Gastrointestinal System

Dr. Srinath.Chandramani

Anatomy

The gastrointestinal (GI) tract extends from the mouth to the

anus and comprises several organs with distinct functions.
Gut compartmentalization : The organs are separated by
specialized & independently controlled thickened sphincters
that aid in gut compartmentalization.
Functionally the gut wall is organized into :
The mucosa serves as a barrier to luminal contents and as a
site for transfer of fluids or nutrients.
Gut smooth muscle mediates propulsion from one region to
the next.
Serosal layer provides a supportive foundation and permits
external input.

Anatomical levels in the GIT :

Oral cavity
Oesophagus
Stomach
Small intestinal
Large intestinal
Peritoneum

Oesophageal disorders

Motility disorders

Inflammatory

Bleeding related

Reflux disorder

Neoplastic
Miscellaneous

:
:

Achalasia Cardia
Diffuse Oesophageal spasm (DES)
Scleroderma Oesophagus
Viral HSV, Varicella Zoster, CMV, HIV
Fungal Candidiasis
Drug induced, Corrosive poisoning
Iatrogenic - sclerotherapy
Oesophageal varices
Mallory Weiss tear
Boerheeves syndrome
GERD
Barretts oesophagus
Hiatus hernia
Malignancy
Plummer-Vinson syndrome
Oesophageal webs/strictures
Diverticuli, Schatzki ring

Achalasia Cardia
Achalasia is a motor disorder of the esophageal smooth muscle in which the LES
does not relax normally with swallowing, and the esophageal body undergoes
nonperistaltic contractions.

Epidemiology : 1:1,00,000 population. 2nd-4th decade. No gender preponderance.

PATHOPHYSIOLOGY : loss of intramural neurons.
Inhibitory neurons containing VIP and nitric oxide synthase are predominantly
involved, but cholinergic neurons are also affected in advanced disease.
Types : Primary idiopathic achalasia accounts for most of the patients.
Secondary achalasia may be caused by gastric carcinoma that infiltrates the
esophagus, lymphoma,Chagas disease, certain viral infections, eosinophilic
gastroenteritis, and neurodegenerative disorders.

Achalasia Cardia

CLINICAL FEATURES : Dysphagia, chest pain, and regurgitation are the main symptoms.
Dysphagia appears early, occurs with both liquids and solids, and is worsened by
emotional stress and hurried eating.
Various maneuvers designed to increase intraesophageal pressure, including the Valsalva
maneuver, may aid the passage of the bolus into the stomach.
Regurgitation and pulmonary aspiration are complications.
Achalasia associated with carcinoma is characterized by severe weight loss and a rapid
downhill course if untreated.
Risk of carcinoma is increased 10 times.
DIAGNOSIS A chest x-ray shows absence of the gastric air bubble and an air-fluid level in
the mediastinum in the upright position represents retained food in the esophagus.
Barium swallow shows proximal esophageal dilation, Birds Beak Sign.
Cholecystokinin (CCK), which normally causes a fall in the sphincter pressure,
paradoxically causes contraction of the LES (the CCK test).
Endoscopy is helpful in excluding the secondary causes of achalasia.

Achalasia
TREATMENT : Medical line unsatisfactory.

Endoscopic intrasphincteric injection of botulinum toxin

Balloon dilatation reduces the basal LES pressure by tearing muscle fibers.
Hellers extramucosal myotomy of the LES, is equally effective.
Laparoscopic myotomy is the procedure of choice.
Reflux esophagitis and peptic stricture may follow successful treatment.
Diffuse Esophageal Spasm :
Diffuse esophageal spasm is characterized by nonperistaltic contractions,
usually of large amplitude and long duration. An esophageal motility
pattern showing hypertensive but peristaltic contractions has been called
nutcracker esophagus.
Diffuse esophageal spasm may progress to achalasia.
CLINICAL FEATURES chest pain, dysphagia, or both.
DIAGNOSIS Barium swallow shows the corkscrew esophagus.
DES is a manometric diagnosis.

