General Medicine gastrointestinal chapter overview. Summarised form.

1. 1
GIT
Plain x-rays:
 Intestinal obstruction
 Paralytic ileus: dilated loops of bowel , erect position fluid levels visible
 Calcified lymph nodes, renal stones, gallstones
 Suspected perforation (sub diaphragmatic free air)
Contrast studies:
 Detect filling defects eg tumors
 Strictures
 Ulcers
 Motility disorders
Barium swallow meal:
 Possible motility disorder eg achalasia / gastroparesis
 Suspected perforation / fistula
Barium follow through
 Diarrhea
 Abdominal pain of small bowel origin
 Obstruction by strictures
 Malabsorption
 Crohn’s disease assessment
Barium enema:
 Altered bowel habit
 Strictures, diverticular disease
 Megacolon
 Chronic constipation
 Suspected colon cancer
Ultrasound:
 Abdominal masses eg cysts, tumors, abscesses
 Ascites
 Biliary tract dilatation
 Gallstones
 Guided biopsy of lesions

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CT:
 Assess pancreatic disease
 Hepatic tumor
 Tumor staging
 Vascularity of lesions
 Abscesses and collections
MRI
 Hepatic tumor staging
 Pelvic / peri anal disease
 Crohn’s fistulas
 Small bowel visualization
PET
 Metastases detection
Upper GI endoscopy:
 Dyspepsia (over 55 yrs with alarming symptoms)
 Atypical chest pain
 Dysphagia
 Vomiting
 Weight loss
 Acute / chronic GI bleeding
 Suspicious barium meal
Dysphagia:
 Food sticking after swallowing with or without regurge – esophageal dysphagia –
endoscopy / biopsy
o Stricture: benign= peptic, malignant= carcinoma of esophagus, stomach; extrinsic
compression
o Esophagitis: peptic, candidiasis
o Dysmotility (manometry, barium swallow)= achalasia, motility disorder
 Difficulty initiating swallow with / without choking , aspiration – oropharyngeal
dysphagia – endoscopy, and neurological investigation
o Neurological disease: bulbar palsy, myasthenia gravis
Dyspepsia:
 Upper GI disorders:
o Peptic ulcer

3. 3
o Acute gastritis
o Gallstones
o Motility disorders
 Other GI disorders:
o Pancreatic disease
o Hepatic disease
o Colonic carcinoma
 Systemic disease
o Renal failure
o Hypercalcemia
 Drugs:
o Nsaids
o Iron / potassium supplements
o Corticosteroids
o Digoxin
 Others:
o Alcohol
o Anxiety, depression
 Alarm features in dyspepsia: weight loss, anemia, vomiting, hematemesis, malena,
dysphagia, palpable abdominal mass
Diarrhea:
 Passage of 200g of stool daily
 Measure stool volume to confirm this
Acute diarrhea:
 Due to fecal oral transmission of bacteria, their toxins, viruses, or parasites
 Drugs: antibiotics, cytotoxic drugs, PPIs, NSAIDS
Chronic / relapsing diarrhea:
 Irritable bowel syndrome: increased frequency of defecation and loose, watery, pellety
stools. Stool contains mucus, never blood.
 Colonic chronic diarrhea: blood / mucus in stool, cramping lower abdominal pain
 Malabsorption chronic diarrhea: steatorrhea, undigested food, weight loss, nutritional
disturbances
 Small bowel problems chronic diarrhea: large vol water stool, abdominal bloating,
cramping mid abdominal pain
Weight loss causes:
 Psychosocial:

4. 4
o Deprivation starvation
o Eating disorders
 Resp:
o COPD
o Pulmonary tb
o Malignancy
 GIT:
o Dysphagia
o Malabsorption
o Malignancy
o IBD
cirrhosis
 Chronic infection:
o HIV AIDS
o Tb
o Gut infections
 Endocrine
o DM
o Hyperthyroidism
o Addison’s disease
o Diabetes insipidus
 Cardiac
o CHD
o IE
 Renal
o Chronic renal failure
 Rheumatological
o Rheumatoid arthritis
Investigation:
 Urinalysis for blood, protein, sugar
 Blood tests, lfts, random blood glucose, thyroid function tests
 ESR may be raised in infections
GERD
Factors associated with dev. of GERD:
 Obesity, dietary factors
 Defective esophageal clearance (esophagitis= healed by acid suppressing drug therapy)
still persists

