Gastro Intestinal Tract

Gastro Intestinal Tract
Organs of GIT
 Oral cavity  Pharynx  Esophagus  Stomach  Small intestine  Large intestine

Gastro Intestinal Tract
Accessory Organs
Liver Gallbladder Pancreas Spleen

Gastro Intestinal Tract
Esophagus
 Esophagus is a muscular, collapsible tube about 10 inches long, extending from the pharynx to the stomach.

Lower Esophageal Sphincter
 It is the physiological not the anatomical sphincter at the lower end of esophagus that joins the stomach.  There is only thick layer of circular muscle that relaxes only on swallowing to propel the food to the stomach otherwise it is tonically contracted.

Gastro Intestinal Tract

Gastro Intestinal Tract
Stomach
Dilated part of the GIT between the esophagus and small intestine. A J-shaped distended organ. Has two openings; cardiac and pyloric openings. Has two curvatures; greater and lesser curvatures.

Gastro Intestinal Tract
Parts of Stomach Fundus Body Pylorus

Gastro Intestinal Tract
Small Intestine  Duodenum  Jejunum  Ileum Large Intestine  Caecum  Ascending colon  Transverse colon  Descending colon  Sigmoid colon  Rectum  Anal canal

Gastro Intestinal Tract
Wall of the GIT
A hollow system throughout. Right from esophagus till rectum, the wall of GIT has three layers : Mucosa (inner most) Muscular Layer (middle) Serosa (outer most)

Layers of GI Tract

Gastro Intestinal Tract
LIVER
The largest gland in the body. Functions  Production and secretion of bile.  Involvement in many metabolic activities.  Filtration of blood.  Synthesis of blood clotting factors.

Digestion and Absorption

Digestion and Absorption
Digestion is the process by which the large and complex food substances are broken down into the simpler and smaller form, so that they can be easily absorbed. Food on which the body mainly lives consists of the following: Carbohydrates Proteins Fats

Digestion and Absorption
These substances can not be absorbed in their natural forms so they are broken down into smaller particles with the help of various enzymes and secretions.
Carbohydrates Glucose, Galactose, Fructose Proteins Amino acid Fats Fatty acids

These substances are then absorbed in the small intestine.

Digestion and Absorption
Throughout the GIT, secretory glands are present that secrete various secretions and serve many functions for digestion and absorption of food. They are Saliva Pancreatic secretion Bile Gastric secretion

Digestion and Absorption
 It is the secretion of the stomach.  The stomach mucosa has two important types of tubular glands:  Pyloric Gland  Oxyntic gland

Pyloric Glands
Pyloric glands are located in the pylorus of the stomach. They secrete : Mucus (secreted by Mucus Cells) Pepsinogen (secreted by Chief Cells) Gastrin (secreted by G - Cells)

Oxyntic Glands
Oxyntic glands are located in the mucous membrane of the body and fundus of the stomach. An Oxyntic gland is composed of three different types of cells: Mucous neck cells Peptic (chief) cells Parietal (oxyntic) cells

Oxyntic Glands
Mucous Cells secrete mainly mucus. Chief Cells secrete pepsinogen. Parietal Cells mainly secrete HCl.

Oxyntic Glands

The Parietal Cell

Parietal Cell

Cl- H+ ClNa+ Na+ Na+ Na+ Na+ Na+

H+/K+ ATPase
Na+

K+ ClNa+

Na+

Gastrin

Histamine

Acetylcholine

Parietal Cell

Parietal Cell
Receptors on a parietal cell
Three receptors are present on the membrane of a parietal cell:  Histamine receptors  Acetylcholine receptors  Gastrin receptors

Parietal Cell
Stimulation of gastric acid (HCl) secretion
• The Parietal cells are stimulated by three different things:  Nervous stimulation  Histamine  Gastrin

Parietal Cell
Inhibition Of Gastric Acid Secretion
LOW pH

• Low pH , less than 3.0 in the stomach inhibits Gastrin secretion and thereby inhibits acid secretion.
Drugs  Atropine  H2 receptor blockers  Proton Pump Inhibitors

 When parietal cell is stimulated, a series of changes take place in the cell.

Mechanism of HCl secretion by parietal cell

Step 1  Chloride ions ( Cl -) are transported from cytoplasm into the lumen of the canaliculi to create a negative potential.  The initial stimulation for the transport of these chloride ions is not known however histamine appears to be an important factor.

Mechanism of HCl secretion by parietal cell
Step 2
This negative potential causes diffusion of positively charged potassium ions (K +) from the cell cytoplasm into the canaliculi.

