digestive system and its disease
DESCRIPTION
Digestive system and diseaseTRANSCRIPT
Digestive system & its diseases
Pooja Goswami
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
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
Digestive system
How food moves into GI tract
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
Peristalsis: Invoulntary wave like muscles contraction moving down along the GI tract
(modified from McPhee, Lingappa, Ganong & Lange, Pathophysiology of Disease, 1997, 2nd ed.
Upper esophagealsphincter
Lower esophageal sphincter
Sphincters
- 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
Functional anatomy of the GI system
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.
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
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
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
Small Intestine
Colon• Reabsorb water from food and digestive
juices
• Defecation– Elimination of indigestible substances
from body as feces
GI- tract & its diseaseGERD, Achalasia, cardia, Barret esophagus, esophageal cancer
Dyspepsia, Gastritis, gastric ulcer, Gastric cancer
Duodenal ulcer, Celiac disease, CD, ITb
Diarrhea, Constipation, IBS, IBD, CRC
Billiary tract
GERD, Achalasia, cardia, Barret esophagus, esophageal cancer
Dyspepsia, Gastritis, gastric ulcer, Gastric cancer
Duodenal ulcer, Celiac disease, IBD, Diarrhea, Constipation, IBS,
IBD, CRC
Acute pancreatitisChronic pancreatitis , Ca pancreas
ALD, NAFLD, CLD, Cirrhosis, Liver cancer
GB, stone, Ca-Gall bladder
Disease of GE system
Upper GI endoscopy• Diagnostic
• GI bleeding
• Dysphagia, Gastro esophageal reflux
• ulcers
• Intestinal disease
• Suspicion of neoplasm (weight loss, etc.)
• Therapeutic• treatment of variceal and nonvariceal GI bleeding
• removal of polyps, early neoplasms
• dilation of strictures
• placement of feeding tube
• removal of foreign bodies
Ascending colon
How to study colonic disease
Lower GI endoscopyColonoscopy, 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
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
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
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
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
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
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
Gastric Ulcer : Due to NSAID, pH imbalance & H. Pylori
Normal
Gastric cancer Chronic
ulcer
Erosion and acute ulcer
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,
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..
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
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
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.
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
Symptoms and diagnosisClinical 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
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
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
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
UCCD
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
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)
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
Normal vs CD colon
Normal colonCD colon
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
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
Thanking You