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1
Q

Anatomically, the stomach is usually
divided into two major parts:

A
  1. The body 2. The antrum.
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2
Q

Physiologically, it is more appropriately
In
divided into:

A
  1. The “orad” portion, comprising about
    the first two thirds of the body
  2. The “caudad” portion, comprising the remainder of the body plus the
    antrum.
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3
Q

Motor Functions of the Stomach

A

1) Storage of large quantities of food until the food can be processed in the stomach, duodenum, and lower intestinal tract.
(2) Mixing of food with gastric secretions
until it forms a semifluid mixture called “chyme”.
(3) Slow emptying of the chyme from the stomach into the small intestine at rate suitable for proper digestion and absorption by the small intestine.

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4
Q

he body of the stomach contains:

A
  1. Chief or peptic cells (pepsinogens).
  2. Oxyntic or parietal cells (Hcl &
    intrinsic factor).
  3. Mucous cells (Mucus alkaline
    secretion which protects the mucosa).
  4. Argentaffin cells or enterochromaffin
    like cells; ELC (unknown function).
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5
Q

Innervation of stomach
Parasympathetic , Sympathetic

A
  1. Parasympathetic (vagus).
    - Secretory to juice rich in acid & mucus.
    - Motor to wall & inhibitory to sphincters.
  2. Sympathetic (greater splanchnic nerve)
    - No effect on secretion.
    - Inhibitory to wall & motor to sphincters.
    - VC to blood vessels with decreased blood
    flow which returns back to normal by
    autoregulatory escape mechanism (effect increaseactivityof VC
    of local metabolic vasodilators).
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6
Q

Composition of gastric juice

1 . Volume 2. pH 3. Specific Gravity 4.Water 5. Inorganic 6. Organic

A

1 . Volume : about 2.5 L /day.
2. pH : acidic (1).
3. Specific Gravity: 1002 – 1004 .
4.Water: 99 %.
5. Inorganic: Hcl, Na+, K +, Mg+, So4-, Po4-
6. Organic: enzymes , mucin &
intrinsic factor.

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7
Q

Gastric enzymes

A
  1. Pepsinogens: proteolytic enzymes which digest proteins into peptones & proteoses.
    - It causes digestion of milk proteins.
    (Caseinogen + Hcl + Ca2+ calcium paracaseinate = milk clot.
    - It has 3 Types (I,II and III). - Optimum pH: 1.5 – 3 (it doesn‟t act in the intestine „‟alkaline‟‟ medium).
    2 . Chymosin or Rennin
    Proteolytic enzyme (milk clotting enzyme).
    Not present in human. Present in young animals.
    Optimum pH 6.
  2. Lipase: - It doesn‟t act in the stomach as its optimum pH is 5 (pH of the stomach is 1.5 ).

4-Lysozyme: antibacterial enzyme.

5-Intrinsic factor - Glucoprotein which combines with vitamin B12
(extrinsic factor) to help its absorption in
the terminal ileum.
6-Mucin: (soluble & insoluble). - Is a mucopolysaccharide which protects
the gastric mucosa.

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8
Q

Mechanism of gastric secretion

A

Cephalic phase brains
(Nervous)

  1. Gastric phase
  2. Intestinal phase (Hormonal)
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9
Q

Cephalic phase
(Nervous)

A

Conditioned reflex - Proved by Pavlov „ s experiment.
Cortex:
Diencephalon
Limbic system
Anterior hypothalamus
Vagal efferent impulses

Unconditioned reflex:
Stimulus: presence of food in the mouth
• Receptors: Taste buds.
• Afferent: 7 th & 9th cranial nerves.
• Centre: dorsal vagal nucleus in medulla
oblongata
• Efferent: Vagus nerve.
Proved by “ sham feeding experiment”

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10
Q

Gastric phase

A

1- Occurs when food reaches the stomach.
1. Mechanical distension of the pyloric antrum.
2. Chemical stimulation of the pyloric mucosa by products of protein digestion.
• lead to secretion of GASTRIN hormone from
G cells of the pyloric antrum (direct or by local axon reflex) i.e. hormonal.

  1. Nervous mechanism including the vagus
    nerve reflexes and local nervous reflexes.
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11
Q

Intestinal phase (Hormonal)

A

1-Intestinal gastrin:secreted from the duodenal mucosa in response to chemical stimuli (direct or by local axon reflex).
2. Gastric gastrin: - secreted in response to secretagogues absorbed from the small intestine.
- Secretagogues are chemical substances (products of digestion) which are absorbed into the blood from the small intestine and reaches the G cells in the pyloric antrum to stimulate gastrin H. secretion

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12
Q

Regulation of Gastric Secretion
Gastric secretion is stimulated by
…….,…….,…….

