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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+ K+ Cl-
H+/K+ ATPase
Cl- Na+
Na+ Na+ Na+
Na+

Na+ Na+ Na+


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
Mechanism of HCl secretion by
parietal cell
 When parietal cell is
stimulated, a series of changes
take place in the 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

HCO3
Pepsin
Prostaglandins

Gastric Mucosal
Gastric Acid 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 anti-
inflammatory 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 Cyclo-


Oxygnase 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 400 mg BD or 800 mg at night
Available Brands Cimet , Tagamet, Ulcerex

• Ranitidine
Dose 150 mg BD or 300 mg at night
Available Brands Zantac, Anzol, Renulcid,
Ranax
• Famotidine
Dose 20 mg BD or 40 mg at night
Available Brands Famopsin, Polypep, Nocid,
Peptiban
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 Selanz, Inhibitol, lanzac

• Pantoprazole
Dose40 mg OD
Available Brands Zotonix, Zopent, Protium, Pantazol

• Esomeprazole
Dose20 – 40 mg OD
Available Brands Espra, Esopra, Nexium, Esso

• Rebprazole
Dose10-20 mg OD
Available Brands Bepra, Rabicid, Zechin, Prompto