This document provides information on several gastrointestinal conditions: 1. Achalasia is a motility disorder of the esophagus characterized by loss of peristalsis and failure of the lower esophageal sphincter to relax properly. 2. Esophageal cancer can be squamous cell carcinoma or adenocarcinoma, with risk factors including smoking, alcohol, and Barrett's esophagus. Treatment depends on cancer stage and may include surgery, chemotherapy, or radiation. 3. Peptic ulcer disease is caused by a bacterial infection with H. pylori in most cases. Treatment involves eradicating H. pylori with antibiotic therapy and proton pump inhibitors.

1. GIT CONDITIONS 1
ACHALASIA, ESOPHANGEAL Ca, PEPTIC ULCER

2. Achalasia

3. DEFINITION
• An oesophageal motility disorder, characterized by loss of
peristalsis and failure of relaxation of the lower oesophageal
sphincter (LOS).

4. AETIOLOGY
• Degeneration of ganglion cells of the myenteric plexus in the
oesophagus due to an unknown cause.
• Oesophageal infection with Trypanosoma cruzi seen in Central and
South America produces a similar disorder (Chagas disease).

5. EPIDEMIOLOGY
• Annual incidence is about 1 in 100 000.
• Usual presentation age: 25–60 years.

6. CLINICAL MANIFESTATION

7. HISTORY
• Insidious onset and gradual progression of:
• intermittent dysphagia involving solids and liquids;
• difficulty belching;
• regurgitation (particularly at night);
• heartburn;
• chest pain (atypical/cramping, retrosternal);
• weight loss.

8. EXAMINATION
• May reveal signs of complications (see the following text).

9. INVESTIGATIONS
• CXR may show a widened mediastinum and double right heart border
(dilated oesophagus), an air-fluid level in the upper chest and
absence of the normal gastric air bubble.
• Barium swallow: Dilated oesophagus which smoothly tapers down to
the sphincter (beak shaped).
• Endoscopy: To exclude malignancy which can mimic achalasia.

10. • Manometry:
• Elevated resting LOS pressure (>45 mmHg);
• incomplete LOS relaxation;
• absence of peristalsis in the distal (smooth muscle portion) of the
oesophagus.
• Serology for antibodies against T. cruzi if Chagas’disease is suggested
by epidemiology and symptoms.
• Blood film might detect parasites.

11. MANAGEMENT
• Pneumatic balloon dilation of the LOS: Up to 80% short-term success
rate, 2–6% risk of oesophageal perforation.
• Surgical myotomy via an abdominal or thoracic approach: The LOS is
weakened by cutting its muscle fibres using a modified Heller
approach.
• Surgery can be complicated by reflux oesophagitis and some surgeons
combine it with a fundoplication procedure to prevent reflux.
• More recently, laparoscopic and thoracoscopic techniques have been
used to perform the myotomy.

12. • Botulinum toxin injected into the LOS inhibits acetylcholine release
from the excitatory neurons that increase smooth muscle tone. The
long-term safety and efficacy remain uncertain.
• Medical treatment: Nitrates and calcium channel blockers (e.g.
nifedipine) may be used to relax the smooth muscle of the LOS.
• Medical treatment is often ineffective, and may be associated with
side effects (e.g. headache, hypotension) and tachyphylaxis.

13. COMPLICATIONS
• If untreated,
• aspiration pneumonia,
• malnutrition and
• weight loss may result.
• Increased risk of oesophageal malignancy: 15 times
that of the general population (on average 15 years
after diagnosis).

14. PROGNOSIS
• Good if treated.
• If untreated, oesophageal dilation may worsen
causing pressure on mediastinal structures.

15. Oesophageal carcinoma

16. DEFINITION
• Malignant tumour arising in the oesophageal mucosa.
• Two major histological types: squamous cell carcinoma and
adenocarcinoma.

17. AETIOLOGY
• Squamous: Alcohol, tobacco, certain nutritional deficiencies
(vitamins, trace elements), HPV infection, achalasia, Paterson–Kelly
(Plummer–Vinson) syndrome, tylosis (Howel–Evans syndrome),
scleroderma, coeliac disease, lye stricture, history of previous thoracic
radiotherapy or upper aerodigestive squamous cancer, dietary
nitrosamines.
• Adenocarcinoma: GORD, Barrett’
s oesophagus (intestinal metaplasia
of the distal oeso_x0002_phageal mucosa with _x0002_ 0.5–0.7%
incidence of adenocarcinoma per year).

