2. AIM OF DISCUSSION
• Anatomy of Stomach
• Physiology of Stomach
• Definition of PUD
• Aetiology of PUD
• Types of PUD
• Symptoms
• Treatment and Complications.
3. ANATOMY OF STOMACH
Stomach is a J-shaped organ in upper lt. region of abdominal cavity.
In adult life , Stomach is located between T10 to L3 vertebrae.
It is the dilated part of alimentary canal between oesophagus and
duodenum
It is divided into 4 parts :
- CARDIA
- FUNDUS
- BODY (CORPUS)
- PYLORIC ANTRUM
10. NERVE SUPPLY
SYMPATHETIC
T6 to T10 spinal segments
Motor to pyloric sphincter
Carry pain sensation from stomach
PARASYMPATHETIC
Vagus nerve & its branches
Gastric motility
Gastric secretion
11. MICROSCOPIC ANATOMY
Gastric glands:
1. Mucous glands- Located at cardia and secrets mucous.
2. Chief cells – Secrets pepsinogen and stimulated by Vagus.
3. Parietal cells- Secrets HCl and Intrinsic factor and stimulated by Ach,
Gastrin, Histamine.
4. Gastrin cells – Located at distal part, secrets Gastrin and stimulated by
Amino acids.
5. D cells- Secrets Somatostatin which inhibits gastric emptying,
pancreatic secretion and GB contraction.
12.
13.
14. PHYSIOLOGY OF STOMACH
FUNCTION OF STOMACH : -
Reservoir for food
Digestion
Gastric acid production
Slows food entering into duodenum
Absorption of VitB12
15. Stomach contains a number of biologically active peptides in nerves and
endocrine cells.
These are :-
- Gastrin
- Somatostatin
- Vasoactive intestinal peptides (VIP )
- Substance P
16. GASTRIN
Produced by G- cell
Synthesized as prepropeptide and undergo post translational processing
to produce biologically active Gastrin.
Stimulus for secretion are :-
- Amino acids produced from proteolysis
- Gastric distention due to food
- Lumen pH>3.
17. Inhibitors of Gastrin secretion :
- Somatostatin
- Lumen Ph<3
Action of Gastrin :-
Act on parietal cells to secrets HCl in gastric phase
Once gastric distention decreases, there is stimulation of Somatostatin
occurs and attenuating Gastrin secretion.
18. SOMATOSTATIN
It is produced by D-cell.
It is a 14 amino acid peptide.
Actions :-
- Inhibits parietal cell acid secretion directly.
- Inhibition of Gastrin release.
- Downregulation of Histamine release from ECL cells.
Stimulator :- lumen Ph<3.
Inhibitors :- Ach.
19. HISTAMINE
It plays important role in gastric acid secretion by stimulating parietal
cells.
It is stored in acidic granules of ECL cells and Mast cells.
Stimulator :-
-Gastrin
- Ach
- Epinephrine.
Inhibitor :- Somatostatin.
20. GHRELIN
It is a 28 amino acid peptide.
Produced by endocrine cells of the oxyntic mucosa of the stomach.
Some amounts from bowel, pancreas.
It enhances appetite and increase food intake.
It promotes glycolysis and prevent fatty acid oxidation.
Used in treatment and prevention of obesity.
21. COMPOSITION OF GASTRIC SECRETION
Approx. secretion of gastric juice is 1.5 – 2 liter per day
When meal is consumed, it stimulates release of gastric juice from
gastric glands.
Contain water and solutes.
Solutes are inorganic and organic
HCL Pepsin
Sodium intrinsic factor
potassium gastric lipase
bicarbonate
23. Basolateral membrane of parietal cells contain specific receptors for
three major stimulant of acid production.
These are :-
- Histamine
- Gastrin
- Ach
Each stimulant have their own 2nd messenger .
25. CEPHALIC PHASE
It occurs even before food enters the stomach
It results from sight, smell, thought of food.
It accounts for 30% of gastric secretion.
Neurogenic signal transmit through vagus nerve (dorsal
motor nuclei).