SCLERODERMA ESOPHAGUS

The esophageal lesions in systemic sclerosis consist of atrophy of

smooth muscle, manifested by weakness in the lower two-thirds of
the esophageal body and incompetence of the LES.
These patients usually also complain of heartburn, regurgitation, and
GERD
Mucosal changes due to esophageal ulceration and esophageal
stricture may be present. Motility studies show a marked reduction in
the amplitude of smooth-muscle contractions, The resting pressure
of the LES is subnormal, but sphincter relaxation is normal.
Dietary adjustments with the use of soft foods are helpful in
management.
GERD and its complications should be treated aggressively.

Mallory- Weiss tear :

It is a Longitudinal partial thickness tear at the GE-Junction.
Follows prolonged retching/vomiting.
Bleeding mild/moderate. Self-limiting.
Classical history with Endoscopy is diagnostic.
Treatment is conservative. Supportive. Endoscopic.

Boerhaaves syndrome : complete thickness tear with rupture of

oesophagus.
Often seen in alcoholics.
Immediate and urgent surgery in Boerhaaves syndrome.

GERD/Hiatus hernia :
Reflux of gastric contents into the oesophagus is GERD.
Usually due to inappropriate LES relaxation. Dilated stomach. Drugs.
Often associated with hiatus hernia.
Hiatus hernia are of 2 types : Sliding/Paraoesophageal type.
Commoner of the 2 is : Sliding.

Barretts oesophagus :
Replacement of Squamous epithelium to Columnar epithelium in the lower 1/3rd of the
oesophagus constitutes Barretts oesophagus. (more acid/pepsin-resistant)
Barretts esophagus is more common in men, particularly white men.
Barretts esophagus is arbitrarily divided into : long (_23 cm) or short-segment (_23
cm) disease;
Long segment disease is present in 0.5% of population and short-segment disease in
15%.
Barretts epithelium progresses through a dysplastic stage before developing into
adenocarcinoma. The rate of cancer development is 0.5% per year; those with longsegment disease have a risk of developing esophageal cancer that is 30 to 125 times
the risk of the general population.
Barretts esophagus can also lead to chronic peptic ulcer of the esophagus with high
(midesophageal) and long strictures.
Established metaplasia does not regress with treatment; thus, acid suppression and
fundoplication are indicated only when active esophagitis is also present.
The need and frequency of surveillance endoscopies in patients is debated.
The risk of developing esophageal adenocarcinoma is related to the length involved.
Once high-grade dysplasia is detected, treatment of choice is esophagectomy of the
Barretts segment.

Misc
Plummer-Vinson syndrome / Schatzki ring :
The combination of symptomatic hypopharyngeal webs and irondeficiency anemia in middle-aged women constitutes PlummerVinson syndrome.
The clinical importance of this syndrome is uncertain.
A lower esophageal mucosal ring (Schatzki ring) is a thin, weblike
constriction located at the squamocolumnar mucosal junction at or
near the border of the LES.
It commonly produces dysphagia when the lumen diameter is <_1.3
cm.
Asymptomatic rings may be present in <_10% of normal individuals.
A lower esophageal ring is one of the common causes of dysphagia.
Symptomatic webs and lower esophageal rings are easily treated by
dilatation.
Muscular rings are not suitable for dilatation.

Stomach - Anatomy
Consists of Antrum, body and pylorus.
Lined by columnar epithelium.
Consists of 2 Cells : Chief and Parietal cell.

Gastric motor activities exhibit regional variability:

(1) the proximal stomach serves a storage function by relaxing
(2) the distal stomach exhibits phasic contractions that propel
solid food residue against the pylorus, where it is repeatedly
propelled proximally for further mixing before it is emptied into
the duodenum.
Transit time 3-5 hours

Gastric protective mechanisms

Pre-Epithelial : Mucous layer, Bicarbonate
layer, Phospholipid layer.
Epithelial : Prostaglandins, Restitution,
Immune cells
Post-epithelial : Vascularity, immune cells.

Peptic Ulcer Disease

PUD encompasses both gastric and duodenal ulcers.

Ulcers are defined as a break in the mucosal surface > 5 mm in size,
with depth to the submucosa.
Duodenal ulcers (DUs) and gastric ulcers (GUs); share many common
features in terms of pathogenesis, diagnosis, and treatment, but
several factors distinguish them.
NSAID induced PUD : Prostaglandin Physiology.
NSAID non dose-dependant. No class effect.
Incidence is high due to OTC sale of NSAID and wide its therapeutic
usage.
Classical history is usually diagnostic.
Pathophysiology is direct (ION trapping) and indirect (inhibition of PG
synthesis. )
Treatment is symptomatic.

