Primary biliary cirrhosis is associated with a raised level of:ia

x A.A IgMia
B.A IgEia
C.A IgDia
D.A IgAia
E.A IgGia
Next question
Primary biliary cirrhosis
sqweqwesf erwrewfsdfs adasd dhe
Primary biliary cirrhosis is a chronic liver disorder typically seen in middle-aged
females (female:male ratio of 9:1). The aetiology is not fully understood although it is
thought to be an autoimmune condition. Interlobular bile ducts become damaged by a
chronic inflammatory process causing progressive cholestasis which may eventually
progress to cirrhosis. The classic presentation is itching in a middle-aged woman
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Associations
• Sjogren's syndrome (seen in up to 80% of patients)he
• rheumatoid arthritishe
• systemic sclerosishe
• thyroid diseasehe
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Diagnosis
• anti-mitochondrial antibodies (AMA) M2 subtype are present in 98% of patients
and are highly specifiche
• smooth muscle antibodies in 30% of patientshe
• raised serum IgMhe

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Management
• pruritus: cholestyraminehe

• fat-soluble vitamin supplementationhe

• ursodeoxycholic acidhe

• livertransplantation e.g. if bilirubin > 100 (PBC is a major indication) -

recurrence in graft can occur but is not usually a problemhe
A 25-year-old man presents with lethargy and increased skin pigmentation. Blood test
reveal deranged liver function tests and impaired glucose tolerance. Given the likely
diagnosis of haemochromatosis, what is the most appropriate initial investigation?ia
 x A.A Transferrin saturation
B.A Haematocritia
C.A Liver biopsy with Perl's stainia
D.A Serum ironia
E.A Serum ferritinia
Next question
Screening for haemochromatosis
• general population: transferrin saturation
• family members: HFE genetic testing

The British Committee for Standards in Haematology (BCSH) guidelines recommend

measuring the transferrin saturation as this is the most specific and sensitive test for
iron accumulation
Haemochromatosis: investigation
sqweqwesf erwrewfsdfs adasd dhe
Haemochromatosis is an autosomal recessive disorder of iron absorption and
metabolism resulting in iron accumulation. It is caused by inheritance of mutations in
the HFE gene on both copies of chromosome 6*. The British Committee for
Standards in Haematology (BCSH) published guidelines for the investigation and
management of haemochromatosis in 2000
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There is continued debate about the best investigation to screen for
haemochromatosis. The 2000 BCSH guidelines suggest:
• general population: transferrin saturation is considered most useful markerhe
• testing family members: genetic testing for HFE mutationhe
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These guidelines may change as HFE gene analysis become less expensive
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Diagnostic tests
• molecular genetic testing for the C282Y and H63D mutationshe
• liver biopsy: Perl's stainhe
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Typical iron study profile in patient with haemochromatosis
• transferrin saturation > 55% in men or > 50% in womenhe
• raised ferritin (e.g. > 500 ug/l) and ironhe
• low TIBChe
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Joint x-rays characteristically show chondrocalcinosis
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there are rare cases of families with classic features of genetic haemochromatosis but*
no mutation in the HFE gene
Which of the following antibiotics is most likely to cause cholestasis?ia
x A.A Co-amoxiclav
B.A Gentamicinia
C.A Ciprofloxacinia
D.A Trimethoprimia
E.A Ceftazidimeia
Next question
Drug-induced liver disease
sqweqwesf erwrewfsdfs adasd dhe
Drug-induced liver disease is generally divided into hepatocellular, cholestatic or
mixed. There is however considerable overlap, with some drugs causing a range of
changes to the liver
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The following drugs tend to cause a hepatocellular picture:
• paracetamolhe
• sodium valproate, phenytoinhe
• MAOIshe

• halothanehe
• anti-tuberculosis: isoniazid, rifampicin, pyrazinamidehe
• statins, fibrateshe
• alcoholhe
• amiodaronehe
• methyldopahe

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The following drugs tend to cause cholestasis (+/- hepatitis):
• oral contraceptive pillhe
• antibiotics: flucloxacillin, co-amoxiclav, erythromycin*, nitrofurantoinhe
• anabolic steroids, testosteroneshe
• phenothiazines: chlorpromazine, prochlorperazinehe

• sulphonylureashe
• rare reported causes: nifedipinehe
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Liver cirrhosis
• methotrexatehe
• methyldopahe
• amiodaronehe
 he earaer aeraer asdsadas eerw dssdfsselleds
risk may be reduced with erythromycin stearate*

A 46-year-old man is being investigated for indigestion. Jejunal biopsy shows

deposition of macrophages containing PAS-positive granules. What is the most likely
diagnosis?ia
A.A Bacterial overgrowthia
B.A Coeliac diseaseia
C.A Tropical sprueia
x D.A Whipple's disease
E.A Small bowel lymphomaia
Next question
Whipple's disease
sqweqwesf erwrewfsdfs adasd dhe
Whipple's disease is a rare multi-system disorder caused by Tropheryma whippelii
infection. It is more common in those who are HLA-B27 positive and in middle-aged
men
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Features
• malabsorption: diarrhoea, weight losshe
• large-joint arthralgiahe
• lymphadenopathyhe
• skin: hyperpigmentation and photosensitivityhe
• pleurisy, pericarditishe
• neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia,
myoclonushe
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Investigation
• jejunal biopsy
shows deposition of macrophages containing Periodic acid-Schiff
(PAS) granules he
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Management
• varies e.g. IV penicillin then oral co-trimoxazole for a yearhe
Which one of the following is most strongly associated with coeliac disease?ia
A.A HLA A5ia
x B.A HLA-DQ2
C.A HLA-DR2ia
D.A HLA-DR4ia
E.A HLA-B27ia
Next question
Coeliac disease
sqweqwesf erwrewfsdfs adasd dhe
Coeliac disease is caused by sensitivity to the protein gluten. Repeated exposure leads
to villous atrophy which in turn causes malabsorption. Conditions associated with
coeliac disease include dermatitis herpetiformis (a vesicular, pruritic skin eruption)
and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis). It is
strongly associated with HLA-DQ2 (95% of patients) and HLA-B8 (80%) as well as
HLA-DR3 and HLA-DR7
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Complications
• anaemia: iron, folate and
vitamin B12 deficiency (folate deficiency is more
common than vitamin B12 deficiency in coeliac disease)he
• hyposplenismhe
• osteomalacia (vitamin D deficiency)he
• lactose intolerancehe
• enteropathy-associated T-cell lymphoma of small intestinehe
• rare: oesophageal cancer, other malignancieshe
Which of the following is the best prognostic marker in paracetamol overdose?ia
A.A ALTia
x B.A Prothrombin time
C.A Paracetamol levels at presentationia
D.A Paracetamol levels at 12 hoursia
E.A Paracetamol levels at 24 hoursia
Next question
An elevated prothrombin time signifies liver failure in paracetamol overdose and is a
marker of poor prognosis
Paracetamol overdose: metabolic pathways
sqweqwesf erwrewfsdfs adasd dhe
The liver normally conjugates paracetamol with glucuronic acid/sulphate. During an
overdose the conjugation system becomes saturated leading to oxidation by P450
mixed function oxidases*. This produces a toxic metabolite (N-acetyl-B-
benzoquinone imine)
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Normally glutathione acts as a defense mechanism by conjugating with the toxin
forming the non-toxic mercapturic acid. If glutathione stores run-out, the toxin forms
covalent bonds with cell proteins, denaturing them and leading to cell death. This
occurs not only in hepatocytes but also in the renal tubules
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N-acetyl cysteine is used in the management of paracetamol overdose as it is a
precursor of glutathione and hence can increase hepatic glutathione production
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*this explains why there is a lower threshold for treating patients who take P450
inducing medications e.g. phenytoin or rifampicin
A 54-year-old female presents with a 3 month history of dysphagia affecting both
food and liquids from the start, along with symptoms of heartburn. What is the most
likely underlying diagnosis?ia
A.A Pharyngeal pouchia
B.A Gastric adenocarcinomaia
C.A Benign strictureia
D.A Oesophageal canceria
x E.A Achalasiaia
Next question
Dysphagia affecting foods and solids from the start - think achalasia
This is a classic history of achalasia, particularly dysphagia affecting both solids and
liquids from the start
Achalasia
sqweqwesf erwrewfsdfs adasd dhe
Failure of oesophageal peristalsis and of relaxation of lower oesophageal sphincter
(LOS) due to degenerative loss of ganglia from Auerbach's plexus i.e. LOS
contracted, oesophagus above dilated. Achalasia typically presents in middle-age and
is more common in women
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Clinical features
• dysphagia of BOTH liquids and solidshe
• typically variation in severity of symptomshe
• heartburnhe
• regurgitation of food - may lead to cough, aspiration pneumonia etche
• malignant change in small number of patientshe
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Investigations
• manometry: excessive LOS tone which doesn't relax on swallowing - considered
most important diagnostic testhe
• barium swallow shows grossly expanded oesophagus, fluid levelhe
• CXR: wide mediastinum, fluid levelhe
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Treatment
• cardiomyotomyhe
• balloon dilationhe
• i.e. drug therapy not particularly usefulhe
A 54-year-old man with a long history of heartburn is proven to have Barrett's
oesophagus on biopsy (histology report states non-dysplastic columnar-lined
oesophagus). What is the most suitable management?ia
A.A Reassure and dischargeia
 B.A Fundoplicationia
C.A Laser ablationia
D.A Ivor-Lewis oesophagectomyia
x E.A High-dose proton pump inhibitor
Next question
The 2005 British Society of Gastroenterology guidelines state that high-dose proton
pump inhibitor therapy is first-line treatment in such patients. There is yet insufficient
evidence to support the use of endoscopic ablation.
Barrett's oesophagus
sqweqwesf erwrewfsdfs adasd dhe
Barrett's refers to the metaplasia of the lower oesophageal mucosa, with the usual
squamous epithelium being replaced by columnar epithelium. There is an increased
risk of oesophageal adenocarcinoma, estimated at 50-100 fold.
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Histological features
• the columnarepithelium may resemble that of either the cardiac region of the
stomach or that of the small intestine (e.g. with goblet cells, brush border)he
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Management
• endoscopic surveillance with biopsieshe

• high-dose PPIhe
A 49-year-old female is referred to the gastroenterology out-patient clinic with a 3
month history of epigastric pain and diarrhoea. Her GP initially prescribed
lansoprazole 30mg od but this didn't alleviate her symptoms. The only past medical
history of note is hyperparathyroidism.
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Endoscopy revealed multiple duodenal ulcerations. What is the likely diagnosis?ia
A.A Gastric carcinomaia
B.A Coeliac diseaseia
x C.A Zollinger-Ellison syndrome
D.A Menetrier's diseaseia
E.A Crohn's diseaseia
Next question
Zollinger-Ellison syndrome typically presents with multiple gastroduodenal ulcers
causing abdominal pain and diarrhoea. High-dose proton pump inhibitors are needed
to control the symptoms. Around a third of patients may have multiple endocrine
neoplasia type I (MEN-I), explaining the hyperparathyroidism in this patient
Zollinger-Ellison syndrome
sqweqwesf erwrewfsdfs adasd dhe
Overview
 • gastrin secreting tumour usually of pancreatic originhe
• causes multiple gastroduodenal ulcershe
• 30% occur as part of MEN type I syndromehe
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Features
• multiple gastroduodenal ulcershe
• diarrhoeahe
• malabsorptionhe
A 35-year-old man who is usually fit and well presents to his GP with a 2 month
history of indigestion. His weight is stable and there is no history of dysphagia.
Examination of the abdomen is unremarkable. Of the following options, what is the
most suitable initial management?ia

A.A Three month course of a H2 receptor antagonistia

B.A H pylori eradication therapyia
C.A Proton pump inhibitor and immediate referral for endoscopyia
D.A Three month course of a proton pump inhibitoria
x E.A Urea breath testing and treat for H pylori if positive
Next question
This question highlights the NICE guidelines for the management of dyspepsia.
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It is slightly unfair question as there is no evidence to suggest whether a one month
course of a PPI or 'test and treat' strategy should be adopted first line. Many clinicians
prefer to test for H pylori first as this cannot be done within 2 weeks of acid-
suppression therapy, as false-negative results may occur
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Given the options available, only the answer is in line with current NICE guidelines
Dyspepsia
sqweqwesf erwrewfsdfs adasd dhe
In 2004 NICE published guidelines for the management of dyspepsia in primary care.
These take into account the age of the patient (younger or older than 55 years) and the
presence or absence of 'alarm signs':
• chronic gastrointestinal bleedinghe
• progressive unintentional weight losshe

• progressive difficulty swallowinghe

• persistent vomitinghe
• iron deficiency anaemiahe
• epigastric masshe
• suspicious barium mealhe
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Deciding whether urgent referral for endoscopy is needed
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Urgent referral (within 2 weeks) is indicated for patients with any alarm signs
irrespective of age
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Routine endoscopic investigation of patients of any age, presenting with dyspepsia
and without alarm signs is not necessary, however
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Patients aged 55 years and over should be referred urgently for endoscopy if
dyspepsia symptoms are:
• recent in onset rather than recurrent and he
• unexplained (e.g. new symptoms which cannot be explained by precipitants such
as NSAIDs) and he
• persistent: continuing beyond a period that would normally be associated with
self-limiting problems (e.g. up to four to six weeks, depending on the severity
of signs and symptoms)he
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Managing patients who do not meet referral criteria ('undiagnosed dyspepsia')
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This can be summarised at a step-wise approach
• 1. Review medications for possible causes of dyspepsiahe
• 2. Lifestyle advicehe
• 3. Trial of full-dose PPI for one month*he
• 4. 'Test and treat' using carbon-13 urea breath testhe
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*it is unclear from studies whether a trial of a PPI or a 'test and treat' should be used
first
A 26-year-old male blood donor is noted to have the following results:
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Bilirubin 41 µmol/L
ALP 84 U/L
ALT 23 U/L
Albumin 41 g/L

