Gastroenterology

Dr. Emtiaz Zaman

MD Phase-B Resident
Hepatology
BSMMU
1.A 60-year-old man presented with dysphagia for 3 months. How would you evaluate him? ( January 25)

2.A 31-year-old woman presented with passage of blood-mixed loose stool with abdominal cramps for
the last six months.

a) Write important clinical clues you would look for related to the underlying diagnosis. ( January 25 )

b) What is your plan of investigations to reach the underlying cause?

3.A 55-year-old man presents with difficulty in swallowing for 6 months. Mention the plan of
investigations with reasoning for their selection. ( july 24 )

4.A 31-year-old woman presented with passage of mixed loose stool with abdominal cramps for the last
6 months. Write the pertinent clinical clues and plan of investigations to reach the underlying
diagnosis.(july 24)

5.A 42-year-old man presented with complaints of abdominal pain and passage of blood mixed stool for
9 (nine) months. Write a clinical checklist to evaluate him with expected findings. (January 2024)

6.A 30-year-old man presented with chronic diarrhea and weight loss for 4 months. Make a plan of
investigations with expected findings hinting the underlying diagnosis. ( July 2023 )

7.A 28-year old man presented with proximal muscle weakness with difficulty in swallowing for 6
months. Make a clinical checklist to reach the probable diagnosis. ( July 2023 )

8.A 45-year-old woman presented with massive hematemesis. Write the principles of management for
this patient. ( July 2023 )

9.A 60-year-old man presented with unintentional weight loss. Make a clinical checklist to establish the
cause of this presentation. ( January 2023 )

10.A 32-year-old man presented with recurrent bloody diarrhea for last 2 months. Write a plan of
investigations with expected findings to reach the underlying diagnosis. ( july 22 )

11.A 28-year-old obese man presented with heart burn specially after meal. How would you advise him
to minimize his symptoms? ( july 22 )

12. A 32-year-old man presented with recurrent bloody diarrhea for the last 2 months. Write a plan of
investigations with expected findings to reach the underlying diagnosis. January 22

13. A 45-year-old man presented with difficulty in swallowing for 3 months. How would you evaluate
him? July 21, July 16

14. A 65-year-old man presented with chronic constipation. How would you evaluate him? July 21

15. A 35-year-old woman came with a history of recurrent oral ulcer. How would you evaluate her
clinically? July 21, July 20, July 16, July 15, January 15

16. A 60-year-old man presented with dyspepsia (with alarming sign). How would you assess and
investigate him? July 20, January 20
17. Discuss in brief about abdominal angina. July 20

18. How would you evaluate a patient with cachexia? July 20

19. How would you evaluate a 45-year-old woman with dysphagia? July 19

20. Enumerate the plan of investigation with findings for a patient with chronic diarrhea. July 19

21. Mention the alarming signs of dyspepsia. January 19

22. How would you evaluate a 35-year-old patient presented with severe upper abdominal pain? January
19, July 17

23. Discuss the emergency management of non-variceal gastrointestinal hemorrhage. July 18, July 14

24. How would you manage a patient with intractable hiccup? July 18, July 16, January 15, January 14

25. A 40-year-old man presented with blood-mixed diarrhea for 3 months. How would you evaluate him
to establish the diagnosis? January 18

26. A 45-year-old man presented with recurrent upper abdominal pain. Write a clinical checklist hinting
the etiology. July 17

27. How would you manage a patient of chronic dyspepsia with normal upper GI endoscopy findings?
January 17

28. How would you evaluate a 55-year-old woman with unexplained weight loss? January 17, January 15

29. How would you treat abdominal pain due to pancreatic malignancy? January 17

30. Outline the management and complications of acute pancreatitis. July 16

31. A 50-year-old man presented with chronic lower GI bleeding. How would you evaluate him? July 16

32. How would you evaluate a 60-year-old man presented with recurrent central abdominal pain? July 16

33. How would you approach a 30-year-old man presenting with a white patch in the oral cavity? January
16

34. Describe the role of USG in evaluating an adult patient presented with acute abdomen. January 16

35. What are the causes and complications of acute pancreatitis? January 16

36. How would you evaluate a patient presenting with malabsorption syndrome? January 16

37. Mention the alarm features of IBS. July 15

38. Describe the role of upper GI endoscopy in clinical practice. July 15, July 13

39. A 40-year-old man presented with recurrent bloody diarrhea for 3 months. How will you manage
him? January 15

40. Write in short about functional dyspepsia. January 15

41. A 30-year-old woman has presented with chronic diarrhea. Give a checklist of clinical information to
reach a diagnosis. July 14

42. How will you evaluate a 25-year-old woman presenting with vomiting for the last 2 weeks. January 14

43. A 30-year-old man presented with fever for 6 weeks. He had a lump in the right lower abdomen. How
would you diagnose him? January 14 (consider cancer, tuberculosis)

44. How will you manage a 50-year-old man presenting with melaena? July 13

45. What information can you get by bedside examination of the testis? July 13

46. How will you manage a case of aphthous ulcer? July 13

47. What is steatorrhoea? Enumerate the causes of malabsorption? July 13

48. Clinically, how can you differentiate chronic pancreatitis from peptic ulcer disease? Enumerate the
common causes of acute pancreatitis. January 13

Pictorial:
Imaging:
Imaging in gastroenterology
Ultrasound Computed tomography Magnetic resonance Positron
(CT) imaging (MRI) emission
tomography-CT
(PET-CT)
Indications Abdominal Assessment of Hepatic tumour Detection of
and major masses pancreatic staging metastases not
uses Organomegaly disease MRCP seen on
Ascites Hepatic tumour Pelvic/perianal ultrasound or
Biliary tract deposits disease CT
dilatation CT colonography Crohn’s fistulae Images can be
Gallstones (‘virtual Small bowel fused with CT
Guided biopsy colonoscopy’) visualisation to form
of lesions Tumour staging composite
Small bowel Assessment of lesion image
imaging vascularity
Abscesses and
collections
Limitations Low sensitivity Cost Claustrophobic Signal
for small lesions Radiation dose patients detection
Little functional Contraindicated in depends on
information presence metabolic
Operator- of metallic activity
dependent prostheses, cardiac within tumour
Gas and pacemaker, cochlear – not all are
obesity may implants metabolically
obscure view active
(MRCP = magnetic resonance cholangiopancreatography

Upper gastrointestinal endoscopy

Indications
• Dyspepsia in patients > 55 years of age or with alarm symptoms
• Atypical chest pain
• Dysphagia
• Vomiting
• Weight loss
• Acute or chronic gastrointestinal bleeding
• Screening for oesophageal varices in chronic liver disease
• Abnormal CT scan or barium meal
• Duodenal biopsies in the investigation of malabsorption and confirmation of a diagnosis of
coeliac disease prior to commencement of gluten-free diet
• Therapy, including treatment of bleeding lesions, banding/injection of varices, dilatation of
strictures, insertion of stents, placement of percutaneous gastrostomies, ablation of Barrett’s
 oesophagus and resection of high-grade dysplastic lesions and early neoplasia in the upper
gastrointestinal tract

Contraindications
• Severe shock
• Recent myocardial infarction, unstable angina, cardiac arrhythmia
• Severe respiratory disease*
• Atlantoaxial subluxation*
• Possible visceral perforation

Complications
• Cardiorespiratory depression due to sedation
• Aspiration pneumonia
• Perforation

*These are ‘relative’ contraindications; in experienced hands, endoscopy can be safely performed.
(CT = computed tomography)
Wireless capsule endoscopy
Indications
• Obscure gastrointestinal bleeding
• Small bowel Crohn’s disease
• Assessment of coeliac disease and its complications
• Screening and surveillance in familial polyposis syndromes
Contraindications
• Known or suspected small bowel stricture (risk of capsule retention)
• Caution in people with pacemakers or implantable dfibrillators
Complications
• Capsule retention (< 1%)
Double balloon enteroscop
Indications
Diagnostic
• Obscure gastrointestinal bleeding
• Malabsorption or unexplained diarrhoea
• Suspicious radiological findings
• Suspected small bowel tumour
• Surveillance of polyposis syndromes
Therapeutic
• Coagulation/diathermy of bleeding lesions
• Jejunostomy placement
Contraindications
• As for upper gastrointestinal endoscopy
Complications
• As for upper gastrointestinal endoscopy
• Post-procedure abdominal pain (≤ 20%)
• Pancreatitis (1%–3%)
• Perforation (especially after resection of large polyps)

