The digestive system has the gastrointestinal or GI tract, consisting of the mouth, pharynx, esophagus, stomach, small intestine, and large intestine (1).
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Accessory organs and tissues consist of salivary glands, liver, gallbladder, and exocrine pancreas.
The GI tract is a 9m tube that runs from the mouth to the anus. The tract’s lumen connects to the external environment, and billions of bacteria live in the large intestine. Most are harmless and beneficial. However, severe infections may occur if bacteria enter the lumen’s internal environment due to the GI tract structure (1).
Some Important Definitions:
Digestion– is the dissolving and breakdown process of food.
Amylase– is an enzyme that initiates polysaccharide digestion.
Lipase -has its uses for triglyceride digestion.
Proteases– digest proteins.
Secretion– is the process of enzymes released into the GI tract’s lumen, and exocytosis allows these enzymes to release into ducts connecting to the GI tract.
Carbohydrates– consist of polysaccharides, which include starch and glycogen. The amylase molecules convert to maltose molecules and break down into monosaccharides. The breakdown of these molecules is glucose, fructose, and galactose (1).
Disaccharides– consist of sucrose and lactose molecules.
Proteins– consist of polypeptides like pepsin, trypsin, and chymotrypsin.
These molecules convert to peptide fragments such as carboxypeptidase and aminopeptidase. The conversion of these amino acids has 20 different types (1).
Triglycerides– consist of glycerol molecules that connect to lipase, which break into monoglycerides with fatty acids.
Absorption– is a process in which molecules do not require digestion and instead move from the GI tract’s lumen across a layer of epithelial cells and enter the interstitial fluid.
The hepatic portal vein– is the vein in which all other absorbed nutrients enter directly into capillaries that drain into veins and the liver.
Motility– are the GI tract’s contractions. The contractions move in a wavelike fashion and are called peristaltic waves.
Four critical processes of the digestive system include secretion, digestion, absorption, and motility.
Digestion will break down food and begin the process in the mouth. Salivary glands secrete to break down the food into small particles—the food forms into a bolus and transfers into the pharynx and esophagus. From there, the food prepares to go into the stomach (1).
Hydrochloric acid or HCL are acidic gastric secretions in the stomach. These gastric secretions refer to as chyme.
The small intestine is the location in which the majority of the digestive process occurs. The small intestine has three parts; the duodenum, jejunum, and ileum.
The duodenum receives chyme from the stomach. The jejunum is the middle section, and the ileum is the terminal region from which the chyme enters the large intestine (1).
The small intestine also has increased finger-like projections called villi and aids secretions via ducts from the liver and pancreas. Lymphatic nodules line the small intestine and act as immune cells to kill microorganisms. The liver also metabolizes and aids in the elimination of foreign and toxic substances ingested with a meal.
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At the end of digestion, feces forms when the metabolic end-products excrete through the gastrointestinal tract.
Average American adults consume 500-800 g of food and 1200 ml of water per day, but only a fraction of the material enters the GI tract’s lumen.
Structure of the Gastrointestinal Tract Wall
There are invaginations of the epithelium in the underlying tissue. These invaginations allow the secretion of acid, HCO3 enzymes, water, ions, and mucus into the lumen. Surrounding the epithelium is the lamina propria, a loose connective tissue layer that allows the passage of small blood vessels, neurons, and lymphatic vessels (1).
The lamina propria separates from the mucosa’s underlying tissues. A thin layer of smooth muscle is involved in the mucosal surface’s, allowing small movements (1).
The mucosa has a combination of three layers; the epithelium, lamina propria, and mucosa (1).
The function of the Digestive System
- Ingestion of foods and liquids containing nutrients.
- Digestion of large molecules in ingested food into absorbable molecular forms.
- Absorption of nutrients from the gut into the body’s internal environment.
- Metabolic transformation of fuel molecules and detoxification of foreign substances in the liver.
- Elimination of small amounts of metabolic end-products excreted by the liver.
- Carrying out various immune functions, like producing antibodies and fighting microorganisms not destroyed by the stomach’s acidity.
Outside of the mucosa is the submucosa, which is a second connective tissue layer. The submucosal plexus is a layer in which a network of neurons contains blood and lymphatic vessels (1).
The plexus holds a thick inner layer of muscle and a thin outer layer of longitudinal muscle (1).
The myenteric plexus is the second network of neurons connected with the submucous plexus and projects into the surrounding smooth muscle layers. The myenteric nerves innervate from the sympathetic and parasympathetic divisions of the autonomic nervous system (1).
The tube’s outer surface is called the serosa and has a thin layer of connective tissue. This tissue supports the GI tract in the abdominal cavity. Enteroendocrine cells secrete hormones and provide various gastrolienal functions, including motility and exocrine pancreatic secretions (1).
How is the GI process regulated?
The enteric nervous system is a part of the autonomic nervous system that comprises the two nerve plexus—neurons synapse with other neurons within a given plexus near smooth muscles, glands, and epithelial cells.