18. • Pathology: Squamous cell carcinomas are more common in the mid-
upper oesophagus.
• Adenocarcinoma usually develops in the lower oesophagus or,
increasingly, the gastro_x0002_oesophageal junction. Barretts
intestinal metaplasia can progress to low-grade dysplasia, high-grade
dysplasia and invasive carcinoma. Spread is typically initially direct
(oesophagus has no serosa) and longitudinal via an extensive network
of submucosal lymphatics to tracheobronchial, mediastinal, coeliac,
gastric or cervical nodes. Rare oesophageal tumours include
lymphoma, melanoma and leiomyosarcoma.

19. EPIDEMIOLOGY
• Eighth most common malignancy (UK 7000–8000 per year).
3–4 : 1 male : female.
• Worldwide squamous carcinoma is more common (95%),
with considerable geographical variation (high incidence in
northern China, Iran, southern Russia).
• Adenocarcinoma is more common in westernized countries
(65% cases in the UK) and increasing by 5–10% per year.
• Peak incidence 60–70 years.

20. CLINICAL MANIFESTATIONS

21. HISTORY
• Early: symptomatic/symptoms of reflux.
• Later: dysphagia, initially worse for solids, regurgitation, cough or
choking after food, pain (odynophagia), weight loss, fatigue, voice
hoarseness (may indicate recurrent laryngeal nerve palsy).

22. EXAMINATION
• No physical signs may be evident, signs of weight loss.
• With metastatic disease there may be supraclavicular
lymphadenopathy, hepatomegaly.
• Respiratory signs may be due to aspiration or direct tracheobronchial
involvement.

23. INVESTIGATIONS
• Endoscopy: Tumour location and biopsy. Early high-grade dysplasia
and cancer detection is improved by endoscopic techniques such as
narrow band imaging or magnification, staging.
• Imaging: Barium swallow, CT (chest, abdomen, pelvis), PET can detect
previously occult distant metastases.

24. Other:
• Bronchoscopy (if risk of trancheobronchial invasion), bone scan is
symptoms of bony involvement.
• Laparoscopy and peritoneal washings, thoracoscopy.
• Careful cardiac and respiratory assessment if surgery planned.

25. MANAGEMENT

26. TREATMENT
• Best managed at specialist centres with multidisciplinary expertise.
• For early (mucosal) localized disease endoscopic therapies are
increasing, e.g. endoscopic mucosal resection, endoscopic
submucosal dissection.
• Surgical: only 30% are suitable for surgical resection.
• Neoadjuvant chemoradiotherapy (e.g. cisplatin, 5-fluorouracil) can be
beneficial in downstaging tumours prior to surgery.

27. Surgery:
• Operative approach depends on tumour location and extent of
proposed lymphadenectomy.
• Minimally invasive approaches are increasingly used, i.e. laparoscopic
and thorascopic dissection.

28. Radiotherapy/chemotherapy:
• Squamous cell carcinomas are more radiosensitive than
adenocarcinomas.
• Radical radio or chemoradiotherapy can be performed in localized
disease in patients are unfit for surgery.
• Neoadjuvent and adjuvant chemotherapy using a cisplatin-based
regimen is used where tolerated.

29. Palliation:
• Is tailored to individual patient’s tumour and symptoms.
• Luminal recannulization can be achieved by expandable stents or
laser ablation or photodynamic therapy techniques.
• Radiotherapy and/or chemotherapy is associated with variable
response rates, e.g. epirubicin, cisplatin and 5-fluorouracil.

30. COMPLICATIONS

31. Of tumour:
• Malnutrition,
• aspiration pneumonia,
• haematemesis,
• oesophageobronchial fistula,
• of metastatic disease: ascites, pleural effusions.

32. Of oesophagectomy:
•Mortality < 5% in specialized centres, morbidity up to
40%:
•pulmonary complications are the most common, e.g.
•atelectasis,
•pneumonia,
•serious complications include anastomotic leakage (5–
15%) or conduit failure,
•others: chylothorax, recurrent laryngeal nerve damage.

