Week 7: Gastroenterology (1) (GI bleeding and disorders)

Question 1

taking a bowel habit history

Answer 1

• How often are they going to the toilet?
• Has this changed from their usual?
• Has the form changed?
• Are they waking overnight to open their bowels?
• Is there any blood in the motion?
• Do they have tenesmus?
• Do they have faecal urgency or incontinence?
• Do the motions flush away easily?

Question 2

IBD treatment

Answer 2

• Steroids
  
  • Topical (suppositories or enemas)
  • Oral (prednisolone, or in small bowel disease, budesonide)
  • IV (hydrocortisone 100mg qds)
• If steroids don’t work: rescue therapy=ciclosporin, biologics or surgery
• Immunosuppressant medication
  
  • UC specifically: Mesalazine (5-ASAs)
    
    • Maintain remission in UC
    • No role in Crohns
  • Crohns specifically: Azathioprine and biologics (UC not on mesalazine)
• Regular blood tests to monitor FBC, U and E and LFTRs

Question 3

two main types of IBD and risk factors

Answer 3

Risk factors

• Age <30
• Whites highest risk
• Family history
• Cig smoking
• NSAIDs medication

Two main types

• Crohns
• Ulcerative colitis

Question 4

crohns characters

Answer 4

• can affect anywhere from mouth to the anus
• skip lesions
• transmural inflammation
• fissuring ulcers
• lymphoid and neutrophil
• non-caseating granulomas
• increased incidence in smokers

Question 5

ulcerative colitis character

Answer 5

• always affects the rectum and extends proximally varying distances
• continous
• mucosal and sub mucosal inflammation only
• crypt abscesses
• decreased incidence in smokers

Question 6

investigations for IBD

Answer 6

• Blood tests
  
  • FBC- anaemia/ raised platelet count
  • U and E- deranged electrolytes due to AKI due to GI losses
  • CRP
• Stool tests
  
  • Stool cultures- exclude infective colitis
  • Faecal calprotectin- raised in active disease and negative in irritable bowel or IBD in remission, but not specific to IBD and shouldn’t be used if blood is present as the presence of blood requires further investigation
• Simple imaging
  
  • AXR
    
    • Used less commonly but used if suspicion of toxic megacolon and can be useful to assess for proximal constipation
• Endoscopy
  
  • Flexible sigmoidoscopy- safest test in bloody diarrhoea
  • Colonoscopy- needed to look for more proximal disease
  • Capsule endoscopy- useful to view small bowel mucosa
• Cross sectional imaging
  
  • Acute complications
  • MRI enterography when looking for small bowel crohns, fistulas or to map the extent of small bowel crohns
  • MRI rectum is image perianal crohns

Question 7

crohns disease presentation

Answer 7

• Diarrheal – non bloody
• Smoker
• Mildly anaemic
• Low grade fever
• Any inflammations stops us absorbing things diarrhoea  weight loss
  
  • Osmotic pressure drawing water out into the lumen
• Crohns unlikely to have bleeding
  
  • Deeper but less widespread
• Tender mass RLQ
  
  • Terminal ileum common site
• Low grade fever arthritis?
• Mild perianal inflammation  fistulas and strictures

Question 8

crohns presentation in the bowel

Answer 8

• Diarrheal – non bloody
• Smoker
• Mildly anaemic
• Low grade fever
• Any inflammations stops us absorbing things diarrhoea  weight loss
  
  • Osmotic pressure drawing water out into the lumen
• Crohns unlikely to have bleeding
  
  • Deeper but less widespread
• Tender mass RLQ
  
  • Terminal ileum common site
• Low grade fever arthritis?
• Mild perianal inflammation  fistulas and strictures

Question 9

ulcerative colitits presentation

Answer 9

Ulcerative colitis presentation

• Inflammatory bowel disease characterised by diffuse inflammation of the colonic mucosa*
• It affects the rectum and extends proximally : distal (proctitis), left sided (splenic flexure) and extensive (beyond splenic flexure)*
• Can be up to 40 bloody stools a day
• Blood and mucous= affecting mucosa
• Weight loss  inflammation uses a lot of calories and diarrhoea can make you lose appetite
• Mild lower abdominal pain
• Normal temp
• Painful red eye extraintestinal problem
• Nocturnal symptoms
• Urgency
• tenesmus