5. 5
 Hiatus hernia
 Abnormal lower esophageal sphincter: reduced tone, inappropriate relaxation
 Delayed gastric emptying
 Increased intra-abdominal pressure (pregnancy, obesity) weight loss may improve
symptoms
Clinical features:
 Heartburn, regurgitation, provoked by bending, straining, lying down
 Waterbrash, salivation due to reflex salivary gland stimulation as acid enters gullet
 Pt often overweight
 Pts sometimes woken at night by choking as refluxed fluid irritates larynx
 Odynophagia, dysphagia
 Atypical chest pain mimic angina, may be due to reflux induced esophageal spasm
 Acid laryngitis
 Recurrent chest infections
 Chronic cough
 Asthma
Complications:
1) Esophagitis:
a. Endoscopic findings: mild redness to severe bleeding ulceration with stricture
formation
2) Barret’s esophagus
a. Premalignant condition
b. Normal squamous lining of lower esophagus replaced by columnar mucosa
(columnar lined esophagus CLO) containing areas of metaplasia
c. Adaptive response to chronic GERD
d. Cancer risk more closely related to severity and duration of reflux rather than
presence of CLO
e. Importance of duodenogastro-esophageal reflux containing bile, pancreatic
enzymes and pepsin in addition to acid.
f. Diagnosis: multiple systemic biopsies maximizing chance of detecting intestinal
metaplasia or dysplasia
g. Management: treatment only indicated for symptoms of reflux or complications
such as strictures. Regular endoscopic surveillance can detect dysplasia and
malignancy at early stage may improve survival. Esophagectomy widely
recommended for high grade dysplasia as resected specimen harbours cancer up
to 40% of the time.
3) Anemia:
a. Iron deficiency anemia due to chronic insidious blood loss caused by esophagitis

6. 6
b. Hiatus hernia
c. Colorectal cancer
4) Benign esophageal stricture
a. Fibrous strictures develop as result of long standing esophagitis
b. Diagnosis is by endoscopy, biopsies of strictures to exclude malignancy
c. Long term therapy with PPI to reduce risk of recurrent esophagitis and stricture
formation
Investigations of GERD:
 Young pts presenting with typical symptoms of GERD, no worrying features eg
dysphagia, wt. loss, or anemia, can be treated empirically without investigations
 Endoscopy investigation of choice in middle or late age people, atypical symptoms, or
suspected complications.
Management of GERD:
 PPIs treatment of choice
 Proprietary antacids and alginates provide symptomatic benefit
 H2 receptor antagonist help symptoms without healing esophagitis
Other causes of esophagitis:
 Infection
o Esophageal candidiasis in old pts. those taking broad spectrum antibiotics.
Cytotoxic drugs.
o Problem in AIDS pts.
 Corrosives:
o Suicide attempt by strong household bleach or battery acid followed by painful
burns of mouth and pharynx
o Extensive erosive esophagitis
o At time of presentation, treatment is conservative. Analgesia and nutritional
support
o Vomiting and endoscopy avoided initially.
o Following acute phase, barium swallow should be performed to demonstrate
extent of stricture formation
 Drugs:
o Potassium supplements and NSAIDS may cause esophageal ulcers
o Tablets trapped above esophageal strictures
 Eosinophilic esophagitis

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Achalasia of the esophagus
 Hypertonic lower esophageal sphincter fails to relax in response to swallowing wave
 Failure of propagated esophageal contraction leading to progressive dilatation of gullet
Clinical features:
 Presents with dysphagia
 Develops slowly, intermittent, worse for solids, eased by liquids
 Standing and moving around after eating
 Episodes of chest pain due to esophageal spasm
 Achalasia predisposes to squamous carcinoma of esophagus
Investigations:
 Endoscopy always carried out because carcinoma of cardia always mimics presentation
and radiological / manometric features of achalasia
 Barium swallow shows tapered narrowing of lower esophagus
 Late disease, esophagus is dilated, aperistaltic, and food filled.
Management:
 Endoscopic:
o Forceful pneumatic dilatation
o Those requiring frequent dilatation are best treated surgically
 Surgical:
o Surgical myotomy (Heller’s operation) performed laparoscopically or open
operation. PPI therapy often necessary after surgery
Gastritis
Acute gastritis
 Often erosive and hemorrhagic
 Neutrophils predominant cells in superficial epithelium
 Result from aspirin or NSAIDS ingestion commonly.
 Other causes:
o H. pylori initial infection
o Bile reflux
o Viral infections
o Alcohol
 Dyspepsia, anorexia, vomiting, nausea, hematemesis, malena
 Endoscopy / biopsy required to exclude peptic ulcer or cancer