Colonoscopy
Indications
• Suspected infiammatory bowel disease
• Chronic diarrhoea
• Altered bowel habit
• Rectal bleeding or iron deficiency anaemia
• Assessment of abnormal CT colonogram or barium enema
• Colorectal cancer screening
• Colorectal adenoma and carcinoma follow-up
• Therapeutic procedures, including endoscopic resection, dilatation of strictures,
laser, stent insertion and argon plasma coagulation
Contraindications
• Acute severe ulcerative colitis (unprepared dfiexible sigmoidoscopy is preferred)
• As for upper gastrointestinal endoscopy
Complications
• Cardiorespiratory depression due to sedation
• Perforation
• Bleeding following polypectomy
*Colonoscopy is not useful in the investigation of constipation. (CT = computed
tomography)
Endoscopic retrograde cholangiopancreatography (ERCP)
Indications
Diagnostic
• Biliary or pancreatic disease where other imaging is equivocal or contraindicated
• Ampullary biopsy or biliary cytology

Therapeutic
• Biliary disease:
Removal of common bile duct calculi*
Palliation of malignant biliary obstruction
Management of biliary leaks/damage complicating surgery
Dilatation of benign strictures
Primary sclerosing cholangitis
• Pancreatic disease:
Drainage of pancreatic pseudocysts and fistulae
Removal of pancreatic calculi (selected cases)
Contraindications
• Severe cardiopulmonary comorbidity
• Coagulopathy
Complications
• Occur in 5%–10% with a 30-day mortality of 0.5%–1%
General
• As for upper endoscopy
Specific
• Biliary disease:
Bleeding following sphincterotomy
Cholangitis (if biliary obstruction is not relieved by ERCP)
Gallstone impaction
• Pancreatic disease:
Acute pancreatitis
Infection of pseudocyst
* Laparoscopic surgery is preferred in fit individuals who also require cholecystectomy.
Tests of gastrointestinal function
Process Test Principle Comments

Absorption Lactose H2 breath test Measurement of Non-invasive and

Lactose breath H2 content accurate. May
after 50 g oral provoke pain and
lactose. Undigested diarrhoea in sufferers
sugar is metabolised
by colonic bacteria in
hypolactasia and
expired hydrogen is
measured
Fructose Fructose H2 breath Measurement of Results can be
test breath H2 content difficult to interpret
after 25–50 g oral as breath testing does
fructose. Unabsorbed not refiect fructose
fructose is fermented ingestion in everyday
by colonic bacteria life
with expired
hydrogen measured
Bile acids Isotopic Accurate and specific
75
SeHCAT test quantification of 7- but requires two visits
Serum day whole-body and involves
7α- retention of oral dose radiation. Results can
hydroxycholestenone Se-labelled be equivocal. Serum
homocholyltaurine 7α-
(>15% = normal, 5%– hydroxycholestenone
15% borderline, < 5% is almost as sensitive
= abnormal) and specific Simple
Intermediate test to perform and
metabolite of the bile only marginaly less
acid synthetic sensitive and specific
pathway. Serum than 75SeHCAT test
levels indicate activity
of the pathway and
are elevated in bile
acid diarrhoea
Pancreatic exocrine Faecal elastase Immunoassay of Simple, quick and
function pancreatic enzymes avoids urine
on stool sample collection. Does not
detect mild disease
Mucosal Faecal calprotectin Proteins secreted Useful screening test
inflammation/permeability or lactoferrin non-specifically by for gastrointestinal
neutrophils into the inflammation and for
colon in response to monitoring patients
inflammation or with Crohn’s disease
neoplasia and ulcerative colitis.
Poor sensitivity for
cancer
Tests involving radioisotopes
Test Isotope Major uses and principle of test
99m
Gastric emptying study Tc-sulphur Assessment of gastric emptying,
111
In-DTPA particularly for possible
gastroparesis
13
Urea breath test C-urea Non-invasive diagnosis of
Helicobacter pylori. Bacterial
urease enzyme splits urea to
ammonia and CO2, which is
detected in expired air
99m
Meckel’s scan Tc pertechnetate Diagnosis of Meckel’s
diverticulum in cases of obscure
gastrointestinal bleeding.
Isotope is injected
intravenously and localises in
ectopic parietal mucosa within
diverticulum
111
Somatostatin receptor In-DTPA octreotide Staging neuro-endocrine
99m
scintigraphy (SRS) 18 Tc-tektrotyd tumours.
Labelled somatostatin
analogues
bind to cell surface
somatostatin
receptors on neuro-endocrine
cancer cells
18
Positron emission F-FDG Staging high-grade cancers
68
tomography-CT (PET-CT) Ga-labelled somatostatin More sensitive and specific
analogue than
SRS for staging neuro-endocrine
tumours
Dysphagia:

Dyspepsia:
Alarm features in dyspepsia
Unintentional weight loss
• Anaemia
• Persistent vomiting
• Haematemesis and/or melaena
• Dysphagia
• Palpable abdominal mass
Vomiting:

Acute upper gastrointestinal bleeding:

Causes of acute upper gastrointestinal haemorrhage:

Management:
Intravenous access:
• Ideally using two large-bore cannulae.

Initial clinical assessment:

Define circulatory status:

• Severe bleeding causes tachycardia, hypotension and oliguria.
• The patient is cold and sweating, may be agitated.

Seek evidence of liver disease:

• Jaundice, cutaneous stigmata, hepatosplenomegaly and ascites may be present in
decompensated cirrhosis.

Identify comorbidity:
• Presence of cardiorespiratory, cerebrovascular or renal disease

Basic investigations:

Full blood count:

• Chronic or subacute bleeding leads to anaemia, but the haemoglobin concentration may be
normal after sudden, major bleeding until haemodilution occurs.
• Thrombocytopenia may be a clue to the presence of hypersplenism in chronic liver disease.

Urea and electrolytes:

• Evidence of renal failure.
• An elevated blood urea with normal creatinine concentration implies severe bleeding.

Liver function tests:

• May show evidence of chronic liver disease.

Prothrombin time:
• Check when there is a clinical suggestion of liver disease or patients are anticoagulated.

Cross-matching:
• At least 2 units of blood should be cross-matched if a significant bleed is suspected.

Resuscitation:
• Intravenous crystalloid fluids should be given to raise the blood pressure, with a 500 ml bolus
recommended over less than 15 minutes in haemodynamically unstable patients.

• In most patients, blood should be transfused when haemoglobin is less than 70 g/L.

Oxygen:
 • Oxygen saturations should be monitored with pulse oximetry, with a target saturation of 94%–
98%.

Antithrombotic drugs:

• Aspirin can be continued during an upper gastrointestinal bleed.

• P2Y12-receptor antagonists (e.g. clopidogrel) should be temporarily stopped (unless prescribed

following coronary artery stenting) as well as Warfarin and direct oral anticoagulant therapy.

• Early reintroduction of these medications should occur after haemostasis has been achieved to
reduce thrombotic events and death.

Proton pump inhibitor (PPI) therapy:

• Intravenous PPI infusion, in individuals who have a high-risk ulcer post endoscopy (e.g. ulcers
with a clot and/or requiring endoscopic haemostasis).

PPIs work by:

• Reducing gastric acid secretion
• Neutralising intragastric pH
• Promoting clot stability by reducing pepsin-induced clot lysis
• Increasing platelet aggregation

• While intravenous PPI infusion is most frequently used, intermittent intravenous PPI and oral
high-dose PPI can be considered as alternatives.

Common proton pump inhibitors (PPIs) and dosage for peptic ulcer disease
Oral administration
Standard dose High dose
Lansoprazole 30 mg OD 30 mg BD

Omeprazole 20 mg OD 40 mg OD

Pantoprazole 40 mg OD 40 mg BD

Rabeprazole 20 mg OD 20 mg BD

Esomeprazole 20 mg OD 40 mg OD

Intravenous infusion
Dose
Omeprazole 80 mg IV bolus, followed by 8 mg/hr for 72 hrs
Pantoprazole
 Esomeprazole
(BD = twice daily; IV = intravenous; OD = once daily
Endoscopy:

• This should be carried out after adequate resuscitation, ideally within 24 hours.

• Treated endoscopically using a thermal or mechanical modality, such as a ‘heater probe’ or

endoscopic clips, combined with injection of dilute adrenaline (epinephrine) into the bleeding
point (‘dual
• therapy’).

• A biologically inert haemostatic mineral powder (TC325, ‘haemospray’) can be used as rescue
therapy when standard therapy fails.

• Newer techniques, such as ‘over-the-scope clips’, may also be used as a rescue therapy when
standard therapy fails, treating large vessels or fibrotic lesions.

