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A. Parts of the stomach

Cardia or cardiac orifice :

The part where the oesophagus enters the stomach is called the cardiac orifice or cardia. Fundus :

The portion of stomach which lies above the cardiac orifice is called the fundus.

Body :

The portion of the stomach below he fundus is called the body of the stomach. Pyloric antrum or antrum/pyloric sphincter

At the end of the body of the stomach is the pyloric antrum or simply called the antrum. The pyloric antrum leads into the pyloric canal. The pyloric canal opens into the duodenum and the opening is guarded by a sphincter called pyloric sphincter.

Incisura angularis

A small notch on the lesser curvature between the body and the pyloric antrum is called incisura angularis.

A straight line from the incisura angularis to the greater curvature separates the pyloric antrum from the body.

3. Gastric glands

The shape and structure of the gastric glands is different in different parts of the stomach. In the fundus and the

body, the glands are long and straight. In the pylorus and in the cardiac area, the glands are short and tortuous.


Four different types of cells are present in the gastric glands; these are :

  1. Parietal or oxyntic cells
  2. Chief or zymogen cells
  3. Mucous cells
  4. Argentaffin cells
  5. In the cardiac and pyloric regions

Here, the glands secrete mucous

In the body and fundus

Here, the glands also contain parietal (or oxyntic cells) à which secrete HCl and intrinsic factor and chief or zymogen or peptic cells  à which secrete pepsinogensThese secretions mix with mucus secreted by the cells in the neck of the glands. Many such glands open on the gastric pit; the gastric pit in turn opens on the surface of the mucosa. 


iii. Surface epithelium

The surface epithelium contains mucous cells; these secrete mucous and bicarbonate. Food is stored in the stomach, mixed with acid, mucus and pepsin, and released at a controlled steady rate into the duodenum.


4. Function of HCl

  1. Kills many ingested bacteria
  2. Provides the necessary ph for pepsin to start protein digestion
  3. Stimulates the flow of bile
  4. Activates pepsinogen to pepsin 

5. Blood supply and lymphatic supply

The stomach has a very rich blood and lymphatic supply.  Blood is supplied by the cardiac arteries. Lymph drains into the gastro-duodenal group and celiac group of lymph glands. Nerve supply


6. Sympathetic

This is from the celiac plexus; the sympathetic supply causes

  1. Relaxation of the muscle
  2. Contraction of the sphincters
  3. Vasoconstriction  

7. Parasympathetic

This comes from the dorsal nucleus of the vagi located in the floor of the fourth ventricle.  The right vagus supplies the posterior surface and the left vagus supplies the anterior surface. They synapse with the myenteric and Meissner’s plexuses. Post-ganglionic fibres start from here and supply the gastric glands.


8. The parasympathetic supply causes

  1. Contraction of the muscle
  2. Relaxation of the sphincter

9. Local nervous system

These are the myenteric and Meissner’s plexuses. Peristalsis is mainly coordinated by the local plexus.

Gastric juice Amount = about 2500 ml per day; During meals, the gastric secretion is maximum and during sleep, it is minimum.

pH = about 1.0 Composition


The contents of the normal gastric juice in the fasting state are

a. Inorganic :

Cations are Na, K, Mg, H;

Anions are Cl-, HPO42-SO42-


b. Organic

Pepsins, lipase, mucus, intrinsic factor

HCI Secretion

As mentioned above, HCl is secreted by the parietal cells.  Content of H in parietal cell secretion Pure parietal secretion has pH of about 0.87 and contains 0.17 N HCl. It is isotonic with plasma (with 150 meq of H and 150 meq of Cl per liter).


Note : The pH of the cytoplasm of the parietal cells is 7.0 to 7.2


Plasma : H concentration = 0.00004 meq/L ; Cl concentration = 100 meq/L

The above-mentioned figures show that there is a very large H gradient against which the parietal cell has to secrete H; thus, the transport mechanism is active. The active transporter is H – K ATPase. Structure of the parietal cell

The parietal cell has

i. Apical membrane

This faces the lumen of the gastric glands; it contains the H-K ATPase

ii. Canaliculi

The resting cell has intracellular canaliculi, which open on the apical membrane of the cell

iii. Tubulo-vesicular structures

At rest The parietal cells contain abundant tubulo-vesicular structures; these structures contain H-K ATPase in their walls.


