Gastroenterology Tutorial

By Lucy Havard & Suroosh Madanipour

Session plan

3 key topics (45 mins) IBD (UC & Crohn’s) + IBS; Dyspepsia & peptic ulcer disease; Liver disease;

OSCE practice (15 mins) SBAs (20 mins) Suggested further revision topics

IBD Ulcerative colitis vs Crohn’s disease

Features? Extra-intestinal? Complications? Pathology? Histology? Endoscopy? Radiology?

IBDCrohn’s disease Ulcerative colitis

(overall higher incidence)

Features Weight loss more prominent Upper gastrointestinal symptoms, mouth ulcers, perianal disease e.g. fistulas, fissures etc. Abdominal mass palpable in the right iliac fossa

Bloody diarrhoea more commonAbdominal pain in the left lower quadrantTenesmus

Extra-intestinal Primary sclerosing cholangitis (PSC) more common

Complications Obstruction, fistula, colorectal cancer

Risk of colorectal cancer higher in UC than CD

Pathology Lesions may be seen anywhere from the mouth to anusSkip lesions may be present

Inflammation always starts at rectum and never spreads beyond ileocaecal valveContinuous disease

CD UC

Histology Inflammation in all layers from mucosa to serosaIncreased goblet cellsGranulomas

No inflammation beyond submucosa (unless fulminant disease) - inflammatory cell infiltrate in lamina propriaGranulomas are infrequent

Endoscopy Deep ulcers, skip lesions - 'cobble-stone' appearance

Widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps ('pseudopolyps')

Radiology Small bowel enema - high sensitivity & specificity for examination of the terminal ileum; strictures - ‘Kantor’s string sign’; proximal bowel dilation; ‘rose thorn’ ulcers.

Barium enema - loss of haustrations; superficial ulceration ‘pseudopolyps’; in long-standing disease, colon is narrow & short - ‘drainpipe colon’.

IBS

Clinical features? Red flags? Ix?

IBSNICE guidelines 2008

A Dx of IBS should be considered if the pt has had the following for >6m: abdo pain &/or bloating &/or change in bowel habit.

Red flag features = rectal bleeding; unexplained/unintentional weight loss; FHx bowel/ovarian Ca; o/set >60yrs.

Suggested Ix = FBC, ESR/CRP, coeliac disease screen (TTG abs).

Coeliac disease

Pathology? Assoc. conditions? Ix? Findings on Bx?

Coeliac diseaseNICE guidelines 2009

Caused by sensitivity to gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption.

Assoc. conditions = dermatitis herpetiformis (a vascular, pruritic skin eruption); autoimmune disorders (DMT1, autoimmune hepatitis).

Ix = tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE; endomyseal ab (IgA); antigliadin ab (IgA or IgG) tests not recommended by NICE; anti-casein abs are also found in some pts.

Jejunal Bx = villous atrophy, crypt hyperplasia, inc. in intraepithelial lymphocytes, lamina propria infiltration w/ lymphocytes.

Dyspepsia

Red flags? Urgent referral criteria? ‘Undiagnosed dyspepsia’ Mx?

DyspepsiaNICE guidelines 2004

Red flags = chronic GI bleeding; progressive unintentional weight loss; progressive difficulty swallowing; persistent vomiting; IDA; epigastric mass, suspicious barium meal.

Urgent referral for endoscopy = red flag Sx; pts >55yrs w/: recent (rather than recurrent) & unexplained OR persistent (4-6wks).

Undiagnosed dyspepsia Mx: Review medications for possible causes Lifestyle advice Trial of full-dose PPI for 4wks ‘Test & treat’ using carbon-13 urea breath test.

Helicobacter pylori

What is it? Associations? Mx?

Helicobacter pylori

A gram -ve bacteria assoc. w/ a variety of GI problems, principally peptic ulcer disease.

Associations = peptic ulcer disease (95% of duodenal ulcers, 75% gastric ulcers); B cell lymphoma of MALT tissue; atrophic gastritis.

Mx = eradication may be achieved w/ a 7 day course of PPI + amoxicillin + clarithromycin OR PPI + metronidazole + clarithromycin.

