DIGESTIVE
SYSTEM 1 (Physiology)
4 Processes
Motility
- Contraction of smooth muscle in the digestive tract
- Mixing and Moving the contents in the GIT
Secretion
- Both exocrine and endocrine secretions
- Mucus – along entire digestive tract
- Saliva, acid, enzymes, bile, bicarbonate, hormones et
Digestion
- Food that we consume are generally large molecules
- Cannot cross the plasma membrane of the intestinal epithelial cells
- Chemically break down complex macromolecules into smaller absorbable molecules
Absorption
Digested material transferred from GIT lumen into blood or lymph. Occurs mainly in small intestine
Regulation
Intrinsic nerve plexuses
Submucosal plexus
Myenteric Plexus
Oral Cavity
Entrance to the digestive tract. Muscular lips help procure, guide and contain food in the mouth
Functions
Mastication
Involves the mechanical action of slicing, tearing, grinding, and mixing of ingested food by the teeth
Salivary secretion
99.6% water, 0.5% electrolytes, proteins and
mucus
Taste
Initiation of swallowing (deglutition)
Functions
- Breaks food into smaller pieces
- Facilitate swallowing
- Increases surface area of food particles
- Mixes food with saliva
- Expose food to taste buds
- Increases secretions to prepare for the arrival of food
Functions
- Initiates digestion of dietary starch by salivary amylase
- Initiates digestion of some lipids by lingual lipase
- Some antibacterial effect (lysozyme and salivary IgA)
- Dissolving molecules (taste buds)
- Helps in swallowing, speech and oral health
Pharynx
Common passageway for digestive and respiratory tract
Swallowing
Oropharyngeal stage
- Initiated by tongue voluntarily pushing bolus of food to pharynx
- Note functions of uvula, tongue, glottis and epiglottis
Esophageal stage
Primary peristaltic wave sweeps from the beginning to end of the esophagus, forcing the bolus ahead of it toward the stomach
Stomach
Storage
- Body of stomach
- Receptive relaxation
- Expansion of stomach cavity with little change in intragastric pressure
Mixing
- Mainly in the pyloric antrium where the peristaltic contractions are stronger and more vigorous
- Retropulsion – Churning action breaks the food into smaller pieces producing chyme
Emptying
Controlled propulsion of chyme into the duodenum with each peristaltic wave
- A peristaltic contraction originates in the upper fundus and sweeps down toward the pyloric sphincter.
- The contraction becomes more vigorous as it reaches the thick-muscled antrum (just before the pyloric sphincter).
- The strong antral peristaltic contraction propels the chyme forward.
- A small portion of chyme is pushed through the partially open sphincter into the duodenum. The stronger the antral contraction, the more chyme is emptied with each contractile wave.
- When the peristaltic contraction reaches the pyloric sphincter, the sphincter is tightly closed and no further emptying takes place.
- When chyme that was being propelled forward hits the closed sphincter, it is tossed back into the antrum. Mixing of chyme is accomplished as chyme is propelled forward and tossed back into the antrum with each peristaltic contraction, a process called retropulsion.