H-Pylori related PUD

Gram negative rod, Flagellate, micro-aerophilic bacilli. Resistant
Cocci form.
Epidemiology : Usually > 80% population infected before 20 years
of age.
Diagnosis :
Non-Invasive : Urease Breath test.
Invasive : Rapid Urease test , Staining, Culture.

Treatment : Triple Drug therapy :

Category 1 : Azithromycin/Clarithromycin.
Category 2 : Amoxacillin/ Metronidazole.
Category 3 : Proton pump inhibitor Omeprazole.

Gastritis

Types A Gastritis : Autoimmune, Antral sparing

Common in females
Presentation with PUD symptoms and symptoms of autoimmune disease viz.
Anaemia Pernicious anaemia. Hashimotos thyroiditis.
Anti parietal cell antibody vs anti-Intrinsic factor antibody > 80%.
Increased risk of MALTomas.Treatment supportive.
Prognosis good.

Type B gastritis. : NSAID and H.Pylori related.

Common in males.
Refractory. High recurrence. Risk of adenocarcinoma.
Prognosis worse.

Medical treatment : Diet , Posture

H2 blockers, Proton pump inhibitors
Antacids, Cytoprotective agents.

Zollinger-Ellison syndrome

Gastrinoma Sporadic vs MEN 1

Intractable peptic ulcers
Severe diarrhea
Very high acid output
Valuable provacative test is Secretin Stimulation
test.
Fasting Gastrin levels > 200 is common.
Octreotide scan
Drug of Choice is PPI.

Test 1
1.

Bernstein test is useful in the diagnosis of cause of

(A) Pyrosis
(B) Odynophagia
(C) Dysphagia
(D) Dyspepsia

2.

Which is true about achalasia cardia?

(A) Failure of relaxation of lower oesophageal sphincter
(B) Associated with Vit. A deficiency
(C) Not a premalignant condition
(D) It is a normal phenomenon

3.

Connective tissue disorder which is associated with gastroesophageal reflux

is.
(A) SLE
(B) Scleroderma
(C) Behcets syndrome
(D) Dermatomyositis

Test 1
4.

Following is true about Barrets esophagus except

(A) Occurs in 3rd decade
(B) Lined by transitional epithelium
(C) Not reversible by medical therapy
(D) It is a physiological condition.

5.

Oesophagitis in immuno compromised person is caused by all except is

(A) HSV
(B) HIV
(C) Varicella
(D) CMV

6.

True about plummer-vinson syndrome except

(A) Microcytic hypochronic anemia
(B) More common in females
(C) Common in old age
(D) Post cricoid web is common

Test 1
7.

True about H. Pylori is all except

(A) It splits urea and produces ammonia to survive
(B) Produces Gastric Ca
(C) Gram ve curved rods
(D) Cag-A gene is not associated with risk of duodenal ulcer

8.

Gastric Ulcer is caused due to

(A) Bile acid Reflux
(B) Recurrent trauma
(C) Hyperacidity
(D) Decreased mucosal resistance

9.

Treatment of choice for Zollinger Ellison Syndrome (ZES) is..

(A) PPI
(B) Somatostatin analogues
(C) Streptozocin
(D) Sucralfate

Test 1
10.

All of the following drugs are used for eradication of Helicobacter pylori except.
(A) Bismuth subcitrate
(B) Sucralfate
(C) Metronidazole
(D) Amoxycillin

11.

A patient with H. Pylori infection is treated with drugs. The best method to detect
presence of residual H. Pylori infection in this person is
(A) Rapid urease test
(B) Urea breath test
(C) Endoscopy and biopsy
(D) Serum anti H. Pylori titre

12.

Ulcer in lesser curvature in 65 year old male biopsy negative for malignancy not
healing after 6 weeks of H2 blocker next treatment is..
(A) Repeat biopsy
(B) Total gastrectomy
(C) Partial gastrectomy
(D) Hydrogen blocker for another 6 weeks

Test 1
13.

The most common complication of

(A) Diarrhoea
(B) Dryness of mouth
(C) Tachycardia
(D) Bleaching

vagotomy is

14.