Step 3
Water (H2O) in the cytoplasm dissociates in to hydroxyl ions (OH-) and hydrogen ions (H+)

Mechanism of HCl secretion by parietal cell
Step 4
Hydrogen ions ( H +) are then exchanged in the canaliculi for potassium ions ( K + ). This exchange process is brought about through the presence of an enzyme ( H +, K + , adenosine triphosphatase ), which is also called PROTON PUMP.

Mechanism of HCl secretion by parietal
Thus potassium ions are reabsorbed in to cell the cell cytoplasm and hydrogen ions take their place in the canaliculi. Hydrogen ions then combine with Chloride ions to make HCl. The final secretion in the canaliculi is extremely high in HCl.

Acid Related Diseases

Acid Related Diseases
• Peptic ulcer • Gastroesophageal reflux disease (GERD) • Gastritis • NSAIDs and Peptic Ulcer

Ulcer
Ulcer can be defined as breach in the continuity of the superficial epithelium and exposure of deeper tissues to the external environment.

Ulcer

Ulcer
• Ulcer is an imbalance between Aggressive and Defensive factors The Aggressive Factors (gastric acid secretion) & The Defense Mechanisms (mucosal resistance to acid) of the GI-mucosa

Aggressive

Defensive

Mucus

Pepsin

HCO3
Prostaglandins

Gastric Acid

Gastric Mucosal Blood Flow

Peptic Ulcer
Sites
Duodenum 90 -95 % of duodenal ulcers occur in first portion of duodenum Stomach More than 90% of gastric ulcers occur in the lesser curvature

Esophagus Lower end of Esophagus in reflux esophagitis Jejunum In zollinger Ellison syndrome

Peptic Ulcer

Peptic Ulcer
ETIOLOGY Heredity Acid pepsin vs mucosal resistance. Factors reducing mucous resistance Association with other diseases

Peptic Ulcer
Heredity
Peptic ulcer tends to run in families. Gastric and duodenal ulcers are inherited as separate disorder. In case of family history, duodenal ulcer develops below the age of 20.

Peptic Ulcer
Acid Pepsin Vs Mucosal Resistance
• An ulcer forms when there is imbalance between the aggressive factors (e.g. acid and pepsin) and defensive forces (e.g. mucus, HCO3 and Prostaglandins) a) Abnormal Acid Pepsin Secretion
• Increase secretion of acid is due to the increase secretion of  Gastrin  Histamine  Acetylcholine.

Peptic Ulcer
b. Reduced mucous resistance • Gastric cells secrete mucus , bicarbonates and prostaglandins as protective agents against the acid. • Following factors reduce the mucus resistance
    Helicobacter Pylori NSAIDs Smoking Reflux of bile and intestinal secretions.

Peptic Ulcer
Association With Other Diseases Or Known Factors • Higher incidence in patients with COPD, CRF, Cirrhosis. • Steroids in higher dose. • Severe burns

Peptic Ulcer
Signs & Symptoms
• • • • • • • Pain in epigastrium Heart burning Nausea Anorexia Haematemesis due to ulcer perforation Weight loss Vomiting

Peptic Ulcer
• Both duodenal and gastric ulcer has the same signs & symptoms but they differ in the character of pain.
– In Gastric ulcer pain starts within 15 -20 min after eating. – In Duodenal ulcer pain starts 2-3 hours after eating.

Gastro- Esophageal Reflux Disease (GERD)
• GERD develops when esophageal mucosa is exposed to the gastric contents for prolonged period of time resulting in inflammation and heart burn.

Gastro- Esophageal Reflux Disease (GERD)
Signs & Symptoms • Heart burn • Regurgitation of food in mouth • Iron deficiency anemia

Gastro- Esophageal Reflux Disease (GERD)
Complications • Esophagitis • Benign esophageal sphincter • Barrett’s esophagus • Anemia • Aspiration

GASTRITIS
It is the inflammation of gastric mucosa and if persists leading to the gastric ulcerations and erosions. Etiology  Aspirin and other NSAIDS  Severe stress  Burns  Excessive alcohol consumption

GASTRITIS
Signs & symptoms
• It may be asymptomatic • Anorexia • Nausea • Epigastric pain • Heart burn • Slow loss of blood may lead to anemia • hemorrhage

NSAIDs and Peptic Ulcer
• Some peptic ulcers are caused by prolonged use of nonsteroidal antiinflammatory drugs (NSAIDs) such as
– – – – – Aspirin Ibuprofen Diclofenac sodium Indomethacin Naproxen sodium

NSAIDs and Peptic Ulcer
• Normally the stomach has three defenses against digestive juices:
– Mucus – The chemical bicarbonate and Prostaglandins – Blood circulation to the stomach lining that aids in cell renewal and repair.