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 Short term symptomatic treatment includes antacids, acid suppression using PPIs or
antiemetics eg metoclopramide
Chronic gastritis:
 Causes:
o H. pylori infection
o Autoimmune (pernicious anemia)
 Predominant inflammatory cells lymphocytes and plasma cells.
 Pts with dyspepsia may benefit from H. pylori eradication
Peptic ulcer
 Ulcer in lower esophagus, stomach, and duodenum
 In stomach or duodenum, may be acute or chronic
 Penetrate muscularis mucosae
 Acute ulcer: no evidence of fibrosis
 Erosions do not penetrate muscularis mucosae
 Chronic gastric ulcer is usually single
Pathophysiology:
 PU strongly associated with H. pylori infection
 H. pylori is gram negative and spiral, with multiple flagellae at one end making it motile.
Burrows deep beneath the mucosal layer closely adherent to epithelial surface.
 Bacteria spread by person to person contact via gastric refluxate or vomit
 Bacterium stimulates chronic gastritis provoking local inflammatory response in
underlying epithelium
 In one percent of infected ppl, H. pylori causes pangastritis leading to gastric atrophy and
hypochlorhydria. Allows bacteria to proliferate within stomach
 Effects of H. pylori more complex in gastric ulcer pts. ulcer occurs most probably by
impaired mucosal defence resulting from combo of H. pylori infection, NSAIDS,
smoking
Clinical features:
 Chronic condition, natural history of spontaneous relapse and remission lasting for
decades
 Common presentation of recurrent abdominal pain with three notable characteristics:
o Localization to epigastrium
o Relationship to food
o Episodic occurrence
 Occasional vomiting. Persistent daily vomiting occurs in gastric outlet obstruction

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 Sometimes history less characteristic. True in elderly under treatment with NSAIDS. Pain
may be absent, or experienced as vague sense of epigastric unease.
Investigations:
 Endoscopy is the preferred investigation
 Gastric ulcers may occasionally be malignant so must be biopsied and followed up to
ensure healing.
 Pts screened for H. pylori infection
Management:
 H. pylori eradication cornerstone of treatment for peptic ulcers
 Treatment based upon taking PPI simultaneously with two antibiotics (amoxicillin,
clarithromycin, and metronidazole) for 7 days
 Second line therapy offered to those pts who remain infected after failure for first
therapy.
 For those still colonized after two treatments, choice lies between third attempt quadruple
therapy (bismuth, PPI, and two antibiotics) or long term maintenance therapy with acid
suppression
 Common side effects of H. pylori eradication therapy:
o Diarrhea
o Flushing and vomiting
o Nausea and vomiting
o Abdominal cramps
o Headache
o Flush
 Smoking, aspirin, NSAIDS avoided
 Operation of choice for chronic non healing gastric ulcer is partial gastrectomy
Indications for H. pylori eradication:
 Peptic ulcer
 MALToma
 H. pylori positive dyspepsia
 GERD
 Long term NSAID users
Complications of gastric resection and vagotomy:
 Dumping:
o Rapid gastric emptying leads to distention of proximal small intestine
o Abdominal discomfort and diarrhea after eating

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 Bile reflux gastritis:
o Duodeno-gastric bile reflux leads to chronic gastritis
o Dyspepsia can occur
o Treat with aluminium containing antacids and sucralfates.
 Diarrhea and maldigestion
o Anti-diarrheal drugs eg codeine phosphate and loperamide may be given
 Weight loss:
 Anemia:
o Iron deficiency anemia most common
o Folic acid and vit B12 deficiency much less frequent
 Metabolic bone disease:
o Osteoporosis and osteomalacia can occur as consequence of calcium and vit. D
malabsorption
 Gastric cancer
Complications of PUD:
 Perforation
o Gastric contents of stomach escape into the peritoneal cavity, leading to
peritonitis
o Common in duodenal than gastric ulcers.
o Usually found with ulcers in anterior wall
o Most striking symptom is sudden, severe pain; distribution follows spread of
gastric contents over peritoneum
o Pain accompanied by shallow respiration due to limitation of diaphragmatic
movements and shock.
o Abdomen held immobile and board-like rigidity
o Bowel sounds absent
o Liver dullness to percussion decreases due to presence of gas under diaphragm
o After resuscitation of the pt. acute perforation treated surgically.
 Gastric outlet obstruction:
o Most common cause ulcer in region of pylorus
o Presentation with nausea, vomiting, abdominal distention
o Large quantities of gastric contents often vomited. Food eaten 24 hours or more
previously might be recognized.
o Evidence of wasting and dehydration
o Visible gastric paralysis diagnostic of gastric outlet obstruction