All of the following are features of Zollinger Ellison syndrome except..

(A) Intractable peptic ulcers
(B) Severe diarrhea
(C) Beta cell tumours of the pancreas
(D) Very high acid output

15.

Most valuable provocative test for Zollinger Ellison syndrome is..

(A) ACTH infusion test
(B) Secretin stimulation test
(C) Ca2+ infusion test
(D) Food stimulation test

Small intestine - Anatomy

Consists of Duodenum,Jejunum and Ileum. (X ray dif. of small
bowel)
Length is 300cms.
The intestinal mucosa exhibits villous architecture to provide
maximal surface area for absorption and is endowed with
specialized enzymes and transporters.
The proximal intestine is optimized for rapid absorption of nutrient
breakdown products and most minerals, while the ileum is better
suited for absorption of vitamin B12 and bile acids.
The small intestine also aids in waste elimination.
The small intestine terminates in the ileocecal junction, a
sphincteric structure that prevents coloileal reflux and maintains
small-intestinal sterility.
Transit time : 6-8 hours.

Symptomatology
Diarrhea
Secretory
Osmotic

Steatorrheoa
Malabsorption

 Malabsorption Syndrome : constitutes a broad spectrum of conditions

due to malabsorption of 1 or more nutrients with multiple etiologies and
varied clinical manifestations.
Almost all of these clinical problems are associated with diminished
intestinal absorption of one or more dietary nutrients. E.g. B12, Iron,
Lactase deficiency.
The only clinical situations in which absorption is increased are
hemochromatosis and Wilsons disease, in which there is increased
absorption of iron and copper, respectively.
Steatorrhea is increase in stool fat excretion of > 6% of dietary fat intake.
Majority of malabsorptive disorders are associated with Steatorrhea
except the following :
Primary lactase deficiency : is associated with lactose malabsorption,
Pernicious anemia : is associated with a marked decrease in intestinal
absorption of Cobalamin (vitamin B12) due to an absence of gastric
parietal cell intrinsic factor required for cobalamin absorption.

Lipid Metabolism
Long chain triglycerides (LCT) : only dietary form.
Steps : Digestion starts with Gastric Lipase requires Acid for optimal
activity
Pancreatic Lipase micelle formation by bile salts mucosal absorption by
jejunal cell transporatation by lipoproteins to storage sites.
Medium chain triglycerides (MCT) : only processed / formulated
preparation.
Doesnot require lipolysis/micelle formation .
Hence the absorption of MCTs is greater than that of LCTs in pancreatic
insufficiency, conditions with reduced intraduodenal bile acid
concentrations, small-intestinal mucosal disease, abetalipoproteinemia,
and intestinal lymphangiectasia.

Etilogy of Fat malabsorption

Pre-mucosal :
1. Achlorhydria
2. Chronic Pancreatitis
3. Bile salt deficiency.
Mucosa :
1. Coeliac disease
2. Tropical sprue
3. Whipples disease.
Post-absorptive :
1. Abetalipoproteinemia
2. Lymphagiomatous telengectasia.

Diagnostic possibilities : 1. Tests directed detecting steatorrhea

2. Tests directed diagnosing cause of steatorrhea
3. Tests directed for specific deficiency states : A,D,E,K.

Coeliac disease :
(nontropical sprue, celiac disease, glutensensitive
enteropathy.)
Celiac sprue has various manifestations, almost all of which are secondary
to nutrient malabsorption.
The symptoms of celiac sprue may appear with the introduction of cereals
in an infants diet, although there is frequently a spontaneous remission
during the second decade of life that may be either permanent or
followed by the reappearance of symptoms over several years.
Alternatively, the symptoms of celiac sprue may first become evident at
almost any age throughout adulthood.
The symptoms range from significant malabsorption to asymptomatic
cases.
Diagnosis : A small-intestinal biopsy is required to establish a diagnosis of
celiac sprue.

Refractory disease
Patients who :
(1) respond to restriction of other dietary protein,
e.g., soy;
(2) respond to glucocorticoids;
(3) are temporary, i.e., the clinical and
morphologic findings disappear after several
months or years; or
(4) fail to respond to all measures and have a fatal
outcome, with or without documented
complications of celiac sprue, such as
development of intestinal T cell lymphoma.

