2. Topics to be cover
• Digestive system
• GI tract & its anatomy
• Billiary tract
• How to assess GI tract
• GI disease
– Esophageal diseases
– Gastric disease
– Small intestinal disease
– Colonic disease
• Billiary diseases
3. Studied material
• Book: Chapters in Harrison
• Book : Chapters in Clark
• Book: Chapters in IBD
• Journal : ECAB clinical updates
• Gastroenterology 2002,
• IBD: 2008
• Can . J. Gastroenterology 2005
6. Layers of GI tract
– Mucosa (Inner most)
• Absorptive and secretary
(mucus)
– Sub mucosa
• Absorbed molecule of
mucosa picked up by BC
– Muscularis
• Controlled peristalsis
– Serosa (outer most)
• Protective layer &
secretary
9. Functional anatomy of the GI system
- Mechanical digestion:
breaking food in small particles
so they are easily broken down
by enzymes mouth and
stomach
Chemical digestion:
pancreas and duodenum
Nutrient absorption:
small intestine
Water reabsorption:
colon
10. Esophagus
• Pharynx, esophagus: passageway
for food (from mouth to stomach)
• Esophageal sphincters
Upper esophageal sphincter (UES):
Prevents entry of air
Lower esophageal sphincter (LES):
Prevents reflux of corrosive acidic
stomach content.
11. Stomach
• J- shaped structure have 4 specific region for digestion, store foods for 4 hours
– Cardiac region, which receive bolus from esophagus via LES
– Fundus upper part
– Later on whole body
– Last is pyloric region which allow chyme to move towards the duodenum via pyloric sphincter,
when it reaches the right consistency
• Different glands secrete diff. enzyme, for digestion of bolus into chyme
– Parietal cells- HCL
– Chief cells -Pepsin (protein-digesting enzyme needing acid environment)
– Goblet cells secrete mucus
– G cells secrete gastrin
• Imbalance b/w mucus and HCL leads to disorder
12. Gastric mixing and emptying
• Gastric glands begin secretion of gastric juices in 3 phases, before food entry
i.e. cephalic , gastric and intestinal phase
• Chyme = mixture of gastric secretion and food content
• Pyloric valve : - regulates emptying of gastric content
• - Prevents regurgitation of duodenal content
13. Small Intestine
Duodenum : 25 cm (10 in.) long &
receive juices from pancreas, liver .
• To receive chyme from
stomach
• To neutralize acids before
they can damage the
absorptive surfaces of the
small intestine
Jejunum 2.5 meters (8.2 ft) long
• Chemical digestion
• Nutrient absorption
Ileum : 3.5 meters (11.48 ft) long
Ends at the IC valve, a sphincter that
controls flow of material from the
ileum into the large intestine
14. Colon
• Reabsorb water from food and digestive
juices
• Defecation
– Elimination of indigestible substances
from body as feces
15. GI- tract & its disease
GERD, Achalasia, cardia, Barret
esophagus, esophageal cancer
Dyspepsia, Gastritis, gastric
ulcer, Gastric cancer
Duodenal ulcer, Celiac
disease, CD, ITb
Diarrhea, Constipation, IBS,
IBD, CRC
21. Lower GI endoscopy
Colonoscopy, rectosigmoidoscopy, rectoscopy
• Diagnostic
– Bleedings (occult blood or, iron deficiency)
– Chronic diarrhea
– Suspicion of cancer
– Suspicion of inflammatory bowel disease
– Screening for cancer (altered bowel habits, risk
groups for colon cancer)
• Therapeutic
• Removal of polyps, early cancers
22. Ba meal follow through: to visulize t. ileum
& caecum
– Small bowel follow through - drink barium and
take pictures as it transits the small bowel
But now fluoroscopy is superceded by CT and MR enterography
23.