Dipstick urinalysis normal

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What is the most likely diagnosis?ia
x A.A Gilbert's syndrome
B.A Dubin-Johnson syndromeia
C.A Rotor syndromeia
D.A Hepatitis C infectionia
E.A Primary biliary cirrhosisia
Next question
An isolated hyperbilirubinaemia in 26-year-old male is likely to be secondary to
Gilbert's syndrome. The normal dipstix urinalysis excludes Dubin-Johnson and Rotor
syndrome as these both produce a conjugated bilirubinaemia
Gilbert's syndrome
sqweqwesf erwrewfsdfs adasd dhe
Gilbert's syndrome is an autosomal dominant condition of defective bilirubin
conjugation due to a deficiency of UDP glucuronyl transferase. The prevalence is
approximately 1-2% in the general population
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Features
• unconjugated hyperbilinaemia (i.e. not in urine)he
• jaundice may only be seen during an intercurrent illnesshe
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Investigation and management
• investigation: rise in bilirubin following prolonged fasting or IV nicotinic acidhe
• no treatment requiredhe
Each one of the following is associated with non-alcoholic steatohepatitis, except:ia
A.A Hyperlipidaemiaia
B.A Obesityia
C.A Sudden weight loss or starvationia
D.A Jejunoileal bypassia
x E.A Type 1 diabetes mellitus
Next question
Obese T2DM with abnormal LFTs - ? non-alcoholic steatohepatitis
Non-alcoholic steatohepatitis
sqweqwesf erwrewfsdfs adasd dhe
Non-alcoholic steatohepatitis (NASH) is a term used to describe liver changes similar
to those seen in alcoholic hepatitis in the absence of a history of alcohol abuse. It is
relatively common, being seen in 5-10% of liver biopsies. There is wide spectrum of
histological changes seen ranging from steatosis to cirrhosis. NASH may be
responsible for a proportion of patients previously labeled as cryptogenic cirrhosis
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Associated factors
• obesityhe
• hyperlipidaemiahe
• type 2 diabetes mellitushe
• jejunoileal bypasshe
• sudden weight loss/starvationhe
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Features
 • usually asymptomatiche
• hepatomegalyhe
• ALT is typically greater than ASThe
A 24-year-old man being investigated for iron-deficiency anaemia is found to have
numerous polyps in his jejunum. On examination he is also noted to have pigmented
lesions on his palms and soles. What is the likely diagnosis?ia
A.A Hereditary non-polyposis colorectal carcinomaia
B.A Gardner's syndromeia
C.A Familial adenomatous polyposisia
x D.A Peutz-Jeghers syndrome
E.A Hereditary haemorrhagic telangiectasiaia
Next question
Hereditary haemorrhagic telangiectasia is associated with mucocutaneous lesions and
iron-deficiency anaemia but intestinal polyps are not a feature
Peutz-Jeghers syndrome
sqweqwesf erwrewfsdfs adasd dhe
Peutz-Jeghers syndrome is an inherited condition characterised by numerous
hamartomatous polyps in GI tract (mainly small bowel) associated with pigmented
freckles on the lips, face, palms and soles. The polyps undergo malignant change in
less than 3% of patients
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Genetics
• autosomal dominanthe
• responsible gene encodes serine threonine kinase LKB1 or STK11he
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Features
• hamartomatous polyps in GI tracthe
• pigmented lesions on lips, oral mucosa, face, palms and soleshe
• intestinal obstruction e.g. intussusceptionhe
• GI bleedinghe
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Management
• conservative unless complications develophe
Each one of the following is a recognised complication of gastro-oesophageal reflux
disease except:ia
A.A Oesophageal carcinomaia
B.A Barrett's oesophagusia
C.A Anaemiaia
x D.A Achalasiaia
 E.A Benign stricturesia
Next question
GORD
sqweqwesf erwrewfsdfs adasd dhe
Management
• no role for H pylori eradicationhe
• give high-dose PPI, reducing laterhe
• anti-reflux surgery has high relapse ratehe
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Complications
• oesophagitishe
• ulcershe

• anaemiahe
• benign strictureshe
• Barrett's oesophagushe
• oesophageal carcinomahe
Crohn's disease is associated with each one of the following findings, except:ia
x A.A Inflammation confined to mucosa and submucosa
B.A Non-caseating granulomasia
C.A Rose-thorn ulcersia
D.A Cobblestone patternia
E.A Fistulasia
Next question
IBD: histology
sqweqwesf erwrewfsdfs adasd dhe
This histological differences between ulcerative colitis and Crohn's are summarised
below:
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Ulcerative colitis
• inflammation in mucosa and submucosa only (unless fulminant disease)he
• widespread ulceration with preservation of adjacent mucosa which has the
appearance of polyps ('pseudopolyps')he
• inflammatory cell infiltrate in lamina propriahe
• crypt abscesses neutrophils migrate through the walls of glands to form he
• depletion of goblet cells and mucin from gland epitheliumhe
• granulomas are infrequenthe
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Crohn's
 • inflammation occurs in all layers, down to the serosa --> strictures, fistulas,
adhesions etche
• oedema of mucosa and submucosa, combined with deep fissured ulcers 'rose-
thorn' --> 'cobblestone' patternhe
• lymphoid aggregateshe
• non-caseating granulomashe
Which of the following conditions is least associated with Helicobacter pylori?ia
A.A Gastric carcinomaia
B.A B cell lymphoma of MALT tissueia
x C.A Gastro-oesophageal reflux disease
D.A Atrophic gastritisia
E.A Peptic ulcer diseaseia
Next question
H Pylori
sqweqwesf erwrewfsdfs adasd dhe
Overview
• Gram negative bacteriahe
• produces ureasehe
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Associations
• peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers)he
• gastric cancerhe
•B cell lymphoma of MALT tissue (eradication of H pylori results causes
regression in 80% of patients)he
• atrophic gastritishe
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The role of H pylori in Gastro-oesophageal reflux disease (GORD) is unclear - there
is currently no role in GORD for the eradication of H pylori

Which one of the following medications is least associated with dyspepsia?ia

A.A Isosorbide mononitrateia
B.A Prednisoloneia
C.A Aminophyllineia
x D.A Atenololia
E.A Amlodipineia
Next question
Drugs causing dyspepsia
sqweqwesf erwrewfsdfs adasd dhe
Causes
• NSAIDshe
• bisphosphonateshe
• steroidshe
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The following drugs may cause reflux by reducing lower oesophageal sphincter
pressure
• calcium channel blockershe
• nitrateshe

• theophyllineshe
Which one of the following is true regarding bacterial exotoxins?ia
x A.A They are mainly produced by Gram positive bacteria
B.A Cholera toxin inhibits cAMP release in intestinal cellsia
C.A Diphtheria toxin necrosis is limited to the pharynx, nasopharynx and
tonsilsia
D.A Staph. aureus exotoxins are not known to cause gastroenteritisia
E.A 'Lockjaw' seen in tetanus is secondary to blockade of the neuromuscular
junction by Botulinus toxinia
Next question
Exotoxins
sqweqwesf erwrewfsdfs adasd dhe
Exotoxins are generally released by Gram positive bacteria with the notable exception
of Vibrio cholerae
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Cholera toxin causes activation of adenylate cyclase leading to increases in cAMP
levels, which in turn leads to increased chloride secretion.
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Diphtheria toxin commonly causes a 'diphtheric membrane' on tonsils caused by
necrotic mucosal cells. Systemic distribution may produce necrosis of myocardial,
neural and renal tissue.
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Staph. aureus exotoxins lead to acute gastroenteritis, toxic shock syndrome and
Staphylococcal scalded skin syndrome
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Lockjaw is caused by Clostridium tetani neurotoxin (tetanospasmin)
A 25-year-old woman develops deranged liver function tests following the
introduction of a new drug. Alb 40, Bilirubin 46, ALT 576, ALP 95, yGT 150. Which
of the following drugs is the most likely cause?ia
A.A Oral contraceptive pillia
x B.A Sodium valproate
C.A Flucloxacillinia
D.A Chlorpromazineia
 E.A Tetracyclineia
Next question
The liver function tests suggest a hepatitis rather than cholestasis. Sodium valproate
may be associated with such a picture
Drug-induced liver disease
sqweqwesf erwrewfsdfs adasd dhe
Drug-induced liver disease is generally divided into hepatocellular, cholestatic or
mixed. There is however considerable overlap, with some drugs causing a range of
changes to the liver
he earaer aeraer asdsadas eerw dssdfsselleds
The following drugs tend to cause a hepatocellular picture:
• paracetamolhe
• sodium valproate, phenytoinhe
• MAOIshe
• halothanehe
• anti-tuberculosis: isoniazid, rifampicin, pyrazinamidehe
• statins, fibrateshe
• alcoholhe
• amiodaronehe
• methyldopahe
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The following drugs tend to cause cholestasis (+/- hepatitis):
• oral contraceptive pillhe
• antibiotics: flucloxacillin, co-amoxiclav, erythromycin*, nitrofurantoinhe
• anabolic steroids, testosteroneshe
• phenothiazines: chlorpromazine, prochlorperazinehe
• sulphonylureashe
• rare reported causes: nifedipinehe
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Liver cirrhosis
• methotrexatehe
• methyldopahe
• amiodaronehe
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risk may be reduced with erythromycin stearate*

Each one of the following statements is true regarding hepatitis A, except:ia

A.A Has an incubation period of 2-4 weeksia
x B.A May cause chronic hepatitis
C.A It is a RNA virusia
D.A May cause hepatosplenomegalyia
E.A Spread by the faeco-oral routeia
Next question
Hepatitis A
sqweqwesf erwrewfsdfs adasd dhe
Hepatitis A is typically a benign, self-limiting disease, with a serious outcome being
very rare
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Overview
• incubation period (weeks) = 2-4, viraemia transienthe
• structure = RNAhe
• transmission = faecal-oral spread, often in institutionshe
• doesn't cause chronic diseasehe

• vaccination available - highly effective with long lasting immunityhe

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Features
• flu-like prodrome he
• jaundice, hepatosplenomegalyhe
A 34-year-old HIV positive man presents to his GP due to jaundiced sclera. Liver
function tests are as follows:
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Albumin 34 g/l
ALP 540 iu/l
Bilirubin 67 µmol/l
ALT 45 iu/l
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What is the most likely diagnosis?ia
A.A Hepatic abscessia
B.A Fungal obstruction of the bile ductia
C.A Duodenal adenomaia
D.A Primary biliary cirrhosisia
x E.A Sclerosing cholangitis
Next question
HIV: biliary and pancreatic disease
sqweqwesf erwrewfsdfs adasd dhe
The most common cause of biliary disease in patients with HIV is sclerosing
cholangitis due to infections such as CMV, Cryptosporidium and Microsporidia
he earaer aeraer asdsadas eerw dssdfsselleds
Pancreatitis in the context of HIV infection may be secondary to anti-retroviral
treatment (especially didanosine) or by opportunistic infections e.g. CMV
Which one of the following causes of diarrhoea has the shortest incubation period?ia
A.A Salmonellaia
B.A Shigellaia
C.A Campylobacteria
D.A E. coliia
x E.A Bacillus cereus
Next question
Gastroenteritis
sqweqwesf erwrewfsdfs adasd dhe
Which organism - clues
he earaer aeraer asdsadas eerw dssdfsselleds
Most common cause of traveller's diarrhoea is E coli
he earaer aeraer asdsadas eerw dssdfsselleds
Incubation period
• 1-6 hrs: Staph aureus, Bacillus cereus he
• 12-48 hrs: Salmonella, E. colihe
• 48-72 hrs: Shigella, Campylobacterhe
•> 7 days: Giardiasis, Amoebiasishe
he earaer aeraer asdsadas eerw dssdfsselleds
Stereotypical histories
• profuse, watery diarrhoea: cholerahe
• prolonged, non-bloody diarrhoea: Giardiahe
• bloody diarrhoea:, vomiting, abdo pain: Shigellahe
• severe vomiting: Staphylococcus aureushe
Which of the following histological findings is not associated with coeliac disease?ia
A.A Villous atrophyia
B.A Crypt hyperplasiaia
x C.A Non-caseating granulomas
D.A Lamina propria infiltration with lymphocytesia
E.A Increase in intraepithelial lymphocytesia
Next question
Non-caseating granulomas are seen in conditions such as Crohn's disease but are not
associated with coeliac disease
Coeliac disease: investigation
sqweqwesf erwrewfsdfs adasd dhe
Coeliac disease is caused by sensitivity to the protein gluten. Repeated exposure leads
to villous atrophy which in turn causes malabsorption. Conditions associated with
coeliac disease include dermatitis herpetiformis (a vesicular, pruritic skin eruption)
and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis)
he earaer aeraer asdsadas eerw dssdfsselleds
Diagnosis is made by a combination of immunology and jejunal biopsy. Villous
atrophy and immunology should reverse on a gluten-free diet
he earaer aeraer asdsadas eerw dssdfsselleds
Immunology
• endomyseal antibody (IgA, 95% specific)he
• alpha-gliadin antibody (IgA/IgG)he
• TTG (tissue transglutinamise) antibodies (IgA)he
• anti-casein antibodies are also found in some patientshe
he earaer aeraer asdsadas eerw dssdfsselleds
Jejunal biopsy
• villous atrophyhe
• crypt hyperplasiahe
• increase in intraepithelial lymphocyteshe
• lamina propria infiltration with lymphocyteshe
he earaer aeraer asdsadas eerw dssdfsselleds
Rectal gluten challenge has been described but is not widely used

A 25-year-old female currently under investigation for secondary amenorrhoea

presents with jaundiced sclera. On examination spider naevi are present along with
tender hepatomegaly. Blood tests show:
he earaer aeraer asdsadas eerw dssdfsselleds
Hb 11.6 g/dl
Plt 145 * 109/l
WCC 6.4 * 109/l

Albumin 33 g/l
Bilirubin 78 µmol/l
ALT 245 iu/l
he earaer aeraer asdsadas eerw dssdfsselleds
What is the most likely diagnosis?ia
A.A Haemochromatosisia
B.A Wilson's diseaseia
C.A Primary biliary cirrhosisia
x D.A Autoimmune hepatitis
E.A Primary sclerosing cholangitisia
Next question
The combination of deranged LFTs combined with secondary amenorrhoea in a
 young female strongly suggest autoimmune hepatitis
Autoimmune hepatitis
sqweqwesf erwrewfsdfs adasd dhe
Autoimmune hepatitis is condition of unknown aetiology which is most commonly
seen in young females. Recognised associations include other autoimmune disorders,
hypergammaglobulinaemia and HLA B8, DR3.Two types of autoimmune hepatitis
have been characterised according to the types of circulating antibodies present
he earaer aeraer asdsadas eerw dssdfsselleds
Type I Type II
Anti-nuclear antibodies (ANA) and/or anti- Anti-liver/kidney microsomal
smooth muscle antibodies (SMA) type 1 antibodies (LKM1)
he earaer aeraer asdsadas eerw he earaer aeraer asdsadas eerw
dssdfsselleds dssdfsselleds
Affects both adults and children Affects children only
he earaer aeraer asdsadas eerw dssdfsselleds
Features
• may present with signs of chronic liver diseasehe
• acute hepatitis: fever, jaundice etc (only 25% present in this way)he
• amenorrhoea (common)he
• ANA/SMA/LKM1 antibodies, raised IgG levelshe
• liverbiopsy: inflammation extending beyond limiting plate 'piecemeal necrosis',
bridging necrosishe
he earaer aeraer asdsadas eerw dssdfsselleds
Management
• steroids, other immunosuppressants e.g. azathioprinehe
• liver transplantationhe
Each one of the following is associated with oesophageal cancer, except:ia
A.A Achalasiaia
B.A Smokingia
C.A Gastro-oesophageal reflux diseaseia
x D.A Helicobacter pylori
E.A Alcoholia