Liver Disease

Objectives

Know what you need to know about:JaundiceDifferentials for CirrhosisLiver Function TestsThe alcoholic patientLiver Failure

Jaundice

Definition?-Yellow skin, sclerae, mucosa due to increased bilirubin

Visible?>35micromol/L

Jaundice

Pre hepatic

Hepatic

Post hepatic

Fava Beans

G6PD Deficiency

Pre Hepatic ANYTHING that causes haemolysis

-Breaks down RBCs and release UNconjugated bilirubin into the bloodstream.

Bilirubin metabolism-Gilbert’s – glucoronyltransferase deficiency-5% of population – doesn’t make you ill - SBA

Pre-Hepatic

Lab tests

- Urine: No bilirubin (conjugation makes bilirubin water soluble)

- Serum: Increased unconjugated bilirubin

Hepatic

Hepatocyte failure:-Hepatitis-Cirrhosis-Cancer

Failure of excretion:-PBC, PSC-Obstruction: Gall stones, pancreatic cancer, atresia-Drug induced cholestatis: Flucloxacillin, Fusidic Acid, Steroids

Hepatic

Lab Tests

- Urine: Bilirubin (conjugated bilirubin is water soluble), making the urine DARK COLOURED

- Stool: Pale – less bilirubin entering the gut

Think BILE OBSTRUCTION – conjugated bilirubin usually excreted into gut via bile.

Urobilinogen absent in urine too. Why?

Post Hepatic

Largely Obstructive-Gallstones-Pancreatic Cancer at the head-Cholangiocarcinoma

Courvoisier’s Law-Painless jaundice suggests a cause other than gallstones

Cirrhosis

What is it?-Consequence of chronic liver disease-Characterised by fibrosis, regenerative nodules and decline in liver function

Cirrhosis - Differential Chronic Hep B Chronic Hep C Haemochromatosis – Celtics/Nordics – Bronze Diabetes – High ferritin + iron,

low TIBC – reverse of Iron Definciency anaemia NAFLD – Insulin Resistance, Amiodarone, Methotrexate Primary bilary cirrhosis – Raised IgM – Antimitochondrial antibodies. Lots of

autoimmune associations. Deadly Sclerosing cholangitis – Ulcerative colitis - cholangiocarcinoma Autoimmune hep – Learn your HLAs, ANA positive Cystic fibrosis Budd-Chiari syndrome – thrombosis/tumour at portal vein – fulminant liver

failure or insidious cirrhosis Wilsons disease – Psych symptoms, Kayser-Fleischer Rings, treat

w/Penicillamine. Tests – low Cu, low caeruloplasmin – because Cu is being sequestered elsewhere

Alpha1 antitrypsin deficiency – low serum levels – young patient with emphysema. “Serpinopathy” – serine protease inhibitor deficiency

Drugs – eg methotrexate

Kayser-Fleischer Ring – Wilson’s Disease

LFTs

AST/ALT/ALP/Gamma GT/Bil/Alb/INR?

A set of results – What do you think?

ALT 32 (10-35) ALP 268 (35-104) Bilirubin 205 (0-20) Albumin 26 (34-50) INR 1.53 Platelets 129 (150-400) HB 11 .9 (11.5-15.5) MCV 102 (80-99)

AST/ALT

Asparate/alanine transaminase Released from “bursting” liver cells If this has already happened then may be normal The person without a liver won’t have elevated

ALT/AST AST not specific to liver – also cardiac/skeletal

muscle

De Ritis Ratio

Ratio of AST/ALT Greater than 2 – more likely Alcoholic

hepatitis Less than 1 – more likely Viral hepatitis

Causes of ALT over 1000

Viral hepatitis Drugs Ischaemia Alcohol may give raised ALT but lower

ALP/Gamma GT/5’NTD

Enzymes of bile canaliculi Raised levels could mean obstruction of bile

duct or intrahepatic cholestasis ALP not specific to liver – can suggest bone

disease eg. mets/osteomalacia Use Gamma GT/5’NTD to see if raised

ALP is biliary or not

INR

Measure of Prothrombin Time and thus Extrinsic Pathway

Demonstrates liver’s ability to synthesise Vitamin K dependent clotting factors II,VII,IX,X