26. GASTRIC PHASE
Once food enters the stomach, it excites local enteric reflex, gastrin
mechanism, which causes stimulation of gastric juice secretion.
It accounts for 60% of gastric secretion.
Gastrin is the most important mediator.
Ends when antral mucosa is exposed to acid as the gastrin release stops
and somatostatin release is increased.
27. INTESTINAL PHASE
Presence of food in duodenum or upper part of small intestine,
stimulate stomach to secrete small amount of gastric juice.
This is due to release of gastrin in duodenal mucosa.
It accounts of 10% of gastric secretion.
28. REGULATION OF GASTRIC ACID SECRETION
Stimulated by – acetylcholine, gastrin, histamine.
Inhibited by-
- presence of food in small intestine.
- presence of acid, fat, protein breakdown product.
- secretin.
- gastric inhibitory peptides
- VIP
- somatostatin
29. GASTRIC MOTILITY AND EMPTYING
When food enters stomach the fundus and upper part of body relax and
accommodate the food.
Peristalsis begins in the lower portion of body, mixing and grinding the food and
permitting chyme pass through pylorus and enter the duodenum.
In regulation of gastric emptying the antrum, pylorus, upper duodenum function
as unit.
Contraction of antrum is followed by sequential contraction of the pyloric region
and duodenum.
30. REGULATION
The rate at which the stomach empties into duodenum depends on the
type of food ingested.
Food rich in carbohydrate empties fast
Protein rich food leaves slowly.
And fat containing food leaves stomach very slowly.
The rate of emptying also depends on osmotic pressure of the chyme.
CCK is also an inhibitor of gastric emptying.
31. PACEMAKER OF GASTRIC PERISTALSIS
The source of myogenic activity in GIT has been tracked down to
INTERSTITIAL CELLS OF CAJAL, which act as pacemaker, that
generates slow wave in smooth muscle.
32. PEPTIC ULCER DISEASE
DEFINITION
- It is a sore or disruption in the lining of stomach and duodenum.
- Peptic refers to Pepsin , a stomach enzyme that breakdown protein.
- An ulcer occurs when the lining of stomach and duodenum is
corroded by acidic digestive juice secreted by stomach cells.
34. TYPES OF PEPTIC ULCER
1. DEPENDING ON THE SITE :-
A. Duodenal Ulcer :- Typically occurs in 1st inch of 1st part of
duodenum
B. Gastric Ulcer :- Occurs in the lesser curvature
C. Combined
35. 2. DEPENDING ON THE DURATION :-
A. Chronic peptic ulcer
B. Acute peptic ulcer
36. RISK FACTORS
H. Pylori infection
Use of NSAIDs or Corticosteroid.
Smoking
Alcohol
Physical stress
Family history of PUD
Increased salivation (water brash).
Gastrinoma (ZE Syndrome)
37. PATHOPHYSIOLOGY
H. PYLORI :-
It is a gram –ve, spiral shaped organism.
Lophoflagellate, so moves rapidly in gastric lumen.
It uses an adhesion molecule (Bab A) to bind to the Lewis AAg on
epithelial cells.
Transmission route is via gastric refluxate.
38. It produces Urease enzyme which cause breakdown of urea and
produces ammonia and thus raising pH .
The bacteria stimulate chronic gastritis by provoking local
inflammatory response underlying epithelium.
Infection occurs in childhood but remain asymptomatic and only few
people develop clinical disease.
39. VIRULENCE FACTOR :-
1. Vacuolating cytotoxin A (vacA) => Increase permeability.
2. Cytotoxin associated gene A (cag A) => Apoptosis.
3. Adhesins (BabA).
4. Outer inflammatory protein A (oipA).
40.
41. NSAIDs :-
Three patterns of mucosal damage are caused by NSAIDs.
These are :-
- Superficial erosion
-Haemorrhages
- Silent ulcers.
42. They acts mainly by inhibiting prostaglandins synthesis.
Inhibits enzyme COX1 & COX2.
Prostaglandin provide a protective layer over gastric mucosa.
43. SMOKING :-
Nicotine increases parasympathetic activity => stimulate G cell and
ECL cells => Increased secretion of gastrin and histamine.