Next question
Oesophageal cancer
sqweqwesf erwrewfsdfs adasd dhe
Overview
• classically squamous
carcinoma is the most common cell type but the incidence
of adenocarcinoma is rising rapidlyhe
• majority of tumours are in the middle thirdhe
he earaer aeraer asdsadas eerw dssdfsselleds
Risk factors
• smokinghe
• alcoholhe
• GORDhe
• Barrett's oesophagushe
• achalasiahe
• Plummer-Vinson syndromehe
• rare: coeliac disease, sclerodermahe
he earaer aeraer asdsadas eerw dssdfsselleds
Management
• CT for staginghe
Each one of the following is a risk factor for gastric cancer, except:ia
A.A Smokingia
x B.A Blood group O
C.A Nitrates in dietia
D.A Chronic atrophic gastricia
E.A H. pylori infectionia
Next question
Gastric cancer
sqweqwesf erwrewfsdfs adasd dhe
Epidemiology
• overall incidence is decreasing, but incidence of tumours arising from the cardia
is increasinghe
• peak age = 70-80 yearshe
• more common in Japan, China, Finland and Columbia than the Westhe
• more common in males, 2:1he
he earaer aeraer asdsadas eerw dssdfsselleds
Associations
• H. pylori infectionhe
• blood group A: gAstric cAncerhe
• chronic atrophic gastriche
• gastric adenomatous polypshe
• pernicious anaemiahe
• smokinghe
• diet: salty, spicy, nitrateshe
• may be negatively associated with duodenal ulcerhe
he earaer aeraer asdsadas eerw dssdfsselleds
Investigation
• diagnosis: endoscopy with biopsyhe
• staging: CT or endoscopic ultrasound - endoscopic ultrasound has recently been
shown to be superior to CThe
A 38-year-old female with a long history of alcohol excess presents with abdominal
pain, weight loss and clay-coloured stools. What is the most suitable investigation to
confirm the diagnosis?ia
A.A Endoscopic ultrasoundia
B.A Endoscopic retrograde cholangiopancreatographyia
C.A Ultrasound abdomenia
x D.A CT abdomen
E.A Endoscopy with D2 biopsyia
Next question
This patient has chronic pancreatitis. CT is the most sensitive method to detect the
characteristic pancreatic calcification which is associated with the condition
Chronic pancreatitis
sqweqwesf erwrewfsdfs adasd dhe
Chronic pancreatitis is an inflammatory condition which can ultimately affect both the
exocrine and endocrine functions of the pancreas. Around 80% of cases are due to
alcohol excess with up to 20% of cases being unexplained
he earaer aeraer asdsadas eerw dssdfsselleds
Features
• pain is typically worse 15 to 30 minutes following a mealhe
• steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5
and 25 years after the onset of painhe
• diabetesmellitus develops in the majority of patients. It typically occurs more
than 20 years after symptom begin. Patients often require lower doses of
insulin than other diabetic patientshe
he earaer aeraer asdsadas eerw dssdfsselleds
Investigation
• abdominal x-ray shows pancreatic calcification in 30% of caseshe
• CT is more sensitive at detecting pancreatic calcificationhe
• functional tests: pancreolauryl and
Lundh tests may be used to assess exocrine
function if imaging inconclusivehe
he earaer aeraer asdsadas eerw dssdfsselleds
Management
• pancreatic enzyme supplementshe
• analgesiahe
• antioxidants: limited evidence base - one study suggests benefit in early
diseasehe
A 42-year-old dentist presents to his GP complaining of persistent lethargy. Routine
bloods show abnormal liver function tests so a hepatitis screen is sent. The results are
shown below:
he earaer aeraer asdsadas eerw dssdfsselleds
Anti-HAV IgG negative
HBsAg negative
Anti-HBs positive
Anti-HBc negative
Anti-HCV positive
he earaer aeraer asdsadas eerw dssdfsselleds
What do these results most likely demonstrate?ia
A.A Hepatitis B infectionia
B.A Hepatitis C infectionia
C.A Previous vaccination to hepatitis B and Cia
x D.A Hepatitis C infection with previous hepatitis B vaccination
E.A Hepatitis B and C infectionia
Next question
Given the deranged liver function tests these results most likely indicate previous
hepatitis B vaccination with active hepatitis C infection. However, around 15% of
patients exposed to the hepatitis C virus clear the infection. It would therefore be
necessary to perform a HCV PCR to see if the virus is still present
he earaer aeraer asdsadas eerw dssdfsselleds
There is currently no vaccination for hepatitis C
Hepatitis C
sqweqwesf erwrewfsdfs adasd dhe
Transmission
• risk of transmission during a needle stick injury is about 2%he
• the vertical transmission rate from mother to child is about 6%he
• breast feeding is not contraindicated in mothers with hepatitis Che
• the risk of transmitting the virus during sexual intercourse is probably less than
5%he
he earaer aeraer asdsadas eerw dssdfsselleds
Features
• after exposure to the hepatitis C virus less than 20% of patients develop an he
acute hepatitis
he earaer aeraer asdsadas eerw dssdfsselleds
Complications
• chronic infection(85%) - only 15% of patients will clear the virus and will hence
the majority will develop chronic hepatitis Che
• cirrhosis (20-30% of those with chronic disease)he
• hepatocellular cancerhe
 • cryoglobulinaemiahe
he earaer aeraer asdsadas eerw dssdfsselleds
Management
• currently a combination of interferon-alpha and ribavirin are usedhe
he earaer aeraer asdsadas eerw dssdfsselleds
Complications of treatment
• ribavirin - side-effects: haemolytic anaemia, cough. Women should not become
he
pregnant within 6 months of stopping ribavirin as it is teratogenic
• interferonalpha - side-effects: fatigue, leukopenia, thrombocytopenia,
depressionhe
Which one of the following is most associated with the development of acute
pancreatitis?ia
x A.A Hyperchylomicronaemiaia
B.A Amyloidosisia
C.A Hypogammaglobulinaemiaia
D.A Hypercholesterolaemiaia
E.A Hypotriglyceridaemiaia
Next question
Hyperchylomicronaemia may be caused by hereditary lipoprotein lipase deficiency
and apolipoprotein CII deficiency. It predisposes to recurrent attacks of acute
pancreatitis
Acute pancreatitis: causes
sqweqwesf erwrewfsdfs adasd dhe
The vast majority of cases in the UK are caused by gallstones and alcohol
he earaer aeraer asdsadas eerw dssdfsselleds
Popular mnemonic is GET SMASHED
• Gallstoneshe
• Ethanolhe
• Traumahe
• Steroidshe
• Mumps (other viruses include Coxsackie B)he
• Autoimmune (e.g. polyarteritis nodosa), Ascaris infectionhe
• Scorpion venomhe
• Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia,
Hypothermiahe
• ERCPhe
• Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, frusemide,
pentamidine, steroids, sodium valproate)he
 he earaer aeraer asdsadas eerw dssdfsselleds
pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine*

A 31-year-old female is admitted to the Emergency Department following a

paracetamol overdose. The paracetamol level comes back as elevated but the doctor is
unsure which treatment line to use. Which one of the following features in the
medical history would classify the patient as high risk?ia
A.A Hypothyroidismia
x B.A Anorexia nervosa
C.A Previous paracetamol overdoseia
D.A Combined overdose with codeineia
E.A Long-term sodium valproate useia
Next question
Paracetamol overdose: risk factors
sqweqwesf erwrewfsdfs adasd dhe
The following groups of patients are at an increased risk of developing hepatotoxicity
following a paracetamol overdose:
• alcoholicshe
• patients on P450 enzyme inducers (rifampicin, phenytoin, carbmazepine)he
• anorexia nervosa: decreased glutathione storeshe
• HIVhe
Which of the following statements is true regarding the genetics of colon cancer?ia

A.A Hereditary non-polyposis colorectal carcinoma is a autosomal

recessive conditionia
B.A The adenomatous polyposis coli gene is located on chromosome 12ia
C.A Around 50% of patients with familial adenomatous polyposis develop
colon canceria
D.A Both hereditary and non-hereditary colon cancers typically present at
60-70 yrs of ageia
E.A Non-inherited colon cancer often involves mutation of the
x
adenomatous polyposis coli geneia
Next question
Colorectal cancer: genetics
sqweqwesf erwrewfsdfs adasd dhe
It is currently thought there are three types of colon cancer:
• sporadic (95%)he
• hereditary non-polyposis colorectal carcinoma (HNCPP, 5%)he
• familial adenomatous polyposis (FAP, <1%)he
he earaer aeraer asdsadas eerw dssdfsselleds
Studies have shown that sporadic colon cancer may be due to a series of genetic
mutations. For example, more than half of colon cancers show allelic loss of the APC
gene. It is believed a further series of gene abnormalities e.g. activation of the K-ras
oncogene, deletion of p53 and DCC tumour suppressor genes lead to invasive
carcinoma
he earaer aeraer asdsadas eerw dssdfsselleds
HNPCC , an autosomal dominant condition, is the most common form of inherited
colon cancer. Around 90% of patients develop cancers, often of the proximal colon,
which are often poorly differentiated and highly aggressive. Currently four gene
mutations have been identified (including in the hMLH1 and hMSH2 genes). The
Amsterdam criteria are sometimes used to aid diagnosis:
he earaer aeraer asdsadas eerw dssdfsselleds
Amsterdam criteria for HNPCC
• at least 3 family members with colon cancerhe
• the cases span at least two generationshe
• at least one case diagnosed before the age of 50 yearshe
he earaer aeraer asdsadas eerw dssdfsselleds
FAP is a rare autosomal dominant condition which leads to the formation of hundreds
of polyps by the age of 30-40 years. Patients inevitably develop carcinoma. It is due
to a mutation in a tumour suppressor gene called adenomatous polyposis coli gene
(APC), located on chromosome 5. Genetic testing can be done by analysing DNA
from a patients white blood cells. Patients generally have a total colectomy with ileo-
.anal pouch formation in their twenties
he earaer aeraer asdsadas eerw dssdfsselleds
Patients with FAP are also at risk from duodenal tumours. A variant of FAP called
Gardener's syndrome can also feature osteomas of the skull and mandible, retinal
pigmentation and epidermoid cysts on the skin

Which one of the following is most suggestive of Wilson's disease?ia

A.A Reduced hepatic copper concentrationia
B.A Reduced 24hr urinary copper excretionia
C.A Increased skin pigmentationia
x D.A Reduced serum caeruloplasmin
E.A Reduced serum copperia
Next question
Wilson's disease
sqweqwesf erwrewfsdfs adasd dhe
Wilson's disease is an autosomal recessive disorder characterised by excessive copper
deposition in the tissues. Metabolic abnormalities include increased copper absorption
from the small intestine and decreased hepatic copper excretion. Wilson's disease is
caused by a defect in the ATP7B gene located on chromosome 13
he earaer aeraer asdsadas eerw dssdfsselleds
The onset of symptoms is usually between 10 - 25 years. Children usually present
with liver disease whereas the first sign of disease in young adults is often
 neurological disease
he earaer aeraer asdsadas eerw dssdfsselleds
Features result from excessive copper deposition in the tissues, especially the brain,
liver and cornea:
• liver: hepatitis, cirrhosishe
• neurological: speech and behavioural problems are often the first manifestations.
Also: tremor, choreahe
• Kayser-Fleischer ringshe
• renal tubular acidosis (esp. Fanconi syndrome)he
• haemolysishe
• blue nailshe
he earaer aeraer asdsadas eerw dssdfsselleds
Diagnosis
• reduced serum caeruloplasminhe
• increased 24hr urinary copper excretionhe
he earaer aeraer asdsadas eerw dssdfsselleds
Management
• D-penicillamine: chelates copperhe
Which one of the following brush border enzymes cleaves glucose and galactose?ia
A.A Dipeptidaseia
B.A A-dextrinaseia
C.A Maltaseia
x D.A Lactaseia
E.A Sucraseia

Next question
Brush border enzymes:
• maltase: glucose + glucose
• sucrase: glucose + fructose
• lactase: glucose + galactose

Gastrointestinal physiology: brush border enzymes

sqweqwesf erwrewfsdfs adasd dhe
The following brush border enzymes are involved in the breakdown of carbohydrates:
• maltase - glucose + glucosehe
• sucrase - glucose + fructosehe
• lactase - glucose + galactosehe
Ulcerative colitis is associated with each one of the following, except:ia
 A.A Pseudopolypsia
B.A Drainpipe colonia
C.A Loss of haustrations on barium enemaia
x D.A Rose thorn ulcers
E.A Crypt abscessesia
Next question
Ulcerative colitis
sqweqwesf erwrewfsdfs adasd dhe
Basics
• always starts at rectumhe
• never spreads beyond ileocaecal valvehe
• continuoushe
he earaer aeraer asdsadas eerw dssdfsselleds
Pathology
• red, raw mucosa, bleeds easilyhe
• no inflammation beyond submucosa (unless fulminant disease)he
• widespread ulceration with preservation of adjacent mucosa which has the
appearance of polyps ('pseudopolyps')he
• inflammatory cell infiltrate in lamina propriahe
• neutrophils migrate through the walls of glands to form crypt abscesseshe
• depletion of goblet cells and mucin from gland epitheliumhe
• granulomas are infrequenthe
he earaer aeraer asdsadas eerw dssdfsselleds
Barium enema
• loss of haustrationshe
• superficial ulceration, 'pseudopolyps'he
• long standing disease: colon is narrow and short -'drainpipe colon'he
The most common type of inherited colorectal cancer:ia
A.A Familial adenomatous polyposisia
B.A Li-Fraumeni syndromeia
x C.A Hereditary non-polyposis colorectal carcinoma
D.A Fanconi syndromeia
E.A Peutz-Jeghers syndromeia
Next question
Colorectal cancer: genetics
sqweqwesf erwrewfsdfs adasd dhe
It is currently thought there are three types of colon cancer:
 • sporadic (95%)he
• hereditary non-polyposis colorectal carcinoma (HNCPP, 5%)he
• familial adenomatous polyposis (FAP, <1%)he
he earaer aeraer asdsadas eerw dssdfsselleds
Studies have shown that sporadic colon cancer may be due to a series of genetic
mutations. For example, more than half of colon cancers show allelic loss of the APC
gene. It is believed a further series of gene abnormalities e.g. activation of the K-ras
oncogene, deletion of p53 and DCC tumour suppressor genes lead to invasive
carcinoma
he earaer aeraer asdsadas eerw dssdfsselleds
HNPCC , an autosomal dominant condition, is the most common form of inherited
colon cancer. Around 90% of patients develop cancers, often of the proximal colon,
which are often poorly differentiated and highly aggressive. Currently four gene
mutations have been identified (including in the hMLH1 and hMSH2 genes). The
Amsterdam criteria are sometimes used to aid diagnosis:
he earaer aeraer asdsadas eerw dssdfsselleds
Amsterdam criteria for HNPCC
• at least 3 family members with colon cancerhe
• the cases span at least two generationshe
• at least one case diagnosed before the age of 50 yearshe
he earaer aeraer asdsadas eerw dssdfsselleds
FAP is a rare autosomal dominant condition which leads to the formation of hundreds
of polyps by the age of 30-40 years. Patients inevitably develop carcinoma. It is due
to a mutation in a tumour suppressor gene called adenomatous polyposis coli gene
(APC), located on chromosome 5. Genetic testing can be done by analysing DNA
from a patients white blood cells. Patients generally have a total colectomy with ileo-
.anal pouch formation in their twenties
he earaer aeraer asdsadas eerw dssdfsselleds
Patients with FAP are also at risk from duodenal tumours. A variant of FAP called
Gardener's syndrome can also feature osteomas of the skull and mandible, retinal
pigmentation and epidermoid cysts on the skin