Question 10

ulcerative colitits presentation in the bowel

Answer 10

• Chronic inflammatory infiltrate of lamina propria
• Crypt abscesses (Neutrophilic exudate in crypts)
• Crypt distortion (bottom image)
  
  • Irregular shaped gland with dysplasia
  • Darker crowded nuclei
• Reduced numbers of goblet cells
• Pseudo polyps can develop after repeated episodes
  
  • Inflammation then healing
  • Nonneoplastic
  • More common in UC ( vs Crohns)
• Loss of haustra
  
  • Inflammation reduces the appeared of haustra on imaging

Question 11

Endocscopy of IBD

Answer 11

Question 12

X-ray of UC

Answer 12

• Left colon looks featureless
• Thumbprinting
• Mucosal oedema – should not be able to see lining of the bowel

Question 13

extraintestinal. manifestations of IBD

Answer 13

erythema nodosum

apthous ulcers

acute arthropathy- sore joints

anteiro uveitis

ankylosing sponylittis

primary sclerosing cholangitis

Question 14

aim of treating UC

Answer 14

• Induce remission in acute disease
• Maintain remission
• Improve quality of life
• Decrease risk of colo-rectal cancer

Question 15

main drugs in treatment of UC

Answer 15

• anticoagulation
• steroids
• DMARDs
  
  • mesalazine
  • azathioprine
  • ciclosporin
  • biologics
  • laxatives

Question 16

anti-coagulation in treatment of UC

Answer 16

• IBD flare lead to prothrombotic state
• Need low molecular weight heparin – prevent micro-vascular occlusion e.g. DVT and PE

Question 17

steroids in treatment of UC

Answer 17

• Induce remission
• Use topically (suppositories and enemas), orally or intravenously
• Remember bone protection
• 40mg prednisolone for 2 weeks followed by weaning of 5mg/week

Question 18

mesalazine in treatment of UC

Answer 18

5-ASA

• Mesalazine is rapidly absorbed from the jejunum and so the drug has to be delivered to the colonic mucosa in one of several ways.
  
  • Topical preparations can be applied PR
  • Oral preparations can have various pharmacological modifications.
    
    • pH sensitive resin or membranes can be used (Pentasa, Asacol)
    • linking to another molecule that is enzymatically cleaved in the colon (Olsalazine, Sulphasalazine)
• Main role is in maintenance of remission, but can escalate dose to treat mild flares (decrease relapse rate by 2/3 compared with placebo)
• Decrease the risk of colo-rectal cancer (75% decreased risk quoted)
• Uncommon side effects include diarrhoea, headache, nausea & rash. Interstitial nephritis & nephritic syndrome are rare occurrences.

Question 19

azathiprine in treatment of UC

Answer 19

• Steroid sparing agents that are used in patients intolerant of corticosteroids, in those who require ≥2 course of steroids per year, relapse once dose of Prednisolone is less than 15mg/day or if the disease relapses within 6 weeks of stopping steroids.
• Onset of action takes at least 6 weeks.
• Adverse reactions include flu like symptoms, GI upset, Leucopenia, Hepatitis, Pancreatitis, Rash & Infections
• Require monitoring of blood tests & use of sun block
• Seems to be effecting and safe in the long term.
• Mercaptopurine is the active metabolite of Azathioprine & is often tolerated by those who cannot tolerate Azathioprine.

Question 20

ciclosporin in treatment of UC

Answer 20

• Calcineurin inhibitor
• Used as salvage therapy in patients with severe refractory colitis
• Has a rapid onset of action (initially IV then PO)
• Short-term it decreases colectomy rate by about 50%, but its use is limited due to toxicity and long term failure rate.
• Main role is bridging to Azathioprine

Question 21

biologics in treatment of UC

Answer 21

• Effective
• Newer drug in UC
  
  • Acute UC if ciclosporin is contraindicated
  • Maintenance treatment in moderate colitis if failed other therapies
    
    • Infliximab
    • Biosimilars
    • Humira
    • Gololumimab
    • Vedoluzamab

Question 22

laxatives in treatment of UC

Answer 22

• Colonic motility is affected by inflammation with rapid transit occurring through the inflamed colon
• In left sided disease the distal transit is rapid but proximal transit is slowed which can result in proximal constipation
• Relief of this proximal constipation may induce remission in left sided disease