Increased rate of gastric emptying.
Decreased pancreatic bicarbonates secretion
Reduce mucosal blood flow.
Inhibition of mucosal PGs.
44.
45. ACID PEPSIN VERSUS MUCOSAL RESISTANCE
An ulcer forms when there is an imbalance between aggressive and
defensive factors.
Aggravating Factor :-
- ACID (HCl)
- PEPSIN
Defensive factor :-
- MUCOSAL BARRIER
46.
47.
48. CLINICAL FEATURES
Epigastric pain (MC)
- Gastric ulcer pain is associated or closely followed by meal.
- Duodenal ulcer pain is relieved by food.
- Duodenal ulcer pain is hunger pain and awaken the pt. at night.
- Burning in nature
- May radiates to back (consider perforation)
Chest discomfort
Dyspepsia
50. INVESTIGATIONS
Routine investigations
Endoscopy +/- biopsy.
H. Pylori detection tests
- urea breath test
- stool antigen test
Radiology
- CXR Digital PA view – if perforation is suspected.
- Double contrast barium radiography.
51. Cont…
Serum Gastrin level – value >200pg/ml is high.
Measurement of gastric acid production.
USG of abdomen
52.
53. UREA BREATH TEST :-
- It is based on urease activity in the stomach.
- Urease hydrolyses urea to form ammonia and CO2.
- Ingest urea labelled with radioactive Carbon.
- Hydrolysis of urea => labelled CO2.
- Rapidly absorbed into blood and within a few minutes, appear in breath
54. COMPLICATIONS
Bleeding Peptic ulcer.
Peptic Perforation.
CDU leading to Pyloric Stenosis
Intractable PUD
ZE Syndrome
62. TRIPLE THERAPY
Omeprazole 20mg/ Lansoprazole 30mg BD
Clarithromycin 500mg BD.
Amoxicillin 1gm/ Metronidazole 400mg BD.
Given for 14 days followed by PPI for 4-6 wks.
65. PROTON PUMP INHIBITORS
Disrupt chemical binding in stomach cell to reduce acid production,
lessening irritation and allowing ulcer to heal.
Drugs include :-
- Omeprazole
- Rabeprazole
- Pantoprazole
- Lansoprazole
- Esomoprazole
66. H2 – RECEPTOR ANTAGONISTS
Commonly prescribed anti-ulcer drugs.
It includes :- Cimetidine, Ranitidine, Famotidine.
Food and antacid reduces absorption.
It acts by blocking Histamine from stimulating acid secreting parietal
cells.
Reduces gastric acid secretion and prevent stress ulcers.
67. ANTACIDS
Work locally in stomach by neutralising gastric acid.
Relieve pain and promote healing
Reduces the total amount of acid in GI Tract
These includes :-
- Magnesium hydroxide and aluminium hydroxide.
- Sodium bicarbonate.
- Calcium carbonate.
- Simethicone.
69. MUCOSAL PROTECTIVE AGENTS
BISMUTH COMPOUNDS :-
Tripotassium dicitratobismuthate
Colloidal Bismuth subcitrate.
SUCRALFATE :-
It is a complex of aluminium hydroxide and sulphated sucrose
Act by protecting the mucosa from acid pepsin attack
70. GENERAL MEASURES
Avoid cigarette smoking
Avoid alcohol
Avoid NSAIDs groups of drug.
Avoidance of coffee and tea.
Uses fibre rich diet.
Wash hand after using bathroom and before eating and cooking food.
71. SURGICAL TREATMENT
INDICATION FOR SURGERY :-
- Peptic Perforation
- Haemorrhage
- Pyloric stenosis
SURGICAL OPTIONS :-
- Billroth II Gastrectomy
- Gastrojejunostomy
- Truncal Vagotomy and drainage.
72. BILLROTH II GASTRECTOMY
Two – third of stomach is removed
Duodenum stump is closed
Stomach anastomosed with jejunum.
73. TRUNCAL VAGOTOMY AND DRAINAGE
Section of Vagus nerve, which are critically involved in secretion of
gastric acid.
Reduces the maximal acid output by 50%