A 34-year-old male is admitted with central abdominal pain radiating through to the
back and vomiting. The following results are obtained:
he earaer aeraer asdsadas eerw dssdfsselleds
Amylase 1,245 u/dl
he earaer aeraer asdsadas eerw dssdfsselleds
Which one of the following medications is most likely to be responsible?ia

A.A Phenytoinia
x B.A Sodium valproate
C.A Metoclopramideia
D.A Sumatriptania
 E.A Pizotifenia
Next question
Sodium valproate induced pancreatitis is more common in young adults and tends to
occur within the first few months of treatment. Asymptomatic elevation of the
amylase level is seen in up to 10% of patients
Acute pancreatitis: causes
sqweqwesf erwrewfsdfs adasd dhe
The vast majority of cases in the UK are caused by gallstones and alcohol
he earaer aeraer asdsadas eerw dssdfsselleds
Popular mnemonic is GET SMASHED
• Gallstoneshe
• Ethanolhe
• Traumahe
• Steroidshe
• Mumps (other viruses include Coxsackie B)he
• Autoimmune (e.g. polyarteritis nodosa), Ascaris infectionhe
• Scorpion venomhe
• Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia,
Hypothermiahe
• ERCPhe
• Drugs(azathioprine, mesalazine*, didanosine, bendroflumethiazide, frusemide,
pentamidine, steroids, sodium valproate)he
he earaer aeraer asdsadas eerw dssdfsselleds
*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine
Which of the following tests is most suitable in screening patients for coeliac disease?
ia
A.A Anti-casein antibodiesia
x B.A Anti-endomyseal antibodies
C.A Anti-gliadin antibodiesia
D.A Xylose absorption testia
E.A CRPia
Next question
Anti-endomyseal antibodies are the most sensitive and specific way to screen for
coeliac disease from the listed options.
Coeliac disease: investigation
sqweqwesf erwrewfsdfs adasd dhe
Coeliac disease is caused by sensitivity to the protein gluten. Repeated exposure leads
to villous atrophy which in turn causes malabsorption. Conditions associated with
coeliac disease include dermatitis herpetiformis (a vesicular, pruritic skin eruption)
and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis)
he earaer aeraer asdsadas eerw dssdfsselleds
Diagnosis is made by a combination of immunology and jejunal biopsy. Villous
atrophy and immunology should reverse on a gluten-free diet
he earaer aeraer asdsadas eerw dssdfsselleds
Immunology
• endomyseal antibody (IgA, 95% specific)he
• alpha-gliadin antibody (IgA/IgG)he
• TTG (tissue transglutinamise) antibodies (IgA)he
• anti-casein antibodies are also found in some patientshe
he earaer aeraer asdsadas eerw dssdfsselleds
Jejunal biopsy
• villous atrophyhe
• crypt hyperplasiahe
• increase in intraepithelial lymphocyteshe
• lamina propria infiltration with lymphocyteshe
he earaer aeraer asdsadas eerw dssdfsselleds
Rectal gluten challenge has been described but is not widely used
A 45-year-old man is noted to have non-tender, smooth hepatomegaly associated
Dupuytren's contracture and parotid enlargement. He recently returned from a holiday
in Thailand. What is the likely diagnosis?ia
A.A Primary hepatomaia
B.A Hydatid diseaseia
x C.A Alcoholic liver disease
D.A Viral hepatitisia
E.A Tricuspid regurgitationia
Next question
Both Dupuytren's contracture and parotitis are associated with alcoholic liver disease
Hepatomegaly
sqweqwesf erwrewfsdfs adasd dhe
Common causes of hepatomegaly
• Cirrhosis: ifearly disease, later liver decreases in size. Associated with a non-
tender, firm liverhe
• Malignancy: metastatic spread or primary hepatoma. Associated with a hard,
irregular. liver edgehe
• Right heart failure: firm, smooth, tender liver edge. May be pulsatilehe
he earaer aeraer asdsadas eerw dssdfsselleds
Other causes
• viral hepatitishe
• glandular feverhe
• malariahe
 • abscess: pyogenic, amoebiche
• hydatid diseasehe
• haematological malignancieshe
• haemochromatosishe
• primary biliary cirrhosishe
• sarcoidosis, amyloidosishe
Each one of the following is associated with vitamin C deficiency, except:ia
x A.A Visual field defects
B.A Lethargyia
C.A Macrocytic anaemiaia
D.A Epistaxisia
E.A Gingivitisia
Next question
Vitamin C deficiency
sqweqwesf erwrewfsdfs adasd dhe
Vitamin C deficiency (scurvy) leads to defective synthesis of collagen resulting in
capillary fragility (bleeding tendency) and poor wound healing
he earaer aeraer asdsadas eerw dssdfsselleds
Features
• gingivitis, loose teethhe
• bleeding from gums, haematuria, epistaxishe
• general malaisehe
• macrocytic anaemia is occasionally notedhe
A 45-year-old man is admitted to the Emergency Department with severe abdominal
pain. He smokes 20 cigarettes a day and drinks approximately 50 units of alcohol per
week. He also complains of sudden deterioration in vision. Fundoscopy reveals shows
multiple micro infarcts (cotton wool spots). Which investigation would best confirm
the most likely diagnosis?ia
A.A Gastroscopyia
B.A Serum glucoseia
x C.A Amylaseia
D.A Biliary USSia
E.A ECGia
Next question
Acute pancreatitis: features
sqweqwesf erwrewfsdfs adasd dhe
Rare features associated with pancreatitis include:
• ischaemic (Purtscher) retinopathy - may cause temporary or permanent
blindnesshe
 A 62-year-old female presents to her GP with a two month history of indigestion. She
is otherwise well, has not had a similar episode before and takes no regular
medication. Of note there is no recent weight loss or vomiting and abdominal
examination is unremarkable. What is the most appropriate initial management?ia
A.A Long-term course of a H2 receptor antagonistia
B.A Lifestyle advice with follow-up appointment in one monthia
x C.A Urgent referral for endoscopy
D.A One month course of a full-dose proton pump inhibitoria
E.A Urea breath testing and treat for H pylori if positiveia

Next question
This patient meets the criteria for urgent referral for endoscopy as she is older than 55
years, has recent onset, persistent and unexplained symptoms
Dyspepsia
sqweqwesf erwrewfsdfs adasd dhe
In 2004 NICE published guidelines for the management of dyspepsia in primary care.
These take into account the age of the patient (younger or older than 55 years) and the
presence or absence of 'alarm signs':
• chronic gastrointestinal bleedinghe
• progressive unintentional weight losshe
• progressive difficulty swallowinghe
• persistent vomitinghe
• iron deficiency anaemiahe
• epigastric masshe
• suspicious barium mealhe
he earaer aeraer asdsadas eerw dssdfsselleds
Deciding whether urgent referral for endoscopy is needed
he earaer aeraer asdsadas eerw dssdfsselleds
Urgent referral (within 2 weeks) is indicated for patients with any alarm signs
irrespective of age
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Routine endoscopic investigation of patients of any age, presenting with dyspepsia
and without alarm signs is not necessary, however
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Patients aged 55 years and over should be referred urgently for endoscopy if
dyspepsia symptoms are:
• recent in onset rather than recurrent and he
• unexplained
(e.g. new symptoms which cannot be explained by precipitants such
as NSAIDs) and he
• persistent: continuingbeyond a period that would normally be associated with
self-limiting problems (e.g. up to four to six weeks, depending on the severity
 of signs and symptoms)he
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Managing patients who do not meet referral criteria ('undiagnosed dyspepsia')
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This can be summarised at a step-wise approach
• 1. Review medications for possible causes of dyspepsiahe
• 2. Lifestyle advicehe
• 3. Trial of full-dose PPI for one month*he
• 4. 'Test and treat' using carbon-13 urea breath testhe
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*it is unclear from studies whether a trial of a PPI or a 'test and treat' should be used
first
A 26-year-old man with a history of speech and behavioural problems presents with
lethargy. On examination he is noted to have jaundiced sclera. What is the most likely
diagnosis?ia
A.A Wiskott-Aldrich syndromeia
B.A Haemochromatosisia
C.A Friedreich's ataxiaia
x D.A Wilson's disease
E.A Acute intermittent porphyriaia
Next question
Wilson's disease
sqweqwesf erwrewfsdfs adasd dhe
Wilson's disease is an autosomal recessive disorder characterised by excessive copper
deposition in the tissues. Metabolic abnormalities include increased copper absorption
from the small intestine and decreased hepatic copper excretion. Wilson's disease is
caused by a defect in the ATP7B gene located on chromosome 13
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The onset of symptoms is usually between 10 - 25 years. Children usually present
with liver disease whereas the first sign of disease in young adults is often
neurological disease
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Features result from excessive copper deposition in the tissues, especially the brain,
liver and cornea:
• liver: hepatitis, cirrhosishe
• neurological: speech and behavioural problems are often the first manifestations.
Also: tremor, choreahe
• Kayser-Fleischer ringshe
• renal tubular acidosis (esp. Fanconi syndrome)he
• haemolysishe
• blue nailshe
he earaer aeraer asdsadas eerw dssdfsselleds
Diagnosis
• reduced serum caeruloplasminhe
• increased 24hr urinary copper excretionhe
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Management
• D-penicillamine: chelates copperhe
Which one of the following is most associated with melanosis coli?ia
A.A Crohn's diseaseia
B.A Angiodysplasiaia
C.A Ulcerative colitisia
x D.A Laxative abuse
E.A Coeliac diseaseia
Next question
Laxative abuse
sqweqwesf erwrewfsdfs adasd dhe
Sigmoidoscopy may show dark brown bowel - melanosis coli (a histological
diagnosis showing pigment-laden macrophages)
Which one of the following may be used to monitor patients with colorectal cancer?ia
A.A CA-125ia
x B.A Carcinoembryonic antigen
C.A Alpha-fetoproteinia
D.A CA 19-9ia
E.A CA 15-3ia
Next question
Carcinoembryonic antigen may be used to monitor for recurrence in patients post-
operatively or to assess response to treatment in patients with metastatic disease
Colorectal cancer: screening
sqweqwesf erwrewfsdfs adasd dhe
Overview
• most cancers develop from adenomatous polyps therefore a screening program
could theoretically reduce mortalityhe
• main techniques being evaluated are faecal occult blood (FOB) testing,
sigmoidoscopy and colonoscopyhe
• FOB testing is the only method to have been proven to reduce mortality (by c.
20%) in trials. Sensitivity can be increased by DNA analysis for the APC
genehe
• trials
looking at screening using flexible sigmoidoscopy are currently
underwayhe
Which of the following is not a recognised complication of coeliac disease?ia
 x A.A Hypersplenismia
B.A Osteomalaciaia
C.A Lactose intoleranceia
D.A Oesophageal canceria
E.A Anaemiaia
Next question
Hypo-, not hypersplenism is seen in coeliac disease
Coeliac disease
sqweqwesf erwrewfsdfs adasd dhe
Coeliac disease is caused by sensitivity to the protein gluten. Repeated exposure leads
to villous atrophy which in turn causes malabsorption. Conditions associated with
coeliac disease include dermatitis herpetiformis (a vesicular, pruritic skin eruption)
and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis). It is
strongly associated with HLA-DQ2 (95% of patients) and HLA-B8 (80%) as well as
HLA-DR3 and HLA-DR7
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Complications
• anaemia: iron, folate and
vitamin B12 deficiency (folate deficiency is more
common than vitamin B12 deficiency in coeliac disease)he
• hyposplenismhe

• osteomalacia (vitamin D deficiency)he

• lactose intolerancehe

• enteropathy-associated T-cell lymphoma of small intestinehe

• rare: oesophageal cancer, other malignancieshe

Which one of the following investigations is considered the gold standard for the
diagnosis of gastro-oesophageal reflux disease?ia
A.A Endoscopyia
x B.A 24hr oesophageal pH monitoring
C.A Oesophageal manometryia
D.A Barium swallowia
E.A CT thoraxia

Next question
24hr oesophageal pH monitoring is gold standard investigation in GORD
GORD: investigation
sqweqwesf erwrewfsdfs adasd dhe
Overview
• poor correlation between symptoms and endoscopy appearancehe
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 Indications for upper GI endoscopy:
• age > 55 yearshe
• symptoms > 4 weeks or persistent symptoms despite treatmenthe
• dysphagiahe

• relapsing symptomshe
• weight losshe

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If endoscopy is negative consider 24-hr oesophageal pH monitoring (the gold
standard test for diagnosis)
Which one of the following is least likely to cause massive splenomegaly?ia
A.A Malariaia
x B.A Felty's syndrome
C.A Visceral leishmaniasisia
D.A Chronic myeloid leukaemiaia
E.A Myelofibrosisia

Next question
The splenomegaly seen in Felty's syndrome is not typically massive. The other
conditions are more likely to cause massive splenomegaly
Splenomegaly
sqweqwesf erwrewfsdfs adasd dhe
Massive splenomegaly
• myelofibrosishe

• chronic myeloid leukaemiahe

• visceral leishmaniasis (kala-azar)he
• malariahe
• Gaucher's syndromehe
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Other causes (as above plus)
• portal hypertension e.g. secondary to cirrhosishe
• lymphoproliferative disease e.g. CLL, Hodgkin'she
• haemolytic anaemiahe