Associated Diseases Celiac sprue is associated with dermatitis herpetiformis (DH).

Tropical Sprue :

Chronic diarrhea in a tropical environment is most often caused by infectious

agents including G. lamblia, Yersinia enterocolitica, C. difficile, Cryptosporidium
parvum, and Cyclospora cayetanensis, among other organisms.

Broad-spectrum antibiotics and folic acid are most often curative.

Folic acid alone will induce a hematologic remission as well as improvement in
appetite, weight gain, and some morphologic changes in small intestinal biopsy.

Whipples disease :

Organism : T.Whippllei. PAS + in biopsy.

Dementia is late complication and poor prognostic indicator.
Septran (Co-Triamoxazole) is drug of choice.

Protein Malabsorption
Protein is present in food almost exclusively as
polypeptides and requires extensive hydrolysis to di- and
tripeptides and amino acids before absorption. Proteolysis
occurs in both the stomach and small intestine; it is
mediated by pepsin secreted as pepsinogen by gastric chief
cells and trypsinogen and other peptidases from pancreatic
acinar cells.
These proenzymes, pepsinogen and trypsinogen, must be
activated to pepsin (by pepsin in the presence of a pH _5)
and trypsin (by the intestinal brush border enzyme
enterokinase). Proteins are absorbed by separate transport
systems for di- and tripeptides and for different types of
amino acids, e.g., neutral and dibasic.

Protein Malabsorption
Three rare genetic disorders involve protein digestionabsorption:
(1) enterokinase deficiency is due to an absence of the
brush border enzyme that converts the proenzyme
trypsinogen to trypsin and is associated with diarrhea,
growth retardation, and hypoproteinemia;
(2) Hartnup syndrome, a defect in neutral amino acid
transport, is characterized by a pellagra-like rash and
neuropsychiatric symptoms; and
(3) cystinuria, a defect in dibasic amino acid transport, is
associated with renal calculi and chronic pancreatitis.

Carbohydrate Malabsorption
Carbohydrates in the diet are present in the form of starch,
disaccharides (sucrose and lactose), and glucose. Carbohydrates are
absorbed only in the small intestine and only in the form of
monosaccharides. Therefore, before their absorption, starch and
disaccharidesvmust first be digested by pancreatic amylase and
intestinal brush border disaccharidases to monosaccharides.
Monosaccharide absorption occurs by a Na-dependent process
mediated by the brush border transport protein SGLT.
Lactose malabsorption is the only clinically important disorder of
carbohydrate absorption. Lactose, the disaccharide present in milk,
requires digestion by brush border lactase to its two constituent
monosaccharides, glucose and galactose.
Lactase is present in almost all species in the postnatal period but
then disappears throughout the animal kingdom, except in humans.
Lactase activity persists in many individuals throughout life.

Lactose intolerance
Two different types of lactase deficiency existprimary and
secondary.
In primary lactase deficiency, a genetically determined
decrease or absence of lactase is noted, while all other
aspects of both intestinal absorption and brush border
enzymes are normal.
In contrast, secondary lactase deficiency occurs in
association with small-intestinal mucosal disease with
abnormalities in both structure and function of other brush
border enzymes and transport processes.
Secondary lactase deficiency is often seen in celiac sprue.

Development of symptoms of lactose intolerance is related to several factors:

1. Amount of lactose in the diet.
2. Rate of gastric emptying. Symptoms are more likely when gastric
emptying is rapid than when gastric emptying is slower. Therefore, it is
more likely that skim milk will be associated with symptoms of lactose
intolerance than will whole milk, as the rate of gastric emptying following
skim milk intake is more rapid. Similarly, the diarrhea observed following
subtotal gastrectomy is often a result of lactose intolerance, as gastric
emptying is accelerated in patients with a gastrojejunostomy.
3. Small-intestinal transit time. Although the small and large intestine
contribute to the development of symptoms, many of the symptoms of
lactase deficiency are related to the interaction of colonic bacteria and
nonabsorbed lactose. More rapid small-intestinal transit makes symptoms
more likely.
4. Colonic compensation by production of SCFAs from nonabsorbed lactose.
Reduced levels of colonic microflora, which can occur following antibiotic
use, will also be associated with increased symptoms following lactose
ingestion, especially in a lactase-deficient individual.

