5 Medicine GIT

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 : Achalasia Cardia

Diffuse Oesophageal spasm (DES)

Scleroderma Oesophagus

• Inflammatory : Viral –HSV, Varicella Zoster, CMV, HIV

Fungal – Candidiasis

Drug induced, Corrosive poisoning

Iatrogenic - sclerotherapy

• Bleeding related : Oesophageal varices

Mallory Weiss tear

Boerheeve’s syndrome

• Reflux disorder : GERD

Barretts oesophagus

Hiatus hernia

• Neoplastic : Malignancy

• Miscellaneous : 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.

• Heller’s 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.

• Boerhaave’s syndrome : complete thickness tear with rupture of oesophagus.

• Often seen in alcoholics.

• Immediate and urgent surgery in Boerhaave’s 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.

Barrett’s oesophagus :

• Replacement of Squamous epithelium to Columnar epithelium in the lower 1/3rd of the oesophagus constitutes Barrett’s oesophagus. (more acid/pepsin-resistant)

• Barrett’s esophagus is more common in men, particularly white men.

• Barrett’s esophagus is arbitrarily divided into : long (_2–3 cm) or short-segment (_2–3 cm) disease;

• Long segment disease is present in 0.5% of population and short-segment disease in 15%.

• Barrett’s epithelium progresses through a dysplastic stage before developing into adenocarcinoma. The rate of cancer development is 0.5% per year; those with long-segment disease have a risk of developing esophageal cancer that is 30 to 125 times the risk of the general population.

• Barrett’s 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 Barrett’s segment.

Misc • Plummer-Vinson syndrome / Schatzki ring :

• The combination of symptomatic hypopharyngeal webs and iron-deficiency anemia in middle-aged women constitutes Plummer-Vinson 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) Behcet’s syndrome

(D) Dermatomyositis

Test 1 4. Following is true about Barret’s 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 vagotomy is…

(A) Diarrhoea

(B) Dryness of mouth

(C) Tachycardia

(D) Bleaching

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 Wilson’s 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.

• Short chain triglycerides (SCT) : only by bacterial activity in colon.

Etilogy of Fat malabsorption • Pre-mucosal :

1. Achlorhydria

2. Chronic Pancreatitis

3. Bile salt deficiency.

• Mucosa :

1. Coeliac disease

2. Tropical sprue

3. Whipple’s 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 infant’s 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. • Whipple’s 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 digestion-absorption:

(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 exist—primary 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) Whipple’s 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 Crohn’s 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 Turner’s 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 Willebrand’s 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 Frequently Rarely

• 2. Pain/Systemic symptoms Rarely Frequently

• 3. Lump in abdomen Rarely Frequently

• 4. Bowel involvement Continous Segmental

Ileum rare Rectal sparing

• 5. Complications Sepsis, Toxic megacolon Stricture,Fistulae

• 6. Barium Fine granularity,continuous “Cobble-stone”

“String sign”

• 7. Serology pANCA +ve ASCA +ve

• 8. Antibiotics Poor Good

• 9. Surgery Rarely required Commonly required

• Recurrence rare recurrence often

• 10. Prognosis Better 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 Crohn’s 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.

• Sweet’s 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, Behcet’s, 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 Crohn’s 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) Crohn’s 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