GI reflexes occur from the distension of the intestinal wall. Chyme osmolarity then concentrates, increasing the acidity of the chyme. The chyme concentrations produce digestion products like monosaccharides, fatty acids, and amino acids (1).
The enteric nervous system contains neurons called adrenergic and cholinergic neurons (1).
These neurons initiate the GI tract’s reflexes. The neurons also rely on other neurotransmitters to digest different molecules (1).
Nitric oxide, neuropeptides, and acetylcholine are essential for digesting molecules. There are two types of neural reflexes. One is through the nerve plexus to effector cells within the GI tract. The other is a long reflex arc from the tract’s receptors to the CNS through afferent nerves and back to the nerve plexus through autonomic nerves (1).
Hormonal Regulation
The four best understood GI hormones are secretin, cholecystokinin CCK, gastrin, and glucose-dependent insulin tropic peptide (GIP).
Most of the hormones participate in a feedback control system that regulates a part of the GI luminal environment, and GI hormones influence more than one type of target cell (1).
A potential ion’s response to a hormone increases when a second hormone is present (1).
Incretins have GI hormones in which they control blood glucose by serving as a feedforward signal from the GI tract to the endocrine pancreas (1).
Phases of GI Control
The cephalic phase initiates when sensory receptors in the head are stimulated by sight, smell, taste, and chewing.
The gastric phase distends, regulates acidity and amino acids for digestion.
The intestinal phase initiates by stimuli of small vibrations, including distension, acidity, osmolarity, and digestive products (1).
Mouth, Pharynx, and Esophagus
Saliva releases through a series of short ducts from three pairs of salivary glands- the parotid, sublingual, and submandibular glands (1).
These glands contain mucus, water, HCO3, and several enzymes (1).
Mucus is a viscous, slippery, glycoprotein-rich, protective secretion produced by epithelial cells throughout the GI tract (1).
Lysozyme is a salivary enzyme that protects against harmful bacteria (1).
The secretion of saliva regulates by sympathetic and parasympathetic innervation. Both stimulate salivary secretion, and parasympathetic innervation produces increased saliva (1).
Swallowing is a complex flexion initiated when pressure receptors in the pharynx walls receive stimulation by food or are forced into the rear of the mouth by the tongue. The swallowing center is a receptor in the medulla oblongata of the brainstem (1).
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The glottis is the area around the vocal cords and the space between them. It keeps food from moving into the trachea (1).
The tongue forces the food farther back into the pharynx, and the epiglottis is the flap of tissue that sends the food to the glottis (1).
Aspiration is when food travels down the trachea and causes choking when the stomach regurgitates contents (1).
The upper esophageal sphincter is a ring of skeletal muscle that surrounds the esophagus below the pharynx. The lower esophageal sphincter is the last portion of the esophagus (1).
When saliva glands are not working correctly, many conditions can occur. Sjogren’s syndrome is an immune disorder in which exocrine glands are nonfunctional due to white blood cells’ infiltration (1).
Summary
Food starts in the mouth, moves into the pharynx, the glottis, and esophagus, and is pushed down by a neural wave of muscle contractions called peristalsis (1).
The upper esophageal sphincter allows the food into the esophagus. The lower esophageal sphincter remains relaxed while swallowing (1).
The esophagus’ maintains distension by the bolus activating receptors that initiate reflexes, causing repeated waves of peristaltic activity (1).
Food from the stomach to the esophagus creates a lot of acidity in the gut that breaks down the food. Sometimes if the lower esophageal sphincter does not close properly, there are small amounts of acid during the periods of esophageal relaxation that reflux (1).
This response is known as gastroesophageal reflux or acid reflux. Smoking and alcohol, or even caffeine, contribute to this process (1).
The process even increases a condition known as heartburn because the pain appears to be in the heart when, in fact, it stems from the stomach (1).
The Stomach
Food is mixed with gastric secretions to form the solution defined earlier as chyme. Chyme is molecular fragments of proteins and polysaccharides, droplets of fat and ions, water, and various other molecules ingested in the food (1).
Anatomy
The stomach has three parts, the body, and the uppermost position, which refers to the fundus. The lower portion of the stomach, the antrum, has a thicker smooth muscle layer and is responsible for mixing and grinding the stomach contents (1).
The pyloric sphincter is a ring of smooth contractile muscle of the small intestine. An epithelial layer lines the stomach that invaginates into the mucosa, forming many tubular glands (1).
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Secretions of the Stomach
Gastric glands have a protective coating of mucus and HCO3. The glands are parietal cells that secrete acid and intrinsic factors, and chief cells secrete pepsinogen (1).
An intrinsic factor is a protein that binds and allows the absorption of vitamin B12 (1).
There are unique parts of the apical membrane of parietal cells; these are called canaliculi. The gastric glands in the antrum contain enteroendocrine cells called G cells, which secrete gastrin (1).