10. During stimulation of the parietal cells

  1. The tubulovesicular structures move to the apical membrane and fuse with it; this helps in inserting many more H-K ATPase molecules into the apical membrane. These H-K ATPase molecules are now exposed to the K in the ECF; this activates the H-K ATPase and the H-K exchange begins.
  2. Many microvilli project into the canaliculi; this greatly increases the surface area of the cell membrane in contact with the gastric lumen.

Basolateral membrane

This is in contact with the interstitial fluid.


11. Mechanism of HCl secretion

  1. Secretion of H secretion
    As mentioned above, this is done by H-K ATPase.
    The H is initially formed inside the parietal cell as follows :
    CO2 + H2 O    -- H2 CO3    --  H+  HCO3-                                                            

The above reaction is catalyzed by carbonic anhydrase; the parietal cells a high content of carbonic anhydrase. The HCO3-  is extruded from the basolateral membrane into the interstitial fluid in exchange for Cl- (by HCO3 Cl antiport).

Because of the efflux of HCO3 into the blood, the stomach has a negative respiratory quotient; in other words, the amount of CO2 in the arterial blood is greater than the amount in gastric venous blood. When gastric acid
secretion is elevated after a meal, sufficient H may be secreted to raise the pH of systemic blood and make the urine alkaline (post-prandial alkaline tide)


b. Secretion of Chloride

i. Chloride is extruded down its electrochemical gradient into the lumen through channels that are activated by cAMP. 

ii. In the gastric lumen, the H and Cl combine to form HCl.


12. Factors affecting HCl secretion

a. HCl stimulants

  1. Histamine
    This stimulates acid secretion by acting via H2 receptors the H2 receptors stimulate Gs protein increases adenylyl cyclase activity increases intracellular cAMP stimulates protein kinases stimulates H-K ATPase increases HCl output
  2. Acetylcholine
    This stimulates acid secretion by acting via M3 muscarinic receptors this in turn increases intracellular free calcium stimulates protein kinases stimulates H-K ATPase increases HCl output.
  3. Gastrin
    Gastrin increases HCl output in two ways :
  4. Direct action :
    via the gastrin receptors on the parietal cells this in turn increases intracellular free calcium stimulates protein kinases stimulates H-K ATPase increases HCl output.
  5. Indirect action (via ECL cells)
    This is the main way by which gastrin increases HCl secretion. Gastrin stimulates the gastrin receptors on the enterochromaffin-like (ECL) cells. 

13. ECL cells :

  1. These are the vesicle- and granule containing cells; the ECL cells are the predominant endocrine cell type in the
  2. acid-secreting portion of the stomach.
  3. Stimulation of ECL cells stimulates histamine secretion which in turn stimulates HCl secretion.
  4. ECL cells undergo hypertrophy when gastric acid secretion is suppressed for prolonged periods.
  5. The different intracellular mediators interact with each other; thus, activation of one receptor type potentiates the response of another receptor type. 

i. HCl inhibitors

  • Somatostatin : this inhibits ECL cells.
  • PGE2 : acts via Gi to decrease adenylyl cyclas222e activity and decrease intracellular cAMP.
  • EGF and TGF : these also act via Gi.
  • High acidity, H2 blockers, and atropine also decrease
  • HCl secretion.

Organic constituents of the gastric juice

1. Mucous

This is of two types

  1. insoluble or visible mucous : it is a polymer of glycoprotein with a high viscosity; it is secreted by the surface epithelial cells and forms a 0.5 to 2.5 mm thick layer. It protects the gastric mucosa from the acid.
  2. Non-parietal secretion includes the mucous, enzymes, and electrolytes. When HCl combines with either salts or other substances, it gets neutralized and produces neutral chloride.
  3. soluble mucous : this is secreted by the mucous neck cells and acts as a vehicle for HCl and other enzymes secreted by the gastric glands.       

2. Intrinsic factor

This is secreted by the parietal cells. It is a glycoprotein required for the absorption of vitamin B12. Its deficiency leads to pernicious anaemia. Its secretion is stimulated by acetylcholine, gastrin and histamine.


