1/42
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai | Chat |
|---|
No analytics yet
Send a link to your students to track their progress
What is the function of salivary amylase?
Parotid salivary glands - Located inferior and anterior to the ears between the skin and masseter muscles – its duct empties into vestibule opposite upper second molar
cells secrete watery serous liquid containing salivary amylase
70% of saliva
Chemical digestion in the mouth - initiates the digestion of starches (polysaccharides), breaking them down into disaccharides
What is the function of lingual lipase?
Secreted by glands on the dorsum of the tongue
In newborns, it plays an important role in digesting milk fats, breaking triglycerides into free fatty acids and monoglycerides
Has an optimal pH around 4, allowing it to remain active in the acidic environment of the stomach
In adults, lingual lipase has limited physiological significance
What is the submucosal nerve plexus and what does it do?
In submucosal layer
Regulates secretion and local blood flow
This autonomic nerve plexus regulates the local movements of the muscularis mucosae, which cause folding or wrinkling of the mucosal surface
These subtle contractions do not propel food, but rather agitate and reposition the mucosa to:
Enhance secretion from mucosal glands
Improve contact between the mucosal surface and luminal contents for absorption
What is the myenteric nerve plexus and what does it do
In muscularis layer
Lies between the 2 smooth muscle layers
The nerve plexus consists of fibers from both autonomic divisions and functions to coordinate GI motility
Parasympathetic activation - increase motility
Sympathetic activation - decrease motility
The submucosal plexus regulates chemical secretions and local blood flow, while the myenteric plexus controls gut movement and muscle contractions. The submucosal plexus helps change local muscle fibers in the lining (like the muscularis mucosae) to alter surface area for absorption
What are the differences between the submucosal and myenteric nerve plexuses? What nervous system structure regulates surface area in the GI tract?
The submucosal plexus regulates chemical secretions and local blood flow, while the myenteric plexus controls gut movement and muscle contractions. The submucosal plexus helps change local muscle fibers in the lining (like the muscularis mucosae) to alter surface area for absorption
What cell delivers antigen to the submucosal GI lymph nodes?
What substance is secreted by parietal cells?
Hydrochloric acid
Note: H+ and Cl- are secreted independently from the apical surface of the cell and combine in the lumen of the stomach to form HCl • H+ and K+ exchange via counter transport • HCO3 _ is secreted from the basolateral surface of the parietal cell and enters blood
What are 3 functions of HCl?
Converts pepsinogen → pepsin
Denatures/unfolds proteins by breaking hydrogen bonds
Stimulates secretion of hormones that promote flow of bile and pancreatic juice
Destroys microbes
What are at least 3 stimuli for release of the substance?
Gastrin, ACh, histamine
What substance is secreted by chief cells?
Produce and secrete pepsinogen, the inactive precursor of pepsin, which digests proteins
What is the function of pepsinogen?
Gets converted to pepsin by HCl
Pepsin helps digest proteins by breaking peptide bonds
What is the stimuli for release of pepsinogen?
ACh, gastric acid, gastrin, secretin
What substance is secreted by the ECL cells?
Secrete histamine in response to ACh and gastrin
What is the function of histamine?
Enhancing acid secretion by parietal cells - stimulate HCl by binding to H2 receptors
What are the stimuli for release of histamine?
gastrin
What substance is secreted by G cells
Gastrin
What is the function of gastrin
Stimulates both chief and parietal cells to release their respective secretions. Triggers ECL cell to secrete histamine
Causes increase of protein pump activity - increase production HCl in parietal cell
What is the stimuli for release of gastrin?
digestion of proteins by HCl, pepsin leads to increase of stomach pH
secretion happens when the pH of the stomach goes up or when theres many small peptide units
Under normal circumstances would the pH of blood leaving the stomach be: >, ~, < 7.4?
>, because as parietal cells secrete H+ into the stomach lumen, bicarbonate (HCO3-) is released into the bloodstream, making blood leaving the stomach slightly alkaline
What stimulates the release of CCK?
Released in response to fatty acids and partially digested proteins
What are the target tissues of CCK?
Stimulates pancreatic enzyme secretion
Lipase, amylase, and proteases
Triggers gallbladder contraction and relaxation of the hepatopancreatic sphincter, promoting bile and enzyme entry into the duodenum
What is the stimulus for release of GIP?
Glucose-Dependent Insulinotropic Peptide
Released in response to fatty acids and glucose-rich chyme
What is the target tissue of GIP?
Decreases gastric secretion of HCl and slows gastric emptying
Stimulates insulin release from the pancreas in response to elevated glucose levels
What is the stimulus for release of secretin?
Released primarily in response to acidic chyme (and to a lesser extent, fatty acids, and peptides)
What are the target tissues of secretin?
Decreases gastric secretions and motility
Stimulates pancreatic ducts to release bicarbonate-rich (alkaline) juice, helping neutralize acid in the duodenum
What is the gastric phase of digestion?