Enterochromaffin-like (ECL) cells release the paracrine substance histamine and other cells called D cells. D cells secrete the polypeptide somatostatin.
HCL Production and Secretion
The stomach secretes about 2 L of hydrochloric acid per day (1).
Carbonic anhydrase catalyzes CO2 with water to produce carbonic acid, dissociating to H+ and HCO3(1).
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H+/K+ ATPase pumps in the parietal cells’ apical membrane, pump hydrogen ions into the stomach’s lumen (1).
The pump pumps K+ into the cell, then leaks back into the lumen through K+ channels (1).
H+ secretes into the lumen, and HCO3 moves across the basolateral membrane and into the capillaries through Cl-(1) exchange.
Three chemical messengers stimulate the insertion of H+/K+ ATPases into the plasma membrane, thereby increasing acid secretion: gastrin, acetylcholine, and histamine (1).
The cephalic and gastric phases alter the release of the four chemical messengers.
During the cephalic phase, increased activity of efferent parasympathetic neural input to the stomach’s enteric nervous system results in ACh’s release from the plexus neurons, gastrin from the gastrin-releasing G cells, and histamine from ECL cells (1).
The concentration of acid in the gastric lumen is an essential determinant of acid secretion rate because H+ directly inhibits gastrin secretion (1).
This inhibition will also stimulate somatostatin from D cells. Then the parietal cells increase to inhibit acid secretion and also inhibit gastrin and histamine (1).
During the cephalic phase, food enters the stomach, and H+ concentration in the lumen increases because of a few buffers present to bind the secreted H+ (1).
Summary
Cephalic phase stimuli–initiates in the brain and will increase enteric neural activity (1).
That activity increases gastric secretion, stimulates histamine secretion, and acts on parietal cells to increase acid secretion, increasing HCL (1).
HCL also inhibits gastrin secretion and simultaneously increases somatostatin secretion to decrease acid secretion (1).
Summary of HCL
Cephalic initiates by sight, smell, taste, and chewing of food. Then the parasympathetic nerves to the enteric nervous system increase HCL secretion (1).
Gastric initiates by distension, peptides increase, H+ concentration decreases, and long and short neural reflexes and direct stimulation of gastrin secretion increase HCL secretion (1).
Intestinal contractions initiated by distention will increase H+ concentration, increase osmolarity, and increase nutrient concentrations. CCK and duodenal hormones assist with these reflexes and ultimately will decrease HCL secretion (1).
Enterogastrone hormones released by the intestinal tract inhibit gastric activity and include secretin and CCK (1).
Pepsin Secretion
Pepsin secretes by chief cells, and the precursor is pepsinogen (1).
When there is low pH in the lumen, the stomach will increase pepsin (1).
Zymogens are synthesized and stored intracellularly in inactive forms and do not act on proteins inside the cells that produce them, thereby protecting the cell from proteolytic damage (1).
Pepsin is active only in the presence of high H+ concentration or low pH. It inactivates when HCO3 secretes the small intestine, and the pancreas neutralizes the H+ (1).
Gastric Motility
Smooth muscle in the stomach wall relaxes before the arrival of food. This relaxation forms by parasympathetic nerves that innervate the stomach’s enteric nerve plexus. The stomach also has peristaltic waves that help food break down and move through to the small intestine (1).
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Summary
Increasing sympathetic efferent innervation can decrease stomach digestion and will decrease gastric emptying (1).
Plasma enterogastrones will also decrease gastric emptying (1).
Duodenum activity will increase acidity and increase fat. The movement of amino acids, hypertonicity, and distention will also increase. As well, secretion of enterogastrones and stimulation of neural receptors (1).
Feedback loops will affect long neural reflexes back to the CNS (1).
Basic Electrical Rhythm
Smooth muscle cells undergo spontaneous depolarization-repolarization in the stomach. Initiation of reflexes controls gastric motility and deepens upon the contents of the stomach and small intestine. The stomach’s distention also increases the force of antral contractions through long and short reflexes triggered by mechanoreceptors in the stomach wall (1).
These slow waves conduct through gap junctions, and the stomach’s longitudinal muscle layer will induce similar slow waves in the overlying circular muscle layer. In the absence of neural or hormonal input, these depolarizations are too small to cause significant contractions (1).
Initiation of reflexes controls gastric motility and deepens upon the contents of the stomach and small intestine. The stomach’s distention also increases the force of antral contractions through long and short reflexes triggered by mechanoreceptors in the stomach wall (1).
Gastric emptying inhibits the duodenum’s distension, fat content, acidity, and hypertonic solutions in the duodenum’s lumen. This reflex refers to the intragastric reflex. These factors also inhibit acid and pepsin secretion in the stomach (1).
The Small Intestine
Anatomy
The macro and microscopic structure of the wall of the small intestine is incredibly elaborate. The circular folds cover with finger-like projections called villi. Each villus’ surface covers a layer of epithelial cells whose surface membranes form small projections called microvilli (1).
