PEPTIC ULCER 1

SECRETIN

This hormone is released from the proximal duodenal mucosa into

the blood stream.

- The hormones causes a secretion from the pancreas of bicarbonate,

a similar increase of bicarbonate is also caused in the bile.

- Pepsinogen secretion of gastric mucosa is increased.

- Gastrin and acid secretion from stomach is decreased.

Secretin

Secretin is the hormone that is the main stimulant of bicarbonate and water secretion from the centroacinar cells lining the proximal pancreatic ducts.

Secretin is produced by the S cell in the duodenum and jejunum. This action is stimulated of the release of secretion when the luminal pH of 4.5 or less. Circulating secretin stimulates bicarbonate-rich fluid from the centroacinar cells of the pancreas and from Brunner’s glands in the duodenum.

PEPTIC ULCER

A peptic ulcer is an erosion (break down) of the mucosa of the

gastrointestinal tract located adjacent to acid-secreting cells

and it occurs in the;

*  Lower oesophagus (Barrett's Ulcer)

*  The antrum of the stomach(Gastric ulcer)

*  Duodenum first part(Duodenal ulcer)

*  The jejunum at the margin of a gastrojejunostomy

*  In the ileum at the outlet of a Meckel's diverticulum  bearing

   aberrant gastric mucosa

Duodenal and Gastric ulcer are types of ulcers most often

seen in practice.

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DUODENUM 1 physiology

 

3. DUODENUM

The  duodenum begins at the pylorus and ends to the left  of  the

midline at the level of second lumbar vertebra.

The duodenum is divided into four parts(fig above)

-  the first part is the duodenal bulb and is related posteriorly

   to the common bile duct

-  and opens into the second part

-  The third part crosses the midline

-  and ends in the fourth part to the left of the midline and

   leads into the Duoeno-jejunal junction.

The mucosa of the duodenum has a special feature of many branched

coiled secretory tubules which opens into the crypts, these are

the Brunner's glands, they secrete an alkaline mucus.

- The secretion contains a precursor of trypsin and is activated by

hydrochloric acid,the trypsin is required to break the fibrous

framework of ingested food.

- The duodenum also receives the secretions of the liver (bile) and

pancreas through the ampulla of Vater.

ENDOCRINE FUNCTION Fig.above

Cholecystokinin (CCK)

The arrival of chyme (fats and acids) acts as a stimulant for

release of CCK from distal duodenum into the blood stream.

- This causes contraction of the gallbladder and relaxation of the

sphincter of Oddi.

- It also causes a release of enzyme rich secretion of the

pancreas.

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GASTRIC Physiology 2 Phases of secretion

PHASES

*  The  primary cephalic phase (central) involves a reflex where

   the C.N.S. participates.

   -  The sight, smell or taste of food excites secretion of

      gastric juice through impulses along the vagus nerve.

   -  This mechanism is also brought into action by a fall of

      blood glucose.

   -  This gastric juice is rich in acid and pepsin.

*  The  secondary phase is initiated by the presence of food in

   the stomach.

   -  This reflex is stimulated by the distension of the stomach

      and certain chemical substances (peptones, amino acids,

      caffeine etc.)

   -  This juice secreted is rich in acid.

The transmitter in both these reflexes is acetylcholine, this

local reflex in secondary gastric phase can be prevented by local

anaesthetic application to the antral mucosa.

This action is through histamine and is executed through H2

receptors and is not affected by antihistamine

*  The third phase is hormonal by the liberation of a  polypeptide

   gastrin from antral mucosa.The normal plasma levels of

   gastrin  are 30-60 pg/ml, after feeding they increase to 200-

   400 pg/ml

Gastrin Release

The G cells in the antrum synthesize the peptide gastrin. The release of gastrin is stimulated by intraluminal amino acids as well as di- and tripeptides. The most powerful amino acids are aromatic: tryptophane and phenylalanine. Antral distention also causes the release of gastrin.

During the cephalic phase of acid secretion, stimulated by the senses (sight, smell, and taste) gastrin is released into the systemic circulation through a long neural network involving the vagal nucleus in the thalamus. The neural transmitter for this is the gastrin-releasing peptide (GRP) released from the postganglionic neurouns terminating on the G cell.

There are also D cells in the antrum, that contain somatostatin. Somatostatin acts as a paracrine agent to inhibit the release of gastrin, when the antral lumen is acidified, serving as a negative feedback mechanism to inhibit the release of gastrin. There are some data suggesting that the colonization of the antrum by Helicobacter pylori is associated with increased rate of acid secretion in some patients. One of the mechanisms suggested is related to the ability of H pylori to interfere with this negative feedback mechanism.

There is some evidence that colonistion of antral mucosa by H pylori inhibits release of somatotstatin thus blocking the negative feed back, these patients have hyper gastrinemia and huperacidity.

-  Gastrin is also produced by pancreatic tumors and the high

   levels thus produced give rise to Zollinger-Ellison Syndrome

   leading to peptic ulceration.

HISTAMINE

It seems that Gastrin response of the gastric mucosa is also

mediated through the release of histamine in the vicinity of

parietal cells.

This action of histamine is executed through H2 receptors and is

not affected by antihistamines.

GASTRIN INHIBITORS

*  Gastric inhibitory peptide (GIP) released from duodenum.

   Its initial peak is stimulated by blood glucose and later

   sustained release is evoked by fat in the lumen of duodenum.

*  Vasoactive intestinal peptide (VIP) is present in the entire

   gastrointestinal tract.

   It inhibits gastric secretion.

   This hormone also stimulates secretion of water and

   electrolyte by the pancreas.

