DR MOHAMMAD NASIR

MBBS(AMC)
LECTURER
PHYSIOLOGY DEPARTMENT
PHYSIOLOGY OF GI DISORDERS
 DISORDERS OF OESOPHAGUS
• PARALYSIS OF SWALLOWING MECHANISMS:

• CAUSES:

Damage to 5th 9th and 10th cranial nerve

• Poliomyelitis
• Encephalitis
• Muscle dystrophy
• Myasthenia gravis
• Botulism
• anesthesia
• EFFECTS:
• No swallowing
• Food enter lungs
• Food enter posterior naries

• ACHALASIA AND MEGA OESOPHAGUS:

• Failure of lower oesophageal sphinctor to
relax
• CAUSE:
• Non functioning of the myenteric plexus in
lower third of oesophagus

• MEGAOESOPHAGUS:
• Distended oesophagus associated with
achalasia
DISORDERS OF THE STOMACH
• GASTRITIS:
• Inflammation of the gastric mucosa

• TYPES:
• Acute and chronic
• Superficial and deep
• CAUSES
• Chronic bacterial infections
• Alcohol
• Aspirin

• CONCEPT OF GASTRIC BARRIER:

• Consist of mucus cell and their tight
junctions
GASTRIC ATROPHY:

• CAUSES:
• Chronic gastritis
• Autoimmune

• EFFECTS OF GASTRIC ATROPHY:

• Hypochlorhydria
• Achlorhydria
• Pernicious anemia
 PEPTIC ULCER
• Excoriated are of mucosa caused mainly
by gastric juices

• COMMONLY EFFECTED AREAS:

• First few cms of duodenum
• Lesser curveture
• Gastroesophageal sphinctor
• BASIC PHYSIOLOGY OF PEPTIC ULCERATION:
• Imbalance between rate of secretion and degree of
protection
•
• PROTECTIVE FACTORS:
• Mucus production
• Bicarbonates of pancreatic juices
• Bile from the liver
• Reverse enterogastric reflex
• secretin
• CAUSES OF PEPTIC ULCERS:
• H pylori
• Alcohol
• Smoking
• Aspirin

• MARGINAL ULCER:
• Ulcer after gastroduodenostomy of
gastrojejunostomy
 PHYSIOLOGFY OF TREATMENT
OF PEPTIC ULCER
• MEDICAL:
• Antibiotics
• H2 receptor blockers
• PPI’S
• Mucaine sucralfates etc

• SURGICAL:
• Vagotomy
• Removal of portion of stomach
 DISORDERS OF SMALL
INTESTINE
• ABNORMAL DIGESTION OF FOOD BY THE
SMALL INTESTINE:
• Failure of the pancreas to secrete pancreatic
juices

• OCCURS IN:
• Pancreatitis:acute and chronic
• Pancreatic duct blokage by gallstone
• Pancreas removal
 MALABSORBTION BY SMALL
INTESTINE-SPRUE
• NONTROPHICAL SPRUE:
• Celiac disease or gleuten enteropathy

• CAUSE:
• Toxic effects of gluten present in wheat and rye

• EFFECTS:
• Direct destructive effects on microvilli and villi
• TROPHICAL SPRUE:
• Occurs in trophical areas

• CAUSE:
• Infectious agent and treated with antibiotics

• MALABSORBTION IN SPRUE:
• Fats called steatorrhea
• Proteins vitamins

• EFFECTS:
• Nutriional deficency,osteomaslacia and anemia
 DISORDERS OF LARGE
INTESTINE
• CONSTIPATION:
• HIRSCHPRUNG DISEASE:
• DIAHORREA:
• Enteritis
• Psychogenic diahorrea
• Ulcerative colitis and crohn disease
 OTHER GI DISORDERS
• VOMITING:
• The process by which the GIT get rid of its
content when almost any part of the upper
GI become excessively irritated over
distended or over excitable.
• TRANSMISSION OF IMPULSES:
• AFFARENT IMPULSES: from vagus and
symphathetic nerves bilateral
vomiting centre of medulla
• EFFERENT IMPULSES:
• Vomiting centre 5th,7th,9th,10th and
12th upper GI
• Vomiting centre spinal nerves
diaphram and abdominal muscles
Connections of vomiting centre
• ANTIPERISTALSIS:
• The start of vomiting

• THE VOMITING ACT:

• Deep breath
• Upper oesophageal sphinctor open
• Glottis closed
• Posterior nares closed
• Diaphram and abdominal muscles contract
• CHEMORECEPTOR TRIGGER ZONE:
• Area located bilaterally on the floor of fourth
ventricle
• Its excitation cause vomiting
• EXCITING FACTORS:
• Electrical
• Drugs like opiods
• Motion sickness
• MOTION SICKNESS:
• Vomiting due to rapidly changing
directions
• MECHANISM:
• Labyrinthine receptors vestibular
nuclei cerebellum CTZ
Vomiting centre