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Goblet cells also secrete mucus that lubricates and protects the inner surfaces of the small intestine wall. A combination of circular folds, villi, and microvilli increases the small intestine’s surface area by about 600-fold (1).
Lacteal is a lymphatic vessel in which the lacteals absorb material and reach the general circulation by emptying the lymphatic system into large veins through a thoracic duct structure (1).
The pancreas and liver connect to the small intestine via ducts and produce secretions essential to the small intestine’s function (1).
The pancreas is an elongated gland located behind the stomach (1).
The liver, a large organ located in the abdomen’s upper-right portion, secretes bile into small ducts that join to form the common hepatic duct. Between meals, secreted bile stores in the gallbladder, a small sac underneath the liver that branches from the common hepatic duct (1).
Oddi’s sphincter is a sphincter in the duodenum where the gallbladder walls stimulate, and they cause bile to flow down the common bile duct (1).
Secretions
1500 mL of fluid secretes by cells in the small intestine. These secretions, along with mucus, lubricate the intestinal tract’s surface and help protect the epithelial cells from excessive damage by the lumen’s digestive enzymes (1).
Pancreatic Secretions
The pancreas has endocrine and exocrine functions, but only the latter is directly involved in the gastrointestinal processes (1).
The enzymes secrete from lobules called acinar cells at the end of the pancreatic duct system. HCO3 secretes by epithelial cells lining the pancreatic ducts (1).
While HCO3 and H+ are produced and exchanged for extracellular Na+ on the cell’s basolateral side, the H+ enters the pancreatic capillaries to eventually meet up in the venous blood containing the HCO3 produced by the stomach during the generation of luminal H+ (1).
The energy for the secretion of HCO3 stems from Na+/K+ ATPase pumps on the basolateral membrane (1).
Sometimes there is a dependence on Cl- and there will be mutations in the CFTR that cause a disease called cystic fibrosis resulting in decreased pancreatic HCO3 secretion (1).
CFTR cystic fibrosis transmembrane conductance regularly recycles ions into the lumen. This recycling leads to clogging of the pancreatic ducts and pancreatic damage (1).
The cystic and fibrotic appearance of the diseased pancreas was the origin of this disease’s name (1).
Enterokinase is a proteolytic enzyme that splits off a peptide from pancreatic trypsinogen, forming the active enzyme trypsin. Trypsin is also a proteolytic enzyme; once activated, it activates the other pancreatic zymogens by splitting off peptide fragments (1).
Summary Pancreatic Enzymes
Trypsin, chymotrypsin, and elastase break peptide bonds in proteins to form peptide fragments (1).
Carboxypeptidase proteins split off terminal amino acids from the carboxyl end of the protein (1).
Lipase is known as triglycerides that split off two fatty acids from triglycerides, forming free fatty acids and monoglycerides (1).
Amylase is a polysaccharide that splits polysaccharides into maltose (1).
Ribonuclease, deoxyribonuclease are nucleic acids that split nucleic acids into free nucleotides (1).
Pancreatic secretion increases during a meal, and CCK releases from enteroendocrine cells of the small intestine. Secretin is the primary stimulant for HCO3 secretion, whereas CCK mainly stimulates acinar cell secretion (1).
Note that there are inactive enzymes in the pancreases that turn into active enzymes in the intestinal lumen. Trypsinogen turns into trypsin by entering kinase in the intestinal lumen (1).
CCK stimulates the secretion of digestive enzymes, including those for fat and protein digestion. It is appropriate that the stimuli for its release are fatty acids and amino acids in the duodenum. Luminal acid and fatty acids also act on afferent neuron endings in the intestinal wall, initiating reflexes that work on the pancreas to increase enzyme and HCO3 secretion (1).
Bile Formation and Secretion
Exocrine secretions from the liver enter the small intestine and are essential for normal digestion (1).
Bile contains HCO3, cholesterol, phospholipids, bile pigments, several organic wastes, and a group of substances collectively termed bile salts. HCO3, like that from the pancreas, neutralizes the acid from the stomach, whereas the bile salts, as we shall see, solubilize dietary fat (1).
Substances absorbed from the small intestine wind up in the hepatic sinusoid and either reach the vena cava via the central vein or are taken up by the hepatocytes or liver cells. Hepatocytes rid the body of substances by secretion into the bile canaliculi. This location converges to form the common hepatic bile duct (1).
Bile contains six significant components; bile salts, phospholipids, HCO3, and other ions, cholesterol, bile pigments, and a small amount of other metabolic end-products and trace metals (1).
Bile salts help to solubilize fat in the small intestine. Bile salts are the most critical digestive components of bile and absorb by specific Na+ coupled transports in the ileum (1).
The bile salts return to the portal vein to the liver. Uptake of the salts drives by secondary active transport coupled to Na+. This recycling pathway is called enterohepatic circulation (1).