D-xylose test
D-Xylose excretion test is used to detect
monosachharide malabsorption
False positive is seen in Ascitis and Blind loop
syndrome.

Schilling test

Parenteral B12 injection to saturate stores

Give oral radioactive cobalamine
Urinary excretion is < 10% in malabsorption
After giving Intrinsic factor pernicious anaemia
recovers
Defect persists in blind loop syndrome.

Test 2
16.

6-year old Arun participitated in an ice-cream eating competition and developed

bloating diarrhoea and moderate dehydration. He used to get similar episodes on
consuming ice-cream and milk in the past. The likely diagnosis is.
(A) Lactase deficiency
(B) Sucrase deficiency
(C) Maltase deficiency
(D) Amylase deficiency

17.

Patient with congenital lactose deficiency will experience distension, flatulence and
diarhoea on ingestion of
(A) Glucose
(B) Sucrose
(C) Milk
(D) Eggs

18.

The urinary excretion of Radioactive vitamin B12 after oral administration in vitamin
B12
malabsorption is..
(A) > 50%
(B) 30 to 40%
(C) 20 to 30%
(D) < 10%

Test 2

19.

Xylose excretion test used to assess.

(A) Liver function
(B) Kidney function
(C) Pancreatic function
(D) Monosaccharide absorption

20.

False positive D-xylose test is seen in

(A) Ascites
(B) Renal failure
(C) Aspirin
(D) Hepatic failure

21.

Xylose absorption tests are good screening test for.

(A) Fat absorption
(B) Pernicious anaemia
(C) Carbohydrate absorption
(D) Amino acid absorption

Test 2
22.

Jejunal biopsy is diagnostic in.

(A) Celiac Sprue
(B) Tropical Sprue
(C) Whipples disease
(D) Radiation enteritis

23.

Abnormal schilling test which persists after intrinsic factor is given suggests
(A) Blind loop syndrome
(B) Pernicious anaemia
(C) Defective marrow
(D) Total gastrectomy

24.

Non-tropical sprue is characterized by.

(A) Elongation of intestinal villi
(B) Current jelly stools
(C) Hypertriglyceridaemia
(D) Poor absorption of lipids

Test 2
25.

After extensive small bowel resection, increased

incidence of renal stones is due to.
(A) Increased Vit. D absorption
(B) Increased calcium oxalate absorption
(C) Increased acid loss duodenum
(D) Increased oxalate absorption

26.

Whipples disease is associated with all except

(A) Cerebellar ataxia
(B) Seizure
(C) Dementia
(D) Supranuclear ophthalmoplegia

Colon - Anatomy

Consists of ascending colon, transverse colon and descending colon.

Length is 80cms.
Mucosa has Haustrations.
The colonic mucosa dehydrates the stool, decreasing daily fecal volumes
from the 1000 to 1500 mL delivered from the ileum to the 100 to 200 mL
expelled from the rectum.
The colonic lumen possesses a dense bacterial colonization that ferments
undigested carbohydrates and short-chain fatty acids.
Colonic motor patterns exhibit a to and- fro character that facilitates slow
fecal desiccation. The proximal colon serves to mix and absorb fluid,
the distal colon exhibits peristaltic contractions and mass actions that
function to expel the stool.
The colon terminates in the anus, a structure with volitional and
involuntary controls to permit retention of the fecal bolus until it can be
released in a socially convenient setting.
Transit time in hours to days 18-30 hours.

Symptomatology

Tenesmus
Hematochezia
Lump in abdomen
Peri-anal itching
Incontinence

IBD
Inflammatory bowel disease (IBD) is an idiopathic and
chronic intestinal inflammation. Ulcerative colitis (UC)
and Crohns disease (CD) are the two major types of IBD.
Epidemiology : Bimodal presentation : 1. between 15
and 30 yrs. 2.between 60 and 80yrs.
The male to female ratio for UC is 1:1 and for CD is 1.1 to
1.8:1.
Cigerrete smoking protects UC and OCP increase risk of
UC and CD.
IBD runs in families. Incidence and site of bowel
involvement both correlate.
UC and CD are both associated with Turners syndrome.