• NSAIDs hinder all of these protective mechanisms, therefore digestive juices can damage the stomach lining and cause ulcers.

NSAIDs and Peptic Ulcer
• Prostaglandins are the chemical mediators of Inflammation and Pain • NSAIDs inhibit the enzyme CycloOxygnase that plays an important for the production of Prostaglandins • Some Prostaglandins are gastro-protective and work as house keeping enzyme

NSAIDs and Peptic Ulcer
• Inhibition of those PGs is associated with a decrease in GMBF, HCO3 and Mucus • Ultimately when the defenses of the stomach are weak, Ulcer can occur • NSAID-induced ulcers usually heal once the person stops taking the medication.

ZOLLINGER ELLISON’S SYNDROME
In this uncommon disorder, ulceration occurs due to gastric acid hypersecretion as a result of gastrin secreting tumor mainly arising in pancreas. Signs & symptoms
    Diarrhea may be the presenting feature Epigastric pain Heart burn Bleeding and perforations are common

Helicobacter Pylori & Peptic Ulcer
• H.Pylori infection is the most important factor in peptic ulcer disease. • It is spiral shaped, flagellated, bacteria found in stomach and duodenum. • It accounts for 90% of duodenal ulcer and 70% of gastric ulcer.

Helicobacter Pylori & Peptic Ulcer
H. Pylori causes its effects by: • Increase in fasting and meal stimulated gastrin release. • Increase in parietal cell mass. • Increase in pepsinogen.

Management of Acid Related Diseases

General Measures
Peptic Ulcer  No smoking  Avoid alcohol  Avoid aspirin

General Measures
• GERD
Weight reduction Stop smoking Meals should be of in small volume Avoid heavy lifting and bending after meals  Avoid late night meals to reduce reflux during sleep.    

Pharmacological Treatment
It can be divided into the : • Drugs enhancing the mucosal defense • Acid suppression drugs.

a. Drugs enhancing the mucosal defense
• These drugs act by strengthening the defensive forces of gastric mucosa by increasing the prostaglandin synthesis , increase in mucus and bicarbonate production. • They include the following groups :
 Sucralfate  Antacids  Prostaglandin analogues

a. Drugs enhancing the mucosal defense
Sucralfate
Mechanism Of Action • It forms an adherent complex with proteins in the ulcer base and protects it from further digestion . • It also stimulates mucus , prostaglandin and mucus production.
• Available Brands

• Ulsanic, Ulcocid, Sucrafate, Sucemed.

a. Drugs enhancing the mucosal defense
Antacids
Mechanism Of Action • They contain the Aluminium Hydroxide, calcium carbonate , magnesium salts , sodium bicarbonate. They cause the neutralization of gastric acid and local cooling effect. Available Brands

• Gaviscon, Tricil, Aluphagel, Magalcid

a. Drugs enhancing the mucosal defense
Prostaglandin analogues • Misoprostol is a prostaglandin analogue that promotes ulcer healing by stimulating mucus and bicarbonate secretion and inhibition of acid secretion.

b. Acid Suppression Drugs
• H2 receptor antagonists • Proton Pump Inhibitors

H2 Receptor Antagonists
Mechanism Of Action They are the competitive inhibitors of histamine at H2 receptors on the parietal cells there by decreasing the acid production. They inhibit about 60 – 65% acid production.

H2 Receptor Antagonists
Major drugs Available • Cimetidine Dose Available Brands Ranitidine Dose Available Brands Ranax Famotidine Dose Available Brands Peptiban 400 mg BD or 800 mg at night Cimet , Tagamet, Ulcerex

150 mg BD or 300 mg at night Zantac, Anzol, Renulcid,

20 mg BD or 40 mg at night Famopsin, Polypep, Nocid,

Proton Pump Inhibitors
Mechanism Of Action They bind with the acid secreting enzyme called H+ K+ ATPase (Proton Pump) and inactivate it, thereby inhibiting acid secretion. The PPIs inhibit approximately 90 – 95% of acid production.

Proton Pump Inhibitors
Major Drugs Available • Omeprazole Dose 20 mg OD Available Brands Risek, Omega , Ruling, Omezol • Lansoprazole Dose30 mg OD Available Brands Pantoprazole Dose40 mg OD Available Brands Esomeprazole Dose20 – 40 mg OD Available Brands Rebprazole Dose10-20 mg OD Available Brands

Selanz, Inhibitol, lanzac

Zotonix, Zopent, Protium, Pantazol

Espra, Esopra, Nexium, Esso

Bepra, Rabicid, Zechin, Prompto

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