The liver also secretes cholesterol extracted from the blood into the bile. Bile secretion, followed by the excretion of cholesterol in the feces, is one mechanism for maintaining cholesterol homeostasis in the blood and is also the process by which some cholesterol-lowering drugs work. Cholesterol is insoluble in water, and its solubility in bile achieves by incorporating tiny fat droplets called micelles (1).
In blood, cholesterol will turn into lipoproteins. Bile pigments are substances formed from the central portion of hemoglobin when old or damaged erythrocytes break down in the spleen and liver (1).
Bilirubin is a predominant bile pigment extracted from the blood by hepatocytes and actively secreted into the bile. Bilirubin is yellow and contributes to the color of urine (1).
Bacterial enzymes modify bilirubin to form the brown pigments that give feces their characteristic color (1).
Hepatocytes secrete bile salts, cholesterol, phospholipids, and bile pigments (1).
Secretin stimulates the secretion of HCO3. Bile secretion is significant during and just after a meal (1).
The sphincter of Oddi remains close, and dilute bile is shunted into the gall bladder where there are organic components of bile that become concentrated as some NaCl and water in the blood (1).
Summary
Polysaccharides get converged into maltose by pancreatic amylase in the lumen. There are brush border enzymes that ingest these disaccharides and convert them into monosaccharides. The monosaccharides separate into fructose, glucose, and galactose (1).
The fructose, glucose, and galactose get pushed into the intestine epithelial cell in the apical brush border (1).
The glucose and galactose are pushed through secondary transport by Na+. The process uses the SGLT enzyme to transport the glucose and galactose ions into the intestinal epithelial cell (1).
Fructose is sent to the intestinal epithelial cell by GLUT enzymes (1).
Glucose, galactose, and fructose will be sent to the interstitial fluid by GLUT enzymes. The process occurs across the basolateral membranes (1).
Potassium and Sodium channels work as Na+ in the intestinal epithelial cell and go into the interstitial fluid. In contrast, K+ from the interstitial fluid goes into the intestinal epithelial cell using ATP converting to ADP (1).
Excess K+ ions from the intestinal epithelial cell get transported into the intestinal fluid (1).
Summary of CCK
In the duodenum, CCK secretes ion increases and allows the gallbladder to contract and the sphincter of Oddi to relax (1).
The gallbladder will increase bile flow into the common bile duct, and the sphincter of Oddi will expand bile flow into the duodenum(1).
Carbohydrate
Carbohydrates consumption is about 250 to 300g per day in the American diet. Dietary fiber is known as cellulose and presents in other polysaccharides vegetable matter. These do not break down by the small intestine enzymes and pass on to the large intestine, where bacteria partially metabolize them (1).
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The digestion of starch by salivary amylase begins in the mouth but accounts for only a tiny fraction of total starch digestion (1).
Protein
In the lumen, pancreatic proteases and peptidases convert proteins to small peptides and amino acids (1).
Brush border peptidases use the amino acids and Na+ to convert to amino acids in the intestinal epithelial cell (1).
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Brush border peptidases convert to small peptides, and H+ in the lumen convert that to intestinal epithelial cells across the apical brush border membrane (1).
Small peptides, H+, amino acids, and Na+, are peptidases (1).
Small peptides take peptidases and convert them into amino acids (1).
Amino acids convert into the interstitial fluid by amino acid transporters across the basolateral membranes.
The potassium channel uses K+ in the intestinal epithelial cell to take the K+ in the interstitial fluid (1).
Na+/K+ transporter aims to pump Na+ from the intestinal epithelial cell and convert it to Na+ in the interstitial fluid. At the same time, K+ from the interstitial fluid passes to the intestinal epithelial cell. ATP converts to ADP and drives this transporter (1).
Summary
Proteins are first partially broken down into peptide fragments in the stomach by the enzyme pepsin. Further breakdown is completed in the small intestine by the enzymes trypsin and chymotrypsin. The pancreas’ major proteases secrete during this process (1).
These peptide fragments absorb if they are small enough. The peptides allow free amino acids by carboxypeptidases and aminopeptidases to fully digest. These amino acids are on the small intestine’s apical membranes epithelial cells (1).
FAT
The average daily intake of lipids is 70 to 100 g per day.
Pancreatic lipase is the primary digestive enzyme in this process, catalyzing the splitting of bonds linking fatty acids to the first and third carbon atoms of glycerol, producing two free fatty acid monoglycerides products (1).
Triglyceride uses pancreatic lipase and converts it into monoglyceride and two fatty acids (1).
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Emulsification is the process in which a small number of lipid droplets break down as an emulsion (1).
Emulsification of fat requires mechanical disruption of the large lipid droplets into smaller droplets. Additionally, an emulsifying agent prevents the smaller droplets from reaggregating back into large droplets (1).
The mechanical disruption is provided by the GI tract’s motility, accruing into the lower portion of the stomach and in the small intestine, which grinds and mixes the luminal contents (1).