24. Gastro esophageal reflux disease
• Stomach tolerates high acid
content but esophagus
doesn’t – when stomach
contents refluxes into
esophagus (heartburn;
GERD)
• Esophageal: heartburn, chest
pain, regurgitation, acidic
taste in mouth, dysphagia,
Extraesophageal: chr.cough,
asthma, noncardiac chest
pain
25. Peptic ulcer (duodenal, gastric)
• Defect in GI muscularis mucosae
• Dependent on acid peptic activity
• Caused by majorly 2 reason
– H. Pylori
– NSAID
• PUD occurs in gastric & duodenal mucosa
– Gastric
– Duodenal ulcer
• Diagnosis: endoscopy
26. H. Pylori mechanism
– H. Pylori is gram negative, its niche is stomach
– Mechanism involves elucidation of primary
defense i.e. gastric acidity & to counteract
peristalsis to establish persistent infection
– Ph. Imbalance , counteract to peristalsis ,
flagella of H. pylori colonize to stomach, &
duodenum leads to urease production for
persistent infection & cause gastric ulcer,
duodenal ulcer, maltoma & gastric cancer
27. Detection & treatment of H. pylori
• Invasive (Endoscopic Bx)
– RUT
– Urea converted to NH3 by urease containing Bx in 30 min,
detect by pH indicator
• Non-invasive
• Urea breath test
• Treatment
• Triple therapy: PPI (Ranitidine)+ Clarithomycin+
amoxicillin or metrotindazole
28. Pathology of peptic ulcers
• Defend mechanism of GI tract : Acid pepsin secretion
create a balance between inputs from neural, endocrine,
paracrine, & autocrine pathway.
• Imbalance b/w the acid pepsin secretion leads to erosion and
ulcer
• Erosion: Superficial mucosal defect
• Ulcer : Defect extends into submucosa
• Acute lesion: Generally multiple & shallow with minimal
inflammation or fibrosis, but heal early
• Gastritis: Microscopic inflammation of Stomach due to fall
in acid secretion facilititate H. Pylori to colonize which leads
to gastric atrophy
• Chronic Ulcer: Usually Single & surrounded by inflammation
& fibrosis & heal slowly . And reoccur at same location
29. Gastric Ulcer : Due to NSAID, pH imbalance & H.
Pylori
Normal
Erosion and
acute ulcer
Gastric
cancer Chronic
ulcer
30. Diarrhea
• Diarrhea is an increase in the volume of
stool or frequency of defecation.
– Osmotic: Malabsorption , excessive amounts
of solutes are retained in the intestinal lumen,
water will not be absorbed.
– Secretory: Large volumes of water is
efficiently absorbed before reaching the large
intestine. Ex v. cholera
– Inflammatory/ Infectious : defected intestinal
barrier function due to microbial or viral
pathogens lead to in-efficient absorption of
water . Ex, bacteria ( salomonella, shigella)
virus ( rota , corona, hepatitis), parasitic
(amoeba, giardia)
– Deranged Motility: For efficiently absorption,
the intestinal contents must be adequately
exposed to the mucosa. Disorders in motility
accelerate transit time which decrease water
absorption,
31. Constipation
• Constipation usually is caused by the slow movement of stool
through the colon.
• Due, delay in bowel movement more water get absorbed,
which makes stool tight & difficult to defecate..
32. Dyspepsia ( problem of upper gut)
Dyspepsia is discomfort in the upper abdomen, bloating, satiety, &
nausea.
• Pathophysiology
– A delay in emptying the stomach contents into the duodenum may be a
factor
– Acute H. pylori infection
– Anxiety, depression, or stress
– The most common NSAID is ibuprofen and aspirin.
• Treatment
– To, ↓ stomach acid - proton pump inhibitors (PPIs) and H2-receptor
antagonists to be used.
– PPIs include: omeprazole, lansoprazole, pantoprazole, rabeprazole, and
esomeprazole.
– H2-receptor antagonists include: cimetidine, famotidine, nizatidine,
and ranitidine
33. Lactose intolerance
• Inability to digest dairy product containing lactose
due to lack of lactase enzyme
• The lactase enzyme converted lactose into glucose
and galactose — which can be absorbed into
bloodstream.
– congenital ( with birth)
– Primary ( disappear after milk withdrawal from diet)
– Secondary ( due to traumatic or intestinal disease)
• Diagnosis
• H2 breath test
• Lactose tolerance
34. Malabsorption
• Food nutrients are not adequately absorbed in the small
intestine ,
– Protozoal infection (Giardia intstinalis), Helminthis , bacterial
infection ( M. tuberculosis), viral infection & autoimmune mediated.
• Carbohydrate malabsorption
• Fat malabsorption
• Nutrient malabsorption
• Diagnosis : UGIE
– D-xylose test
– Iron deficiency
• Treatment: Antibiotics course
Mucosal malabsorption get resolved with antibiotics If problem still persist, look for
non mucosal causes, celiac, pancreatitis, hepatitis etc.