A

Gastric secretion is stimulated by neural, paracrine and endocrine

• Acetylcholine stimulates HCl
secretion by acting on muscarinic
cholinergic receptors (increase intracellular calcium). • Also, it stimulates the secretion of
mucus, pepsinogen and gastrin

Histamine stimulates HCl
secretion By acting on H2
receptors in gastric mucosa
(increase cAMP)

• Gastrin stimulates HCl secretion
(1500 times more powerful
compared to histamine)

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13
Q

Regulation of Gastrin Secretion

A

Vagal control
- Antrum acidification
- peptides and amino acids

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14
Q

Regulation of Histamine Secretion

A
  • Gastrin and acetylcholine stimulate histamine release from enterochromaffin- like (ECL) cells
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15
Q

Functions of gastrin hormone

A
  1. Stimulation of: a. growth of gastric mucosa.
    b. gastric acid & pepsin secretion.
    c. gastric motility.
    d. bile secretion & pancreatic secretion (both exocrine & endocrine).
    e. gall bladder evacuation.
    f. calcitonin hormone secretion.
  2. Contraction of the cardia (LES).
  3. VD of gastric blood vessels.
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16
Q

Functions of gastric
HCl

A
  1. Activates pepsinogens into pepsin.
  2. Has antibacterial activity.
  3. Hydrolysis of food material.
  4. Stimulates bile flow & pancreatic
    secretion (by release of secretin
    hormone from the upper part of small intestine).
  5. Helps absorption of calcium (as it ionizes
    ca2+ & prevents its precipitation)
  6. Helps absorption of iron (as it reduces;with vit C; ferric into ferrous ions which are easily absorbed).reduce It
  7. Regulates evacuation of the stomach as
    excessive duodenal acidity delays gastric emptying.
  8. Causes clotting of milk in the stomach to stay for long time to be digested by the proteolytic enzymes.
17
Q

Inhibition of gastric secretion

  1. Enterogastric reflex:
A
  1. Enterogastric reflex:
    Stimulus: - Distension of the small intestine.
    • Presence of acid & products of protein
      digestion in the upper part of the Inhibition small intestine or irritation of its
      mucosa.
      Effect:
      inhibition of gastric motility & acidity.
      • This reflex is mediated by myenteric
      plexus, sympathetic & vagus.
18
Q

Inhibition of gastric secretion

  1. Enterogastrone hormone:
A

other inhibitory intestinal hormones
e.g. secretin, cholecystokinin (CCK),
gastric inhibitory polypeptide (GIP) and
vasoactive intestinal polypeptide (VIP).

  • Stimulus: Presence of fats & hypertonic solutions
    (as glucose) in the upper part of the
    small intestine.
19
Q

The protective gastric mucosal barrier
is mainly caused by two specific
features of the gastric mucosa:

A
  1. It is lined with highly resistant mucous
    cells that secrete a viscid and adherent mucus.
  2. It has tight junctions between the
    adjacent epithelial cells.
20
Q

Mucosal Barrier-Integrity of Mucosal Barrier

Weakens

A

Helicobacter pylori, aspirin, ethanol, NSAIDs, and bile salts

21
Q

Mucosal Barrier-Integrity of Mucosal Barrier

Strengthens

A

secretion, gastrin PGs and epidermal growth factor (EGF) , Mucus, HCO3

22
Q

Gastric movements

A
  1. Fasting movements.
  2. Receptive movements.
  3. Digestive movements.
23
Q

Fasting movements

A
  1. Tonus rhythm: - Insensible gastric contraction that
    occurs during fasting at a rate of 2-4 /min.
  2. Hunger contraction:- Sensible mildly painful contractions associated with hunger sensation.
    - It occurs in the body)) of the stomach.
    - Tonus rhythmic contraction is changed
    to strong rhythmic contraction.
    - It occurs in groups (30-40 sec)
    alternate with peroids of rest.

When the successive contractions
become extremely strong, they often
fuse to cause a continuing tetanic
contraction that sometimes I
lasts for 2 to 3 minutes.

Hunger contractions are due to strong
vagal stimulation due to hypoglycemia.
Hunger sensation is due to stimulation of feeding center by hypoglycemia.

24
Q

Receptive relaxation

A

Is initiated by movements of the pharynx
& esophagus during swallowing &
increases when food enters the stomach.

It occurs mainly in the (fundus & body) of
the stomach (proximal part).

25
Q

Digestive movements

A

Peristaltic movements:
- It occur after food intake.
- It start from the middle of the body)) of the stomach to the pylorus in the form of peristaltic wave (wave of contraction preceded by wave of relaxation).
- They reach the pylorus in about 15- 30 sec.
2. Antiperistaltic movements: - It start from the pylorus towards the fundus.

26
Q

Functions of peristalsis:

A

1 . Mixing the gastric contents with digestive juices.
2. Grinding the food.

27
Q

Functions of antiperistalsis:

A
  1. Return of undigested food to the stomach.
  2. Mixing the gastric contents with digestive juices. 3. Grinding the food.
28
Q

Factors affecting emptying (evacuation) of the stomach

A
  1. Nervous factors (innervation): **increased Vagus
    ** decreases Sympathetic
  2. Emotions: decreased due to Sympathetic overactivity. Chronic emotions cause nervous dyspepsia.
  3. Pain decreases
  4. Degree of gastric distension: (Starling law of the stomach)
    - Increased in Moderate distension in -decrease in Overdistension
  5. Consistency of the diet:increased Fluids pass very rapidly followed by semisolid food then solid food.
  6. Nature of the diet: decreased in Fats & concentrated sugars
    Carbohydrates are rapidly evacuated followed by proteins & then fats.
  7. Enterogastric reflex & enterogastrone hormone decreases
  8. Chemical factors:
    Increased Insulin, parasympathomimetic drugs, alcohol, caffeine & bicarbonate
    Decrease Smoking, adrenergic drugs & anticholinergic drugs

Physo GIT (9 decks)

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