3. Enzymes : pepsin, gelatinase, carbonic anhydrase, rennin, lipase, urease

  1. Pepsin : this is secreted by the chief cells in the inactive form as pepsinogen. Pepsinogen is activated to pepsin by HCl and pepsin itself. Molecular weight = 35000; optimum pH for activity is 1. 5 to 3.5. Beyond 3.5, pepsin is inactivated. Secretion of pepsin is stimulated by vagus, acetylcholine, gastrin, histamine and insulin. Pepsin is an endopeptidase; it acts on denatured proteins and converts them into proteoses, peptones and a few amino acids. It attacks the peptide linkages in which the amino groups are attached to the aromatic amino acids.
  2. Rennin : this is important in calves and human infants. Origin is not known. It is suggested to be produced by chief cells. It acts on milk in the presence of calcium and causes its precipitation. It is absent in adult humans and cows where its function is taken over by HCl and pepsin
  3. Gelatinase : causes digestion of gelatin
  4. Lipase : acts chiefly on tributyrin and other low molecular weight triglycerides. Its origin in humans is not known. It is active between 4 to 5 pH and is inactive below pH 2.5. It is a weak fat-splitting enzyme and becomes important for fat digestion only when there is pancreatic insufficiency.
  5. Carbonic anhydrase : derived from the parietal cells
  6. Urease : origin not known; converts urea into ammonia

Note : Salivary amylase can act in the stomach and converts starch into maltose till it is inactivated by gastric
acidity. It is inactivated within 30 to 60 minutes.


4. Gastric mucosal barrier

This protects the stomach from getting damaged by the acid in gastric juice. The mucosal barrier is made by The mucus and The HCO3


a. Mucus :

Source :

i. Neck cells of the gastric glands and

ii. surface mucosal cells.


Composed of Mucus is made up of glycoproteins called mucins; the mucins form a flexible gel on the gastric mucosa.


Source :

Surface mucosal cells

HCO3- trapping

Most of the secreted HCO3 is trapped in the mucus gel.

Because of this, a pH gradient is established at the epithelial cells as follows :

  1. on the luminal side : the pH is 1.0 to 2.0
  2. at the surface of the epithelial cells : the pH is 6.0 to 7.0.
  3. HCl secreted by the parietal cells in the gastric glands crosses this barrier in finger-like channels, leaving the rest of the gel layer intact.
  4. Mucus and HCO3- secreted by mucosal cells also play an important role in protecting the duodenum from
  5. damage when acid-rich gastric juice is secreted into it.
  6. Factors affecting mucus/HCO3- secretion
  7. Prostaglandins stimulate mucus secretion.
  8. HCO3- secretion is also stimulated by prostaglandins and by local reflexes.
  9. Other factors which protect the gastric mucosa
  10. Trefoil peptides
  11. Some of the resistance of the mucosa of the GIT to autodigest is also provided by trefoil peptides in the gastric mucosa.
  12. These are of several types and are acid-resistant.

Other places where trefoil peptides are found

  1. Hypothalamus
  2. Pituitaryand
  3. In rapidly proliferating tissues.  

6. Structure

They are characterized by a three-loop structure that looks like a three-leaf clover.

In mice in which the gene for one of these peptides has been knocked out, the gastric and intestinal mucosa are histologically abnormal and there is a high incidence of benign and malignant mucosal tumours.


7. Factors which tend to damage the mucosal barrier

  1. Regurgitated bile salts acting as detergents
  2. Alcohol
  3. Nicotine
  4. Salicylates and other drugs that decrease mucus and hco3- secretion
  5. Lyso lecithin in the regurgitated food
  6. Ischaemia of gastric mucosa
  7. adrenergic agonists like adrenaline and noradrenaline by decreasing HCO3- secretion. 

8. Gastric Motility

  1. Receptive relaxation
  2. When food enters the stomach, the fundus and the upper portion of the body of the stomach relax and accommodate the food (without any increase of pressure). This relaxation of the stomach is called receptive relaxation.

9. Mechanism

Receptive relaxation is vagally mediated; it is triggered by movement of the pharynx and oesophagus.


10. Peristalsis

  1. This is controlled by the gastric BER.  Peristalsis begins immediately after the receptive relaxation and helps in mixing and grinding the food.
  2. Peristalsis begins in the lower portion of the body and goes toward the pylorus.  The contraction of the distal stomach caused by each wave is called antral systole; the contraction waves occur at the rate of 3 to 4 per minute and each contraction wave can last up to 10 seconds. 