• Variceal bleeding:
• Band ligation
• Balloon tamponade
• Transjugular intrahepatic portosystemic shunt (TIPSS)
• Removable, self-expanding, covered metal oesophageal stents

Monitoring:
• Hourly measurements of pulse, blood pressure, oxygen saturations and urine output.

Radiology and surgery:

• Patients who have recurrent bleeding, where endoscopic attempts at haemostasis have failed,
should be considered for radiological or surgical intervention.

• If available, angiographic control of bleeding is generally preferred to surgery in older, frail

patients.

• If surgery is required, the choice of operation depends on the site and diagnosis of the bleeding
lesion.

• Duodenal ulcers are treated by under-running, with or without pyloroplasty.

• Under-running for gastric ulcers can also be carried out (a biopsy must be taken to exclude
carcinoma).

• Local excision may be performed, but when neither is possible, partial gastrectomy is required.

Eradication:
• All patients should avoid non-steroidal anti-inflammatory drugs (NSAIDs)

• Those who test positive for H. pylori infection should receive eradication therapy.
 • Successful eradication should be confirmed by urea breath or faecal antigen testing.

Causes of lower gastrointestinal bleeding

Severe acute
• Diverticular disease
• Angiodysplasia
• Ischaemia
• Meckel’s diverticulum
• Infiammatory bowel disease (rarely)
Moderate, chronic/subacute
• Fissure
• Haemorrhoids
• Infiammatory bowel disease
• Carcinoma
• Large polyps
• Angiodysplasia
• Radiation enteritis
• Solitary rectal ulcer

Chronic or relapsing diarrhoea:

Chronic or relapsing diarrhoea
Colonic Malabsorption Small bowel
Clinical features Blood and mucus in Steatorrhoea Large-volume, watery
stool Cramping lower Undigested food in the stool
abdominal pain stool Abdominal bloating
Weight loss and Cramping mid-
nutritional disturbances abdominal pain
Some causes Infiammatory bowel Pancreatic: Crohn’s disease
disease Chronic pancreatitis Neuro-endocrine
Microscopic colitis Cancer of pancreas tumour
Neoplasia Cystic fibrosis Small bowel carcinoid
Ischaemia Enteropathy: VIPoma
Irritable bowel Coeliac disease Drug-induced:
syndrome Tropical sprue NSAIDs
Lymphoma Aminosalicylates
Lymphangiectasia SSRIs
Investigations Faecal calprotectin Faecal elastase Faecal calprotectin
Ileocolonoscopy with Ultrasound, CT and Stool volume
biopsies MRCP Serum gut hormone
Small bowel biopsy profile and 24 hr urine
Barium follow-through 5HIAA
or small bowel MRI Barium follow-through
or small bowel MRI
Routine blood test abnormalities in malabsorption
Haematology
• Microcytic anaemia (iron deficiency)
• Macrocytic anaemia (folate or B
• deficiency)
• Increased prothrombin time (vitamin K deficiency)
Biochemistry
• Hypoalbuminaemia
• Hypocalcaemia
• Hypomagnesaemia
• Hypophosphataemia
• Low serum zinc
Investigations for suspected Malabsorption:
Weight loss: Weight loss of more than 5% of usual body weight over 6–12 months is clinically important
and can indicate the presence of an underlying disease.

Constipation:
Causes of constipation
Gastrointestinal causes
Dietary
• Lack of fibre and/or fluid intake

Motility
• Slow-transit constipation
• Irritable bowel syndrome
• Drugs (see below)
• Chronic intestinal pseudo obstruction

Structural
• Colonic carcinoma
• Diverticular disease
• Hirschsprung’s disease

Defecation
• Anorectal disease (Crohn’s, fissures,
• haemorrhoids)
• Dyssynergic defecation
Non-gastrointestinal causes
Drugs
• Opiates
• Anticholinergics
 • Calcium antagonists
• Iron supplements
• Aluminium-containing antacids

Neurological
• Multiple sclerosis
• Spinal cord lesions
• Cerebrovascular accidents
• Parkinsonism

Metabolic/endocrine
• Diabetes mellitus
• Hypercalcaemia
• Hypothyroidism
• Pregnancy

Others
• Any serious illness with immobility, especially in old age
• Depression
Initial investigations:
• A thorough history and physical examination should be performed.

• Careful digital rectal examination and inspection of the perineum is essential.

• A full blood count, routine biochemistry, including serum calcium and thyroid function tests,
should be carried out.

• If these are normal, then dietary and lifestyle modifications should be advised, such as increased
fluid intake, dietary fibre supplementation and exercise.

• Laxatives should be commenced if individuals fail to respond.

• Organic causes should be explored using colonoscopy in individuals with concerning symptoms
(e.g. rectal bleeding, pain or weight loss).

Further investigations:
• If no cause is found and disabling symptoms are present, then specialist referral for investigation
of possible dysmotility may be necessary.

• The problem may be due to delayed transit of stool in the colon (slow transit constipation) or
from functional abnormalities in the pelvic oor and anal sphincter muscles (dyssynergic
defecation).

• Intestinal marker studies

• Anorectal manometry
• Electrophysiological studies
• Magnetic resonance proctography
Extra-intestinal causes of chronic or recurrent abdominal pain
Retroperitoneal
• Aortic aneurysm
• Malignancy
• Lymphadenopathy
• Abscess
Psychogenic
• Depression
• Anxiety
• Hypochondriasis
• Somatisation
Locomotor
• Vertebral compression/fracture
• Abdominal muscle strain
Metabolic/endocrine
• Diabetes mellitus
• Acute intermittent porphyria
• Hypercalcaemia
Drugs/toxins
• Glucocorticoids
• Azathioprine
• Lead
• Alcohol
Haematological
• Sickle-cell disease
• Haemolytic disorders
Neurological
• Spinal cord lesions
• Tabes dorsalis
• Radiculopathy
Causes of oral ulceration
Aphthous
• Idiopathic
• Premenstrual
Infection
• Fungal (candidiasis)
• Viral (herpes simplex, HIV)
• Bacterial, including syphilis, tuberculosis
Gastrointestinal diseases
• Crohn’s disease
• Coeliac disease
Dermatological conditions
• Lichen planus
• Immunobullous disorders (Ch. 27)
• Dermatitis herpetiformis
• Erythema multiforme
Drugs
• Nicorandil, NSAIDs, methotrexate, penicillamine, losartan, ACE inhibitors
• Stevens–Johnson syndrome (Ch. 27)
• Cytotoxic drugs
Systemic diseases
• Systemic lupus erythematosus (Ch. 26)
• Behçet’s disease (Ch. 26)
Neoplasia
• Carcinoma
• Leukaemia
• Kaposi’s sarcoma
Gastro-oesophageal reflux disease:

Clinical features:
• Major symptoms are heartburn and regurgitation, often provoked by bending, straining or lying
down.
• Odynophagia or dysphagia
• Atypical chest pain that may be severe and can mimic angina; it may be due to reflux-induced
oesophageal spasm
• Hoarseness (‘acid laryngitis’)
• Recurrent chest infections
• Chronic cough and asthma.

Complications:
• Oesophagitis
• Barrett’s oesophagus
• Anaemia
• Benign oesophageal stricture
• Gastric volvulus

Investigations:
• Endoscopy is the investigation of choice.
• Oesophageal pH monitoring: pH of less than 4 for more than 6% of the study time is considered
diagnostic for reflux disease.
Management:

Lifestyle advice:
• Weight loss
• Avoidance of dietary items that worsen symptoms
• Elevation of the bed head in those who experience nocturnal symptoms
• Avoidance of late meals
• Cessation of smoking
Side effects of prolonged PPI therapy:
• Parietal cell hyperplasia and hypertrophy, leading to acid rebound on withdrawal of PPIs after
long-term usage.
• Reduced absorption of iron, B12 and magnesium
• Enteric infections with Salmonella, Campylobacter and possibly Clostridioides difficile
• Microscopic colitis, Acute interstitial nephritis
• Risk of Helicobacter-associated progression of gastric mucosal atrophy

Hiatus hernia:
Important features of hiatus hernia
• Herniation of the stomach through the diaphragm into the chest
• Occurs in 30% of the population over the age of 50 years
• Often asymptomatic
• Heartburn and regurgitation can occur
• Gastric volvulus may complicate large hernias
Barrett's Oesophagitis:
Pathology:

• Pre malignant condition

• Normal squamous lining of lower oesophagus is replaced by columner mucosa (columner lined
oesophagus, CLO)

High prevelance:
• Men (white)
• Obese
• More than 50 years of age
• Smoking

Investigations:
• Upper GI endoscopy with multiple systematic biopsies: detect intestinal metaplasia and/or
dysplasia.