   Certain intestinal tumours secreting this hormone cause watery

   diarrhoea and hypokalemia.

*  Glucagon secreted by cells of the islets of Langerhans in the

   pancreas, inhibits gastric secretion and motility of the

   gastrointestinal tract.

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STOMACH secretions cell variety & function

2. GASTRIC(physiology)

 

The stomach functions as three distinct units. 

The fundus and proximal part act as a reservior with absence of motor activity and a volume capacity of 1-1.5 liters. 

The antrum with major motor activity acts as the grinder and separator with wave pattern of 3 per minute. 

The pylorus controls the emptying through its sphincter action. Acid bathing, fats with CCK release hypertonic content decrease gastric emptying 4-6 hours after meal the wave pallers changes to frequent 1-5 per minute lasting 10-20 minutes this last phase effectively empties the stomach.

 

The fundus is the portion of the stomach that secretes acid and intrinsic factor produced by the parietal cells.

 

The distal portion of the stomach, the antrum, contains G cells that secrete gastrin the  endocrine hormone for parietal cell stimulation.

 

Both the fundus and the antrum contain epithelial cells that line the surface mucosa. The primary products of these cells are mucus and bicarbonate, which provides protection against the secreted acid in the gastric lumen.

 

CELL FUNCTIONS AND CONTROL

The cardia, antrum and pylorus produce an alkaline viscid  mucus,

this secretion is not controlled by the stimulus of food.

 

CHIEF CELLS

The  peptic  cells  are serous cells and  show  zymogen  granules

containing pepsinogen the precursor of pepsin.

 

Chief Cell Secretion

The chief cell of the gastric fundus synthesizes pepsinogen. The chief cell can be stimulated by vasoactive intestinal polypeptide (VIP)/ secretin, epinephrine, acetylcholine, and gastrin.

 

In addition to activation of any of these receptor, acid bathing the lumen also stimulates the release of pepsinogen. Pepinogen, on entering the acidic environment of lumen of the stomach, is converted to the active form of the proteolytic enzyme, pepsin.

 

 

THE PARIETAL CELLS 

 

The secretion of these cells closely resembles plasma except that

Na is replaced by H+.

The  H+  and chloride ions are actually  transported  across  the

brush border of the parietal cells.

The control of gastric secretions is in three phases

 

Parietal cell secretion & control;

The secretory surface of the parietal cells is lined with a number of H⁺, K⁺-ATPase units.

 

It is thought that the parietal cell is the only cell in the body that contains this H⁺, K⁺-ATPase.

 

The parietal cell has three main receptors that, when activated, result in stimulation of H⁺, K⁺-ATPase units. These receptors are:

 

1.     The Gastrin receptor also referred to as the cholecystokinin B receptor (CCKB).

2.     The cholinergic (M₃) receptor

3.     The histamine₂ (H₂) receptor

 

It has been found recently, that a primary effector cell for stimulation of acid secretion is the (entero chromofin / ike) ECL cell, which is placed in close proximity to the parietal cells. It also contains the gastrin/CCKB receptor, as well as the cholinergic muscarin M₁ receptor, both of which, when activated, cause the ECL cell to release histamine. Histamine acts as a paracrine agent to activate the H₂ receptor on the parietal cell.

 

The parietal cell can be inhibited by two classes of compounds. The H₂ receptor antagonists block the H₂ receptor on the parietal cell. These are compounds that are similar in structure to histamine, allowing them to bind to the H₂ receptor without activating the cell.

 

A second group of compounds, the substituted benzimidazoles, are direct inhibitors of H⁺, K⁺-ATPase. They are weak bases that enter the lumen, where they are acidified. The acidified form of the substituted benzimidazole then binds irreversibly to a portion of H⁺, K⁺-ATPase, thus inhibiting all forms of stimulation of acid secretion.

 

The parietal cell also synthesizes and releases intrinisic factor which combines with B₁₂ a complex, forming which moves down the gastrointestinal tract where, in the terminal ilium, the components are dissociated and there is active transport of vitamin B₁₂ across the enterovte, into the portal circulation.

 

Patients who have had a near-total gastrectomy or have has resection of their terminal ilium are likely to require parenteral vitamin B₁₂ administration on a routine basis to replace this function, and to prevent the development of a macrocytic anemia.

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STOMACH & DUODENUM 2 lymphatics cell variety & function

1.2 LYMPHATIC DRAINAGE

The  lymphatics follow the arteries and thus the lymph  from  the

upper lesser currature flows to the left gastric and  paracardial

lymphnodes.   Similarly, the antral vessal from lesser  curvature

flow  to the right gastric and suprapancreatic  lymphnodes.   The

greater curvature drains into gastroenpiploic artery lymph  nodes

(Rt  +  Lt).  This knowledge helps to predict  the  direction  of

spread  if  the  site of a tumour is know.  This  also  helps  to

define  the minimum limits of surgery required so as  the  tumour

draining lymph nodes and the lymphatics.

1.3  The parasympathetic supply is through the vagus  nerves  and

stimulates motility and secretion of acid and pepsin (fig16.2a).

1.4  The  wall  of  the stomach has  four  distinct  layers  from

outwards -  the serosa (visceral peritoneum)

-  muscle

-  submucosa

-  and mucosa the inner most layer.

The mucosal structure varies, the fundus has (fig above)

- parietal cells that secrete acid and intrinsic factor.

- Chief cells that secrete pepsinogen

The antral mucosa has

- G cells that secrete gastrin

- Delta cells that secrete somatostatin.

There are in addition in the mucosa

- Goblet cells that secrete mucus.

- Mast cells that store heparin and histamine

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