Factors
Autonomous smooth
muscle function
Self excitable
Extrinsic autonomic
nerves
- E.g Vagus nerve
GI hormones
Lower Oesophageal Sphincter or Gastroesophageal spincter
Stomach
Duodenum
Outside the digestive system
Volume of chyme
Degree of fluidity
Distension has a direct effect on gastric smooth muscle excitability, as well as acting through the intrinsic plexuses, the vagus nerve, and gastrin
Increased volume stimulates motility and
emptying
Direct effect; contents must be in a fluid form to
be evacuated
Increased fluidity allows more rapid emptying
Presence of fat, acid,
hypertonicity, or distension
Initiates the enterogastric reflex or triggers the
release of enterogastrones (secretin, cholecystokinin)
These factors in the duodenum inhibit further gastric motility and emptying until the duodenum has coped with factors already present
Emotion
Intense pain
Alters autonomic balance
Stimulates or inhibits motility and emptying
Increases sympathetic activity
Inhibits motility and emptying
Vomitting
- Not a function of retroperistalsis in the stomach
- Contraction of respiratory muscles and abdominal muscles
- Stomach, esophagus and sphincters relaxed
- Controlled by vomiting center (area postrema – medulla of brainstem)
- Causes
- Throat stimulation, irritation of stomach, elevated intracranial pressure etc
Gastric Secretion
Body and Fundus
Pyloric Antrum
Exocrine Cells
Chief Cells
Parietal cells
Hydrochloric acid
Mucous cells
Alkaline mucus
Mechanical stimulation by contents
Effect
Modes of Regulation
Produces
Stimuli
Function
Pepsinogen
ACh, gastrin
When activated, begins
protein digestion
ACh, gastrin,
histamine
Activates pepsinogen, breaks down connective tissue, denatures proteins, kills microorganisms
Intrinsic factor
Facilitates absorption
of vitamin B12
Endocrine/Paracrine Cells
D cells
Enterochromaffinlike
(ECL) cells
Histamine
G cells
Somatostatin
ACh, gastrin
Gastrin
Acid
Stimulates parietal cells
Protein products,
ACh
Inhibits parietal, G,
and ECL cells
Protects mucosa against mechanical, pepsin, and acid injury
Stimulates parietal,
chief, and ECL cells. Increases gastric motility
Gastric Acid Secretion
- Luminal membrane on one end
- Basal lateral membrane on the other end
- CO2 +H20 <-> HCO3- + H+ happening within the parietal cell, catalysed by carbonic anhydrase (ca)
- H+-K+ ATPase pump moves H+ across luminal membrane, against concentration gradient
- Luminal K+ channel allow K+ to passively leak back
- There is an accumulation of HCO3-, hence driving the Cl- - HCO3- antiporter and out via the basal lateral membrane.
- Cl- is also brought into the cell. It then diffuses out of the cell and through the luminal membrane via the Cl- channel
- HCL is then produced
Functions of HCL
- Formation of pepsin
- Pepsinogen to Pepsin
- Breakdown of connective tissue and muscle fibers
- So that it's easier for pepsin to break down proteins
- Denaturation of protein
- Killing of microorganisms
Control
Cephalic Phase
Prepare stomach for arrival of food
Gastric Phase
- Increased secretion started in previous phase
- Initiates digestion of proteins
Intestinal Phase
- Control rate of gastric emptying
Prepare stomach for arrival of food
Short phase (minutes)
Directed by CNS via vagus nerve and submucosal plexus
Increased production of gastric juice (mucous, Chief and parietal cells) and release of gastrin (G cells)
Increased secretion of gastric juice
Long phase (3 – 4hr)
Stimulation of stretch and chemoreceptors
Effects of gastrin
(↑ HCl, pepsinogen, gastric motility)
Release of histamine and its local effect
Sustained increased production of gastric juice and increased motility (mixing)
Submucosal and myenteric plexus
Mucous
Chief
Parietal
G Cells
Control rate of gastric emptying
Long duration
Distension of duodenum trigger enterogastric reflex (inhibits gastric motility)
- ↓ gastric contraction
- ↓ gastrin production
Stimulation of CCK,GIP and secretin release, due to presence of lipids and carbohydrates, and the reduction of pH
Feedback inhibition of pepsinogen and HCl production and gastric motility
Inhibits Chief and parietal cells
↓ Gastric motility and secretion
Liver
Secretion of bile salts
Metabolic processing of nutrients
Detoxifying or degrading
Synthesizing plasma proteins
Storing glycogen, fats, vitamins etc
Activating vitamin D
Hormone secretion
Excrete cholesterol and bilirubin
Remove bacteria and worn-out RBCs
Bile salts
Process nutrients
Detoxifying
Produce proteins
Store nutrients
Vit D
Hormone
Cholesterol Bilirubin
RBCs
Programme
Directors
Praise
Students
Very
Helpful
Cheerful
Radiant, and
Beautiful
Blood Supply
Arterial blood, which provides the liver’s O2 supply and carries blood-borne metabolites for hepatic processing, is delivered by the hepatic artery.
Venous blood draining the digestive tract is carried by the hepatic portal vein to the liver for processing and storage of newly absorbed nutrients.
Blood leaves the liver via the hepatic vein.