Management:
Indications:
• Symptoms of reflux or complications eg. Strictures
• For high grade dysplasia/ Intramucosal carcinoma > Oesophagectomy/ Endoscopic therapy with
combination of Endoscopic resection of visibly abnormal areas & Radiofrequency ablation of
remaining barrettic mucosa as an “Organ preserving” alternative to surgery.
• Alternative ablative therapies to RFA: are in development, Cryoablation

Follow Up:
Without dysplasia:
• Length of barretic segment < 3 cm: 3-5 yearly Endoscopy
• Length of barretic segment > 3 cm: 2-3 yearly Endoscopy
Low grade dysplasia:
• Endoscopy 6 monthly

Eosinophilic oesophagitis:
Pathology:
• Eosinophilic infiltration of the oesophageal mucosa.

6 Endoscopic features: (FREONS)

• Mucosal rings, longitudinal furrows, exudates, oedema, strictures or a narrow-calibre
oesophagus

Biopsy findings:
• Increase in eosinophil density (≥ 15 eosinophils per high-powered field (HPF))
4 Management options:
• Dietary modifications

• Empiric 8-week trial of high-dose PPI

• 8–12 weeks of therapy with topical glucocorticoids, such as fluticasone and budesonide

• Endoscopic oesophageal dilatation in individuals with strictures or mucosal rings that have failed
to respond to medical therapy.

Carcinoma of the oesophagus:

Squamous carcinoma: aetiological factors
• Smoking
• Alcohol excess
• Chewing betel nuts or tobacco
• Achalasia of the oesophagus
• Coeliac disease
• Post-cricoid web
• Post-caustic stricture
• Tylosis (familial hyperkeratosis of palms and soles)

Clinical features:
Symptoms:
• Progressive, painless dysphagia for solid foods.
• Weight loss
• Chest pain or hoarseness suggests mediastinal invasion
• Fistulation between the oesophagus and the trachea or bronchial tree leads to coughing after
swallowing, pneumonia and pleural effusion.

Signs:
• Cachexia
• Cervical lymphadenopathy
• Evidence of metastatic spread
Investigations:

• The investigation of choice is upper gastrointestinal endoscopy with biopsy.

• Investigations for staging the tumour:

• Thoracic and abdominal CT, often combined with positron emission tomography (PET-CT)
• EUS to determine the depth of penetration of the tumour into the oesophageal wall and to
detect locoregional lymph node involvement
Management:

• Endoscopic mucosal resection

• Endoscopic submucosal dissection with or without radiofrequency ablation
• Oesophagectomy is the treatment of choice for limited and locally advanced tumours
• For locally advanced tumours, neoadjuvant and perioperative chemotherapy or
chemoradiotherapy (e.g. cisplatin and capecitabine) can reduce the tumour bulk and increase
the chances of complete (R0) surgical resection.

5 Palliative treatment options:

• Palliative radiotherapy
• Stent placement can be used for symptom control.
• Palliative chemotherapy can be used for selected patients, particularly for those with
adenocarcinoma.
• Nutritional support
• Appropriate analgesia

Achalasia of the oesophagus:

Pathophysiology:

Achalasia is characterised by:

• A hypertonic lower oesophageal sphincter, which fails to relax in response to the swallowing
wave
• Failure of propagated oesophageal contraction, leading to progressive dilatation of the gullet.

Defective release of nitric oxide by inhibitory neurons in the lower oesophageal sphincter has been
reported, and there is degeneration of ganglion cells within the sphincter and the body of the
oesophagus. Loss of the dorsal vagal nuclei within the brainstem can be demonstrated in later stages.

4 Associations:
• Type 1 diabetes mellitus
• Systemic lupus erythematosus
• Rheumatoid arthritis
• Sjogren syndrome
 3 C/F:

• Dysphagia, typically to solids and liquids.

• Chest pain due to oesophageal spasm.
• Pulmonary aspiration

Investigations:

• Endoscopy should always be carried out because carcinoma of the cardia can mimic the
presentation and radiological and manometric features of achalasia (‘pseudo-achalasia’)

• Barium swallow shows tapered narrowing of the lower oesophagus and, in late disease, the
oesophageal body is dilated, aperistaltic and food-filled.

• Manometry confirms the high-pressure, non-relaxing lower oesophageal sphincter with poor
contractility of the oesophageal body.

Management:

Endoscopic:
• Forceful pneumatic dilatation
• Endoscopically directed injection of botulinum toxin into the lower oesophageal sphincter
• Peroral endoscopic myotomy (POEM)
Surgical:
• Surgical myotomy (Heller’s operation), accompanied by a partial fundoplication anti-reflux
procedure.
• PPI therapy is often necessary after surgery.

Methods for the diagnosis of Helicobacter pylori infection

Test Advantages Disadvantages
Non-invasive
Serology Rapid office kits available Good Lacks specificity Cannot differentiate
for population studies current from past infection
13
C-urea breath test High sensitivity and specificity Requires expensive mass
spectrometer
Faecal antigen test Cheap, specific (> 95%) Acceptability
Invasive (antral biopsy)
Histology Specficity False negatives Takes several days to
process
Rapid urease test Cheap, quick, specific (> 95%) Sensitivity 85%

Microbiological ‘Gold standard’ Defines Slow and laborious Lacks sensitivity

culture antibiotic sensitivity

Common side-effects of Helicobacter pylori eradication therapy

• Diarrhoea: 30%–50% of patients; usually mild, but Clostridioides difficileassociated diarrhoea
can occur
• Flushing and vomiting when taken with alcohol (metronidazole)
• Nausea, vomiting
• Abdominal cramps
• Headache
• Rash
 Indications for Helicobacter pylori testing
Definite
• Active or past history of peptic ulcer disease
• Extranodal marginal-zone lymphomas of MALT type
• Previous endoscopic resection for early gastric cancer
• Dyspepsia
• Long-term NSAID or low-dose aspirin users
• Extragastric disorders:
Idiopathic thrombocytopenic purpura
Unexplained iron deficiency anaemia
• Unexplained Vitamin B
Not indicated
• Gastro-oesophageal reflux disease
• Asymptomatic people
Indications for surgery in peptic ulcer
Emergency
• Perforation
• Hemorrhage
Elective
• Gastric outflow obstruction
• Persistent ulceration despite adequate medical therapy
• Recurrent ulcer following gastric surgery

Zollinger–Ellison syndrome:

Triad:
• Gastric acid hypersecretion
• Severe peptic ulceration
• Gastrin-secreting neuro-endocrine tumour (‘gastrinoma’)

Pathophysiology:
• Elevated gastrin stimulates acid secretion to its maximal capacity and increases the parietal cell
mass three- to sixfold.
• The acid output may be so great that it reaches the upper small intestine, reducing the luminal
pH to 2 or less.
• Pancreatic lipase is inactivated and bile acids are precipitated > Diarrhoea and steatorrhoea
result.
• Around 90% of tumours occur in the pancreatic head or proximal duodenal wall.
• Between 20% and 60% of patients have multiple endocrine neoplasia (MEN) type 1.

Clinical features:
• Severe and often multiple peptic ulcers in unusual sites, such as the post-bulbar duodenum,
jejunum or oesophagus.
• Poor response to standard ulcer therapy.
• History is usually short, and bleeding and perforations are common.
• Diarrhoea is seen in one-third or more of patients and can be the presenting feature.
Investigations:
• Serum gastrin levels: grossly elevated (10- to 1000-fold).
• Paradoxical and dramatic increase in gastrin following Injection of hormone secretin
• Tumour localisation (and staging) is best achieved by a combination of CT and EUS; radio-
labelled somatostatin receptor scintigraphy and 68gallium DOTATATE PET scanning may also be
used for tumour detection and staging.

Management:

• Unifocal tumours may be resected

• Surgery may not be appropriate when there are multi-focal tumours or if there is metastatic
disease.
• Continuous therapy with a PPI in high dose can be successful in healing ulcers and alleviating
diarrhoea.
• Somatostatin analogue therapy may reduce gastrin secretion and have an anti-tumour effect.

Prognosis:
• Overall 5-year survival is 60%–75% and all patients should undergo genetic screening for MEN 1.