Phospholipids in food, phospholipids, and bile salts are secreted in the bile and provide the emulsifying agents (1).
Phospholipids are amphipathic molecules consisting of two nonpolar fatty acid chains attached to glycerol, with a charged phosphate group located on glycerol’s third carbon. Bile salts are formed from cholesterol in the liver and are also amphipathic (1).
However, the coating of the lipid droplets with these emulsifying agents impairs the accessibility of the water-soluble pancreatic lipase to its lipid substrate (1).
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The pancreas secretes a protein known as colipase. Colipase is amphipathic (1).
The formation of micelles cluster together with each molecule’s polar ends and increase absorption by producing fat-digesting products free in solution (1).
In summary, micelles are continually breaking down and reforming as more lipids decrease because of their diffusion into epithelial cells. Small lipids replenish micelles (1).
Chylomicron
Chylomicrons are 1-micron diameter extracellular fat droplets that contain diglycerides and other lipids (1).
They absorb through the same process that led to fatty acid and monoglyceride movement into the small intestine’s epithelial cells (1).
Chylomicrons released from the epithelial cells pass into lacteals lymphatic vessels into the intestinal villi rather than into the blood capillaries. The chylomicrons cannot enter the blood capillaries. This barrier results because the basement membrane is too large for chylomicrons’ diffusion (1).
Vitamins
Vitamins are small molecules, like vitamins A, D, E, and K. The vitamins are soluble in micelles (1).
Malabsorption is when an interface with the secretion of bile or bile salts in the intestine decreases the absorption (1).
Celiac disease is due to an autoimmune-mediated loss of intestinal brush border surface area due to sensitivity to the wheat proteins collectively known as gluten. Vitamins absorb by diffusion or mediated transport (1).
Pernicious anemia is when vitamin B12 provides for erythrocyte formation, but there are deficiencies. This anemia may occur when the stomach is absent and removed due to ulcers or cancer (1).
The absorption obtains B12 in the lower part of the ileum, and removal or dysfunction of this segment due to disease can also result in pernicious anemia (1).
Healthy individuals absorb oral vitamin B12, and it is not very useful in patients with pernicious anemia because of the absence of intrinsic factor. Treatment of pernicious anemia requires injections of vitamin B12 (1).
Water Minerals
Water is the most abundant substance in the chyme. Water gets absorbed in the stomach, but the stomach has a much smaller surface area (1).
The small intestine’s epithelial membranes are very permeable to water and, after diffusion, occurs across the epithelium whenever the active absorption of solutes establishes a water concentration defense (1).
Na+ accounts for many active modes of transport since it is a primary active transporter; as Na+/K+ pumps Na+ out and K+ in, water reabsorption follows (1).
Other ions, such as potassium, magnesium, phosphate, and calcium ions, are also absorbed.
Iron
Iron is necessary since it is the O2 binding component of hemoglobin (1).
Iron ions actively transport into intestinal epithelial cells, where most of them turn into ferritin, the protein-iron complex that functions as an intracellular iron store (1).
The absorbed iron that does not bind to ferritin is released on the blood side, circulating throughout the body attached to the plasma protein transferrin (1).
Iron binds to ferritin in the epithelial cells and releases back into the intestinal lumen when the cells at the villi’s tips disintegrate, and the iron excretes into the feces (1).
Hemochromatosis is a condition in which skin pigmentation changes, causing absorption of large portions of iron that overwhelm the body and cause toxic effects (1).
Phlebotomy is a blood withdrawal method that removes iron in red blood cells or hemoglobin from the body (1).
Iron absorption depends on the types of food ingested because it binds to many negatively charged ions in food, which can retard its absorption (1).
The absorption of iron is typical of that of most trace metals in two significant respects. Cellular storage proteins and plasma carrier proteins are involved. The control of absorption rather than urinary excretion is the primary mechanism for the homeostatic control of the body’s content of the trace metal (1).
Summary
Fat droplets break down into bile salts, and the bile salts use pancreatic lipase to break down into free molecules of fatty acids and monoglycerides (1).
Emulsion droplets use the bile salts to break down into bile salts and pancreatic lipase. Micelles use the bile salts to convert into free molecules of fatty acids and monoglycerides (1).
Diffusion occurs in the lumen’s epithelial cell. Then amphipathic proteins coat the fatty acids and monoglycerides. Finally, the triglycerides’ droplet secretes into lacteal and forms into the lacteal cell’s chylomicron (1).
Absorption Pathways
Nutrients absorbed across the intestinal epithelial enter circulating blood by two different pathways (1).
Fats first enter the lymphatic system. Lymph vessels from the small intestine eventually converge and empty into a large vein near the heart. Lastly, chylomicrons circulate throughout the bloodstream and deliver lipids and fat-soluble vitamins to all body cells (1).
The hepatic portal system delivers nutrients to the liver and produces the pancreatic hormones insulin and glucagon to the liver, regulating the metabolic processing of nutrients (1).