Activated partial thromboplastin time (ApTT) measure of Intrinsic Pathway

In liver failure PT will be prolonged first

Hypoalbuminaemia Chronic malnutrition – no protein input Liver disease – dysfuctional synthesis Nephrotic syndrome - lost in urine

Consequence – loss of oncotic pressure >generalised oedema

Note – ascites NOT due to loss of oncotic pressure, it is due to aberrant activation of the RAA system and therefore nephrogenic Na retention. And/or vasodilation of splanchnic circulation. Mechanisms are still unclear

Hypoalbuminaemia often telling sign of impending death on COOP wards

Take home message for LFTs

How well is this person’s liver? Assess the SYNTHETIC FUNCTION

which comprises: INR Bilirubin Albumin

When these are compromised, the liver can said to be “decompensating”

A set of results – What do you think?

ALT 32 (10-35) ALP 268 (35-104) Bilirubin 205 (0-20) Albumin 26 (34-50) INR 1.53 Platelets 129 (150-400) HB 11 .9 (11.5-15.5) MCV 102 (80-99)

The Alcoholic Patient

Complications

Withdrawal Nutritional Deficiency Clotting Function Portal Hypertension Hepatorenal Syndrome Encephalopathy

Withdrawal

Alcohol depresses neurotransmitters Removal of depressant leads to

hyperexcitable state – potential for neurotoxicity and seizures

Chlordiazepoxide – start with 20mg

Nutrition

Calorie Rich Low Fat 1.5kg/day of protein Vitamin supplementation

Carnitine to reverse fatty liver Vitamin C, glutamine/acamprosate – reduce

cravings Vitamin K - clotting Thiamine – vitamin B1 – Wernicke - Korsakoff

Wernicke’s Encephalopathy Ataxia Ophthalmoplegia Nystagmus Confusion Korsakoff’s if untreated

Be wary of “sub-dural” history in SBAs

Bleeding Disorder

Liver synthetic function compromised

Give Vitamin K regardless - 10mg/day IV for 3 days

Give platelets/FFP as needed esp. in portal hypertention – splenic pooling

Portal Hypertension

Portal pressure gradient (difference between portal vein and hepatic vein) of greater than 10mmHg

Varices – backpressure leads to overdilatation of veins at anastomotic sites.

Varices

Bleeding episodes – 30-50% mortality rate B-blocker propanolol maintenance and

banding ligation

Emergency – Terlipressin, Sengstaken-Blakemore balloon tamponade, antibiotics – quinolone

Ultimatley transjugular intrahepatic portosystemic shunt may relieve pressure

Hepatorenal Syndrome

40% of cirrhotics within 5 years of diagnosis

Follows portal hypertension Splanchnic vasodilation – reduced renal

bloodflow Indicated by worsening creatinine clearance

Hepatic Encephalopathy

Liver responsible for metabolism of toxins.

Ammonia particularly important

Lactulose - clear gut flora and bind NH3 Rifaxamin – non-absorbable antibiotic to

clear gut flora

Orthotopic Liver Transplant

• Gum Hypertrophy – Ciclosporin use• Incisional Hernias

1 year after admission for alcoholic hepatitis 40% of people are dead

A sobering thought

OSCE scenario

Mrs Jones has come into hospital to have an operation to repair a hernia. Please consent her for this operation.

OSCE mark scheme – consenting a patient for an operation

Introduction Introduce with name and grade Discuss aim of Consultation “I’ve come to discuss the options

we have ahead in your case” Check Understanding “Tell me about what you understand

what’s happened so far” Elicit patient’s concerns “what are you particularly

worried about” Explain indication of Proc’/Op’ “You’ve got …. Which

means….”“We’ve discussed your case So we need to do…to investigate/treat/etc” Explain preparation required before “the procedure involves”

Explain the implications of not doing“If you don’t have… then….”

Talk through procedure Before “First we…” During “then during…” [Describe Procedure/Op] After “After you will… until results/stable/free to

go/etc”

Discuss Risks and benefits “there are some common Risks which you should be aware of”

Discuss Alternatives “Just so that you’re sure we should discuss other options

Describe out come likelihood of success“In the majority of cases….”