11. Regulation of gastric emptying

  1. For this, the antrum, pylorus, and upper duodenum function as a unit. First, there is contraction of the antrum; this is followed by sequential contraction of the pyloric region and then the duodenum. 
  2. Importance of the initial antral contraction
  3. The initial contraction of the antrum prevents solid masses from entering the duodenum; instead of being ‘prematurely’ pushed into the duodenum, the food particles are allowed to be mixed and crushed. Thus, the more liquid gastric contents are sent in small quantities into the duodenum.
  4. Normally, there is no regurgitation of food from the duodenum; the reasons are :
    1. The contraction of the pyloric segment persists slightly longer than that of the duodenum
    2. CCK and secretin may constrict the pyloric sphincter. 

12. Hunger Contractions

These are the gastric contractions that occur between meals; they are presumably associated with the migrating motor complexes (MMCs). Hunger contractions can sometimes be felt and may even be mildly painful. They are so called because they are associated with the sensation of hunger. However, they have no role in the regulation of food intake.

Regulation of Gastric motility and secretion

This is by neural and humoral mechanisms.

Neural mechanisms :

This is by

  1. local autonomic reflexes (involving cholinergic neurons) and
  2. impulses from the CNS by way of the vagus nerves.

Vaga1 stimulation increases gastrin secretion by release of GRP (see above). Other vagal fibers release acetylcholine; the released acetylcholine acts directly on the cells in the glands in the body and the fundus to increase acid and pepsin secretion. Stimulation of the vagus nerve in the chest or neck increases acid and pepsin secretion, but vagotomy does not abolish the secretory response to local stimuli.


Humoral mechanisms

Discussed above.

Gastric juice is secreted continuously throughout the day. During the resting state, only a small amount is secreted ; during digestion, the secretion increases.


14. Gastric juice secretion can thus be divided into two main phases :

  1. Digestive phase
  2. Inter-digestive (or resting) phase  

15. The digestive phase is further sub-divided into

  1. Cephalic phase
  2. Gastric phase
  3. Intestinal phase

Both neural and humoral mechanisms regulate the secretion of gastric juice during the digestive phase. Neural control mechanisms dominate in the cephalic phase; humoral control mechanisms dominate in the gastric



a. Cephalic phase

This is the initial reflex phase. These are vagally mediated responses induced by activity in the CNS.

The presence of food in the mouth reflexively stimulates gastric secretion. The efferent fibers for this reflex are in
the vagus nerves. Thus, even before the food enters the stomach, there is stimulation of gastric secretion.

This vagally mediated reflex can be easily conditioned. For example, the sight, smell, and thought of food
increase gastric secretion. Cephalic influences are responsible for one third to one half of the acid secreted in response to a normal meal.

  1. Psychological states
    Psychologic states can affect gastric secretion and motility; these changes are mediated principally via the vagi
  2. William Beaumont made observations on a patient called Alexis St. Martin. Martin (a Canadian) had a permanent gastric fistula resulting from a gunshot wound; thus, William Beaumont could study the stomach in various psychological states of the patient. He noted the following :
  • anger and hostility :
  • This was associated with turgor, hyperemia, and hypersecretion of the gastric mucosa
  • fear and depression :
  • This was associated with decrease in gastric secretion, blood flow and gastric motility.

Note : vagotomy abolishes the cephalic phase.


b. Gastric phase

The gastric phase of secretion begins when the food enters the stomach. Food in the stomach potentiates the increase in gastric secretion produced by the sight and smell of food and the presence of food in the mouth.


  • The gastric phase is controlled by both neural and humoral mechanisms.
  • Neural mechanisms
  • Presence of food in the stomach stretches the gastric mucosa. This leads to stimulation of secretion in two ways :
  • long vago-vagal reflex mechanism
  • Vagal nerve endings are stimulated à impulses travel via vagal afferents to the vagal nucleus à then relayed through vagal efferents à to stimulate gastric juice secretion
  • local gastric reflexes in the intrinsic submucous (or Meissner’s) plexus
  • Receptors in the gastric mucosa are activated by stretch and chemical stimuli, mainly amino acids and related products of digestion. This in turn activates the submucous (or Meissner’s) plexus and causes acid secretion.
  • The products of protein digestion also bring about increased secretion of gastrin, and this augments the flow of acid.

