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