Scribd
Upload
13 views25 pages

Gastric Juice

The document provides an overview of gastric juice, including its composition, secretion mechanisms, and the gastric mucosal barrier. It discusses factors affecting gastric secretion, gastric emptying, and hunger contractions, as well as the role of intrinsic factor in vitamin B12 absorption. Additionally, it covers the phases of gastric secretion and the migrating motor complex involved in intestinal motility.

Uploaded by

farej4345
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
13 views25 pages

Gastric Juice

The document provides an overview of gastric juice, including its composition, secretion mechanisms, and the gastric mucosal barrier. It discusses factors affecting gastric secretion, gastric emptying, and hunger contractions, as well as the role of intrinsic factor in vitamin B12 absorption. Additionally, it covers the phases of gastric secretion and the migrating motor complex involved in intestinal motility.

Uploaded by

farej4345
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
You are on page 1/ 25

Gastric juice

Learning objectives
• By the end of this lecture students should be able to:

• List the composition of gastric juice.


• Describe the gastric mucosal barrier and its damaging factors.
• List types of gastric gland.
• Understand the mechanism of HCL secretion.
• Describe factors that stimulate and inhibits gastric secretion.
• Discuss the phases of gastric secretion
• Describe gastric emptying and how gastric and duodenal factors
affects it.
• Define hunger contractions and list its causes.
• Discuss migrating motor complex.
Gastric juice
• It is secreted by gastric gland
• 2 liters of gastric juice is secreted daily
• PH 1.5-3.5 (strongly acidic)
• Composition of gastric juice :
• 1.Water.
• 2.Mineral salts.
• 3.Mucos .
• 4. Hydrochloric acid.
• 5.Intrinsic factor.
• 6.Enzyme pepsin.
• Intrinsic factor secreted by parietal cells of gastric
glands plays an important role in erythropoiesis.

• It is necessary for the absorption of vitamin B12 from


GI tract into the blood.

• Vitamin B12 is an important maturation factor during


erythropoiesis.

• Absence of intrinsic factor in gastric juice causes


deficiency of vitamin B12, leading to pernicious
anemia
Gastric mucosal barrier
1. Alkaline mucous, 1 millimeter thick.
2. The mucosal cell membrane protects the stomach wall
and prevent diffusion of HCL thus (preventing auto
digestion).

3. The mucus gel layer together with the HC03- secreted


by the surface mucosal cells constitute a mucosal barrier
that protects the gastric mucosa against damage by
gastric HCI (through increasing the pH from 1-2 at the luminal
side to 6-7 at the surface of the epithelial cells).
Damaging factors are
• Helicobacter pylori (H. pylori).
• nonsteroidal antiinflammatorydrugs (NSAIDs)
• Stress.
• Smoking.
• alcohol.
• Zollinger Ellison syndrome
(tumor in pancreas which produce excessive
amount of HCL)
Gastric glands
• Gastric glands that secrets gastric juice:
a) Oxyntic (Gastric) glands:
• 1. Mucous neck cells.
• 2.Oxyntic (parietal) cells.
• 3.Peptic (chief) cells.
• 4. Enteroendocrine cells.
• B) pyloric gland
• Secrets mucous and gastrin
Mechanism of Hydrochloric acid (HCL)
secretion

• The main driving force for hydrochloric acid


secretion by parietal cells is hydrogen-
potassium pump adenosine triphosphates (H+
-K+ ATPase).
Mechanism of gastric HCL secretion
Parietal cells secrete HCl into the lumen of the stomach and absorb
HCO3 - into the bloodstream as follows:

(1) C02 combines with H20 forming H2C03 by activity of the carbonic
anhydrase enzyme (which is abundant in the parietal cells). The formed
H2C03 then dissociates into H+ and HC03-.

(2) H+ is pumped into the lumens of the canaliculi in exchange for K+ by


activity of H+ K + ATPase. while HC03- is extruded into the interstitial
fluid in exchange for CL- (by an antitiport).

(3) CL- then diffuses into the canaliculi (where it combines with H+
forming HCL which enters the gastric lumen).
Mechanism of Hydrochloric acid (HCL)
secretion
Factors that stimulate gastric
secretion
 Food ingestion (specially if associated with increased
appetite)
 Food entry into the stomach (mainly through liberation of
the gastrin hormone) as well as taking alcohol or caffeine
(directly stimulate the gastric mucosa)
 Certain emotions e.g. anger and anxiety (through
impulses from the hypothalamus that stimulate the vagus
nucleus in the medulla).
 Hypoglycemia (through stimulating the feeding centre in
the hypothalamus which in turn stimulates the vagus
nucleus).
Factors that inhibit gastric
secretion
• Reduction of the PH in the pyloric antrum below 2 , which
inhibits release of the gastrin hormone.