• infection: hepatitis, glandular feverhe

• infective endocarditishe

• sickle-cell*, thalassaemiahe
• rheumatoid arthritis (Felty's syndrome)he
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 *the majority of adults patients with sickle-cell will have an atrophied spleen due to
repeated infarction
A 36-year-old man is seen the gastroenterology clinic. He has recently been started on
mesalazine 400mg tds for ulcerative colitis. Which of the following adverse effects is
least likely attributable to mesalazine?ia
A.A Interstitial nephritisia
B.A Headachesia
C.A Acute pancreatitisia
D.A Agranulocytosisia
x E.A Infertilityia

Next question
Oligospermia is seen in patients taking sulphasalazine due to the sulphapyridine
moiety, which is not present in mesalazine
Aminosalicylate drugs
sqweqwesf erwrewfsdfs adasd dhe
5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts
locally as an anti-inflammatory. The mechanism of action is not fully understood but
5-ASA may inhibit prostaglandin synthesis
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Sulphasalazine
• a combination of sulphapyridine (a sulphonamide) and 5-ASAhe
• manyside-effects are due to the sulphapyridine moiety: rashes, oligospermia,
headache, Heinz body anaemiahe
• other side-effects are common to 5-ASA drugs (see mesalazine)he
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Mesalazine
• a delayed release form of 5-ASAhe
• sulphapyridine side-effects seen in patients taking sulphasalazine are avoidedhe
• mesalazine is
still however associated with side-effects such as GI upset,
headache, agranulocytosis, pancreatitis*, interstitial nephritishe
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Olsalazine
• twomolecules of 5-ASA linked by a diazo bond, which is broken by colonic
bacteriahe
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*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine
Each one of the following is a recognised complication of hepatitis C infection,
except:ia
x A.A Diffuse proliferative glomerulonephritis
 B.A Chronic infectionia
C.A Cryoglobulinaemiaia
D.A Cirrhosisia
E.A Hepatocellular canceria
Next question
Hepatitis C
sqweqwesf erwrewfsdfs adasd dhe
Transmission
• risk of transmission during a needle stick injury is about 2%he
• the vertical transmission rate from mother to child is about 6%he
• breast feeding is not contraindicated in mothers with hepatitis Che
• the risk of transmitting the virus during sexual intercourse is probably less than
5%he
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Features
• after exposure to the hepatitis C virus less than 20% of patients develop an he
acute hepatitis
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Complications
• chronic infection(85%) - only 15% of patients will clear the virus and will hence
the majority will develop chronic hepatitis Che
• cirrhosis (20-30% of those with chronic disease)he
• hepatocellular cancerhe
• cryoglobulinaemiahe

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Management
• currently a combination of interferon-alpha and ribavirin are usedhe
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Complications of treatment
• ribavirin - side-effects: haemolytic anaemia, cough. Women should not become
he
pregnant within 6 months of stopping ribavirin as it is teratogenic
• interferonalpha - side-effects: fatigue, leukopenia, thrombocytopenia,
depressionhe
A 29-year-old man presents with a 4 day history of watery diarrhoea one week after
returning from India. On examination he is apyrexial and his abdomen is soft and
non-tender. What is the most likely causative organism>ia
A.A Amoebiasisia
x B.A Giardiasisia
 C.A Campylobacteria
D.A Shigellaia
E.A Salmonellaia
Next question
The incubation period and prolonged, non-bloody diarrhoea point towards giardiasis
Gastroenteritis
sqweqwesf erwrewfsdfs adasd dhe
Which organism - clues
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Most common cause of traveller's diarrhoea is E coli
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Incubation period
• 1-6 hrs: Staph aureus, Bacillus cereus he
• 12-48 hrs: Salmonella, E. colihe
• 48-72 hrs: Shigella, Campylobacterhe
•> 7 days: Giardiasis, Amoebiasishe
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Stereotypical histories
• profuse, watery diarrhoea: cholerahe
• prolonged, non-bloody diarrhoea: Giardiahe
• bloody diarrhoea:, vomiting, abdo pain: Shigellahe
• severe vomiting: Staphylococcus aureushe
Primary sclerosing cholangitis is most associated with:ia
A.A Primary biliary cirrhosisia
B.A Crohn's diseaseia
C.A Hepatitis C infectionia
x D.A Ulcerative colitis
E.A Coeliac diseaseia
Next question
Primary sclerosing cholangitis
sqweqwesf erwrewfsdfs adasd dhe
Primary sclerosing cholangitis is a biliary disease of unknown aetiology characterised
by inflammation and fibrosis of intra and extra-hepatic bile ducts
he earaer aeraer asdsadas eerw dssdfsselleds
Associations
• ulcerative colitis: 5% of patients with UC have PSC, 80% of patients with PSC
have UChe
• Crohn's (much less common association than UC)he
• HIVhe
he earaer aeraer asdsadas eerw dssdfsselleds
Features
• cholestasishe

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Investigation
• ERCP show multiple biliary strictures giving a 'beaded' appearancehe
• liver biopsy: fibrous, obliterative cholangitis often described as ‘onion skin’he
• ANCA may be positivehe
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Complications
• cholangiocarcinoma (in 10%)he
• increased risk of colorectal cancerhe
The increased risk of oesophageal malignancy in patients with Barrett's oesophagus is
approximately:ia
A.A No increased riskia
B.A Twice riskia
C.A 5 times riskia
x D.A 50 - 100 times risk
E.A 500 - 1,000 times riskia
Next question
Barrett's oesophagus
sqweqwesf erwrewfsdfs adasd dhe
Barrett's refers to the metaplasia of the lower oesophageal mucosa, with the usual
squamous epithelium being replaced by columnar epithelium. There is an increased
risk of oesophageal adenocarcinoma, estimated at 50-100 fold.
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Histological features
• the columnar epithelium may resemble that of either the cardiac region of the
stomach or that of the small intestine (e.g. with goblet cells, brush border)he
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Management
• endoscopic surveillance with biopsieshe
• high-dose PPIhe

Which one of the following tests is considered the gold standard in the investigation
of achalasia?ia
A.A Barium swallowia
x B.A Oesophageal manometry
C.A Plain chest x-rayia
D.A Endoscopyia
 E.A CT thoraxia
Next question
The gold standard test for achalasia is oesophageal manometry
Achalasia
sqweqwesf erwrewfsdfs adasd dhe
Failure of oesophageal peristalsis and of relaxation of lower oesophageal sphincter
(LOS) due to degenerative loss of ganglia from Auerbach's plexus i.e. LOS
contracted, oesophagus above dilated. Achalasia typically presents in middle-age and
is more common in women
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Clinical features
• dysphagia of BOTH liquids and solidshe
• typically variation in severity of symptomshe
• heartburnhe
• regurgitation of food - may lead to cough, aspiration pneumonia etche
• malignant change in small number of patientshe
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Investigations
• manometry: excessive LOS tone which doesn't relax on swallowing - considered
most important diagnostic testhe
• barium swallow shows grossly expanded oesophagus, fluid levelhe
• CXR: wide mediastinum, fluid levelhe
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Treatment
• cardiomyotomyhe
• balloon dilationhe
• i.e. drug therapy not particularly usefulhe
Where do the majority of VIPomas arise from?ia
A.A Small intestineia
B.A Pituitaryia
x C.A Pancreasia
D.A Antrum of stomachia
E.A Pylorus of stomachia
Next question
VIPoma
sqweqwesf erwrewfsdfs adasd dhe
VIP (vasoactive intestinal peptide)
• source: small intestine, pancreashe
• stimulation: neuralhe
 • actions: stimulates
secretion by pancreas and intestines, inhibits acid and
pepsinogen secretionhe
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VIPoma
• 90% arise from pancreashe
• large volume diarrhoeahe
• weight losshe

• dehydrationhe
• hypokalaemia, hypochlorhydiahe

Which one of the following statements is incorrect regarding Dubin-Johnson

syndrome?ia
A.A Runs a benign courseia
B.A Due to a defect in the canillicular multispecific organic anion
transporteria
C.A Causes defective hepatic bilirubin excretionia
D.A It is an autosomal recessive disorderia
x E.A Results in an unconjugated hyperbilirubinaemia
Next question
Dubin-Johnson syndrome
sqweqwesf erwrewfsdfs adasd dhe
Dubin-Johnson syndrome is a benign autosomal recessive disorder resulting in
hyperbilirubinaemia (conjugated, therefore present in urine). It is due to a defect in
the canillicular multispecific organic anion transporter (cMOAT) protein. This causes
defective hepatic bilirubin excretion
A 64-year-old female with a past history of COPD and hypertension presents with
pain on swallowing. Current medication includes a salbutamol and becotide inhaler,
bendrofluazide and amlodipine. What is the most likely cause of the presentation?ia
A.A Myasthenia gravis precipitated by bendrofluazideia
B.A Oesophageal webia
C.A Achalasia secondary to amlodipineia
x D.A Oesophageal candidiasis
E.A Oesophageal canceria
Next question
Pain on swallowing (odynophagia) is a typical of oesophageal candidiasis, a well
documented complication of inhaled steroid therapy
Dysphagia
sqweqwesf erwrewfsdfs adasd dhe
Mechanical/structural causes
• neoplasia: oesophageal, gastric, pharyngealhe
• strictures: oesophageal webhe
 • pharyngeal pouchhe
• extrinsic pressurehe

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Motility/functional causes
• achalasiahe

• oesophageal spasmhe
• myasthenia gravishe

• systemic sclerosishe
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Clues to cause
• more problems with solids - oesophageal causehe
• more problems with liquids - pharyngeal causehe
• solids and liquids from start - motility disorderhe
• odynophagia - achalasia, oesophagitis, neoplasiahe
A 17-year-old girl presents to her GP with a 6 week history of nausea and abdominal
discomfort. Routine blood tests reveal the following. asdsadas eerw dssdfsselleds
Hb 10.9 g/dl
WBC 6.7 *109/l
Platelets 346 *109/l
Calcium 2.43 mmol/l
Bilirubin 7 µmol/l
ALP 962 u/l
ALT 45 u/l
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What is the most likely diagnosis?ia
A.A Alcoholic liver diseaseia
B.A Cholangiocarcinomaia
x C.A Pregnancyia

D.A Gallstonesia
E.A Primary biliary cirrhosisia
Next question
Alkaline phosphatase is significantly elevated in pregnancy
Alkaline phosphatase
sqweqwesf erwrewfsdfs adasd dhe
Causes of raised ALP
• Paget'she
• osteomalaciahe

• bone metastaseshe
 • hyperparathyroidismhe

• renal failurehe
• cholestasishe

• physiological: pregnancy, growing children, healing fractureshe

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Causes of raised ALP and raised Ca2+
• Paget'she
• bone metastaseshe

• hyperparathyroidismhe
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Causes of raised ALP and low Ca2+
• osteomalaciahe

• renal failurehe

A 30-year-old man presents to his GP enquiring about screening for

haemochromatosis as his brother was diagnosed with the condition 2 years ago. The
patient is currently well with no features suggestive of haemochromatosis. What is the
most appropriate investigation?ia

A.A Serum total iron-binding capacityia

x B.A HFE gene analysis
C.A Serum transferrin saturationia
D.A Serum ferritinia
E.A Serum ironia
Next question
Screening for haemochromatosis
• general population: transferrin saturation
• family members: HFE genetic testing

Serum transferrin saturation is currently the preferred investigation for population

screening. However, the patient has a sibling with haemochromatosis and therefore
HFE gene analysis is the most suitable investigation. In clinical practice this would be
combined with iron studies as well
Haemochromatosis: investigation
sqweqwesf erwrewfsdfs adasd dhe
Haemochromatosis is an autosomal recessive disorder of iron absorption and
metabolism resulting in iron accumulation. It is caused by inheritance of mutations in
the HFE gene on both copies of chromosome 6*. The British Committee for
Standards in Haematology (BCSH) published guidelines for the investigation and
management of haemochromatosis in 2000
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There is continued debate about the best investigation to screen for
haemochromatosis. The 2000 BCSH guidelines suggest:
• general population: transferrin saturation is considered most useful markerhe
• testing family members: genetic testing for HFE mutationhe
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These guidelines may change as HFE gene analysis become less expensive
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Diagnostic tests
• molecular genetic testing for the C282Y and H63D mutationshe
• liver biopsy: Perl's stainhe
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Typical iron study profile in patient with haemochromatosis
• transferrin saturation > 55% in men or > 50% in womenhe
• raised ferritin (e.g. > 500 ug/l) and ironhe
• low TIBChe
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Joint x-rays characteristically show chondrocalcinosis
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*there are rare cases of families with classic features of genetic haemochromatosis but
no mutation in the HFE gene
What percentage of patients with primary sclerosing cholangitis have ulcerative
colitis?ia
A.A 5%ia
B.A 10%ia
C.A 20%ia
D.A 40%ia
x E.A 80%ia
Next question
5% of patients with UC have PSC, 80% of patients with PSC have UC
Primary sclerosing cholangitis
sqweqwesf erwrewfsdfs adasd dhe
Primary sclerosing cholangitis is a biliary disease of unknown aetiology characterised
by inflammation and fibrosis of intra and extra-hepatic bile ducts
he earaer aeraer asdsadas eerw dssdfsselleds
Associations
• ulcerative colitis: 5% of patients with UC have PSC, 80% of patients with PSC
have UChe
• Crohn's (much less common association than UC)he
• HIVhe
he earaer aeraer asdsadas eerw dssdfsselleds
Features
 • cholestasishe
he earaer aeraer asdsadas eerw dssdfsselleds
Investigation
• ERCP show multiple biliary strictures giving a 'beaded' appearancehe
• liver biopsy: fibrous, obliterative cholangitis often described as ‘onion skin’he
• ANCA may be positivehe
he earaer aeraer asdsadas eerw dssdfsselleds
Complications
• cholangiocarcinoma (in 10%)he
• increased risk of colorectal cancerhe
Which of the following symptoms is least associated with irritable bowel syndrome?ia

A.A Dyspareuniaia
x B.A Weight loss
C.A Back painia
D.A Depressionia
E.A Nauseaia
Next question
Weight loss is not a feature of IBS and underlying malignancy needs to be excluded
IBS: features
sqweqwesf erwrewfsdfs adasd dhe
Features
• abdominal pain: relieved by defecationhe
• bloatinghe
• change in bowel habit: constipation/diarrhoea - mucous may be passedhe
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Less common features
• nausea/vomiting may occasionally be seenhe
• associatedsymptoms include fibromyalgia, dyspareunia, back pain, depressionhs
eerw dssdfsselleds
Features not attributable to IBS
• investigate all those > 40 years oldhe
• acute onset of symptomshe
• weight losshe

• anorexiahe
• rectal bleedinghe
 • nocturnal symptomshe

A 54-year-old man who is known to have gastric cancer is reviewed in clinic. He asks
you about a rash he has developed. Which of the following skin disorders is most
associated with gastric cancer?ia
A.A Erythema gyratum repensia
B.A Necrolytic migratory erythemaia
C.A Migratory thrombophlebitisia
D.A Acquired ichthyosisia
E.A Acanthosis nigricansia