Gastric carcinoma:
Risk factors for gastric cancer
• Helicobacter pylori
• Smoking
• Alcohol
• Dietary associations (see text)
• Autoimmune gastritis (pernicious anaemia)
• Adenomatous gastric polyps
• Previous partial gastrectomy (> 20 years)
• Ménétrier’s disease
• Hereditary diffuse gastric cancer families (CDH1 mutations)
• Familial adenomatous polyposis (p. 831)

Clinical features:

C/F:
• Asymptomatic, but may be discovered during endoscopy for investigation of dyspepsia.
• Weight loss
• Ulcer-like pain
• Anorexia and nausea occur in one-third, while early satiety, haematemesis, melaena and
dyspepsia alone are less common.
• Dysphagia occurs in tumours of the gastric cardia that obstruct the gastro-oesophageal junction.
• Anaemia from occult bleeding is also common.
Signs:

• Weight loss
• Anaemia
• Palpable epigastric mass
• Jaundice or ascites > metastatic spread
• Supraclavicular lymph nodes (Virchow’s node), umbilicus (Sister Joseph’s nodule) or ovaries
(Krukenberg tumour)

Paraneoplastic phenomena:
• Acanthosis nigricans
• Thrombophlebitis (Trousseau’s sign)
• Dermatomyositis

• Metastases arise most commonly in: liver, lungs, peritoneum and bone marrow.

Investigations:
• Upper gastrointestinal endoscopy is the investigation of choice
• EUS and CT can be used to stage locally advanced gastric cancer; laparoscopy may be required to
assess for peritoneal metastatic disease.

Management:

Surgery:

• Resection offers the only hope of cure and this can be achieved in about 90% of patients with
early gastric cancer.
• Endoscopic mucosal resection or endoscopic submucosal dissection can be considered for very
early tumours.
• For locally advanced disease, total gastrectomy with lymphadenectomy is the operation of
choice, preserving the spleen if possible.
• Proximal tumours involving the oesophago-gastric junction also require a distal
oesophagectomy.
• Small tumours sited distally can be managed by a partial gastrectomy with lymphadenectomy
and either a Billroth I or a Rouxen-Y reconstruction.
• Those who cannot be cured, palliative resection may be necessary when patients present
with bleeding or gastric outflow obstruction.
• Perioperative chemotherapy is recommended for patients with locally advanced disease (e.g.
epirubicin, cisplatin and 5-fluorouracil).
• For individuals who did not receive pre-operative chemotherapy, post-operative
chemoradiotherapy (e.g. 5-flurouracil and leucovorin with radiotherapy) or adjuvant
chemotherapy (e.g. 5-fluorouracil) is recommended.
Palliative treatment:
• Palliative chemotherapy
• Biologic agent trastuzumab is recommended in conjunction with chemotherapy for patients
whose tumours overexpress HER2
• Endoscopic laser ablation for control of dysphagia or recurrent bleeding
• Carcinomas at the cardia or pylorus may require endoscopic dilatation or insertion of expandable
metallic stents for relief of dysphagia or vomiting.
• Nasogastric tube may offer temporary relief of vomiting due to gastric outlet obstruction.

Zollinger–Ellison syndrome

gastrin-secreting neuro-endocrine tumour (‘gastrinoma’)

Clinical features
The presentation is with severe and often multiple peptic ulcers in unusual sites, such as the post-bulbar
duodenum, jejunum or oesophagus. There is a poor response to standard ulcer therapy. The history is
usually short, and bleeding and perforations are common. Diarrhoea is seen in one-third or more of
patients and can be the presenting feature.

Investigations

Serum gastrin levels are normally grossly elevated

Injection of the hormone secretin normally causes no change or a slight decrease in circulating gastrin
concentrations, but in Zollinger–Ellison syndrome it produces a paradoxical and dramatic increase in
gastrin.

CT and EUS

Management

Unifocal tumours may be resected

continuous therapy with a PPI in high dose

Somatostatin analogue therapy

screening for MEN 1

Coeliac disease:
Clinical features:

In children:
• Diarrhoea
• Malabsorption
• Failure to thrive
• Delayed growth
• Features of malnutrition
• Abdominal distension
• Growth and pubertal delay > short stature in adulthood.
In adults:
• Disease usually presents during the third or fourth decade and females are affected twice as
often as males.
• Florid malabsorption
• Non-specific symptoms: such as tiredness, weight loss, folate deficiency or iron deficiency
anaemia.
• Oral ulceration, dyspepsia and bloating
• Osteoporosis.

Q: 3 Malignancies/ 5 Neurological/ 3 Endocrine Association:

Disease associations of coeliac disease
• Type 1 diabetes mellitus (2%–8%)
• Thyroid disease (5%)
• Primary biliary cholangitis (3%)
• Sjögren syndrome (3%)
• Immunoglobulin A deficiency (2%)
• Pernicious anaemia
• Sarcoidosis
• Neurological complications:
Encephalopathy
Cerebellar atrophy
Peripheral neuropathy
Epilepsy
• Myasthenia gravis
• Dermatitis herpetiformis
• Down syndrome
• Enteropathy-associated T-cell lymphoma
• Small bowel carcinoma
• Squamous carcinoma of oesophagus
• Ulcerative jejunitis
• Pancreatic insufficiency
• Microscopic colitis
• Splenic atrophy

D/D of Coeliac disease:

• Giardiasis
• Tropical sprue
• Lymphoma
• HIV enteropathy

IgA deposition:
• Henoch-scholein Purpura
• Ig A Nephropathy
 • Dermatitis herpetiformis

Investigations:
Investigations: Findings:
FBC Anemia
PBF Macrocytic (Folate deficiency)
Microcytic (Iron deficiency)
F/O Hyposplenism: (TSH)
• Target cell
• Howell-jolly body
• Spherocyte
Endoscopy of Upper GIT with biopsy Four biopsies from the second part of the duodenum
plus one from the duodenal bulb > Sub total villous
atrophy
tTG • Serological test of choice in many countries
• It is easier to perform
• Is semi-quantitative
• Has more than 95% sensitivity and specificity
• More accurate in patients with IgA deficiency.
Anti endomyseal antibody: Anti-endomysial antibodies of the IgA class are
detectable by immunofluorescence in most untreated
cases.
They are sensitive (85%–95%) and specific
(approximately 99%) for the diagnosis, except in very
young infants.
IgG antibodies, however, must be measured in
patients with coexisting IgA deficiency.
BMD Osteoporosis
S. IgA/ Ca2+/ Mg2+/ S. albumin
Vitamin D level
Vitamin B 12 & Folate level
Iron profile
Management:

• Correct existing deficiencies of micronutrients, such as iron, folate, calcium and/or vitamin D,
• To achieve mucosal healing through a life-long gluten-free diet.
• Frequent dietary counselling
• Mineral and vitamin supplements

5 Factors for F/up:

• Assessment of symptoms
• Weight
• Nutritional status
• tTG
• Anti-endomysial antibodies.

2 indications for repeat small bowel biopsies:

• Symptoms fail to improve

• Antibody levels remain high

Refractory coeliac disease (RCD):

• Type 1: characterised as a normal intraepithelial lymphocyte phenotype
• Type 2: characterised by an abnormal expansion of a subset of small intestinal intraepithelial
lymphocytes.

Type 2 RCD has a 5-year survival of around 50%, compared to 90% in type 1 RCD.
Dermatitis herpetiformis:

This is characterised by crops of intensely itchy blisters over the elbows, knees, back and buttocks.
Investigations:
• Skin biopsy with DIF: Immunofluorescence shows granular or linear IgA deposition at the dermo-
epidermal junction.
• Duodenal biopsy: partial villous atrophy.

Treatment:
• Gluten-free diet
• Dapsone (100–150 mg daily)

Small intestinal bacterial overgrowth:

Causes of smal intestinal bacterial overgrowth
Mechanism Examples

Hypo- or achlorhydria Pernicious anaemia

Partial gastrectomy
Long-term proton pump inhibitor therapy
Impaired intestinal motility Systemic sclerosis
Diabetic autonomic neuropathy
Structural abnormalities Gastric surgery (e.g. blind loop after
Billroth II operation)
Jejunal diverticulosis
Enterocolic stulae*
Extensive small bowel resection
Strictures*
Impaired immune function Hypogammaglobulinaemia

Investigations:
• Culture of small bowel aspirate, obtained at endoscopy, is the gold standard for diagnosis.
• Hydrogen breath tests/ Lactulose breath tests
Management:
• Underlying cause of small intestinal bacterial overgrowth should be addressed.
• A course of broad-spectrum antibiotic for 2 weeks is the first-line treatment.
• Examples include: rifaximin, as well as systemic antibiotics such as ciprofloxacin, metronidazole
and amoxicillin.
• Some patients require up to 4 weeks of treatment and, in a few, continuous rotating courses of
antibiotics are necessary.
• Intramuscular vitamin B12 supplementation > in chronic cases.
• Patients with motility disorders, such as diabetes and systemic sclerosis > antidiarrhoeal drugs
(diphenoxylate or loperamide orally)
• Giardiasis should be controlled in patients with hypogammaglobulinaemia, using metronidazole
• or tinidazole, but if symptoms fail to respond adequately, immunoglobulin infusions may be
required.