33. PROGNOSIS
• Depends on stage, overall 5-year survival is 20–25%,
for advanced disease 5-year survival < 5%.

34. Peptic ulcer disease

35. DEFINITION
• Ulceration of areas of the GI tract caused by exposure to
gastric acid and pepsin.
• Most commonly gastric and duodenal (can also occur in
oesophagus and Meckel’s diverticulum).

36. AETIOLOGY
• Cause is an imbalance between damaging action of acid and
pepsin and mucosal protective mechanisms.
• There is a strong correlation with Helicobacter pylori
infection, but it is unclear how the organism causes
formation of ulcers.

37. Common:
• Very strong association with H. pylori (present in 95% of duodenal
and 70–80% of gastric ulcers),
• NSAID use.
• Rare: Zollinger–Ellison syndrome.

38. EPIDEMIOLOGY
• Common.
• Annual incidence is about 1–4/1000.
• More common in males.
• Duodenal ulcers have a mean age in the thirties, while
gastric ulcers have a mean age in the fifties.
• H. pylori is usually acquired in childhood and the
prevalence is roughly equivalent to age in years.

39. CINICAL MANIFESTATION

40. HISTORY
• Epigastric abdominal pain: relieved by antacids.
• Symptoms have a variable relationship to food:
• If worse soon after eating, more likely to be gastric ulcers;
• If worse several hours later, more likely to be duodenal.
• May present with complications (e.g. haematemesis,
melaena).

41. EXAMINATION
• May be no physical findings.
• Epigastric tenderness.
• Signs of complications (e.g. anaemia, succession splash in
pyloric stenosis).

42. INVESTIGATIONS

43. Bloods:
• FBC (for anaemia), cross-match if actively bleeding
• Amylase (to exclude pancreatitis),
• U&Es,
• Clotting screen (if GI bleeding),
• LFT,
• Secretin test; if Zollinger–Ellison syndrome is suspected: IV
secretin causes a rise in serum gastrin in ZE patients but not
controls.

44. • Endoscopy: Four quadrant gastric ulcer biopsies to rule out
malignancy; duodenal ulcers need not be biopsied.
• Histology of biopsies: Difficult to visualize H. pylori so of limited
value.

45. Testing for H. pylori:
• C-Urea breath test: Radio-labelled urea given by mouth and detection
of 13C in the expired air.
• Serology: IgG antibody against H. pylori, confirms exposure but not
eradication.
• Stool antigen test. Campylobacter-like organism test: Gastric biopsy is
placed with a substrate of urea and a pH indicator.
• If H. pylori is present, ammonia is produced from the urea and there
is a colour change (yellow to red).

46. MANAGEMENT

47. Acute:
• Resuscitation if perforated or bleeding (IV
colloids/crystalloids), close monitoring of vital signs, and
proceeding endoscopic or surgical treatment.
• Patients with upper GI bleeding should be treated with IV PPI
(e.g. omeprazole or pantoprazole) at presentation until the
cause of bleeding is confirmed.
• Patients with actively bleeding peptic ulcers or ulcers with
high-risk stigmata (e.g. visible vessel or adherent clot) should
continue IV PPI.
• Switch to oral PPI If there is no rebleeding within 24 hours.

48. • Endoscopy: Haemostasis by injection sclerotherapy, laser or
electrocoagulation.
• Surgery: If perforated or ulcer-related bleeding cannot be controlled.

49. H. pylori eradication
• with “triple therapy” for 1–2 weeks: Various combinations are
recommended made up of one proton pump inhibitors and two
antibiotics (e.g.clarithromycin or amoxicillin, metronidazole or
tetracycline).
• If not associated with H. pylori: Treat with PPIs or H2-antagonists.
• Stop NSAID use (especially diclofenac), use misoprostol (prostaglandin
E1 analogue), if NSAID use is necessary.

50. COMPLICATIONS
• Rate of major complication is 1% per year including haemorrhage
(haematemesis, melaena, iron-deficiency anaemia),
• Perforation,
• Obstruction/pyloric stenosis (due to scarring, Penetration,
Pancreatitis).