IBD-etiopathogenesis

A consensus hypothesis is that in genetically predisposed individuals, both

exogenous factors (e.g., infectious agents, normal lumenal flora) and host factors
(e.g., intestinal epithelial cell barrier function, vascular supply, neuronal activity)
cause a chronic state of dysregulated mucosal immune function that is further
modified by specific environmental factors (e.g., smoking).

Once initiated in IBD, the immune inflammatory response is perpetuated as a

consequence of Tcell activation. A sequential cascade of inflammatory mediators
acts to extend the response; each step is a potential target for therapy.

Inflammatory cytokines, such as IL-1, IL-6, and TNF, have diverse effects on tissue.
They promote fibrogenesis, collagen production, activation of tissue
metalloproteinases, and the production of other inflammatory mediators; they
also activate the coagulation cascade in local blood vessels (e.g., increased
production of von Willebrands factor).

These cytokines are normally produced in response to infection, but are usually
turned off or inhibited at the appropriate time to limit tissue damage. In IBD their
activity is not regulated, resulting in an imbalance between the proinflammatory
and anti-inflammatory mediators.

Clinical Presentation :

UC

CROHNS DISEASE

1. Blood in stools
2. Pain/Systemic symptoms
3. Lump in abdomen
4. Bowel involvement

5. Complications
6. Barium

Frequently
Rarely
Rarely
Continous
Ileum rare
Sepsis, Toxic megacolon
Fine granularity,continuous

7. Serology
8. Antibiotics
9. Surgery
required
Recurrence
10. Prognosis

pANCA +ve
Poor
Rarely required

Rarely
Frequently
Frequently
Segmental
Rectal sparing
Stricture,Fistulae
Cobble-stone
String sign
ASCA +ve
Good
Commonly

rare
Better

recurrence often
Poor

EXTRAINTESTINAL MANIFESTATIONS
1.DERMATOLOGIC :
Erythema nodosum (EN) occurs in up to 15% of CD patients and 10%
of UC patients. Attacks usually correlate with bowel activity.
Pyoderma gangrenosum (PG) is seen in 1 to 12% of UC patients and
less commonly in Crohns colitis. Although it usually presents after
the diagnosis of IBD, PG may occur years before the onset of bowel
symptoms, run a course independent of the bowel disease, respond
poorly to colectomy, and even develop years after proctocolectomy.
Sweets syndrome, a neutrophilic dermatosis, and metastatic CD, a
rare disorder defined by cutaneous granuloma formation.
Psoriasis affects 5 to 10% of patients with IBD and is unrelated to
bowel activity.

Extra-intestinal manifestations
2. RHEUMATOLOGIC :
Peripheral arthritis develops in 15 to 20% of IBD patients, is more common in
CD, and worsens with exacerbations of bowel activity.
It is asymmetric, polyarticular, and migratory and most often affects large
joints of the upper and lower extremities. Treatment is directed at reducing
bowel inflammation. In severe UC, colectomy frequently cures the arthritis.
Ankylosing spondylitis (AS) occurs in about 10% of IBD patients and is more
common in CD than UC. About two-thirds of IBD patients with AS test positive
for the HLA-B27 antigen. The activity of AS is not related to bowel activity and
does not remit with glucocorticoids or colectomy.
Sacroiliitis is symmetric, occurs equally in UC and CD, is often asymptomatic,
does not correlate with bowel activity, and does not always progress to AS.
Other rheumatic manifestations include hypertrophic osteoarthropathy,
pelvic/femoral osteomyelitis, and relapsing polychondritis.

Extra-intestinal syndrome
3. OCULAR : The most common are conjunctivitis, anterior uveitis/iritis,
and episcleritis.
4. HEPATOBILIARY : Hepatic steatosis & fatty liver. Cholelithiasis is more
common in CD than UC and occurs in 10 to 35% of patients with ileitis or
ileal resection.
Primary sclerosing cholangitis (PSC) is characterized by both intrahepatic
and extrahepatic bile duct inflammation and fibrosis, frequently leading to
biliary cirrhosis and hepatic failure; 1 to 5% of patients with IBD have PSC,
but 50 to 75% of patients with PSC have IBD.
4. UROLOGIC The most frequent genitourinary complications are calculi,
ureteral obstruction, and fistulas. The highest frequency of nephrolithiasis
(10 to 20%) occurs in patients with CD following small-bowel resection.
Calcium oxalate stones develop secondary to hyperoxaluria, which results
from increased absorption of dietary oxalate.