Next question
Skin disorders associated with malignancy
sqweqwesf erwrewfsdfs adasd dhe
Paraneoplastic syndromes associated with internal malignancies:
• acanthosis nigricans - gastrointestinal cancerhe
• acquired ichthyosis - lymphomahe
• acquired hypertrichosis lanuginosa - gastrointestinal and lung cancerhe
• dermatomyositis - bronchial and breast cancerhe
• erythema gyratum repens - lung cancerhe
• erythroderma: lymphomahe
• migratory thrombophlebitis - pancreatic cancerhe
• necrolytic migratory erythema - glucagonomahe
• pyoderma gangrenosum (bullous and non-bullous forms) - myeloproliferative
disordershe
• Sweet's syndrome - haematological malignancy e.g. myelodysplasia - tender,
purple plaqueshe
Which one the following disorders is most strongly associated with primary biliary
cirrhosis?ia
A.A Systemic sclerosisia
B.A Thyroid diseaseia
x C.A Sjogren's syndrome
D.A Rheumatoid arthritisia
E.A Systemic lupus erythematousia

Next question
All of the above conditions are associated with primary biliary cirrhosis but Sjogren's
syndrome is the most common, being seen in up to 80% of patients
Primary biliary cirrhosis
sqweqwesf erwrewfsdfs adasd dhe
 Primary biliary cirrhosis is a chronic liver disorder typically seen in middle-aged
females (female:male ratio of 9:1). The aetiology is not fully understood although it is
thought to be an autoimmune condition. Interlobular bile ducts become damaged by a
chronic inflammatory process causing progressive cholestasis which may eventually
progress to cirrhosis. The classic presentation is itching in a middle-aged woman
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Associations
• Sjogren's syndrome (seen in up to 80% of patients)he
• rheumatoid arthritishe
• systemic sclerosishe
• thyroid diseasehe
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Diagnosis
• anti-mitochondrial antibodies (AMA) M2 subtype are present in 98% of patients
and are highly specifiche
• smooth muscle antibodies in 30% of patientshe
• raised serum IgMhe

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Management
• pruritus: cholestyraminehe

• fat-soluble vitamin supplementationhe

• ursodeoxycholic acidhe

• livertransplantation e.g. if bilirubin > 100 (PBC is a major indication) -

recurrence in graft can occur but is not usually a problemhe
Autoimmune hepatitis type 1 is most strongly associated with which one of the
following antibodies?ia
x A.A Anti-smooth muscle antibody
B.A Anti-ribonuclear protein antibodyia
C.A Anti-liver/kidney microsomal type 1 antibodyia
D.A Rheumatoid factoria
E.A Anti-microsomal antibodyia

Next question
Autoimmune hepatitis
sqweqwesf erwrewfsdfs adasd dhe
Autoimmune hepatitis is condition of unknown aetiology which is most commonly
seen in young females. Recognised associations include other autoimmune disorders,
hypergammaglobulinaemia and HLA B8, DR3.Two types of autoimmune hepatitis
have been characterised according to the types of circulating antibodies present
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Type I Type II
Anti-nuclear antibodies (ANA) and/or anti- Anti-liver/kidney microsomal
smooth muscle antibodies (SMA) type 1 antibodies (LKM1)
he earaer aeraer asdsadas eerw he earaer aeraer asdsadas eerw
dssdfsselleds dssdfsselleds
Affects both adults and children Affects children only

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Features
• may present with signs of chronic liver diseasehe
• acute hepatitis: fever, jaundice etc (only 25% present in this way)he
• amenorrhoea (common)he
• ANA/SMA/LKM1 antibodies, raised IgG levelshe
• liverbiopsy: inflammation extending beyond limiting plate 'piecemeal necrosis',
bridging necrosishe
he earaer aeraer asdsadas eerw dssdfsselleds
Management
• steroids, other immunosuppressants e.g. azathioprinehe
• liver transplantationhe
Which one of the following decreases gastric acid secretion?ia
A.A Gastrinomaia
x B.A Secretinia
C.A Small bowel resectionia
D.A Systemic mastocytosisia
E.A Basophiliaia
Next question
Gastrointestinal physiology: acid secretion
sqweqwesf erwrewfsdfs adasd dhe
Principle mediators of acid secretion
• gastrinhe
• vagal stimulationhe

• histaminehe
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Factors increasing acid secretion
• gastrinomahe
• small bowel resection (removal of inhibition)he
• systemic mastocytosis (elevated histamine levels)he
• basophiliahe

he earaer aeraer asdsadas eerw dssdfsselleds

Factors decreasing acid secretion
• drugs: H2-antagonists, PPIshe
• hormones: secretin, VIP, GIP, CCKhe
Which one of the following is least recognised as a complication of measles
infection?ia

x A.A Infertilityia
B.A Keratoconjunctivitisia
C.A Encephalitisia
D.A Subacute sclerosing panencephalitisia
E.A Pneumoniaia
Next question
Measles
sqweqwesf erwrewfsdfs adasd dhe
Overview
• RNA paramyxovirushe

• spread by dropletshe
• infective from prodrome until 5 days after rash starts he
• incubation period = 10-14 dayshe
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Features
• prodrome: irritable, conjunctivitis, feverhe

• Koplik spots (before rash): white spots ('grain of salt') on buccal mucosahe
• rash: starts
behind ears then to whole body, discrete maculopapular rash
becoming blotchy & confluenthe
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Complications
• encephalitishe
• subacute sclerosing panencephalitishe
• febrile convulsionshe
• pneumoniahe

• keratoconjunctivitishe
• D&Vhe

Which one of the following is least associated with the development of colorectal
cancer in patients with ulcerative colitis?ia
A.A Unremitting diseaseia
B.A Disease duration > 10 yearsia
C.A Onset before 15 years oldia
 D.A Poor compliance to treatmentia
x E.A Disease confined to the rectum
Next question
Ulcerative colitis: colorectal cancer
sqweqwesf erwrewfsdfs adasd dhe
Overview
• risk of colorectal cancer is 10-20 times that of general populationhe
• worse prognosis than patients without UC (partly due to delayed diagnosis)he
• lesions may be multifocalhe
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Factors increasing risk of cancer
• disease duration > 10 yearshe
• patients with pancolitishe
• onset before 15 years oldhe
• unremitting diseasehe
• poor compliance to treatmenthe
Which one of the following organisms is thought to play a key role in the
development of gastric MALT lymphoma?ia
A.A Shigellaia
B.A Staphylococcus aureusia
C.A Epstein-Barr virusia
D.A Orf virusia
x E.A Helicobacter pylori

Next question
Gastric MALT lymphoma
sqweqwesf erwrewfsdfs adasd dhe
Overview
• associated with H. pylori infection in 95% of caseshe
• good prognosishe
• if low grade then 80% respond to H. Pylori eradicationhe
he earaer aeraer asdsadas eerw dssdfsselleds
Features
• paraproteinaemia may be presenthe
Each one of the following may have a role in the treatment of irritable bowel
syndrome, except:ia
 A.A Peppermint oilia
B.A High-fibre dietia
C.A Mebeverineia
D.A Lactuloseia
x E.A Ferrous sulphate
Next question
IBS: management
sqweqwesf erwrewfsdfs adasd dhe
Treatment of IBS is difficult
• reassurancehe

• educate on high-fibre diet (but may worsen symptoms)he

• look for and treat any underlying depressionhe
• exclusion diet if food intolerance is suspectedhe
• if constipation then bulking agent + lactulosehe
• antispasmodics or peppermint oil may helphe
A 29-year-old female is noted to have an elevated bilirubin during a viral illness.
Gilbert's syndrome is suspected. Which one of the following tests may confirm the
diagnosis?ia
A.A Bromsulphthalein excretion testia
B.A Ammonium chloride acidification testia
C.A Urine analysisia
x D.A Nicotinic acid test
E.A Faecal fat excretionia
Next question
Gilbert's syndrome
sqweqwesf erwrewfsdfs adasd dhe
Gilbert's syndrome is an autosomal dominant condition of defective bilirubin
conjugation due to a deficiency of UDP glucuronyl transferase. The prevalence is
approximately 1-2% in the general population
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Features
• unconjugated hyperbilinaemia (i.e. not in urine)he
• jaundice may only be seen during an intercurrent illnesshe
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Investigation and management
 • investigation: rise in bilirubin following prolonged fasting or IV nicotinic acidhe
• no treatment requiredhe
A 39-year-old man with a history of alcohol excess presents to the Emergency
Department with a 2 day history of severe epigastric pain. His amylase is found to be
1260. What is the best marker of severity?ia
x A.A CRPia
B.A Amylase (on admission)ia
C.A Pain scoresia
D.A Lipase (on admission)ia
E.A Number of similar previous admissionsia
Next question
CRP is now a widely used marker of severity in acute pancreatitis. Other methods
which have to correlate with prognosis include the Ranson criteria and APACHE II
score (Acute Physiology And Chronic Health Evaluation)
Acute pancreatitis: causes
sqweqwesf erwrewfsdfs adasd dhe
The vast majority of cases in the UK are caused by gallstones and alcohol
he earaer aeraer asdsadas eerw dssdfsselleds
Popular mnemonic is GET SMASHED
• Gallstoneshe

• Ethanolhe

• Traumahe

• Steroidshe

• Mumps (other viruses include Coxsackie B)he

• Autoimmune (e.g. polyarteritis nodosa), Ascaris infectionhe
• Scorpion venomhe
• Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia,
Hypothermiahe
• ERCPhe

• Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, frusemide,

pentamidine, steroids, sodium valproate)he
he earaer aeraer asdsadas eerw dssdfsselleds
*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine
A 45-year-old man with a history of alcoholic liver disease presents with abdominal
distension. Examination reveals tense ascites which is drained. What is the
appropriate type of diuretic to help prevent reaccumulation of ascites?ia
x A.A Aldosterone antagonist
B.A Loop diureticia
C.A Thiazide diureticia
 D.A Osmotic diureticia
E.A Carbonic anhydrase inhibitoria
Next question
Aldosterone antagonists such as spironolactone are used in high doses to help prevent
the formation of ascites in patients with chronic liver disease
Spironolactone
sqweqwesf erwrewfsdfs adasd dhe
Spironolactone
• aldosterone antagonisthe
• act in distal convolutedtubule, potentiates thiazides/loops by antagonizing
aldosterone, weak diureticshe
• ascites, resistant CCF (with loop), nephrotic syndrome, Conn's syndromehe
he earaer aeraer asdsadas eerw dssdfsselleds
Adverse effects
• hyperkalaemiahe

• gynaecomastiahe
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RALES
• NYHA III + IV, patients already taking ACE inhibitorhe
• low dose spironolactone reduces all cause mortalityhe
Which one of the following causes of gastroenteritis has the longest incubation
period?ia
A.A Campylobacteria
B.A Bacillus cereusia
C.A Shigellaia
x D.A Giardiasisia
E.A Salmonellaia
Next question
Gastroenteritis
sqweqwesf erwrewfsdfs adasd dhe
Which organism - clues
he earaer aeraer asdsadas eerw dssdfsselleds
Most common cause of traveller's diarrhoea is E coli
he earaer aeraer asdsadas eerw dssdfsselleds
Incubation period
• 1-6 hrs: Staph aureus, Bacillus cereus he
• 12-48 hrs: Salmonella, E. colihe
• 48-72 hrs: Shigella, Campylobacterhe
•> 7 days: Giardiasis, Amoebiasishe
he earaer aeraer asdsadas eerw dssdfsselleds
Stereotypical histories
• profuse, watery diarrhoea: cholerahe
• prolonged, non-bloody diarrhoea: Giardiahe
• bloody diarrhoea:, vomiting, abdo pain: Shigellahe
• severe vomiting: Staphylococcus aureushe
A 44-year-old obese female is noted to have gallstones during an abdominal
ultrasound, which was requested due to repeated urinary tract infections. Apart from
the repeated UTIs she is otherwise well. What is the most appropriate management of
the gallstones?ia
A.A Ursodeoxycholic acidia
B.A Extracorporeal Short Wave Lithotripsyia
C.A List for laparoscopic cholecystectomy when 50 years oldia
x D.A Observationia
E.A List now for laparoscopic cholecystectomyia
Next question
Gallstones
sqweqwesf erwrewfsdfs adasd dhe
Asymptomatic gallstones are common and do not require treatment
Which one of the following brush border enzymes cleaves glucose and fructose?ia

A.A Maltaseia
B.A Lactaseia
C.A Dipeptidaseia
D.A A-dextrinaseia
x E.A Sucraseia
Next question
Brush border enzymes:
• maltase: glucose + glucose
• sucrase: glucose + fructose
• lactase: glucose + galactose

Gastrointestinal physiology: brush border enzymes

sqweqwesf erwrewfsdfs adasd dhe
The following brush border enzymes are involved in the breakdown of carbohydrates:
• maltase - glucose + glucosehe
• sucrase - glucose + fructosehe
 • lactase - glucose + galactosehe
A 25-year-old intravenous drug user with chronic hepatitis C becomes pregnant.
Approximately what is the chance of the virus being transmitted to her child?ia
x A.A <10%ia
B.A 10-20%ia
C.A 20-30%ia
D.A 30-40%ia
E.A 40-50%ia
Next question
Hepatitis C
sqweqwesf erwrewfsdfs adasd dhe
Transmission
• risk of transmission during a needle stick injury is about 2%he
• the vertical transmission rate from mother to child is about 6%he
• breast feeding is not contraindicated in mothers with hepatitis Che
• the risk of transmitting the virus during sexual intercourse is probably less than
5%he
he earaer aeraer asdsadas eerw dssdfsselleds
Features
• after exposure to the hepatitis C virus less than 20% of patients develop an he
acute hepatitis
he earaer aeraer asdsadas eerw dssdfsselleds
Complications
• chronic infection(85%) - only 15% of patients will clear the virus and will hence
the majority will develop chronic hepatitis Che
• cirrhosis (20-30% of those with chronic disease)he
• hepatocellular cancerhe
• cryoglobulinaemiahe
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Management
• currently a combination of interferon-alpha and ribavirin are usedhe
he earaer aeraer asdsadas eerw dssdfsselleds
Complications of treatment
• ribavirin - side-effects: haemolytic anaemia, cough. Women should not become
he
pregnant within 6 months of stopping ribavirin as it is teratogenic
• interferonalpha - side-effects: fatigue, leukopenia, thrombocytopenia,
depressionhe
What percentage of patients with Peutz-Jeghers syndrome undergo malignant change?
ia
A.A 0%ia
x B.A 3%ia
C.A 30%ia
D.A 60%ia
E.A 100%ia
Next question
Peutz-Jeghers syndrome
sqweqwesf erwrewfsdfs adasd dhe
Peutz-Jeghers syndrome is an inherited condition characterised by numerous
hamartomatous polyps in GI tract (mainly small bowel) associated with pigmented
freckles on the lips, face, palms and soles. The polyps undergo malignant change in
less than 3% of patients
he earaer aeraer asdsadas eerw dssdfsselleds
Genetics
• autosomal dominanthe