Whipple’s disease:
Clinical features of Whipple’s disease
Gastrointestinal (> 70%)
• Diarrhoea (75%)
• Steatorrhoea
• Weight loss (90%)
• Protein-losing enteropathy
• Ascites
• Hepatosplenomegaly (< 5%)
Musculoskeletal (65%)
• Seronegative large joint arthropathy
• Sacroiliitis
Cardiac (10%)
• Pericarditis
• Myocarditis
• Endocarditis
• Coronary arteritis
Neurological (10%–40%)
• Apathy
• Fits
• Dementia
• Myoclonus
• Meningitis
• Cranial nerve lesions
Pulmonary (10%–20%)
• Chronic cough
• Pleurisy
• Pulmonary infiltrates
Haematological (60%)
• Anaemia
• Lymphadenopathy
Other (40%)
• Fever
 • Pigmentation

Caused by: Gram-positive bacillus Tropheryma whipplei.

Investigations:
Diagnosis is made by the characteristic features on small bowel biopsy, with characterisation of the
bacillus by polymerase chain reaction (PCR).

Management:
• IV ceftriaxone (2 g daily for 2 weeks), followed by oral co-trimoxazole for at least 1 year.
• Long-term follow-up is essential.

Bile acid diarrhoea:

Classification of bile acid diarrhoea

Type Cause
Type 1 Terminal ileal disease leading to malabsorption of bile acids from
terminal ileum, e.g. Crohn’s disease, terminal ileal resection

Type 2 Primary or idiopathic – no anatomical abnormalities or risk factors present

Type 3 Other conditions that affect GI absorption, e.g. chronic

pancreatitis, coeliac disease, small intestinal bacterial overgrowth

Pathology:
• Unabsorbed bile salts pass into the colon, stimulating water and electrolyte secretion and
causing diarrhoea.

• If hepatic synthesis of new bile acids cannot keep pace with faecal losses, fat malabsorption
occurs.

• Another consequence is the formation of lithogenic bile, leading to gallstones.

• Renal calculi, rich in oxalate, develop. Normally, oxalate in the colon is bound to and precipitated
by calcium. Unabsorbed bile salts preferentially bind calcium, leaving oxalate to be absorbed,
with development of urinary oxalate calculi.

• Patients have urgent watery diarrhoea or mild steatorrhoea.

Investigations:
• 75Se-homocholic acid taurine (SeHCAT) test: not available throughout the world
• Serum 7α-hydroxycholestenone: elevated
Treatment:
• Bile acid sequestrants, such as colestyramine or colesevelam, which bind bile salts in the
intestinal lumen.
Consequences of ileal resection:

Disorders of the colon and rectum

Colorectal polyps:
 Neoplastic and non-neoplastic polyps
Neoplastic polyps Non-neoplastic polyps
• Conventional adenoma • Hamartoma
• Sessile serrated lesion • Infiammatory
• Traditional serrated adenoma • Hyperplastic

Risk factors for malignant change in colonic polyps

• Large size (> 2 cm)
• Multiple polyps
• Serrated polyps (excluding small rectal hyperplastic polyps)
• Villous architecture
• High-grade dysplasia

Colorectal cancer:
• Globally, colorectal cancer is the third most commonly diagnosed cancer in males and second in
females.

Risk Factors for Colorectal cancer:

Clinical features:

• Symptoms vary, depending on the site of the carcinoma.

• Tumours of the left colon: fresh rectal bleeding and obstruction occurs early.

• Tumours of the right colon: anaemia from occult bleeding or altered bowel habit occurs early,
but obstruction is a late feature.

• Colicky lower abdominal pain and rectal bleeding occurs in 50%.

• Other features: obstruction or perforation, leading to peritonitis, localised abscess or fistula

formation.

• Carcinoma of the rectum usually causes early bleeding, mucus discharge or a feeling of
incomplete emptying. Patients present with iron deficiency anaemia or weight loss.

On examination:
• Palpable mass
• Signs of anaemia
• Hepatomegaly from metastases
• Low rectal tumours may be palpable on digital examination.

Investigations:

Barium Enema: Apple core deformity: Fixed filling defect with destruction of mucosal pattern in an
angular configuration.

• Colonoscopy is the investigation of choice.

 • CT Colonography (virtual colonoscopy): Patients in whom colonoscopy is incomplete and those
who are at high risk of complications.

For Staging:

• CT of the chest, abdomen and pelvis to detect hepatic metastases, with an increasing role of MRI
for further characterisation of liver lesions.

• Pelvic MRI or endoanal ultrasound for local staging of rectal cancer.

• Serum carcinoembryonic antigen (CEA): CEA testing can be helpful during follow-up to monitor
for recurrence.

• FDG PET-CT

Tumour stage (TNM) at diagnosis is the most important determinant of prognosis.

Management:

Endoscopy:

• Endoscopic mucosal resection, endoscopic submucosal dissection and endoscopic full-thickness

resection.

Surgery:

• Cornerstone of treatment with curative intent.

• Neoadjuvant radiotherapy or chemoradiotherapy
• Colorectal cancer may present as an emergency with obstruction or perforation.
• Obstruction: treated by either a decompressing colostomy or endoscopic stenting.
• Metastatic disease confined to liver or lung: Resection, if there is truly no disease at other sites.
• Metastatic disease confined to the peritoneum: Cytoreductive surgery and hyperthermic
intraperitoneal chemotherapy.
• Postoperatively, patients should undergo colonoscopy after 1 year and then 3 years later to
search for local recurrence or development of new lesions.
Adjuvant therapy:

• Adjuvant chemotherapy: 5-fluorouracil/folinic acid or capecitabine, preferably in combination

with oxaliplatin, can reduce the risk of recurrence.
Palliation of advanced disease:
• Surgical resection of the primary tumour > metastases to treat obstruction, bleeding or pain.
• Systemic anti-cancer treatment
• Palliative chemotherapy: with 5-fluorouracil/folinic acid, capecitabine, oxaliplatin or irinotecan
• Monoclonal antibodies such as panitumumab or cetuximab, which bind to and inhibit the
epidermal growth factor receptor.
• Pelvic radiotherapy: for distressing rectal symptoms, such as pain, bleeding or severe tenesmus.
• Endoscopic laser therapy or insertion of an expandable metal stent: used to relieve obstruction.

Prevention and screening:

• Aims: To detect and remove lesions at an early or pre-malignant stage by screening the
asymptomatic general population.

Several potential methods exist:

Methods Advantages Disadvantages
• Faecal immunochemical • Screening of people
testing (FIT) between the age of 50
to 74 years
• Colonoscopy • Gold standard • Expensive
• Preventive polypectomy • Requires bowel
preparation
• Risks of
Perforation(1:1000)
• Lack of resources
• Flexible sigmoidoscopy • Alternative option
• CT Colonography • Fast • Reduced sensitivity to
• Low risk detect polyp < 6 mm
• Equivalent sensitivity to • Require bowel
colonoscopy preparation
• Exposure to ionizing
radiation
• Inability to offer
therapeutic intent

Hereditary syndromes predisposing to colorectal cancer:

Modified Amsterdam criteria* for hereditary non-polyposis colon cancer

• Three or more relatives with colon cancer (at least one first-degree)
• Colorectal cancer in two or more generations
• At least one member affected under 50 years of age
• Familial adenomatous polyposis excluded
Peutz–Jeghers syndrome:

Mode of inheritance:

• Autosomal dominant ( Trancating mutations in a serine-threonine kinase gene on chromosome

19p (STK 11)
Diagnostic criteria: 2 of 3

• Small bowel polyposis

• Mucocutaneous pigmentation
• Family H/O AD inheritance

C/F:

• Asymptomatic
• Chronic bleeding
• Anemia
• Intussusception

Increased risk of cancer:

• Small bowel/ colonic adenocarcinoma

• Pancreatic carcinoma
• Lung Carcinoma
• Testicular cancer
• Ovary, Breast & Endometrial cancer

Examination:

• Testicular examination for men

• Pelvic exam, cervical smears, regular mammography

Investigations:

• Genetic testing
• Regular upper GI Endoscopy, Colonoscopy, Small bowel & pancreatic imaging

Treatment:
• Polyps > 1 cm: should be removed.