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Celiac disease
 Immunologically mediated inflammatory disorder of small bowel
 Resulting from intolerance to wheat gluten, similar proteins found in rye, barley, and
sometimes oats
 Result in malabsorption and responds to gluten free diet
Pathophysiology:
 Tissue transglutaminase (tTG) now recognized as autoantigen for anti-endomysial
antibodies, often used in serological diagnosis
Clinical features:
 Presents at any age
 Infancy: diarrhea, malabsorption, failure to thrive
 Older children: present with non-specific features such as delayed growth. Malnutrition
features on examination. Mil abdominal distention present. Growth and pubertal delay.
Short stature in adulthood
 Adults: peaks in third-fourth decade, common in females. Symptoms depend on severity
and extent of small bowel involvement. Some pts have florid malabsorption while others
have symptoms of tiredness, weight loss, folate deficiency, iron deficiency anemia. Oral
ulceration, dyspepsia, bloating
Investigations:
1) Duodenal biopsy
a. Endoscopic small bowel duodenal biopsy is gold standard
2) Antibodies:
a. IgA anti-endomysial antibodies detectable by immunofluorescence in most
untreated cases. Sensitive and specific
b. IgG antibodies must be analysed in IgA deficiency
c. tTG assay has replaced other blood tests.
d. These antibody tests constitute valuable screening tool in pts with diarrhea but do
not substitute small bowel biopsy
3) Hematology and biochemistry
a. FBC may show microcytic or macrocytic anemia from iron or folate deficiency.
b. Features of hyposplenism: target cells, spherocytes, Howell-Jolly bodies.
c. Reduced conc. of calcium, magnesium, total protein, albumin, or vit D
4) Other investigations:
a. Measurement of bone density should be considered. Evidence of osteoporosis
Management:
 Correct existing deficiencies of iron, folate, calcium, and / or vit D

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 Commence lifelong gluten free diet. Exclusion of wheat, rye, barley, and initially oats.
Oats can be reintroduced after 6-12 months
 Mineral and vitamin supplements also given when indicated
 Regular monitoring of symptoms, weight and nutrition is essential
Abdominal tb
 Gut infection usually results from human M. tb swallowed after coughing
 No pulmonary symptoms, normal chest x-ray
 Area most commonly affected is ileocecal region.
 Presentation / radiological findings very similar to Crohn’s disease.
 Abdominal pain can be acute or of several months’ duration
 Diarrhea less common in tb than Crohn’s disease
 Low grade fever
Diagnosis:
 Elevated ESR
 Raised serum alkaline phosphatase conc. suggests hepatic involvement
 Histo confirmation sought by endoscopy, laparoscopy, or liver biopsy
 Culture may be helpful but identification in 6 weeks
 Diagnosis possible on biopsy specimens by PCR based techniques
Management:
When presentation suggestive of tb, chemo with four drugs – isoniazid, rifampicin,
pyrazinamide, and ethambutol – commenced even if bacteriological or histological proof is
lacking
Inflammatory bowel disease
 Ulcerative colitis and Crohn’s disease are chronic inflammatory bowel diseases
 Crucial distinction is that ulcerative colitis only involves the colon while Crohn’s disease
can involve any part of the GIT from mouth to anus
Pathophysiology
 IBD develops because of an abnormal host response to an environmental factor in
genetically susceptible individuals.
 Causes inflammation of the intestine and releases inflammatory mediators such as TNF,
IL-12, and IL-23 causing tissue damage
 In both diseases, intestinal wall is infiltrated with acute and chronic inflammatory
mediators