• responsible gene encodes serine threonine kinase LKB1 or STK11he

he earaer aeraer asdsadas eerw dssdfsselleds
Features
• hamartomatous polyps in GI tracthe
• pigmented lesions on lips, oral mucosa, face, palms and soleshe
• intestinal obstruction e.g. intussusceptionhe
• GI bleedinghe
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Management
• conservative unless complications develop
Each one of the following is associated with hepatosplenomegaly, except:ia
A.A Glandular feveria
B.A Chronic myeloid leukaemiaia
C.A Alcoholic liver diseaseia
D.A Amyloidosisia
x E.A Infective endocarditis
Next question
Infective endocarditis causes an isolated splenomegaly
Hepatosplenomegaly
sqweqwesf erwrewfsdfs adasd dhe
Causes of hepatosplenomegaly
• chronic liver disease with portal hypertensionhe
• infections: glandular fever, malaria, hepatitishe
 • lymphoproliferative disordershe

• myeloproliferative disorders e.g. CMLhe

• amyloidosishe

What are the most common type of antibodies seen in pernicious anaemia?ia
A.A Vitamin B12 receptor antibodiesia
x B.A Gastric parietal cell antibodies
C.A Jejunal mucosa antibodiesia
D.A Intrinsic factor antibodiesia
E.A Vitamin B12 antibodiesia
Next question
Pernicious anaemia: investigation
sqweqwesf erwrewfsdfs adasd dhe
Investigation
• anti gastric parietal cell antibodies in 90%he
• anti intrinsic factor antibodies in 50%he
• macrocytic anaemiahe

• low WCC and plateletshe

• LDH may be raised due to ineffective erythropoiesishe
• also
low serum B12, hypersegmented polymorphs on film, megaloblasts in
marrowhe
• Schilling testhe
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Schilling test
• radiolabelled B12 given on two occasionshe
• first on its ownhe
• second with oral IFhe
• urine B12 levels measuredhe
Which one of the following is least useful in assessing the severity of a patient with
liver cirrhosis?ia
x A.A ALTia
B.A Prothrombin timeia
C.A Bilirubinia
D.A The presence of ascitesia
E.A The presence of encephalopathyia
Next question
Child-Pugh classification of liver cirrhosis
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The Child-Pugh classification is a scoring system to assess the severity of liver
cirrhosis
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Score 1 2 3
Bilirubin (µmol/l) <34 34-50 >50
Albumin (g/l) >35 28-35 <28
PT (s) <4 4-6 >6
Encephalopathy none mild marked
Ascites none mild marked
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Summation of the scores allows the severity to be graded either A, B or C:
•< 7 = Ahe
• 7-9 = Bhe
•> 9 = Che
Each one of the following is associated with pancreatic cancer, except:ia
A.A Chronic pancreatitisia
B.A Smokingia
x C.A Blood group A
D.A Diabetesia
E.A BRCA2 geneia
Next question
Pancreatic cancer
sqweqwesf erwrewfsdfs adasd dhe
Associations
• smokinghe

• diabeteshe
• chronic pancreatitishe

• hereditary pancreatitishe
• hereditary non-polyposis colorectal carcinomahe
• multiple endocrine neoplasiahe
• Peutz-Jeghers syndromehe
• BRCA2he

• dysplastic naevus syndromehe

he earaer aeraer asdsadas eerw dssdfsselleds
Management
• less than 20% are suitable for surgery at diagnosishe
• radio and chemotherapy are ineffectivehe
Each one of the following is associated with rabies, except:ia
 A.A Hydrophobiaia
x B.A Opisthotonusia
C.A Pyrexiaia
D.A Headacheia
E.A Hypersalivationia
Next question
Rabies
sqweqwesf erwrewfsdfs adasd dhe
Features
• prodrome: headache, fever, agitationhe
• hydrophobia: water-provoking muscle spasms he
• hypersalivationhe

Each one of the following is a risk factor for gastric cancer, except:ia
A.A Nitrates in dietia
B.A Pernicious anaemiaia
C.A H. pylori infectionia
D.A Smokingia
x E.A Duodenal ulceration
Next question
Gastric cancer
sqweqwesf erwrewfsdfs adasd dhe
Epidemiology
• overall incidence is decreasing, but incidence of tumours arising from the cardia
is increasinghe
• peak age = 70-80 yearshe
• more common in Japan, China, Finland and Columbia than the Westhe
• more common in males, 2:1he
he earaer aeraer asdsadas eerw dssdfsselleds
Associations
• H. pylori infectionhe
• blood group A: gAstric cAncerhe
• chronic atrophic gastriche
• gastric adenomatous polypshe
• pernicious anaemiahe
• smokinghe

• diet: salty, spicy, nitrateshe

• may be negatively associated with duodenal ulcerhe
he earaer aeraer asdsadas eerw dssdfsselleds
Investigation
• diagnosis: endoscopy with biopsyhe
• staging: CT or endoscopic ultrasound - endoscopic ultrasound has recently been
shown to be superior to CThe
What percentage of cases of chronic pancreatitis in the UK are due to alcohol excess?
ia
A.A 35%ia
B.A 50%ia
C.A 65%ia
x D.A 80%ia
E.A 95%ia
Next question
Chronic pancreatitis
sqweqwesf erwrewfsdfs adasd dhe
Chronic pancreatitis is an inflammatory condition which can ultimately affect both the
exocrine and endocrine functions of the pancreas. Around 80% of cases are due to
alcohol excess with up to 20% of cases being unexplained
he earaer aeraer asdsadas eerw dssdfsselleds
Features
• pain is typically worse 15 to 30 minutes following a mealhe
• steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5
and 25 years after the onset of painhe
• diabetes mellitus develops in the majority of patients. It typically occurs more
than 20 years after symptom begin. Patients often require lower doses of
insulin than other diabetic patientshe
he earaer aeraer asdsadas eerw dssdfsselleds
Investigation
• abdominal x-ray shows pancreatic calcification in 30% of caseshe
• CT is more sensitive at detecting pancreatic calcificationhe
• functional tests: pancreolauryl and
Lundh tests may be used to assess exocrine
function if imaging inconclusivehe
he earaer aeraer asdsadas eerw dssdfsselleds
Management
• pancreatic enzyme supplementshe

• analgesiahe

• antioxidants: limited evidence base - one study suggests benefit in early

diseasehe
Ulcerative colitis is associated with each one of the following findings, except:ia
A.A Inflammatory cell infiltrate in lamina propriaia
 B.A Pseudopolypsia
x C.A Non-caseating granulomas
D.A Depletion of goblet cellsia
E.A Inflammation confined to mucosa and submucosaia
Next question
IBD: histology
sqweqwesf erwrewfsdfs adasd dhe
This histological differences between ulcerative colitis and Crohn's are summarised
below:
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Ulcerative colitis
• inflammation in mucosa and submucosa only (unless fulminant disease)he
• widespreadulceration with preservation of adjacent mucosa which has the
appearance of polyps ('pseudopolyps')he
• inflammatory cell infiltrate in lamina propriahe
• crypt abscesses neutrophils migrate through the walls of glands to form he
• depletion of goblet cells and mucin from gland epitheliumhe
• granulomas are infrequenthe
he earaer aeraer asdsadas eerw dssdfsselleds
Crohn's
• inflammationoccurs in all layers, down to the serosa --> strictures, fistulas,
adhesions etche
• oedema of mucosa and submucosa, combined with deep fissured ulcers 'rose-
thorn' --> 'cobblestone' patternhe
• lymphoid aggregateshe
• non-caseating granulomashe
Which one of the following is least likely to cause massive splenomegaly?ia

x A.A Sickle-cell anaemia

B.A Myelofibrosisia
C.A Gaucher's syndromeia
D.A Chronic myeloid leukaemiaia
E.A Visceral leishmaniasisia
Next question
Splenomegaly
sqweqwesf erwrewfsdfs adasd dhe
Massive splenomegaly
• myelofibrosishe
• chronic myeloid leukaemiahe
• visceral leishmaniasis (kala-azar)he
• malariahe

• Gaucher's syndromehe
he earaer aeraer asdsadas eerw dssdfsselleds
Other causes (as above plus)
• portal hypertension e.g. secondary to cirrhosishe
• lymphoproliferative disease e.g. CLL, Hodgkin'she

• haemolytic anaemiahe

• infection: hepatitis, glandular feverhe

• infective endocarditishe

• sickle-cell*, thalassaemiahe
• rheumatoid arthritis (Felty's syndrome)he
he earaer aeraer asdsadas eerw dssdfsselleds
*the majority of adults patients with sickle-cell will have an atrophied spleen due to
repeated infarction
Approximately what percentage of patients who are exposed to hepatitis C will clear
the virus?ia
A.A 5%ia
x B.A 15%ia
C.A 30%ia
D.A 50%ia
E.A 65%ia
Next question
Hepatitis C
sqweqwesf erwrewfsdfs adasd dhe
Transmission
• risk of transmission during a needle stick injury is about 2%he
• the vertical transmission rate from mother to child is about 6%he
• breast feeding is not contraindicated in mothers with hepatitis Che
• the risk of transmitting the virus during sexual intercourse is probably less than
5%he
he earaer aeraer asdsadas eerw dssdfsselleds
Features
• after exposure to the hepatitis C virus less than 20% of patients develop an he
acute hepatitis
he earaer aeraer asdsadas eerw dssdfsselleds
Complications
• chronic infection(85%) - only 15% of patients will clear the virus and will hence
the majority will develop chronic hepatitis Che
• cirrhosis (20-30% of those with chronic disease)he
• hepatocellular cancerhe
• cryoglobulinaemiahe
he earaer aeraer asdsadas eerw dssdfsselleds
Management
• currently a combination of interferon-alpha and ribavirin are usedhe
he earaer aeraer asdsadas eerw dssdfsselleds
Complications of treatment
• ribavirin - side-effects: haemolytic anaemia, cough. Women should not become
he
pregnant within 6 months of stopping ribavirin as it is teratogenic
• interferonalpha - side-effects: fatigue, leukopenia, thrombocytopenia,
depressionhe
Autoimmune hepatitis is most characteristically associated with elevated levels of
which one of the following immunoglobulins?i

A.A IgEia
B.A IgAia
C.A IgDia
D.A IgMia
x E.A IgGia
Next question
Autoimmune hepatitis
sqweqwesf erwrewfsdfs adasd dhe
Autoimmune hepatitis is condition of unknown aetiology which is most commonly
seen in young females. Recognised associations include other autoimmune disorders,
hypergammaglobulinaemia and HLA B8, DR3.Two types of autoimmune hepatitis
have been characterised according to the types of circulating antibodies present
he earaer aeraer asdsadas eerw dssdfsselleds
Type I Type II
Anti-nuclear antibodies (ANA) and/or anti- Anti-liver/kidney microsomal
smooth muscle antibodies (SMA) type 1 antibodies (LKM1)
he earaer aeraer asdsadas eerw he earaer aeraer asdsadas eerw
dssdfsselleds dssdfsselleds
Affects both adults and children Affects children only

he earaer aeraer asdsadas eerw dssdfsselleds

Features
• may present with signs of chronic liver diseasehe
• acute hepatitis: fever, jaundice etc (only 25% present in this way)he
• amenorrhoea (common)he
• ANA/SMA/LKM1 antibodies, raised IgG levelshe
• liver biopsy: inflammation extending beyond limiting plate 'piecemeal necrosis',
bridging necrosishe
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Management
• steroids, other immunosuppressants e.g. azathioprinehe
• liver transplantationhe
Which one of the following is the most likely presentation of Staphylococcus aureus
food poisoning?ia

A.A Tenesmusia
B.A Watery diarrhoeaia
C.A Dysenteryia
x D.A Severe vomiting
E.A Presentation 24-48 hours after eating affected foodia
Next question
Severe nausea and vomiting are caused by enterotoxins A-E
Gastroenteritis
sqweqwesf erwrewfsdfs adasd dhe
Which organism - clues
he earaer aeraer asdsadas eerw dssdfsselleds
Most common cause of traveller's diarrhoea is E coli
he earaer aeraer asdsadas eerw dssdfsselleds
Incubation period
• 1-6 hrs: Staph aureus, Bacillus cereus he
• 12-48 hrs: Salmonella, E. colihe
• 48-72 hrs: Shigella, Campylobacterhe
•> 7 days: Giardiasis, Amoebiasishe
he earaer aeraer asdsadas eerw dssdfsselleds
Stereotypical histories
 • profuse, watery diarrhoea: cholerahe
• prolonged, non-bloody diarrhoea: Giardiahe
• bloody diarrhoea:, vomiting, abdo pain: Shigellahe
• severe vomiting: Staphylococcus aureushe
A 64-year-old man presents to his GP due to lethargy and altered bowel habit. On
examination he is noted to have non-tender hepatomegaly with an irregular, nodular
edge. What is the likely diagnosis?ia
A.A Lymphomaia
B.A Chronic myeloid leukaemiaia
C.A Hydatid diseaseia
x D.A Metastatic cancer
E.A Amoebic liver abscessia
Next question
Hepatomegaly
sqweqwesf erwrewfsdfs adasd dhe
Common causes of hepatomegaly
• Cirrhosis: ifearly disease, later liver decreases in size. Associated with a non-
tender, firm liverhe
• Malignancy: metastatic spread or primary hepatoma. Associated with a hard,
irregular. liver edgehe
• Right heart failure: firm, smooth, tender liver edge. May be pulsatilehe
he earaer aeraer asdsadas eerw dssdfsselleds
Other causes
• viral hepatitishe

• glandular feverhe
• malariahe

• abscess: pyogenic, amoebiche

• hydatid diseasehe
• haematological malignancieshe

• haemochromatosishe
• primary biliary cirrhosishe
• sarcoidosis, amyloidosishe
Each one of the following is associated with Wilson's disease, except:ia
A.A Kayser-Fleischer ringsia
B.A Haemolysisia
x C.A Elevated serum caeruloplasmin
D.A Renal tubular acidosisia
 E.A Choreaia
Next question
Wilson's disease
sqweqwesf erwrewfsdfs adasd dhe
Wilson's disease is an autosomal recessive disorder characterised by excessive copper
deposition in the tissues. Metabolic abnormalities include increased copper absorption
from the small intestine and decreased hepatic copper excretion. Wilson's disease is
caused by a defect in the ATP7B gene located on chromosome 13
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The onset of symptoms is usually between 10 - 25 years. Children usually present
with liver disease whereas the first sign of disease in young adults is often
neurological disease
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Features result from excessive copper deposition in the tissues, especially the brain,
liver and cornea:
• liver: hepatitis, cirrhosishe
• neurological: speech and behavioural problems are often the first manifestations.
Also: tremor, choreahe
• Kayser-Fleischer ringshe
• renal tubular acidosis (esp. Fanconi syndrome)he
• haemolysishe