Screening:

• Asymptomatic relatives of affected patients

Diverticulosis:

• Colonoscopy: Multiple pouches branching out from the colon

• Barium Enema: Tortuosity & narrowing of sigmoid colon with multiple diverticula

Common site:

• Sigmoid colon
• Descending colon

Risk factors:

• Lifelong refined diet

• Relative deficiency of fibre

4 Symptoms:

• Colicky pain in suprapubic region/ left iliac fossa

• Diarrhoea
• Rectal bleeding
• Fever
Signs:
• Palpable mass in Left iliac fossa
• Left sided local tenderness, guarding & rigidity (Left sided appendicitis)

5 complications:

• Bleeding
• Perforation
• Stricture/ Obstruction
• Pericolic abscess
• Fistula formation
4 DD:

• Colorectal cancer
• Ischemic colitis
• IBD
• Infection

4 Modalities of investigations:

• Colonoscopy
• CT abdomen: Perforation, Pericolic abscess
• CT colonography
• Barium enema

Management:

Relieve constipation:
• High fibre diet
• Bulk forming laxatives
• Plenty of fluids

Antispasmodics

Severe cases: IV Fluid, IV antibiotics, Analgesics, NG suction

4 indications of surgery:

• Severe hemorrhage
• Perforation
• Repeated attacks of obstruction
• Percutaneous drainage of pericolic abscess
Inflammatory Bowel disease:
Comparison of ulcerative colitis and Crohn’s disease
Ulcerative colitis Crohn’s disease
Age group Any Any

Gender M=F Slight female preponderance

Incidence Stable Increasing

Ethnic group Any Any; more common in
Ashkenazi Jews
Genetic factors HLA-DR*103; colonic epithelial Defective innate immunity and
barrier function (HNF4α, autophagy (NOD2, ATG16L1,
LAMB1, CDH1) IRGM)
Risk factors More common in non-/ex- More common in smokers
smokers Appendicectomy
protects
Anatomical distribution Colon only; begins at anorectal Any part of gastrointestinal
margin with variable proximal tract; perianal disease common;
extension patchy distribution, skip lesions
Extra-intestinal manifestations Common Common

Presentation Bloody diarrhoea Variable; pain, diarrhoea,

weight loss all common
Histology Inflammation limited to Submucosal or transmural
mucosa; crypt distortion, inflammation common; deep
cryptitis, crypt abscesses, loss fissuring ulcers, fistulae; patchy
of goblet cells changes; granulomas
Management 5-ASA; glucocorticoids; Glucocorticoids; azathioprine;
azathioprine; biologic therapy methotrexate; biologic therapy
(anti-TNF, anti-α4β7 integrin, (anti-TNF, anti-α4β7 integrin,
anti-p40, Janus kinase anti-p40); nutritional therapy;
inhibitor); colectomy is curative smoking cessation; surgery for
complications is not curative; 5-
ASA is not effective
 Assessment of disease severity in ulcerative colitis
Mild Moderate
Daily bowel frequency <4 4–6
Blood in stools +/− +/++
Stool volume < 200 g/24 hrs 200–400 g/24 hrs
Pulse < 90 beats/min < 90 beats/min
Temperature Normal Normal
Haemoglobin Normal Normal
Erythrocyte sedimentation rate Normal Normal
Serum albumin > 35 g/L (> 3.5 g/dL
Abdominal X-ray Normal Normal
Sigmoidoscopy Normal or erythema/granular
ucosa
The Truelove–Witts criteria for acute severe ulcerative colitis are ≥ 6 bloody stools/24 hrs plus one or
more of: anaemia, fever, tachycardia and high inflammatory markers.

Truelove- Witts criteria:

THE MHB (Medicare Hospital Bashurhat):

T= Temperature
H= Heart rate
E= ESR
M= Bowel Movement/ day
H= Hemoglobin
B= Blood in stool
Conditions that can mimic ulcerative or Crohn’s colitis
Infective
Bacterial
• Salmonella
• Shigella
• Campylobacter jejuni
• Escherichia coli O157
• Gonococcal proctitis
• Pseudomembranous colitis
• Chlamydia proctitis

Viral
• Herpes simplex proctitis
• Cytomegalovirus

Protozoal
• Amoebiasis

Non-infective
• Ischaemic colitis
• Collagenous colitis
• Non-steroidal anti-inflammatory drugs
• Diverticulitis
• Radiation proctitis
• Behçet’s disease
• Colonic carcinoma

Differential diagnosis of sma l bowel Crohn’s disease

• Other causes of right iliac fossa mass:
Caecal carcinoma
Appendix abscess
• Infection (tuberculosis, Yersinia, actinomycosis)
• Mesenteric adenitis
• Pelvic inflammatory disease
• Lymphoma
Complications:
Intestinal:

• Life-threatening colonic inflammation

• Haemorrhage
• Fistulae
• Cancer:
 Targeted biopsies of areas that show abnormalities on staining with indigo carmine or
methylene blue increase the chance of detecting dysplasia and this technique (termed
pancolonic chromoendoscopy) has replaced colonoscopy with random biopsies taken
every 10 cm in screening for malignancy.

Extra-intestinal complications:
Investigations:

Name of Inv Findings Comments

Routine:
FBC Anemia Bleeding/ Malabsorption of Iron,
Folic acid & Vitamin B12
Thrombocytosis Chronic inflammation
ESR, CRP Elevated Exacerbation/ Abscess formation
S. Albumin Reduced Protein loosing enteropathy/
Inflammatory disease/ Poor nutrition
Fecal Calprotectin Increased GI inflammation/ Distinguish IBD
from IBS/ Monitor disease activity
Bacteriology:
Stool Microscopy & C/S
Exam for C. difficile/ for
ova & cysts
Blood C/S & Serology
Endoscopy:
Ileo-colonoscopy: UC: Biopsy from each anatomical
• Loss of vascular pattern segment (Terminal ileum, Right
• Granularity colon, Transverse colon, Left colon,
• Friability Rectum):
• Contact bleeding
• With/without ulceration • Confirm diagnosis
CD: • Define disease extent
• Patchy inflammation
• Discrete deep ulcer
• Strictures
• Perianal disease (Fissure,
Fistula, Skin tags)
• Often with rectal sparing
Wireless capsule Small bowel inflammation Avoid in stricture
Endoscopy:
Enteroscopy:
Upper GI Endoscopy:
Radiology:
CT colonogram: Preferred where colonoscopy is
Barium Enema: incomplete > For UC
Barium Follow through: Narrowing, ulceration, multiple For CD
MRI enterography: strictures
Plain X-ray abdomen: Dilatation of colon
 Mucosal edema (Thumb printing)
Evidence of perforation

Management:
Aims:
• Treat acute attacks (induce remission)
• Prevent relapses (maintain remission)
• Prevent bowel damage
• Detect dysplasia and prevent carcinoma
• Select appropriate patients for surgery.

Non-biologic agents used in the treatment of inflammatory bowel disease

Class Drug Indication

Aminosalicylates Mesalazine Induce remission or maintenance in mild/

Olsalazine moderate ulcerative colitis
Sulfasalazine
Balsalazide
Glucocorticoids Prednisolone Induce remission in acute ulcerative colitis or
Hydrocortisone Crohn’s disease
Budesonide
Beclomethasone
Methylprednisolone
Anti-metabolites Azathioprine Maintenance therapy in ulcerative colitis or
Mercaptopurine Crohn’s disease

Methotrexate Maintenance therapy in Crohn’s disease

Calcineurin inhibitors Ciclosporin Severe ulcerative colitis refractory to
glucocorticoids
Antibiotics Ciprofioxacin Peri-anal Crohn’s disease and pouchitis
Metronidazole

Biologic agents used in the treatment of inflammatory bowel disease

Class Drug Indication
Anti-TNF antibodies Infliximab Moderate to severe
Crohn’s disease and ulcerative colitis
Acute severe ulcerative colitis as rescue therapy

Adalimumab Moderate to severe Crohn’s disease and ulcerative

colitis

Golimumab Moderate to severe ulcerative colitis

 Certolizumab Moderate to severe Crohn’s disease

Anti-α4β7 integrin Vedolizumab Moderate to severe Crohn’s disease and ulcerative

colitis
Janus kinase inhibitor Tofacitinib Moderate to severe ulcerative colitis
Anti-p40 antibodies Ustekinumab Moderate to severe
Crohn’s disease and ulcerative colitis

