• Abnormal bleeding- Vit K deficiency
• DERMATITIS HERPETIFORMIS
Complications
• Adenocarcinoma and lymphoma (EATL) of the
small bowel
• Ulcerative jejunitis
• Strictures
Anything to see on examinations?
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Dermatitis herpetiformis
Signs of iron deficiency
Mouth ulcers
Signs of weight loss
How do I investigate it?
• Blood tests WHILE STILL ON GLUTEN:
• Specific autoantibodies:
*IgA anti-tissue transglutaminase antibodies
(tTGAs) *
Endomysial antibodies(EMA)
Deaminated forms gliadin peptides (DGP)
• Full blood count
• LFTs (elevated transaminases)
How do I investigate it?
• HLA DQ2/DQ8 typing
• Biopsy
How do I manage it?
• Gluten free diet!
• Poor compliance-especially in young people
• Refer to dietician and have regular follow ups
to improve compliance
Practice Questions
Practice Question
• A 17-year-old man with coeliac disease since childhood is
non-compliant with his gluten-free diet. He describes passing
oily stools that float in the pan and are difficult to flush away.
• What is the main reason for fat malabsorption in this patient?
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(a) Distortion of the Ampulla of Vater impeding pancreatic secretion
(b) Loss of lipase production by the small intestinal epithelium
(c) Mucosal surface area reduction due to villous atrophy
(d) Obstruction of small intestinal lymphatics by lymphocytes
(e) Reduced intestinal transit time because of autonomic stimulation
The Peer Teaching Society is not liable for false or misleading information…
Practice Question
• A 30-year old man presents 1 week with profuse watery
diarrhoea with blood mixed in. He recently returned from a
holiday to Portugal. What is the most likely diagnosis:
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(a) Diverticulitis
(b) Shigella dysenteriae
(c) Clostridium difficile
(d) Bacillus cereus
(e) Yersinius enterocolitica
Shigella is an infectious cause of blood diarrhoea as well as
enterohaemorrhagic E.coli. Diverticulitis may cause similar symptoms but is
unlikely due to age of the patient. C.difficile may cause bloody diarrhoea
however it is usually preceded by a course of abx. Bacillus and Yersinia
typically cause watery diarrhoea
The Peer Teaching Society is not liable for false or misleading information…
Thanks for listening!!
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