The hepatic portal vein system is also important because the liver contains enzymes that can metabolize harmful compounds that may have been ingested and absorbed, thereby significantly reducing their entry into the systemic circulation (1).
Motility of the Small Intestine
The smooth muscles bring about the motility of the small intestine in its walls. The motility starts by mixing the luminal contents. After mixing, the contents come into contact with the epithelial surface. The surface is where absorption takes place. Then, the advancing of the luminal material takes place toward the large intestine. Most substances absorb into the small intestine, but only small quantities of water, ions, and undigested material pass to the large intestine (1).
Segmentation is the rhythmic contraction and relaxation of the intestine. It produces a continuous dividing and subdivision of the intestinal contents, thoroughly mixing the chyme in the lumen and contacting the intestinal wall (1).
These movements are by electrical activity generated by pacemaker cells in the circular smooth muscle layer (1).
As with the slow waves in the stomach, this intestinal electrical rhythm produces oscillations in the smooth muscle membrane potential (1).
The frequency of segmentation sets by the intestinal electrical rhythm; unlike the stomach, which usually has a single rhythm, the intestinal rhythm varies along the intestine’s length. Each successive region has a slightly lower frequency than the one above (1).
The intensity of segmentation can alter by hormones. The enteric nervous system, autonomic nerves, and parasympathetic activity increase the force of contraction, and sympathetic stimulation decreases it (1).
The cephalic phase also alters intestinal motility (1).
Migrating myoelectrical complex is a prostatitis activity of repeated waves of peristaltic movement (1).
MMC moves any undigested material remaining in the small intestine into the large intestine and prevents bacteria from staying in the small intestine long enough to grow and multiply excessively (1).
Motilin, an enzyme in the intestinal hormone’s plasma concentration, is thought to initiate the MMC (1).
The Large Intestine
The cecum is the first portion of the large intestine. There is a sphincter between the ileum and the cecum is called the ileocecal valve. It has smooth muscle innervated by sympathetic nerves (1).
The circular muscle contracts with distension of the colon and limits colonic contents back into the ileum. This movement prevents bacteria in the large intestine from colonizing the small intestine’s final part (1).
The appendix is a small, finger-like projection that extends from the cecum and may participate in immune function and serve as a reservoir for healthy bacteria when illness alerts the bacterial population into the large intestine (1).
The colon consists of three relatively straight segments – ascending, transverse, and descending portions (1).
The terminal portion of the descending colon is S-shaped, forming the sigmoid colon. The colon empties into a relatively straight segment of the large intestine and the rectum, ending at the anus (1).
Secretion, Digestion, and Absorption in the Large Intestine
1500 mL chyme enters the large intestine from the small intestine (1).
The primary absorptive process into the large intestine is the active transport of Na+ from lumen to extracellular fluid, with the osmotic absorption of water (1).
When there is severe potassium depletion, large volumes of fluid excrete into the feces (1).
There is a net movement of HCO3 into the lumen coupled to Cl- absorption from the lumen, and loss of this HCO3 in patients with prolonged diarrhea causes metabolic acidosis (1).
The large intestine also absorbs some of the products formed by the bacteria colonizing this region (1).
HCO3 secreted by the large intestine helps neutralize the increased acidity resulting from these fatty acids’ formation. These bacteria also produce small amounts of vitamins, especially vitamin K, for absorption into the blood (1).
Other bacterial products include gas or flatus, which is a mixture of nitrogen and carbon dioxide. When bacterial fermentation of undigested polysaccharides produces these gases, certain foods cannot digest (1).
Instead, these enzymes are readily metabolized by bacteria in the large intestine, producing large gas quantities (1).
Motility of the Large Intestine and Defecation
In the large intestine, the circular smooth muscle contractions produce a segmentation motion with a slower rhythm than in the small intestine (1).
The mass movement spreads rapidly over the large intestine’s transverse segment toward the rectum (1).
The anus, the exit from the rectum, is usually closed by the internal anal sphincter, composed of smooth muscle, and the external anal sphincter (1).
The external anal sphincter is composed of skeletal muscle under voluntary control (1).
The distension of the rectum walls initiates the defecation reflex, a conscious urge to defecate (1).
The reflex initiates the relaxation of the internal anal sphincter and the external anal sphincter’s contraction to increase motility in the sigmoid colon (1).
Pathology of the Digestive System
Ulcers
When there is a high concentration of acid and pepsin secreted by the stomach, it is natural to wonder why it does not digest (1).
Several factors protect the walls of the stomach from being digested (1).
The mucus forms a thin layer over the luminal surface—the surface lines with alkaline-producing cells (1).
Mucus then forms a barrier between the lumen’s highly acidic contents and the cell surface (1).
When the protective mechanism is damaged, ulcers of the gastric surface develop (1).
Endoscopy is a video technology to visualize gastric and duodenal mucosa ulcers directly (1).
A tissue biopsy is a treatment option to determine the location of ulcers (1).