Discharge date “Hospital for ..days/free to go”

Follow up “come and see us in…” Restrictions on lifestyle after “rest/do not eat/stay on the ward”

Asks for questions - “Do you have any questions?” Explore concerns - “Is there anything else you’re worried

about” Future management plan - “right now we need to

do.../we’re waiting for…/wait till op’” Offer leaflets - “if you’d like some more information…

leaflet’s available” Summarise key points - “Quickly recap what we’ve talked

about” Formalise consent - “Well if that’s ok then please sign the

consent form to show that you understand what’s about to take place” Mention free withdrawal - “this is not a contract you are

free to withdraw at any stage” Thank patient

SBAs

A 5-year-old boy presents with fever, rash and hepatomegaly.

He was well until seven days before when he developed malaise, headache and fever. Subsequently a maculopapular rash had appeared over the trunk. An enlarged liver was noted by the family doctor.

He had a full term normal delivery with no neonatal problems. His immunisations are up to date. There is no family or social history of note.

Question 1

On examination Temperature 38.2 RR 20 Pulse 100

He has marked cervical lymphadenopathy, a 2 cm tender hepatomegaly and 3 cm spleen. Full blood count shows occasional atypical lymphocytes, and his AST is slightly elevated.

What is the most likely diagnosis?

A) CytomegalovirusB) Epstein-Barr VirusC) Kawasaki diseaseD) ToxoplasmosisE) Hepatitis A Infection

Answer = B – Epstein Barr virus Explanation: Hx of fever, rash

lymphadenopathy and hepatosplenomegaly is in keeping with a mononucleosis-like illness. This suspicion is supported by the atypical lymphocytes and elevated liver enzymes, which suggest a mild hepatitis is present. EBV, CMV & toxoplasmosis can cause this picture; EBV is the most common of these & therefore the most likely.

A 70-year-old male presents with haematemesis and melaena.

His presenting blood pressure is 80/46 mmHg, with a heart rate of 114 bpm. He is known to have idiopathic cirrhosis, and there is mild encephalopathy.

You start to resuscitate him with colloid, blood, FFP and dextrose.

Which of the following is the most appropriate next step at this moment?

Question 2

A) OGD (oesophago-gastro-duodenoscopy)B) CiprofloxacinC) TerlipressinD) Oral Beta BlockersE) Lactulose

Answer = C – Terlipressin Explanation - Terlipressin causes

splanchnic vasoconstriction thereby restricting bleeding from varices, which is the likely cause of bleeding in this patient

Question 3

A 50-year-old woman is seen in the clinic because of deranged liver function tests (LFTs).

She drinks 4 units of alcohol weekly. On examination she is obese with a BMI of

45kg/m2 and her LFTs show: ALT 140 (5-40) AST 150 (10-40) ALP 250 (45-105)

What is the most likely cause of this derangement?

A) DMB) HyperparathyroidC) Drug InducedD) HyperthyroidE) Hypertension

Answer = A – Diabetes Mellitus Explanation – DM associated with obesity

is the most likely cause of non-alcoholic fatty liver disease (NAFLD) in this patient.  It is caused by fatty accumulation in the liver leading to inflammation.

A 24-year-old woman is admitted with vomiting and generalised abdominal pain, six weeks after having undergone emergency abdominal surgery for an acute perforated appendicitis.

Her erect abdominal x ray is shown on the next slide:

Question 4

What is the diagnosis?

A) Crohn’s ColitsB) Ectopic PregnancyC) Ischaemic ColitisD) Small Bowel ObstructionE) Large Bowel Obstruction

Answer = D – small bowel obstruction Explanation - a perforated appendix implies

that peritonitis occurred which increases the risk of future adhesions leading to bowel obstruction. This erect AXR shows the air fluid levels in the small bowel and small bowel diameter exceeding 2.5 cm. Although an ectopic pregnancy should always be a consideration in a woman of child-bearing age, the presentation and x ray features are diagnostic.

Question 5 A 26-year-old female returns from a back packing holiday in

Eastern Europe with diarrhoea. One week ago she developed profuse watery diarrhoea together

with colicky abdominal pain. She goes to the toilet approximately 10 times daily. She occasionally feels nauseous but has had no vomiting. She has lost approximately 5 kg in weight with this illness.

On examination she has a temperature of 37.7C and appears slightly dehydrated. There is some slight tenderness on abdominal examination but no specific abnormalities are detected. PR examination reveals watery, brown faeces.