Note : Thus, stretch stimulates gastric secretion by
i. long vago-vagal reflex
ii. local reflex
iii. Humoral mechanisms
Discussed above (see the effects of gastrin, histamine and acetylcholine)


c. Intestinal influences

  1. Although gastrin-containing cells are present in the mucosa of the small intestine as well as in the stomach, instillation of amino acids directly into the duodenum does not increase circulating gastrin levels.
  2. Fats, carbohydrates, and acid in the duodenum inhibit gastric acid secretion, pepsin secretion and gastric motility via neural and hormonal mechanisms. The hormone involved is probably peptide YY. Gastric acid secretion is increased following removal of large parts of the small intestine. The hypersecretion, which is roughly proportionate in degree to the amount of intestine removed, may be due in part to removal of the source of peptide YY.
  3. Other Influences
  • Hypoglycemia

This acts via the brain and vagal efferents to stimulate acid and pepsin secretion.

  • Caffeine and alcohol

These act directly on the mucosa to increase gastric secretion.

  • Smoking

Nicotine present in the smoke stimulates gastric secretion. Light smoking stimulates and heavy smoking inhibits secretion due to excess nicotine.


C. Regulation of Gastric Motility & Emptying

Rate of gastric emptying

This depends on

the type of food ingested :

  • Carbohydrate-rich food : leaves the stomach in a few hours.
  • Protein-rich food : leaves more slowly(3-4 hrs)
  • Fat-rich food : leaves most slowly(5-6 hrs)

ii. the osmotic pressure of the material entering the duodenum :

Hyperosmolality of the duodenal contents decreases gastric emptying. The hyperosmolality is sensed by "duodenal osmoreceptors"; the effect is probably neural in origin.

D. Peptic Ulcer
Localised erosion and destruction of gastric or duodenal mucosa is called peptic ulcer.

Causes :-

1. Breakdown of gastric mucosal barrier

Peptic ulcer is primarily due to breakdown of the gastric mucosal barrier.  The breakdown can be due to

Infection with the bacterium Helicobacter pylori

Aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs)
These inhibit   the production of prostaglandins and consequently decrease mucus and HC03 secretion (see above).


2. Excess acid secretion

E.g. Zollinger-Ellison syndrome. This syndrome is seen in patients with gastrinomas. Most of the gastrinomas are found in the pancreas (although they can occur in the stomach and duodenum). The gastrin causes prolonged hypersecretion of acid. Lipids and protein digestion are affected due to the high acidity and there is steatorrhoea and diarrhoea.


3. Chronic stress


4. Ischemia of gastric mucosa



  1. Inhibition of acid secretion by :
    1. H2 histamine receptors blockers Drugs e.g. cimetidine block the H2 histamine receptors on parietal cells.
    2. Omeprazole This inhibits the H+-K+ ATPase on the parietal cell.
    3. pylori can be eradicated with antibiotics
    4. Ulcers which are due to NSAIDs can be treated by stopping the NSAID; if for some reason, this is not advisable, then treatment can be done with the prostaglandin agonist misoprostol.

Functions of the Stomach

  1. Storage function : the stomach receives large quantities of food taken in a short time and stores it for 2 to 3 hours.
  2. Digestive function : The stomach mainly helps in the digestion of proteins; pepsin in the gastric juice is an important proteolytic enzyme
  3. Mechanical churning or grinding action : food is broken into smaller particles and converted into chyme; this facilitates the digestive process
  4. Produces intrinsic factor (IF) : IF is 49-kDa glycoprotein ; it binds to cyanocobalamin (vitamin B12) and is necessary for its absorption from the small intestine.
  5. Bacteriolytic : The HCl that is produced in the stomach kills bacteria
  6. Absorption : water, alcohol, saline are absorbed in the stomach to some extent.
  7. Conversion of ferrous to ferric ion : iron present in the colloidal form is liberated from the food. Then it is oxidized to ferric from the ferrous state. This is done by the acid and is later reduced to ferrous by ascorbic acid.