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Ulcerative colitis:
 Inflammation involves the rectum (proctitis) but can spread to involve the sigmoid colon
(proctosigmoiditis), or the whole colon (pancolitis)
 Inflammation is confluent, more severe distally
 Long standing pancolitis, bowel becomes shortened and pseudopolyps form which are
normal or hypertrophied residual mucosa within areas of atrophy
 Inflammatory process limited to mucosa
 Acute and chronic inflammatory cells infiltrate the lamina propria and crypts (cryptitis)
 Crypt abscesses are typical
 Goblet cells lose their mucus and in long standing cases, glands become distorted
 Dysplasia, heaping up of cells within crypts, nuclear atypia, and mitotic rate may herald
development of colon cancer
Crohn’s disease:
 Sites most commonly involved:
o Terminal ileum and right side of colon
o Colon alone
o Terminal ileum alone
o Ileum and jejunum
 Entire wall of bowel edematous and thickened
 Deep ulcers which often appear as linear fissures, mucosa between them is described as
cobblestone
 May penetrate through bowel wall to initiate abscesses or fistulas involving bowel,
bladder, uterus, vagina, and skin of perineum
 Mesenteric lymph nodes are enlarged and mesentery is thickened
 Disease has patchy distribution, inflammatory process is interrupted by islands of normal
mucosa
 Histo examination: bowel wall is thickened, chronic inflammatory infiltrate throughout
all the layers
Clinical features of ulcerative colitis:
 Major symptom is bloody diarrhea
 First attack is usually severe, then disease is followed by relapses and remissions
 Proctitis causes rectal bleeding and mucus discharge, sometimes accompanied by
tenesmus
 Some pts pass frequent small-volume fluid stools, others constipated and pass pellety
stools
 Proctosigmoiditis causes bloody diarrhea with mucus
 Fever, lethargy, abdominal discomfort

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 Extensive colitis causes bloody diarrhea with passage of mucus
 Severe cases: anorexia, malaise, weight loss, abdominal pain. Pt is toxic with fever,
tachycardia, signs of peritoneal inflammation
Clinical features of Crohn’s disease:
 Major symptoms: abdominal pain, diarrhea, weight loss
 Ileal Crohn’s disease may cause subacute or acute intestinal obstruction
 Pain is associated with diarrhea, usually watery, does not contain blood or mucus
 All pts lose weight because they avoid food since eating provokes pain
 Wt loss may be due to malabsorption, pt may present with fat, protein, or vitamin
deficiencies
 Rectal sparing and presence of perianal disease are features favouring diagnosis of
Crohn’s disease
 Physical examination reveals evidence of weight loss, anemia, with glossitis and angular
stomatitis
 Abdominal tenderness, markedly over area of inflammation
 Abdominal mass may present due to matted loops of thickened bowel or intra-abdominal
abscesses may occur
 Perianal skin tags, fissures and fistulas may be present
Differential diagnosis:
 Important issue is to distinguish first attack of acute colitis from infection
 Diarrhea lasting longer than 10 days is unlikely to be infection
 History of foreign travel, antibiotic exposure (pseudomembranous colitis) or homosexual
contact increases possibility of infection
 Diagnosis of Crohn’s disease is usually more straightforward on basis of imaging and
clinical presentation
 In atypical cases, biopsy or surgical resection is necessary to exclude other diseases
Complications:
1) Life threatening colonic inflammation
a. Occurs in both ulcerative colitis and Crohn’s disease
b. Most extreme cases, colon dilates (toxic megacolon)
c. Bacterial toxins pass freely into the portal then systemic circulation
d. Abdominal xray should be taken daily because when transverse colon is dilated
more than 6cm, high risk of colonic perforation
2) Hemorrhage
a. Erosion of a major artery
b. Can occur in both conditions
3) Fistulas

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a. Specific to Crohn’s disease
b. Enteroenteric fistulas: cause diarrhea, malabsorption, due to blind loop syndrome
c. Enterovesical fistulation: recurrent urinary infections, pneumaturia
d. Enterovaginal fistulation: feculent vaginal discharge
e. Fistulation from bowel may cause perianal or ischiorectal abscesses, fissures, and
fistulas
4) Cancer
a. Risk of colon cancer is increased in pts with active colitis of more than 8 years’
duration
b. Tumors develop in areas of dyplasia, may be multiple
c. If mild to moderate dysplastic changes are identified, frequency of screening
increased to 1-2-yearly
d. If high grade dysplasia found, panproctocolectomy should be considered due to
high risk of colon cancer
5) Extraintestinal (systemic complications occurring during active phase of IBD:
a. Conjunctivitis
b. Episcleritis
c. Iritis
d. Mouth ulcers
e. Fatty liver
f. Liver abscesses, portal pyaemia
g. Mesenteric or portal vein thrombosis
h. Venous thrombosis
i. Arthralgia of large joints
j. Erythema nodosum
k. Pyoderma gangrenosum
Investigations:
 Necessary to confirm diagnosis, define disease distribution and activity, and identify
complications.
 FBC: anemia resulting from bleeding and malabsorption of iron, folic acid, or vitamin
B12. Serum albumin conc. falls as consequence of protein losing enteropathy,
inflammatory disease, or poor nutrition
 ESR and CRP elevated in exacerbations and response to abscess formation
Bacteriology
 Stool microscopy, culture and examination for Clostridium difficile toxin, or for ova and
cysts
 Blood cultures
 Serological tests should be performed to exclude infection