35. Celiac disease
• Immune mediated enteropathy triggered by gluten in genetically
susceptible individual
• Interplay between genes ( HLA -DQ) & environment (gluten) leads to
intestinal damage
• Extra-intestinal manifestation also responsible for celiac i.e. Skin, liver
and nervous system because genetically susceptible person develop
autoimmune injury of intestine, liver and spleen, skin and other organ
36. Symptoms and diagnosis
Clinical symptom Diarrhea, malabsorption, iron deficiency, short stature,
bloating
Risk Factor ↑ ALT , Seizure, DH, DM, Osteomalacia,
Diagnosis
Serological marker: Anti EMA Ab, Anti-ttg Ab
UGIE: Scalloping of folds in duodenum, cobble stoning in some
Rule out other disease responsible for villous atrophy i.e. tropical sprue,
bacterial growth and parasitic infection
Normal Folds Scalloping of Folds Cobble stoning
37. Disease extent and severity
• Disease severity assessed by Marsh classification
• 1 normal ( C:V-1:3)
• 2 increased IEL
• 3 (3a , 3b, 3c) villous atrophy
• 4 villous atrophy + crypt hyperplasia
• GFD is only treatment with supplement for celiac disease
38. Irritable Bowel Syndrome (IBS) problem of
lower gut
• Abdominal pain associated with disturbed
defecation and relieved with defecation
• Stools looser or more frequent at pain onset
• Feeling of incomplete evacuation
• Mucus per rectum
• Visible abdominal distention (bloating)
• Labs and sigmoidoscopy negative
39. Inflammatory Bowel Disease
• Ulcerative colitis – Effects the
generally mucosa of the colon and
rectum
• Crohn’s disease – This may affect
any segment of the gastrointestinal
tract
• Indeterminate colitis
– 15% patients with IBD
impossible to differentiate
CD UC
40. Ulcerative colitis (UC)
• UC is disease of mucosa and
superficial submucosa, with
deeper layers unaffected
• Symptoms: diarrhea with blood
mucus, diffuse abdominal
discomfort , urgency & tensemus
Diagnosis
Serological test ASCA, & p-ANCA
Colonoscopy
CECT or Ba enema
Rule out infectious causes
41. Ulcerative colitis disease activity & extent
• For disease extent : Three tire
classification
» E1 (Proctotitis)
» E2 ( left sided colitis)
» E3 ( Pancolitits)
• Severity of disease :True love & witts
criteria:
No. of stool ( with or without blood) mucus, fever,
ESR & clinical assessment)
» S0 (Remission)
» S1 (Mild )
» S2 (Moderate)
» S3 (Severe)
42. Crohn’s disease (CD)
– Clinical Symptoms:
• Diarrhea ( 1/4 have blood in stool), oral
ulcer, specific abdominal pain in right
quadrant, fever, arhtlargia, perianl disease
( fistulae or abscess)
– Endoscopic view :
• Disease of skip lesion and deep ulcers
(transmural) , a cobblestone-like mucosal
pattern,
– Radiological view :
• Strictures, thickening of wall
Diagnosis
Serological test , P-ASCA, & ANCA
Colonoscopy, UGIE
CECT or Ba meal follow through
– Rule out infectious causes
44. Crohn’s Disease activity and extent
• For disease extent : Monteral classification
– A (A1, A2 , A3, Age at Diagnosis)
– L (L1, L2, L3, L4 , {TI, C, IC, UGI} Location )
– B (B1, B2, B3 {non- stricture, stricture & penetrating} Behavior)
– P ( P0, P1 { perianl fistulae } Peri-anal disease)
• Severity of disease : Best et al. CDAI score
– On clinical assessment No. and type of stool, extraintesitnal
manifestation, fever, abdominal pain, HCT
– Remission CDAI <150
– Mild CDAI >150-219
– Moderate CDAI >220- 400
– Severe CDAI 400
45. Intestinal tuberculosis ( ITb)
– Clinical Symptoms:
• Diarrhea , specific abdominal pain in right quadrant, fever,
arhtlargia,
• Endoscopic view :
Mostly ulcerative lesion at IC valve
• Radiological view :
Strictures, thickening of wall ( IC valve)
Diagnosis:
Endoscopic, radiologic and histological + clinical symptom
– Rule out infectious causes
– t
– Look like CD BUT, ITb get cure after ATT while CD is
just treatable