Which investigation would be most appropriate for this patient?

A) Analysis for clostridium toxinB) Blood CultureC) ColonoscopyD) Duodenal BiopsyE) Stool Microscopy and Culture

Answer = E – stool microscopy & culture Explanation – this pt has traveller’s

diarrhoea. In view of the Sx & the location of her holiday, giardiasis seems the likely diagnosis. This is best diagnosed through microscopic examination of the faeces where cysts may be seen. Rx = Metronidazole.

A 55-year-old publican presents with a haematemesis.

His wife provides a history that he has consumed approximately four cans of lager per day together with liberal quantities of spirits for many years. He has tried to stop drinking in the past but failed.

Examination reveals that he is oriented but distressed, a pulse of 120 beats per minute, a blood pressure of 108/70 mmHg, he has numerous spider naevi over his chest. Abdominal examination reveals a distended abdomen with ascites.

What would you request next for this patient?

Question 6

A) Abdominal UltrasoundB) Gastrogaffin EnemaC) EndoscopyD) LaparotomyE) Serum AFP

Answer = B – endoscopy This patient with alcohol abuse presents

with features of chronic liver disease and is now shocked due to haematemesis. Bleeding oesophageal varices should be top of the differential list and other diagnoses to consider would include peptic ulceration or haemorrhagic gastritis. An urgent endoscopy should be requested.

Question 7

A 35-year-old female presents with abdominal pain associated with bloating for the past 6 months, Which one of the following symptoms is least associated with a diagnosis of irritable bowel syndrome?

A) TenesmusB) Weight lossC) LethargyD) Back PainE) Nausea

Answer = B – weight loss Explanation – weight loss is not a feature of

IBS & underlying malignancy or IBD needs to be excluded.

Question 8 A 22-year-old man presents with a three week

history of diarrhoea. He says his bowels have not been right for the past few months and he frequently has to run to the toilet. These symptoms had seemed to be improving up until three weeks ago. For the past week he has also been passing some blood in the stool and reports the feeling of incomplete evacuation after going. He has lost no weight and has a good appetite. Examination of his abdomen demonstrates mild tenderness in the left lower quadrant but no guarding. What is the most likely diagnosis?

A) DiverticulitisB) Crohn’s DiseaseC) Ulcerative ColitisD) Colorectal CancerE) Infective Diarrhoea

Answer = C – Ulcerative colitisExplanation – Sx are typical of UC: left lower

quadrant pain, blood in stool, feeling of incomplete evacuation etc.

Question 9

A 26-year-old woman who is known to have type 1 diabetes mellitus presents with a three-month history of diarrhoea, fatigue and weight loss. She has tried excluding gluten from her diet for the past 4 weeks and feels much better. She requests to be tested so that a diagnosis of coeliac disease is confirmed. What is the most appropriate next step?

A) Check her HbA1cB) No need for further investigation as the

clinical response is diagnosticC) Check anti-endomysial antibodiesD) Arrange jejunal biopsyE) Ask her to reintroduce gluten for the next 6

weeks before reassessing

Answer = E – ask her to reintroduce gluten for the next 6wks before further testing

Explanation – serological tests and jejunal biopsy may be negative if the patient is following a gluten-free diet. The patient should eat some gluten in more than one meal every day for at least 6 weeks before further testing.

Question 10

Which one of the following features is more common in Crohn's disease than ulcerative colitis?

A) Abdominal mass palpable in RIFB) TenesmusC) Bloody DiarrhoeaD) Faecal IncontinenceE) Abdominal pain in left lower quadrant

Answer = A – abdominal mass palpable in the RIF

Question 11

Of the following, which one is the most useful prognostic marker in paracetamol overdose?

A) ALTB) Prothrombin TimeC) Paracetomol levels at presentationD) Paracetomol levels at 12hE) Parecetomol levels at 24h

Answer = B – prothrombin time Explanation - an elevated prothrombin time

signifies liver failure in paracetamol overdose and is a marker of poor prognosis. However, arterial pH, creatinine and encephalopathy are also markers of a need for liver transplantation.

Suggested further revision topics

Clostridium difficile GORD Oncology - stomach, colon, liver Dysphagia PBC PSC Wilson’s Pancreatitis

The End!!