Medical management of fulminant ulcerative colitis

• Admit to hospital for intensive therapy and monitoring
• Give IV fiuids and correct electrolyte imbalance
• Consider transfusion if haemoglobin is < 100 g/L (< 10 g/dL)
• Give IV methylprednisolone (60 mg daily) or hydrocortisone (100 mg four times daily)
• Give antibiotics until enteric infection is excluded
• Arrange nutritional support
• Give subcutaneous low-molecular-weight heparin for prophylaxis of venous
thromboembolism
 • Avoid opiates and antidiarrhoeal agents
• Consider infliximab (5 mg/kg) or ciclosporin (2 mg/kg) in stable patients not responding to
3–5 days of glucocorticoids

Monitoring of inflammatory bowel disease (IBD)

• Assess symptoms, including extra-intestinal manifestations
• Examine for abdominal mass or perianal disease
• Perform full blood count, urea and electrolytes, liver function tests, albumin, C-reactive
protein (CRP)
• Check haematinics (vitamin B12 , folate, iron studies) at least annually
• Check faecal calprotectin (to monitor each disease fiare/change in therapy and assess
response)
• Perform stool cultures (at each fiare to exclude infection)
• Assess mucosal healing: surrogate markers (CRP/calprotectin), small bowel capsule,
ileocolonoscopy and/or small bowel magnetic resonance imaging
• Enrol patient in a dedicated IBD clinic (monitoring of stable, uncomplicated patients may be
carried out by a nurse or phone clinic)
• Arrange IBD multidisciplinary meeting for acutely ill or complex patients
• Check vaccinations are up to date; live vaccinations may be given at least 4 weeks before
starting immunosuppressive therapy and at least 3 months after stopping
immunosuppressive therapy. Patients on immunosuppressive therapy should receive
influenza and pneumococcal vaccination
• Ensure surveillance colonoscopy is scheduled where appropriate

How to give anti-tumour necrosis factor (TNF) therapy in in ammatory bowel disease
• Infliximab (5 mg/kg IV infusion) is given as three loading doses (at 0, 2 and 6 weeks), with 8-
weekly maintenance thereafter. Some patients may require dose escalation to 10 mg/kg up
to 4 weekly
• Adalimumab is given as SC injections, which patients can be trained to give themselves.
Loading dose is 160 mg, followed by 80 mg 2 weeks later and 40 mg every second week
thereafter; some patients require dose escalation to 40 mg once weekly
• Concomitant immunosuppression with a thiopurine or methotrexate may be more
efficacious than monotherapy but has more side-effects
• Anti-TNF therapy is contraindicated in the presence of active infection and latent
tuberculosis without appropriate prophylaxis; it carries an increased risk of opportunistic
infections and a possible increased risk of malignancy; rarely, multiple sclerosis may be
unmasked in susceptible individuals. Counselling about the balance of risk and bene t for
each patient is important
• Prior to therapy, latent tuberculosis must be excluded, as well as checking immunisation
status, as well as hepatitis B, hepatitis C, HIV and VZV status
• Live vaccines should not be given
• Golimumab is effective for ulcerative colitis
• Certolizumab is effective for luminal Crohn’s disease, but is not licensed in Europe

Indications for surgery in ulcerative colitis

Impaired quality of life
• Loss of occupation or education
• Disruption of family life
Failure of medical therapy
• Dependence on oral glucocorticoids
• Resistant to drug therapy
• Intolerable side-effects of drug therapy
Fulminant colitis
• Life-threatening bleeding
Toxic megacolon
• Perforation
Colon cancer or severe dysplasia

Pregnancy and inflammatory bowel disease (IBD)

Pre-conception
• Outcomes are best when pregnancy is carefully planned and disease is in remission
• Methotrexate must be stopped 6 months prior to conception; other IBD drugs should be
continued until discussed with a specialist
• Aminosalicylates and azathioprine are safe in pregnancy
• Glucocorticoids are probably safe
• Biologic therapy (in iximab, adalimumab, vedolizumab, ustekinumab) in pregnancy can
continue if established pre-pregnancy
• Tofacitinib should be avoided in pregnancy
• Folic acid (5 mg/day) is recommended pre-conception. Consider high-dose supplements in
small bowel Crohn’s disease with low levels despite 5 mg dose
Pregnancy
• Two-thirds of patients in remission will remain so in pregnancy
• Active disease is likely to remain active
• Severe active disease carries an increased risk of premature delivery and low birth weight
• Perform endoscopy only when absolutely essential for clinical decision-making (ideally in
second trimester)
• X-rays can be performed if clinically indicated, but discuss with the radiologist first.
Ultrasound is preferable but is operator-dependent. MRI small bowel can be performed
without intravenous gadolinium and oral contrast
Labour
• This needs careful discussion between patient, gastroenterologist and obstetrician
• Normal labour and vaginal delivery are possible for most
• Caesarean section may be preferred for patients with perianal Crohn’s or an ileo-anal pouch
to reduce risks of pelvic floor damage, flstulation and late incontinence
• Venous thromboembolism prophylaxis is important if in hospital
Breastfeeding
• This is safe and does not exacerbate IBD
• Data on the risk to babies from drugs excreted in breast milk are limited; most of these drugs
are probably safe
• Patients should discuss breastfeeding and drug therapy with their doctor
Irritable bowel syndrome:
 Alarm features in suspected irritable bowel syndrome
• Age >50 years
• Unintentional weight loss
• Nocturnal symptoms
• Recent change in bowel habit
• Palpable abdominal mass or
Lymphadenopathy
• Family history of colon cancer or inflammatory bowel disease
• Anaemia
• Evidence of overt gastrointestinal bleeding (i.e. melaena or fresh blood in stools
(haematochezia)

6 Differentials of IBS-D:
• Coeliac disease
• Microscopic colitis
• Lactose intolerance
• Bile acid diarrhoea
• Thyrotoxicosis
• Parasitic infection.

Dietary management of irritable bowel syndrome

• Eat regularly and avoid missing meals
• Take time to eat
• Ensure adequate hydration and avoid carbonated and caffeinated drinks
• Reduce alcohol intake
• Reduce intake of ‘resistant’ starch and insoluble fibre
• Avoid foods with artificial sweeteners
• Consider a low FODMAP diet
• Consider a gluten-free diet
• Consider a lactose exclusion diet
Management of irritable bowel syndrome:

Acute small bowel ischaemia:

Causes:

• Embolus from heart/ aorta to superior mesenteric artery (40-50%)

• Thrombosis of atheromatous disease (25%)
• Non-occlusive ischemia due to: Hypotension from MI, Heart failure, Arrhythmias, sudden blood
loss
• Vasculitis
• Venous occlusion
History:

• H/O cardiac disease/ arrhythmia

• Abdominal pain

Signs:

• Abdomen: silent, distended, diminished bowel sound, F/O peritonitis

• CVS: F/O valvular HD/ Heart failure

Investigations:

• Mesenteric/ CT angiography: Occluded/ Narrowed major artery with spasm of arterial arcades
• Plain X-ray abdomen: Thumb printing due to mucosal edema
• FBC: Leukocytosis
• ABG: Metabolic acidosis
• S. Phosphate: Raised
• S. amylase: Raised

Management options:

• Resuscitation
• Mx of cardiac disease
• IV antibiotics
• Laparotomy
• Embolectomy with vascular reconstruction
• 2nd look laparotomy 24 hours later > Resection of necrosed bowel
• Thrombolysis

Complications:

• Nutritional failure
• Short bowel syndrome
Functional dyspepsia
Functional dyspepsia can be diagnosed in patients presenting with dyspepsia where organic disease has
been excluded.

Clinical features

bloating, early satiety, loss of appetite, nausea, vomiting or retching may suggest a diagnosis of
postprandial distress syndrome, whereas symptoms of epigastric pain or epigastric burning may suggest
a diagnosis of epigastric pain syndrome.

Investigations

History

All patients should be checked for H. pylori infection and patients with alarm features should undergo
endoscopy to exclude mucosal disease.

ultrasound scan may detect gallstones

Management

Up to 10% of patients benefit from H. pylori eradication therapy

Drug treatment is targeted on the subtype of functional dyspepsia.

Prokinetic drugs (e.g. metoclopramide), fundus-relaxing drugs (e.g. buspirone) or centrally acting
neuromodulators (e.g. mirtazapine) can be used in postprandial distress syndrome.

Acid suppression medication (e.g. PPI) and tricyclic antidepressants (e.g. amitriptyline) may be used in
epigastric pain syndrome.

Patients with major psychological disorders that result in persistent or recurrent symptoms may require
behavioural or other formal psychotherapy.