Cyanocobalamin is a cobalt-containing vitamin. Deficiency of this vitamin causes megaloblastic anaemia and deterioration of certain sensory pathways in the CNS. If the deficiency of cyanocobalamin is due to lack of the intrinsic factor, oral administration of cyanacobolamin will not be effective but parenteral administration will be effective.

Deficiency due to an inadequate dietary intake of cyanocobalamin is very rare; this is probably because the minimum daily requirements are quite low and the vitamin is found in most foods of animal origin.


E. Mechanism of Vitamin B12 reabsorption

  1. Vitamin B12 normally binds to intrinsic factor and forms a complex with it; this complex is taken up by a protein called cubilin; cubulin is a high-affinity apolipoprotein in receptors in the distal ileum. This triggers absorption of the complex by endocytosis.
  2. In the ileal enterocytes, the cyanocobalamin is transferred to transcobalamin II; transcobalamin II is a cyancobalamin transport protein that transports the vitamin in plasma. 
  3. Causes of cyanocobalamin deficiency
    1. gastrectomy : this removes the intrinsic factor-secreting tissue pernicious anemia,
    2. In this disease, there is autoimmune destruction of the parietal cells.
    3. diseases of the distal ileum. 
  4. Effects of gastrectomy
    1. pernicious anaemia develops; as mentioned above, in such cases, the cyanocobalamin deficiency can only be treated by parenteral injection of cyanocobalamin.
    2. Digestion of food : the gastric juice contains pepsin, which helps in protein digestion; however, the pancreatic enzymes can digest the proteins and thus nutrition can be maintained. Thus, protein digestion is not affected.
    3. These patients are prone to develop iron deficiency anemia and other abnormalities, and they must eat frequent small meals.
    4. Dumping syndrome

Patients with gastrectomy or gastrojejunostomy may have symptoms of weakness, dizziness and sweating after meals; this is referred to as the dumping syndrome. The reasons for the symptoms are :

  1. Hypoglycaemia
  2. This occurs because of the following sequence of events
  3. In gastrectomized patients there is rapid absorption of glucose from the intestine the hyperglycemia causes abrupt rise in insulin secretion   thus they may develop hypoglycemic symptoms about 2 hours after meals.
  4. Rapid entry of hypertonic meals into the intestine this cause the movement of a lot of water into the gut there is significant hypovolemia and hypotension
  5. stimulation of the autonomic reflexes : this occurs secondary to distension of the small intestine and release of hormones from the gut due to rapid entry of gastric contents into the duodenum and jejunum small stomach syndrome 

5. This occurs when partial gastrectomy is done. The symptoms are

  1. there is distension and discomfort on food intake; thus, food intake decreases with consequent loss of weight
  2. vomiting may occur due to entry of bile into the stomach
  3. diarrhoea and steatorrhoea may occur due to failure of fat digestion
  4. palpitation and flushing

