GASTRIC SECRETIONS and PEPTIC ULCER Physiology Slideshow

Surface Mucous Cells

• Line the entire surface of stomach mucosa
• Secrete large quantity of viscoid mucous that coat the stomach mucosa with a gel layer of mucous.
• Provide protection for stomach wall as well as lubrication for food transport.
• This mucous is alkaline in nature so protect stomach wall from acidic secretions—–a part of gastric barrier.

SECRETIONS FROMOXYNTIC/GASTRIC GLAND

Location: In mucosa of fundus and body of

stomach. Cells and their secretions:

PARIETAL CELLS

HCL

SECRETION OF HYDROCHLORIC ACID

STIMULI FOR SECRETION:

1. Parasympathetic stimulation→ release of Acetylcholine
2. Gastrin
3. Histamine

MECHANISM OF HCL SECRETION

1:Water dissociate into OH and H ion,in the cytoplasm of parietal

cell.

2:Hydrogen is actively secreted into the canaliculi in exchange of k (this process is catalyzed by H-K atpase.

3:k normally enter into cell by NA-K atpase pump present on basolateral (extracellular side of member) which then leak into lumen but then recycled back.

1. C02 COMBINE WITH WATER and form carbonic acid in the presence of carbonic anhydrase enzyme WHICH THE DISSOCIATE INTO H AND HCO3.

THIS HCO3 transported into extracellular fluid in exchange of chloride ion.

5:This chloride ion leak into lumen of canaliculi by leak cannels. 6:Water pass into canaliculi from ECF by process of osmosis as canaliculi has more ions

H FORM IN 4^TH STEP COMBINE WITH OH THAT FORM IN 1^ST STEP AND AGAIN FORM WATER

FINAL SECRETION FROM CANALICULI

Final secretion from canaliculi contain:

• Water,
  • Hydrochloric acid (160mmol/L),
  • Potassium chloride and

Small amount of sodium chloride.

INTRINSIC FACTOR

• Intrinsic factor secreted by parietal cells is essential for absorption of vitamin B12 in the ileum.Damage to parietal cell leads to development of achlorhydria (lack of stomach gastric acid secretion) + pernicious anemia (failure of maturation of red blood cells in the absence of vitamin b12 stimulation of bone marrow).

PARIETAL CELLS

PEPSINOGEN

• Secreted by mucous and chief (peptic) cells of oxyntic (gastric) gland.
• When secreted has no digestive activity.
• When come in contact with hydrochloric acid, it is activated and form active pepsin.
• Pepsin functions as proteolytic enzyme in a highly acidic medium (PH 1.8 to 3.5) but above the pH of 5,it has no proteolytic activity and become inactivate.
• Required for protein digestion.

Secrete small amount of pepsinogen and large amount of thin mucus to lubricate food movements as well as to protect the stomach from digestion by the gastric enzymes

PHASES OF GASTRIC SECRETIONS

Gastric secretions occur in three stages:

1. A cephalic phase
2. A gastric phase
3. An intestinal phase
4. Inter digestive phase

GASTRITIS

Gastritis is an inflammation of the protective lining of the stomach

• Inflammation can be
• Superficial (not very harmful) or
• Deep (can lead to atrophy of gastric mucosa, in many long term cases).

What causes gastritis?/pathophysiology

Damage to stomach lining (gastric barrier) allows digestive juices to damage and inflame it , causing gastritis.

Gastric mucosa has two main features:

• it is lined with highly resistant mucous cells that secrete viscid and adherent mucus and
• it has tight junctions between the adjacent epithelial cells.

Together they form gastric barrier

• In gastritis, the permeability of the barrier is greatly increased.

• The hydrogen ions do then diffuse into the stomach epithelium, creating a vicious circle of progressive stomach mucosal damage and atrophy.
• It also makes the mucosa susceptible to digestion by the peptic digestive enzymes, thus frequently resulting in a gastric ulcer

Cause And Risk Factors

The most common cause is helicobacter pylori

It’s a bacterium that infects the lining of the stomach.

Other risk factors include:

1. NSAIDs
2. Tobacco,
3. Increase age,
4. Stress
5. Autoimmune disorders

Complications

• Chronic gastritis can lead to gastric atrophy and loss of stomach secretions.
• Achlorhydria (means simply that the stomach fails to secrete hydrochloric acid).
•    When acid is not secreted, pepsin also usually is not secreted.
• Gastric atrophy may cause pernicious anemia(no intrinsic factor —–no vitamin B12 absorption—RBCs fail to mature)

PEPTIC ULCER

A peptic ulcer is an excoriated area of stomach or intestinal mucosa caused by the digestive action of gastric juice or upper small intestinal secretions.

MOST FREQUENT SITES:

PATHOPHYSIOLOGY

Man basic cause is imbalance between

• The rate of secretion of gastric juice and
• The degree of protection afforded by (1) the gastroduodenal mucosal barrier and (2) the neutralization of the gastric acid by duodenal juices.

Gastroduodenal Mucosal Barrier

Neutralization Of The Gastric Acid ByDuodenal Juices

• Bicarbonate ions secretions from the pancreas Brunner’s glands of duodenum and gall bladder(bile)→neutralize the hydrochloric acid of the gastric juice, thus also inactivating pepsin and preventing digestion of the mucosa.
• When excess acid enters the duodenum, it inhibits gastric secretion both by nervous reflexes and by hormonal feedback system, further ensure neutralization.

Therefore, a peptic ulcer can be caused in

either of two ways:

• excess secretion of acid and pepsin by the gastric mucosa or
• diminished ability of the gastroduodenal mucosal barrier to protect against the digestive properties of the stomach acid–pepsin secretion.

Main Cause Of Peptic Ulcer

• Helicobacter pylori (75% of cases).
• The bacteria penetrate the mucosal barrier by its physical capability to burrow through the barrier and by releasing ammonium that liquefies the barrier and stimulates the secretion of hydrochloric acid.
• As a result, the strong acidic juices of the stomach penetrate into the underlying epithelium and literally digest the gastrointestinal wall, thus leading to peptic ulceration.

Other Causes Of Peptic Ulcer

• Smoking, presumably because of increased nervous stimulation of the stomach secretory glands;
• Alcohol, because it tends to break down the mucosal barrier; and
• Aspirin and other nonsteroidal anti- inflammatory drugs that also have a strong propensity for breaking down this barrier

Treatment Of Peptic Ulcers

• Use of antibiotics along with other agents to kill infectious bacteria and
• Administration of an acid suppressant drug, especially ranitidine, an antihistaminic that blocks the stimulatory effect of histamine on gastric gland histamine2 receptors, thus reducing gastric acid secretion by 70 to 80 percent.

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