Question 23

surgery in UC

Answer 23

• Surgery involves near total colectomy with formation of an ileostomy. This stoma may be permanent, or particularly in younger patients can be rejoined with pouch surgery at a later date.
• There are a number of criteria that can predict the likelihood of colectomy being needed acutely (% with these criteria that require colectomy are in brackets):
  
  • Predicting Colectomy:
    
    • Clinical & Biochemical:
      
      • >12 stools/day on day 2 (55%)
      • >8/day on day 3 of intensive Rx (85%)
      • 3-8/day & CRP >45 on day 3 (85%)
      • >4/day & CRP >25 on day 3 (75%)
      • Albumin <33 before day 4 (55%)
    • Radiological:
      
      • Colonic dilation >5.5cm (55% colectomy)
      • Mucosal islands on plain AXR (85%)
      • 3 or more small bowel loops (5-73%)

Question 24

risk factor of coeliac disease

Answer 24

family hisotry

Question 25

pathophysiology of coeliac

Answer 25

The primary mechanism involved in celiac disease is related to an inappropriate adaptive immune response to gluten-derived peptides. It has been ascertained that prolamines contain critical epitopes presented by either HLA-DQ2 or HLA-DQ8 induce a CD4⁺ T-lymphocytes response.

-→ gliadin

Question 26

signs and symptoms of coeliac disease

Answer 26

• Loose stools
• Bloating
• Wind
• Abdominal cramps
• Weight loss
• Dermatitis herpetiformis
• No symptoms (incidental when investigating iron def anaemia or due to family history of coeliac disease)

Question 27

prognosis of coeliac disease

Answer 27

• Untreated coeliac- increased risk fo small bowel lymphoma, small bowel cancer, osteoporosis and neurological complications such as gluten ataxia and neuropathy

Question 28

diagnosis of coeliac

Answer 28

Diagnosis

• If you suspect coeliac disease it is important that the patient continues eating a normal diet until the diagnosis is made.
  
  • tTG (tissue transglutaminase) is raised in most cases of coeliac disease, but is not a diagnostic test in adult patients
  • OGD and duodenal biopsies is the diagnostic test, and histologically you will see villous atrophy and intra-epithelial lymphocytosis

Question 29

treatment of coeliac disease

Answer 29

Dietitians are key as treatment is a lifelong gluten free diet. Gluten is found in Barley, Rye, Oats and Wheat although some patients are able to reintroduce oats into their diet.

Question 30

Dyspepsia and reflux

• Heartburn, reflux and indigestion are very common symptoms and often used interchangeably.
  
  • It is important that you clarify in your history exactly what the patient’s symptoms are when they use these terms, eg is it abdominal pain, retrosternal burning, waterbrash, vomiting or upper GI wind.
• In the absence of any red-flag symptoms it is reasonable to empirically try a PPI +/- test for H Pylori.
• If there are any red flag symptoms, atypical symptoms, associated dysphagia or weight loss or new onset at an older age investigations are indicated and an OGD (oesophago-gastro-duodenoscopy) should be considered.

Question 31

Dyspepsia and reflux

Answer 31

• Heartburn, reflux and indigestion are very common symptoms and often used interchangeably.
  
  • It is important that you clarify in your history exactly what the patient’s symptoms are when they use these terms, eg is it abdominal pain, retrosternal burning, waterbrash, vomiting or upper GI wind.
• In the absence of any red-flag symptoms it is reasonable to empirically try a PPI +/- test for H Pylori.
• If there are any red flag symptoms, atypical symptoms, associated dysphagia or weight loss or new onset at an older age investigations are indicated and an OGD (oesophago-gastro-duodenoscopy) should be considered.

can treat with antacids and PPIs e.g. omeprazole

Question 32

Dysphagia

Answer 32

Dysphagia can be caused by pathology in a number of different sites.

• A good clinical history is key as this can guide if the dysphagia is due to a problem with the oro-pharyngeal phase of swallowing (patient struggles to get the food to leave the mouth) or the oesophageal phase (things usually leave the mouth ok and then get stuck).
• Patients may also describe difficulty swallowing when in fact they mean that swallowing is painful (odynophagia).

Question 33

Oesophageal Dysphagia

Answer 33

• Either a physical obstruction or neuromuscular problem is present.
  