51. PROGNOSIS
• Overall lifetime risk 10%.
• Generally good as peptic ulcers associated with H. pylori can be cured
by eradication.

52. Ulcerative colitis

53. DEFINITION
• Chronic relapsing and remitting inflammatory disease
affecting the large bowel.

54. AETIOLOGY/ASSOCIATIONS
• Unknown.
• Suggested hypotheses include;
• genetic susceptibility (chromosomes 12, 16),
• immune response to bacterial or self-antigens,
• environmental factors,
• altered neutrophil function, abnormality in epithelial cell
integrity.
• Positive family history of IBD (15%).
• Associated with " serum pANCA, primary sclerosing
cholangitis.

55. EPIDEMIOLOGY
• Prevalence: 1/1500 (in developed world).
• Higher prevalence in Ashkenazi Jews, Caucasians.
• Uncommon before the age of 10 years, peak onset age 20–40 years.
• Equal sex ratio up to age 40, then higher in males.

56. Clinical Features

57. HISTORY
• Bloody or mucous diarrhoea (stool frequency related to severity of
disease).
• Tenesmus and urgency.
• Crampy abdominal pain before passing stool, weight loss, fever.
• Symptoms of extra GI manifestations.

58. EXAMINATION
• Signs of iron-deficiency anaemia,
• dehydration.
• Clubbing.
• Abdominal tenderness,
• tachycardia.
• Blood, mucus and tenderness on PR examination.
• Signs of extra GI manifestations.

59. INVESTIGATIONS
• Bloods: FBC (# Hb, " WCC), " ESR or CRP, # albumin, cross-match if
severe blood loss, LFT.
• Stool: Culture as infectious colitis is a differential diagnosis. Faecal
calprotectin – marker for disease severity.
• AXR: To rule out toxic megacolon (see Toxic megacolon).

60. • Flexible sigmoidoscopy or colonoscopy (and biopsy): Determines
severity, histological confirmation, detection of dysplasia.
• Barium enema: Mucosal ulceration with granular appearance and
filling defects (pseudo_x0002_polyps), featureless narrowed colon,
loss of haustral pattern (leadpipe or hosepipe appearance).
• Colonoscopy and barium enema may be dangerous in acute
exacerbations (risk of perforation).

61. MANAGEMENT

62. Markers of activity:
• Low Hb,
• Low alb,
• High ESR or CRP and
• diarrhoea frequency (< 4 per day is mild, 4–6 per day is moderate, >6
per day is severe),
• bleeding,
• fever.

63. Acute exacerbation:
• IV rehydration, IV corticosteroids, antibiotics, bowel rest, parenteral
feeding may be necessary, and DVT prophylaxis. Monitor fluid balance
and vital signs closely.
• If toxic megacolon develops, low threshold for proctocolectomy and
ileostomy as perforation has a mortality of 30%.
• Mild disease: Oral or rectal 5-aminosalicylic acid derivatives, e.g.
sulphasalazine and/or rectal steroids.
• Moderate to severe disease: Oral steroids and oral 5-ASA.
• Immunosuppression with azathioprine, cyclosporine, 6-
mercaptopurine, infliximab (anti-TNF monoclonal antibody).

64. • Advice: Patient education and support.
• Treatment of complications.
• Regular colonoscopic surveillance.
• Surgical: Indicated for failure of medical treatment, presence of
complications or prevention of colonic carcinoma.
• Proctocolectomy with ileostomy or an ileo-anal pouch formation.

65. COMPLICATIONS

66. Gastrointestinal:
• Haemorrhage,
• Toxic megacolon,
• Perforation,
• Colonic carcinoma (in those with extensive disease for >10 years),
• Gallstones and PSC.

67. Extra-gastrointestinal manifestations (10–20%):
• Uveitis,
• renal calculi,
• arthropathy,
• sacroiliitis,
• ankylosing spondylitis,
• erythema nodosum,
• pyoderma gangrenosum,
• osteoporosis (from steroid treatment),
• amyloidosis.

68. PROGNOSIS
• A relapsing and remitting condition, with normal life expectancy.
• Poor prognostic factors (ABCDEF): Albumin (< 30 g/L), blood PR, CRP
raised, dilated loops of bowel, eight or more bowel movements per
day, fever (>38’C in first 24 h).