16. 16
Endoscopy
 Sigmoidoscopy with biopsy essential in investigating pts presenting with diarrhea
 In ulcerative colitis, sidmoidoscopy always abnormal: loss of vascular pattern,
granularity, irritability, and ulceration
 In Crohn’s disease, patchy inflammation with discrete deep ulcers, perianal disease
(fissures, fistulas, skin tags), rectal sparing occurs
 Colonoscopy may show active inflammation with pseudopolyps or complicating
carcinoma
 Biopsies define disease extent. Seek dysplasia in pts with long standing colitis
 Stricture formation does not occur in absence of carcinoma
 In Crohn’s colitis, endoscopic abnormalities are patchy with normal mucosa in between
the areas of abnormality
 Aphthoid or deep ulcers and strictures are common
Radiology
 Barium enema is less sensitive investigation than colonoscopy in pts with colitis and is
now little used
 Contrast studies of small bowel helpful in investigation of Crohn’s disease, affected areas
narrowed and ulcerated
 Plain abdominal x-rays essential in management of pts with severe active disease
 Dilatation of colon, mucosal edema (thumb-printing) or evidence of perforation may be
found
 Ultrasound may identify thickened bowel loops and abscess development in Crohn’s
disease
Management of ulcerative colitis:
1) Active proctitis:
a. Mild to moderate: mesalazine enemas / suppositories combined with oral
mesalazine effective as first line therapy
b. Topical corticosteroids less effective
c. Pts failing to respond to mesalazine administered with oral prednisolone
2) Active left sided or extensive ulcerative colitis:
a. Mildly active cases: high dose aminosalicylates combined with topical
aminosalicylate and corticosteroids are effective
3) Severe ulcerative colitis:
a. Severe colitis best managed in hospital.
b. Monitor clinically for presence of abdominal pain, temp., pulse rate, stool blood,
frequency of stools
c. Monitor in labs: Hb, white cell count, albumin, electrolytes, ESR, CRP
d. Monitor radiologically: colonic dilatation on plain abdominal x-rays

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e. Supportive treatment: IV fluids to correct dehydration, nutritional support enteral
rather than intravenous feeding for malnourished pts.
f. Intravenous corticosteroids (methylprednisolone) or hydrocortisone as constant
infusion
g. Topical / oral aminosalicylates
h. Pts who develop colonic dilatation (>6cm), those whose clinical / lab
measurements deteriorate, those who do not respond after 7-10 days of maximal
treatment indicated for urgent colectomy
4) Maintenance of remission:
a. Oral aminosalicylates – mesalazine or balsalazide as first line agents
b. Sulfasalazine considered in pts with co-existent arthropathy
Management of Crohn’s disease:
1) Active disease:
a. Pts with active colitis or ileocolitis treated initially same as active ulcerative
colitis
b. Aminosalicylates and corticosteroids both effective in inducing remission in pts
with ileocolitis and colitis
c. Severe disease, intravenous steroids indicated.
d. Nutritional therapy using polymeric or elemental diets induces remission in
Crohn’s disease
e. Pts with isolated ileal disease treated with corticosteroids. Budesonide appropriate
for treating moderately active disease
f. Therapy with anti-TNF antibodies infliximab and adalimumab can induce
remission in pts with active Crohn’s disease at any site within GIT
g. Anti-TNF drugs effectively cure some extraintestinal symptoms as well. CI in
presence of infection such as tb, complicated by allergic reactions
2) Fistulas and perianal disease:
a. Often associated with sepsis in Crohn’s disease
b. Define the site of fistulation by imaging. Surgical intervention is then required.
c. Treatment of underlying active disease with corticosteroids and nutritional
support
d. Simple perianal disease treated by metronidazole and / or ciprofloxacin first line
therapies.
e. Thiopurines used in chronic disease
f. Infliximab and adalimumab heal enterocutaneous fistulas and perianal disease in
many pts.
3) Maintenance of remission:
a. Smoking cessation
b. Pts relapsing more than once a year should be give thiopurines

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c. Pts with aggressive disease managed using combo of immunosuppressives and
anti-TNF therapy