Ulcers form when the mucosa barrier breaks down.
Helicobacter pylori are present in the stomachs of many patients with ulcers or gastritis (1).
Once an ulcer has formed, inhibition of acid secretion with mediation can remove the constant irritation and allow the ulcer to heal (1).
Cimetidine is an H2 receptor antagonist and inhibits histamine. This receptor splits acid secretion and helps to remove the ulcer (1).
Other medications are omeprazole and lansoprazole, which are proton pump inhibitors (1).
Vomiting
Vomiting is a forceful expulsion of the stomach and upper intestine tract contents out of the mouth (1).
The occurrence initiates in the brainstem medulla oblongata.
Many neural inputs initiate the vomiting reflex, and there is excessive distension of the stomach or small intestine (1).
The area is a nucleus in the medulla oblongata. It is outside the blood-brain barrier, which allows it to be sensitive to toxins in the blood and initiates vomiting (1).
Many chemicals are emetics that stimulate vomiting via receptors in the stomach, duodenum, or brain (1).
Vomiting precedes increased salivation, sweating, increased heart rate, and nausea (1).
The events begin with a deep breath and elevation of the soft palate. The abdominal muscles contract and increase the abdominal pressure, making the lower esophageal sphincter relax as high abdominal pressure forces the stomach’s contents into the esophagus (1).
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Retching is when the area expels via the mouth. Vomiting often leads to loss of water and ions and can result in severe dehydration due to the body’s imbalance of ion storage (1).
Gallstones
When the bile concentration becomes high concerning phospholipid and bile salts concentrations, cholesterol crystallizes out of solution, forming gallstones (1).
Gallstones occur when the liver secretes excessive amounts of cholesterol or cholesterol becomes overly concentrated in the gallbladder due to ion and water absorption (1).
Occasionally, bile pigments can cause gallstone formation, but more commonly, the causes are cholesterol gallstones (1).
If a gallstone is small, it may pass through the common bile duct into the intestine with no complications (1).
A larger stone can also become lodged in the gallbladder’s opening, causing decreased bile, fat digestion, and absorption (1).
Vitamins A, D, K, and E deficiency lead to clotting problems and calcium malabsorption (1).
The fat that is not absorbed enters the large intestine and eventually appears in the feces (1).
Jaundice is when bilirubin accumulates in the blood, diffuses into tissues, and produces a yellowish coloration of the skin and eyes (1).
This coloration is an example of some of the nutritional deficiencies of disease that can take place (1).
Cholecystectomy is a surgery in which there is a removal of a gallbladder (1).
However, cholecystectomy can still produce bile and transport it to the small intestine via the bile duct (1).
However, bile secretion and fat intake in the diet no longer couples together (1).
Lactose Intolerance
Lactose is a carbohydrate in milk.
It is absorbed when it breaks down into glucose and galactose through facilitated diffusion. Lactose encounters digestion by the enzyme lactase, which is usually present at birth and allows babies to digest the lactose in milk (1).
All mammals lose the ability to digest lactose, including human beings, known as lactose intolerance. There is an inability to digest lactose in this condition such that its concentration remains high in the small intestine after ingestion (1).
Adults who have diminished lactase levels result in dehydration, vomiting, or diarrhea. Some can avoid these symptoms by drinking milk in which the lactose has added lactase for digestion (1).
Constipation and Diarrhea
When fecal material remains in the large intestine, more water is absorbed, and the feces become firmer and drier, making defecation more difficult and painful. Decreased motility of the large intestine will cause constipation (1).
Dietary fiber is essential and increases distention. People can get this enzyme by eating bran, fruits, and vegetables with high fiber content (1).
Laxatives also increase feces defecation.
They can include mineral oil, salts and lead to more repositions in the large intestine (1).
Diarrhea is known as weary stools—diarrhea results from decreased fluid absorption and increased fluid secretion, or both (1).
A bacterial protozoan and viral disease of the intestine tract cause secretory diarrhea. Cholera is in many parts of the world. The cause is a bacterium that reclassifies a toxin that stimulates cyclic AMP production in the secretory cells at the intestinal villi base (1).
This toxin increases the frequency in the opening of the Cl- channels in the apical membrane and increases secretion of Cl-.
Ions and water loss by this severe diarrhea may recover by ingesting a simple solution containing salt and glucose (1).
Traveler’s diarrhea is common when several bacteria produce secretory diarrhea by the exact mechanism of the cholera bacteria. This form of diarrhea is usually less severe (1).
When diarrhea occurs, blood volume decreases, loss of ions increases, and there is water and potassium depletion. The depletion leads to metabolic acidosis, primarily due to K+ and HCO3 (1).
This section concludes the summary of the digestive system.
Sources
Hill, Richard W., et al. Animal Physiology. Oxford University Press, 2018.
Vander, Arthur J., et al. Vander’s Human Physiology: The Mechanisms of Body Function. McGraw-Hill Education, 2019.