Small Intestine


3 regions: duodenum, jejunum, and ileum                                                              

  1. Mucosa (tunica mucosa): villi (supported by lamina propria) + glands (open into intervillar spaces; embedded in lamina propria) epithelium: wet surface epithelia + goblet (oligomucous) cells (produce mucinogen > mucus). villi: simple columnar; surface absorptive cells with with microvilli forming brush (striated) border and glycocalyx (rich in disaccharidases and dipeptidases); manufacture secretory protein and protein J binding IgA.  Glands: simple tubular (= crypts of Lieberkühn)
  2. Epithelium: simple columnar (resemble surface absorptive cells) basal exocrinocytes (Paneth) cells (apical eosinophilic granules) APUD cells (endocrinocytes; clear cytoplasm; vesicular basal nuclei): Amino Precursor Uptake and Decarboxylation: peptide or amine-secreting cells of gastrointestinal tract and other endocrine organs
  3. lamina propria: underlying loose ct: lacteals take up lipids; capillaries take up amino acids and carbohydrates.
  4. Gut-Associated Lymphoid Tissue (GALT): lymphoid elements (scattered B and T cells, plasma cells, mast cells, macrophages), indivual lymphnodules and aggregated lymnodules in ilium.
  5. muscularis mucosae: thin layer smooth muscle may run up into villi; movement in mucosa
  6. Submucosa: fibroelastic ct; spiral plicae circulares (= folds) especially in jejunum; glands (in duodenum); submucosal (Meissner) nervous plexuses (small parasympathetic ganglia)
  7. functions: absorption of monosaccharides and amino acids via active transport; bile salts emulsify fatty acids and monoglycerides forming micelles which along with glycerol move through sER of surface cells where they are reesterified to triglycerides and coated with protein to form chylomicrons (lipoprotein droplets) that exit cells and are taken up in lacteals (= chyle)
  8. BRUNNER’S GLANDS are compound glands of the duodenum and upper jejunum. They are embedded in the submucous tissue and lined with columnar epithelium They secrete a thick clear alkaline mucinous solution which helps in protecting the duodenal mucosa from gastric acid.
  9. Paneth cells—endocrine cells located in the depths of the crypts of Lieberkuhn—secrete defensins, naturally occurring peptide antibiotics that are also secreted elsewhere in the body .
  10. Defensins: The principal defense molecules secreted by Paneth cells are alpha-defensins, also known as cryptones. These peptides have hydrophobic and positively-charged domains that can interact with phospholipids in cell membranes. This structure allows defensins to insert into membranes, where they interact with one another to form pores that disrupt membrane function, leading to cell lysis. Due to the higher concentration of negatively-charged phospholipids in bacterial than vertebrate cell membranes, defensins preferentially bind to and disrupt bacterial cells, sparing the cells they are functioning to protect. Paneth cells are stimulated to secrete defensins when exposed to bacteria (both Gram positive and negative types) or such bacterial products as lipopolysaccharide, muramyl dipeptide and lipid A.
  11. Other secretions: In addition to defensins, Paneth cells secrete lysozyme, zinc and phospholipase A2, which have clear antimicrobial activity. This battery of secretory molecules gives Paneth cells a potent arsenal against a broad spectrum of agents, including bacteria, fungi and even some enveloped viruses.
  12. Paneth cells secrete a number lysozymes into the lumen of the crypt, thereby contributing to maintenance of the gastrointestinal barrier 
  13. Muscularis externa: two or more muscle layers (inner circular [tight helix]; outer longitudinal [loose helix]); myenteric (Auberbach) plexuses between muscle layers

Large Intestine

  1. No pitts or villi; divided into cecum, appendix, ascending, transverse, descending, and sigmoid colons, rectum, and anal canal. Functions in absorption of water, electrolytes, some vitamins, remaining amino acids, lipids, and carbohydrates; compacts feces.
  2. Mucosa : epithelium simple (surface epithelial cell) columnar absorptive epithelium with abundant goblet (oligomucous) cells, lamina propria: underlying loose ct; glands (= crypts of Lieberkühn) simple columnar epithelium, regenerative cells, and APUD (enteroendocrinocytes) cells in base release paracrine hormones muscularis mucosae: thin layer smooth muscle
  3. Muscularis externa:two muscle layers (inner circular [tight helix; modified in anal sphincters]; outer longitudinal [loose helix]) modified as taniae coli: 3 thickening separate haustra coli (Roman device for hauling water; sacculations); (Auberbachs) myenteric plexuses; sympathetic ganglia and fibers between muscle layers; peristaltic action independent.
  4. Serosa (Adventitia): irregular dense ct surrounded by mesothelium (serosa) or bound to body wall (adventitia); appendices epiploicae = small fat-filled pouches
  5. Appendix: surface epithelium with many goblet cells; glands relatively shallow; lamina propria infiltrated with lymphoid cells; lymph nodules in submucosa
  6. Anorectal junction: abrupt change at anal valves from simple columnar of rectum to stratified squameous epithelium (keratinizing type) of anal canal; rectal glands short; lamina propria infiltrated by lymphoid cells.
  7. Anal Canal: anal columns = longitudinal folds joined at orifice to form anal valves and anal sinuses.
  8. Circumanal glands, hair follicles, and sebaceous glands. Spinincters formed by muscularis externa. 

    More text through MCQs

Which part of the stomach secretes gastrin?
A. Body                               B. Antrum              C. Fundus                               D. Cardia


Body (and also fundus )
i)  Parietal (or oxyntic) cells which produce HCl and intrinsic factor
ii)  Chief (or peptic or zymogen) cells which produce pepsinogens
Mucus is secreted in all parts of the stomach.


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