Extra-intestinal Manifestations

5. Vascular : The risk of thromboembolic disease increases with active IBD.

A spectrum of vasculitidies involving small, medium, and large vessels has also been
observed in IBD patients.

6. Malabsorption related : Patients with IBD have an increased prevalence of osteoporosis

and osteomalacia from vitamin D deficiency, calcium malabsorption, malnutrition,
glucocorticoid use, and the intestinal inflammation itself.
Deficiencies of vitamin B12 and fat-soluble vitamins may occur after ileal resection or with
ileal disease.

7. Miscellaneous :
More common cardiopulmonary manifestations include endocarditis, myocarditis,
pleuropericarditis, and interstitial lung disease. A secondary or reactive amyloidosis can
occur in patients with longstanding IBD, especially in patients with CD.

Pancreatitis is a rare extraintestinal manifestation of IBD and results from duodenal fistulas,
ampullary CD, gallstones, PSC, drugs such as 6-mercaptopurine, azathioprine, or very rarely,
5-ASA agents, autoimmune pancreatitis, and primary CD of the pancreas.

 Conditions that mimic IBD :

Infections : Bacterial,Fungal,Viral and Parasitic

Inflammation : Appendicitis, Diverticultis,
Behcets, Radiation induced
Neoplastic : Lymphoma, familial polyposis
Drugs/Toxins : Cocaine, Gold, OCP, etc.

Treatment
5-ASA agents : The mainstay of therapy for mild to moderate
UC and Crohns colitis is sulfasalazine. These agents are
effective at inducing remission in both UC and CD and in
maintaining remission in UC; whether they have a role in
remission maintenance in CD is unclear.

Gluco-corticoids
Azathioprine
Cyclosporine/Tacrolimus
Infliximab
Surgery
Antibiotics
Supplementary treatment

IBS
ROME II criteria
5HT recptors
Management

Miscellaneous
Mesentric angina
Diverticulosis
Famalial Mediterranean fever pyrin gene
mutation
Volvulus coffee-bean sign
Medical causes of pain porphyria.

GIT Final test

27.

Extra intestinal complication which is more common in Ulcerative Colitis than

Crohns disease?
(A) Uveitis
(B) Pyoderma gangrenosum
(C) Cirrhosis
(D) Cholangiocarcinoma

28.

Which is not true of arthritis associated with inflammatory bowel disease?

(A) Migratory arthritis
(B) Knee joint most common
(C) Deformities are common
(D) Correlates to severity of colitis

29.

In ulcerative colitis, Ca arises from

(A) Pseudopolyps
(B) Dysplastic sites (C) Familial polyposis
(D) Multiple adenomatous polyp

GIT Final test

30.

Kalloo, 65 years presents with complaints of abdominal pain. On examination there was
distension of abdomen and the stools were maroon coloured. He gives a past history of
Cerebro Vascular accident and Myocardial infarction. What would be the probable
diagnosis?
(A) Ulcerative colitis
(B) Crohns disease
(C) Acute mesenteric ischemia
(D) Acute gastric bleed

31.

Intestinal angina is a symptom complex of the following :

(A) Postprandial abdominal pain, weight loss, acute mesenteric vessel occlusion
(B) Postprandial abdominal pain, weight loss, chronic mesenteric vessel occlusion
(C) Preprandial abdominal pain, weight loss, chronic mesenteric vessel occlusion
(D) Preprandia abdominal pain, weight gain, acute mesenteric vessel occlusion

32.

Spastic ileus is seen in..

(A) Porphyria
(B) Retroperitoneai abscess
(C) Hypokalemia
(D) MI

GIT Final test

33.

Coffee bean sign is usually seen in..

(A) Volvulus
(B) Pyloric obstruction
(C) Intussusception
(D) Intestinal obstruction

34.

Which of the following organisms produces signs and symptoms that mimic
acute appendicitis?
(A) Enteropathic Escherichia coli
(B) Enterobius vermicularis
(C) Trichomonas hominis
(D) Yersinia enterocolitica

35.

Least irritant fluid to peritoneum

(A) Blood
(B) Urine
(C) Bile
(D) Pancreatic fluid