  • Obstruction may be a tumour, a benign (peptic) stricture or inflammation from oesophagitis.
  • Neuromuscular problems include achalasia, dysmotility and presbyoesophagus.
• OGD is usually needed to exclude an obstructive cause first and barium swallow or oesophageal manometry will look for neuromuscular problems.
• Treatment depends on the cause; dilatation for benign strictures and surgery or stenting for cancers.

Question 34

Oro-pharyngeal Dysphagia

Answer 34

• Difficulty getting the food to leave the mouth is usually due to problems coordinating the muscles that move the food bolus to the back of the mouth, as a result of neurological disease such as stroke.
• It is important to examine the patient’s cranial nerves and obtain a speech therapy assessment of the safety of their swallow.
• A video-fluoroscopy may be helpful, if their swallow remains unsafe with altered consistencies of food and fluid an enteral feeding tube may be necessary.

Question 35

Taking a GI Bleed history

Answer 35

• Find out what the patient means by passing blood.
  
  • Is this haematemesis (fresh blood vomited),
  • Coffee ground vomit (supposed to indicate altered blood but may in fact be anything that has been in the stomach)
  • Melaena (black, tarry sticky stool)
  • Fresh PR bleeding (usually indicates a lower GI bleed, but may, in a haemodynamically unstable patient suggest a brisk upper GI bleed).
• The next step is thinking about risk factors for bleeding.
  
  • Is the patient known to have varices or chronic liver disease
  • Do they have stigmata of chronic liver disease
  • Have they been on NSAIDs, antiplatelets or anticoagulants?

Question 36

Investigations for Gi bleed

Answer 36

• FBC – to check the level of Haemoglobin and platelet count (thrombocytopenia may be suggestive of chronic liver disease and platelets will need replacing if low and bleeding)
• U&E – a raised urea supports your diagnosis of upper GI bleeding
• Clotting – abnormal clotting should be corrected in order to help control the bleeding
• Group and Save (Cross Match if haemodynamically unstable) – you may need to give a blood transfusion
• LFTs – remember however that normal liver function tests do not exclude chronic liver disease
• Venous Blood gas – this is a quick way to get a haemoglobin result

Question 37

Two assessment scores for GI bleeding

Answer 37

1) ROCKALL score

2) Blatchford score

Question 38

ROCKALL score

Answer 38

• Predicts risk of death and rebleeding from an upper GI bleed
• Split in
  
  • Pre-endoscopy score
  • Post-endoscopy score that can only be completed with endoscopy findings
• Higher the score the more chance of dying

Question 39

blatchford score

Answer 39

• Predicts need for intervention (blood transfusion or therapeutic endoscopy)
• Requires blood tests
• Most useful in deciding if a patient needs admitting or not

Question 40

management of variceal bleeding

Answer 40

Variceal bleeding is a medical emergency and most often presents with fresh

haematemesis +/- melaena.

• Initial action: Fluid resuscitation if haemodynamically compromised (followed by blood)
• IV Terlipressin AND IV antibiotics
• Definitive treatment: endoscopic banding

Question 41

The definitive treatment of variceal bleeding is

Answer 41

• endoscopic banding,
• but if this does not control the bleeding a Linton or Sengstaken tube may be required as a temporary measure, or a TIPSS (trans-jugular intrahepatic porto-systemic shunt) procedure.

Question 42

management of non-variceal bleeding

Answer 42

Non-variceal bleeding covers a whole range of conditions, most commonly ulcer disease but also various vascular malformations such as angiodysplasia and dieulofoys.

These conditions are more likely to stop bleeding on their own than variceal bleeds, and it is important to ensure that the patient is as haemodynamically stable as possible before their endoscopy in order to decrease the risks of this procedure and to increase the likelihood of definitive intervention being possible.

• Initial action: gain IV access. Fluid resuscitation if haemodynamically compromised (followed by blood)
• Prescription: there is no evidence for giving PPI before the endoscopy, but this may be indicated post-endoscopy
• Definitive treatment: Discuss with the gastroenterology team. Dependent on the pathology found there are various different endoscopic treatments possible. If the bleeding cannot be stopped by endoscopy, radiological embolization or surgery may be possible. The Endoscopist will advise on the need for any medications (such as PPI to treat ulcers) after the endoscopy.