Bile
- Continuously secreted by the liver (into the duodenum) and is diverted to the gallbladder between meals
- Contains bile salts, cholesterol, lecithin, bilirubin etc
- Does not contain digestive enzymes
- Bile is concentrated in the gallbladder
Bile salts
- Salts are recycled between the small intestine and the liver via enterohepatic
circulation - Bile salts are derivatives of cholesterol
Enterohepatic
circulation
Bile salts travel from
- Liver
- Common bile duct
- Duodenum, via sphincter of Oddi
- Terminal ileum, where 95% of bile salts are reabsorbed
- 5% lost in faeces
- Hepatic portal vein
- Liver
This is the enterohepatic circulation
Functions
- Aid fat digestion and absorption
- Detergent action of bile salts:
- Bile salts’ ability to convert large fat globules into a lipid emulsion consisting of many small fat droplets suspended in the aqueous chyme
- Formation of micelles: bile salts and lecithin aggregate in small clusters with their fat- soluble parts huddled together in the middle to form a hydrophobic (“water-fearing”) core, hence allowing fats to be absorbed
- Excretion of water insoluble substances
- Cholesterol and the waste product bilirubin for example
- Bilirubin has no role in digestion
- Bile salts stimulate bile secretion
- CCK promotes gallbladder emptying (contraction of gallbladder) and relaxation of Sphincter of Oddi /Hepatopancreatic Sphincter (HPS)
- ↑ CCK secretion
- ↑ Plasma CCK
- Gallbladder contraction and HPS Relaxation
- ↑ bile flow into duodenum
- Aids fat digestion
- Hepatitis and cirrhosis are the most common liver disorders
Pancreas
- The pancreas is a mixture of exocrine and endocrine tissue
- Elongated gland that lies behind and below the stomach
- Exocrine function
- Pancreatic enzymes by the acinar cells
- Aqueous alkaline solution
- Pancreatic enzymes optimal in neutral or slightly alkaline environment
- Neutralize acidic chyme
- High concentration of bicarbonate (HCO3-)
Enzymes
Pancreatic Amylase
- Secreted in active form
- Breaks down complex carbohydrates like starch and glycogen
Pancreatic Lipase
- Main enzyme for fat digestion in GIT
- Hydrolyses dietary triglycerides into monoglycerides and free fatty acids
Pancreatic Proteolytic Enzymes (Proteases)
- Trypsin, chymotrypsin and carboxypeptidase
- Secreted as inactive forms (trypsinogen, chymotrypsinogen and procarboxypeptidase)
- Trypsinogen activated by enteropeptidase (secreted by cells of small intestines)
- Trypsin activates other enzymes and is also autocatalytic (self activation)
Pancreatic insufficiency
- Deficient of pancreatic enzymes
- Dietary fat digestion is seriously impaired
Hormonal Control
Control of pancreatic aqueous NaHCO3 – secretion
Control of pancreatic digestive
enzyme secretion
Acid in duodenal lumen
↑ Secretin release from duodenal mucosa
Activate Pancreatic duct cells
↑ Secretion of aqueous NaHCO3 solution into duodenal lumen
Neutralizes
Fat (especially) and protein products in duodenal lumen
↑ CCK release from duodenal mucosa
Activate Pancreatic acinar
cells
Secretion of pancreatic digestive enzymes into duodenal lumen
Digests
Overview of GI Hormone
Gastrin
- Stimulated by protein in stomach
- ↑ secretion of HCl and pepsinogen
- Enhances gastric motility
Secretin
- Stimulated by acid in duodenum
- Inhibits gastric emptying and gastric secretion
- Stimulates pancreas to produce HCO3-
CCK
- Stimulated by chyme in duodenum
- Inhibits gastric motility and secretion
- Stimulates pancreatic enzyme secretion
- Stimulates contraction of gallbladder and relaxation of hepatopancreatic sphincter
Gastric inhibitory peptide (GIP)
Promotes metabolic processing of
nutrients once they are absorbed
Vasoactive intestinal peptide
Stimulates the secretion of intestinal glands, dilates regional capillaries, and inhibits acid production in the stomach. By dilating capillaries in active areas of the intestinal tract, VIP provides an efficient mechanism for removing absorbed nutrients.
Proteins
G cells
ECL
Chief
Parietal
Converts pepsinogen to pepsin to break down proteins