• blue nailshe

he earaer aeraer asdsadas eerw dssdfsselleds

Diagnosis
• reduced serum caeruloplasminhe
• increased 24hr urinary copper excretionhe
he earaer aeraer asdsadas eerw dssdfsselleds
Management
• D-penicillamine: chelates copperhe
A 54-year-old female is admitted two weeks following a cholecystectomy with
profuse diarrhoea. What is the most likely diagnosis?ia
A.A Campylobacteria
B.A E. coliia
x C.A Clostridium difficile
D.A Salmonellaia
E.A Staphylococcus aureusia
Next question
Clostridium difficile is the most likely cause as the patient would have been given
broad-spectrum antibiotics at the time of the operation
Clostridium difficile
sqweqwesf erwrewfsdfs adasd dhe
Clostridium difficile is a Gram positive rod often encountered in hospital practice. It
produces an exotoxin which causes intestinal damage leading to a syndrome called
pseudomembranous colitis. Clostridium difficile develops when the normal gut flora
are reduced by antibiotics (e.g. clindamycin)
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Features
• diarrhoeahe

• abdo pain he
• if severe toxic dilatationhe
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Diagnosis is made by detecting Clostridium difficile toxin (CDT) in the stool
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Management
• oral metronidazolehe

• if severe or not responding to metronidazole then oral vancomycin may be

usedhe
What percentage of patients with ulcerative colitis have primary sclerosing
cholangitis?ia
A.A 0.25%ia
B.A 0.5%ia
C.A 1%ia
D.A 2%ia
x E.A 5%ia
Next question
5% of patients with UC have PSC, 80% of patients with PSC have UC
Primary sclerosing cholangitis
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Primary sclerosing cholangitis is a biliary disease of unknown aetiology characterised
by inflammation and fibrosis of intra and extra-hepatic bile ducts
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Associations
• ulcerative colitis: 5% of patients with UC have PSC, 80% of patients with PSC
have UChe
• Crohn's (much less common association than UC)he
• HIVhe
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Features
• cholestasishe

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Investigation
• ERCP show multiple biliary strictures giving a 'beaded' appearancehe
 • liver biopsy: fibrous, obliterative cholangitis often described as ‘onion skin’he
• ANCA may be positivehe
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Complications
• cholangiocarcinoma (in 10%)he
• increased risk of colorectal cancerhe
Which one of the following adverse effects is least associated with sulfasalazine?ia
A.A Male infertilityia
B.A Skin rashesia
x C.A Visual disturbance
D.A Diarrhoeaia
E.A Agranulocytosisia
Next question
Aminosalicylate drugs
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5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts
locally as an anti-inflammatory. The mechanism of action is not fully understood but
5-ASA may inhibit prostaglandin synthesis
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Sulphasalazine
• a combination of sulphapyridine (a sulphonamide) and 5-ASAhe
• many side-effects are due to the sulphapyridine moiety: rashes, oligospermia,
headache, Heinz body anaemiahe
• other side-effects are common to 5-ASA drugs (see mesalazine)he
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Mesalazine
• a delayed release form of 5-ASAhe
• sulphapyridine side-effects seen in patients taking sulphasalazine are avoidedhe
• mesalazine isstill however associated with side-effects such as GI upset,
headache, agranulocytosis, pancreatitis*, interstitial nephritishe
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Olsalazine
• two molecules of 5-ASA linked by a diazo bond, which is broken by colonic
bacteriahe
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*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine
Which one of the following is not a feature of Peutz-Jeghers syndrome?ia
A.A Intestinal obstructionia
B.A Pigmented lesions on palmsia
 C.A Malignant change in polypsia
x D.A Osteomasia
E.A Iron-deficiency anaemiaia
Osteomas are a feature of Gardner's syndrome, a variant of familial adenomatous
polyposis
Peutz-Jeghers syndrome
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Peutz-Jeghers syndrome is an inherited condition characterised by numerous
hamartomatous polyps in GI tract (mainly small bowel) associated with pigmented
freckles on the lips, face, palms and soles. The polyps undergo malignant change in
less than 3% of patients
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Genetics
• autosomal dominanthe
• responsible gene encodes serine threonine kinase LKB1 or STK11he
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Features
• hamartomatous polyps in GI tracthe
• pigmented lesions on lips, oral mucosa, face, palms and soleshe
• intestinal obstruction e.g. intussusceptionhe
• GI bleedinghe
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Management
• conservative unless complications develophe
Autoimmune hepatitis type 2 is most strongly associated with which one of the
following antibodies?ia
A.A Anti-microsomal antibodyia
x B.A Anti-liver/kidney microsomal type 1 antibody
C.A Anti-smooth muscle antibodyia
D.A Anti-ribonuclear protein antibodyia
E.A Rheumatoid factoria
Next question
Autoimmune hepatitis
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Autoimmune hepatitis is condition of unknown aetiology which is most commonly
seen in young females. Recognised associations include other autoimmune disorders,
hypergammaglobulinaemia and HLA B8, DR3.Two types of autoimmune hepatitis
have been characterised according to the types of circulating antibodies present
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Type I Type II
Anti-nuclear antibodies (ANA) and/or anti- Anti-liver/kidney microsomal
smooth muscle antibodies (SMA) type 1 antibodies (LKM1)
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dssdfsselleds dssdfsselleds
Affects both adults and children Affects children only

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Features
• may present with signs of chronic liver diseasehe
• acute hepatitis: fever, jaundice etc (only 25% present in this way)he
• amenorrhoea (common)he

• ANA/SMA/LKM1 antibodies, raised IgG levelshe

• liver biopsy: inflammation extending beyond limiting plate 'piecemeal necrosis',
bridging necrosishe
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Management
• steroids, other immunosuppressants e.g. azathioprinehe
• liver transplantationhe
A 72-year-old female is admitted with diarrhoea to the acute medical unit. A
sigmoidoscopy is performed which shows multiple white plaques adhered to the
gastrointestinal mucosa. What is the most likely diagnosis?ia
A.A Crohn's diseaseia
B.A Ulcerative colitisia
C.A Ischaemic colitisia
x D.A Pseudomembranous colitis
E.A Colorectal canceria
Next question
Clostridium difficile
sqweqwesf erwrewfsdfs adasd dhe
Clostridium difficile is a Gram positive rod often encountered in hospital practice. It
produces an exotoxin which causes intestinal damage leading to a syndrome called
pseudomembranous colitis. Clostridium difficile develops when the normal gut flora
are reduced by antibiotics (e.g. clindamycin)
he earaer aeraer asdsadas eerw dssdfsselleds
Features
• diarrhoeahe
• abdo pain he
• if severe toxic dilatationhe
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Diagnosis is made by detecting Clostridium difficile toxin (CDT) in the stool
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Management
 • oral metronidazolehe

• if severe or not responding to metronidazole then oral vancomycin may be

usedhe
Which one of the following is the most common cause of traveller's diarrhoea?ia
A.A Salmonellaia
B.A Shigellaia
C.A Campylobacteria
x D.A E. coliia
E.A Bacillus cereusia
Next question
Gastroenteritis
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Which organism - clues
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Most common cause of traveller's diarrhoea is E coli
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Incubation period
• 1-6 hrs: Staph aureus, Bacillus cereus he
• 12-48 hrs: Salmonella, E. colihe
• 48-72 hrs: Shigella, Campylobacterhe
•> 7 days: Giardiasis, Amoebiasishe
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Stereotypical histories
• profuse, watery diarrhoea: cholerahe
• prolonged, non-bloody diarrhoea: Giardiahe
• bloody diarrhoea:, vomiting, abdo pain: Shigellahe
• severe vomiting: Staphylococcus aureushe
What percentage of patients with chronic pancreatitis have pancreatic calcification on
abdominal x-ray?ia
x A.A 30%ia
B.A 45%ia
C.A 60%ia
D.A 75%ia
E.A 90%ia
Next question
Chronic pancreatitis
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Chronic pancreatitis is an inflammatory condition which can ultimately affect both the
exocrine and endocrine functions of the pancreas. Around 80% of cases are due to
alcohol excess with up to 20% of cases being unexplained
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Features
• pain is typically worse 15 to 30 minutes following a mealhe
• steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5
and 25 years after the onset of painhe
• diabetes mellitus develops in the majority of patients. It typically occurs more
than 20 years after symptom begin. Patients often require lower doses of
insulin than other diabetic patientshe
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Investigation
• abdominal x-ray shows pancreatic calcification in 30% of caseshe
• CT is more sensitive at detecting pancreatic calcificationhe
• functional tests: pancreolauryl and
Lundh tests may be used to assess exocrine
function if imaging inconclusivehe
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Management
• pancreatic enzyme supplementshe

• analgesiahe
• antioxidants: limited evidence base - one study suggests benefit in early
diseasehe
What percentage of patients with chronic hepatitis C will develop liver cirrhosis over
a 20-30 year period?ia
A.A 5-10%ia
B.A 10-20%ia
x C.A 20-30%ia
D.A 40-50%ia
E.A 60-70%ia
Next question
Liver cirrhosis will develop in around 20-30% of patients over 20-30 years
Hepatitis C
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Transmission
• risk of transmission during a needle stick injury is about 2%he
• the vertical transmission rate from mother to child is about 6%he
• breast feeding is not contraindicated in mothers with hepatitis Che
• the risk of transmitting the virus during sexual intercourse is probably less than
5%he
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Features
 • after exposure to the hepatitis C virus less than 20% of patients develop an he
acute hepatitis
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Complications
• chronic infection(85%) - only 15% of patients will clear the virus and will hence
the majority will develop chronic hepatitis Che
• cirrhosis (20-30% of those with chronic disease)he
• hepatocellular cancerhe
• cryoglobulinaemiahe

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Management
• currently a combination of interferon-alpha and ribavirin are usedhe
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Complications of treatment
• ribavirin - side-effects: haemolytic anaemia, cough. Women should not become
he
pregnant within 6 months of stopping ribavirin as it is teratogenic
• interferonalpha - side-effects: fatigue, leukopenia, thrombocytopenia,
depressionhe
Which one of the following increases gastric acid secretion?ia
A.A VIPia
B.A CCKia
x C.A Histamineia
D.A GIPia
E.A Secretinia
Next question
Gastrointestinal physiology: acid secretion
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Principle mediators of acid secretion
• gastrinhe

• vagal stimulationhe

• histaminehe
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Factors increasing acid secretion
• gastrinomahe

• small bowel resection (removal of inhibition)he

• systemic mastocytosis (elevated histamine levels)he
• basophiliahe
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Factors decreasing acid secretion
• drugs: H2-antagonists, PPIshe
• hormones: secretin, VIP, GIP, CCKhe

Which one of the following is least associated with Crohn's disease?ia

A.A Fistulaeia
B.A Kantor's string signia
C.A 'Cobblestone' pattern of mucosaia
x D.A Crypt abscesses
E.A Involvement of all layers of bowel wallia
Next question
Crypt abscesses are sometimes seen in Crohn's disease but they are more commonly
associated with ulcerative colitis
Crohn's disease
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Basics
• anywhere from mouth to anushe
• terminal ileum and colon are most common siteshe
• often discontinuoushe
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Pathology
• oedema of submucosa + mucosahe
• combined with deep fissured ulcers 'rose-thorn' --> 'cobblestone' patternhe
• inflammation occurs in ALL layers, down to the serosa --> strictures, fistulas,
adhesions etche
• majority of patients have granulomashe
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Small bowel enema
• strictures: 'Kantor's string sign'he
• proximal bowel dilationhe

• 'rose thorn' ulcershe

• fistulaehe
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Barium enema
• shows extent of colonic diseasehe
 • deep ulcers and skip areashe
Which one of the following conditions is most associated with angiodysplasia?ia

A.A Aortic regurgitationia

B.A Ventricular septal defectia
x C.A Aortic stenosis
D.A Hypertrophic obstructive cardiomyopathyia
E.A Mitral regurgitationia
Next question
Angiodysplasia is associated with aortic stenosis
The association between angiodysplasia and aortic stenosis is thought to be caused by
von Willebrand factor (vWF) being proteolysed in the turbulent blood flow around the
aortic valve
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vWF is most active in vascular beds with high shear stress, such as angiodysplasia,
and deficiency of vWF increases the bleeding risk from such lesions
Angiodysplasia
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Features
• typically iron deficiency anaemiahe
• associated with aortic stenosishe
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Diagnosis
• colonoscopyhe

• mesenteric angiography if acutely bleedinghe

Which one of the following features is least associated with haemochromatosis?ia
A.A Cardiomyopathyia
B.A Hypogonadismia
x C.A Choreaia
D.A Diabetes mellitusia
E.A Liver cirrhosisia
End session
Haemochromatosis: features
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Haemochromatosis is an autosomal recessive disorder of iron absorption and
metabolism resulting in iron accumulation. It is caused by inheritance of mutations in
the HFE gene on both copies of chromosome 6*. It is often asymptomatic in early
disease and initial symptoms often non-specific e.g. lethargy and arthralgia
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Presenting features
 • 'bronze' skin pigmentationhe
• diabetes mellitushe
• liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular
deposition)he
• cardiac failure (2nd to dilated cardiomyopathy)he
• hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic
hypogonadism)he
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Questions have previously been asked regarding which features are reversible with
treatment:
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Reversible complications Irreversible complications
• Cardiomyopathyhe • Liver cirrhosishe
• Skin pigmentationhe • Diabetes mellitushe
• Hypogonadotrophic hypogonadismhe

• Arthropathy

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*there are rare cases of families with classic features of genetic haemochromatosis but
no mutation in the HFE gene
Key points from session

24hr oesophageal pH monitoring is gold standard investigation in GORD

5% of patients with UC have PSC, 80% of patients with PSC have UC
Angiodysplasia is associated with aortic stenosis
Brush border enzymes:
• maltase: glucose + glucosehe
• sucrase: glucose + fructosehe

• lactase: glucose + galactosehe

Dysphagia affecting foods and solids from the start - think achalasia
Obese T2DM with abnormal LFTs - ? non-alcoholic steatohepatitis
Screening for haemochromatosis
• general population: transferrin saturationhe
• family members: HFE genetic testinghe
The gold standard test for achalasia is oesophageal manometry