• Duodenal distention as well as presence of excess acid, fat,

• Certain emotions e.g. fear and depression (through impulses


from the hypothalamus that inhibit the vagus nucleus).
Pepsinogen
Activation &
Protein
Digestion
Optimum pH for activation of
pepsinogen is below 6.

Protein digestion
starts in stomach 16
Phases of Gastric Secretion

Stimulatory, via vagus account for


30% of gastric acid secretion

Stimulatory via gastrin, account for


60% of gastric acid secretion

Intestinal Fat, acid,


phase of hypertonicity,
Inhibitory via reverse enterogastric
gastric distention reflex,
secretion
CCK and secretin 17
Gastric Emptying

18
Gastric Emptying
Gastric emptying
 The amount of chyme that escapes into the duodenum with each
peristaltic wave before the pyloric sphincter closes depends largely on the
strength of peristalsis.

 Gastric peristalsis occurs at a rate of 3-4 /minute and is coordinated by the Basic
electric rhythm (BER) of the stomach.

 The peristaltic waves start at the upper stomach and proceed towards the antrum
where they become much stronger (pyloric pump)

 They continue in the pyloric canal and result in grinding and propulsion of the
gastric contents into the duodenum through the pylorus.

Gastric mixing
Gastric mixing takes place in the thick-muscled antrum as a result of vigorous
peristaltic contractions against the almost closed pyloric sphincter
19
Regulation of gastric Emptying
(1 ) Gastric factors :

(a) Degree of gastric distention :


 Within limits, the greater the volume or the gastric content, the
more rapid will be the rate of its emptying.
 distention of the stomach initiates both vago vagal and local enteric
Reflexs that stimulate gastric peristalsis and accelerate gastric
emptying.

(b) Consistency of the gastric contents : Fluids are evacuated more


rabidly than solid foods.
B. Duodenal factors: (Enterogastric reflex)

(1) Degree of duodenal distention: Excessive duodenal distention


delays gastric emptying through the enterogastric reflex

(2)Type of food in the duodenum: Presence of excess fat in the


duodenum delays gastric emptying through stimulating release of the
hormones that inhibit gastric motility.

(3) Duodenal acidity execcsive duodenal acidity delays gastric


emptying by both stimulating release of the gastric inhibitory
hormones and initiating the enterogastric reflex.

(4) Duodenal osmolality : hyperosmolality and hypoosmolality (to a


lesser extent) stimulate certain duodenal osmoreceptors that lead to
delayed gastric emptying mainly through initiating the enterogastric
reflex.
This prevents rapid flow of non-isotonic fluids into the small intestine
(which disturbs the electrolyte balance).
C. Other factors :
(1) Stimulation of pain receptors results in reflex inhibition of the
gastric motility (thus delaying its empting).

(2) Emotoinal states : excitcment, anxiety and anger accelerate gastric


emptying while fear and depression slow it.

(3) Chemical factors : Gastric emptying is accelerated by cholinergic


drugs, alcohol, bicarbonate and coffee while it is delayed by adrenergic
drugs, atropine and excessive smoking.

Hormonal :
Hormones from the duodenal mucosa that inhibit gastric secretion and
motility include: CCK, secretin, somatostatin and GIP ( = Gastric
inhibitory polypeptide)
• Hunger contractions:
• stomach has been empty for several hours or
more.
• They are rhythmical peristaltic contractions in the
body of the stomach
• When become successive they fuse to become
continuing tetanic contraction lasts 2-3 minutes
• Greatest intensity in 3-4 days and then weakens.
Causes of hunger contractions

 Hunger contractions are produced as a result of strong vagal


stimulation to the stomach. This occurs as following:

 After several hours of fasting, hypoglycemia tends to occur and


activates the feeding centre in the hypothalamus which stimulates
the vagus nucleus in the medulla oblongata .

 hunger contractions are only associated with the sensation of


hunger but they are not its cause.

 hunger is felt as a result of Stimulation of the feeding centre and


other higher centres.
The migrating motility complex
 Between-meal motility

 Consists of weak, repetitive peristaltic waves that move a short


distance down the intestine before dying out.

 Start at the stomach and migrate down the intestine.

 Intestinal housekeeper: sweeping any remnants of the preceding


meal plus mucosal debris and bacteria forward toward the colon.

 Regulated by hormone motilin

 Absence of MMC associated with gastroparesis, intestinal


pseudo-obstruction, and bacterial overgrowth

25

You might also like