(“Stomach Phase”)
Neural Mechanisms
Stretch of the stomach wall by incoming food activates local parasympathetic reflexes and the enteric (myenteric) plexus
Effect: Enhanced peristaltic contractions and increased gastric gland secretions, promoting thorough mixing of food with gastric juice
Hormonal Mechanisms
The presence of partially digested proteins and buffering of stomach acid stimulates G-cells (in the pyloric antrum) to release gastrin
Main targets of gastrin: Parietal cells, which increase HCl secretion and Chief cells which increase pepsinogen secretion
Feedback regulation:
Gastrin secretion inhibited when gastric pH < 2.0
Gastrin secretion stimulated when gastric pH > 2.0 (less acidic conditions)
Alkaline Tide: As parietal cells secrete H⁺ into the stomach lumen, bicarbonate (HCO₃⁻) is released into the bloodstream, making blood leaving the stomach slightly alkaline
What is the intestinal phase of digestion?
(“Duodenal Phase”)
Initiated when chyme enters the duodenum and initiated by activation of duodenal receptors
Functions primarily to inhibit gastric secretion and motility to prevent duodenal overload
Purpose
Prevents rapid shifts in osmolarity that would draw excess water into the intestinal lumen
Chyme from the stomach is typically hypertonic and overload could result in osmotic water loss from the blood into the intestinal lumen leading to potential low blood volume
Prevents large pH fluctuations that could harm intestinal mucosa
Hormonal Regulation
What are some of the differences between the gastric phase of digestion and the intestinal phase of digestion?
Gastric phase
Takes place inside the stomach. It uses muscle movements and strong acids to turn food into a liquid mix called chyme
Releases gastrin to increase stomach acid and boost mixing.
Intestinal phase
Takes place inside the small intestine. It focuses on finishing food breakdown and absorbing nutrients
Releases hormones like secretin and cholecystokinin (CCK) to slow down the stomach and help the pancreas and gallbladder work
What are the pancreatic enzymes involved in protein digestion? How are they activated?
Enzymes released from exocrine cells
Enzyme release is regulated by
Nervous: Vagus nerve
Hormones: released in response to chyme in duodenum
CHO digesting: pancreatic amylase
Triglyceride digesting: Pancreatic lipase
Cleaves fatty acid from glycerol
Protein digesting
Trypsin: secreted in inactive form trypsinogen
activated by enterokinase secreted by intestinal mucosa
Chymotrypsin: secreted as chymotrypsinogen and activated by trypsin
Carboxypeptidase: secreted as procarboxypeptidase also activated by trypsin
These enzymes are all produced in inactive form, so they don’t digest self-cells
What hormone does the beta cells of the Islets of Langerhan’s release?
Synthesize insulin - A peptide hormone composed of 51 amino acids, produced by the β-cells of the pancreatic islets
What do the beta cells of the Islets of Langerhan’s release their hormone in response to?
Released from endocrine cells
Primary stimulus: An increase in blood glucose concentration
Mechanism of Insulin Secretion
Glucose entry into β-cells via GLUT2 transporters
Intracellular glucose concentration rises and glucose is metabolized to produce ATP
Elevated ATP levels cause ATP-sensitive K⁺ channels to close
The resulting decrease in K⁺ efflux depolarizes the β-cell membrane
Depolarization opens voltage-gated Ca²⁺ channels, allowing Ca²⁺ to enter the cell
Exocytosis: The rise in intracellular Ca²⁺ triggers exocytosis of insulin-containing secretory granules
What is the effect on the target tissue of the hormone released from the beta cells of the Islets of Langerhan’s?
Actions of Insulin
Primary target cells: Skeletal muscle and adipose tissue
Metabolic effects:
Promotes glucose uptake by stimulating GLUT4 translocation to the plasma membrane
Inhibits glycogenolysis (breakdown of glycogen to glucose)
Suppresses gluconeogenesis, the conversion of amino acids or fatty acids into glucose
Promotes anabolic processes such as glycogen synthesis, lipid storage, and protein synthesis
Glucose Uptake Regulation
In the absence of insulin, GLUT4 transporters remain sequestered in intracellular GLUT4 storage vesicles (GSVs), limiting glucose uptake
When insulin binds its receptor, signaling cascades stimulate fusion of GSVs with the plasma membrane, increasing glucose transport capacity
What hormone does the alpha cells of the Islets of Langerhan’s release?
Alpha cells: Synthesize glucagon - A 29 amino acid peptide
What do the alpha cells of the Islets of Langerhan’s release their hormone in response to?
Released from endocrine cells
Glucagon
Major stimulus is for release is a decline in blood glucose levels
Other stimuli include increased plasma amino acid levels and the catecholamines
What is the effect on the target tissue of the hormone released from the alpha cells of the Islets of Langerhan’s?
Major target is liver
Glycogenolysis: conversion of glycogen to glucose via cAMP activation
One molecule of glucagon can cause the release of 100 million molecules of glucose into the blood
Gluconeogenesis: formation of glucose from L.A., F.A. and Amino Acid molecules
What are the disaccharides?
Sucrose, maltose, lactose
What enzymes break disaccharides down?
Salivary Amylase - Initiates the digestion of starches (polysaccharides), breaking them down into disaccharides
Absorption in the small intestine
Brush border enzymes complete digestion of the disaccharides
Sucrase digest sucrose to glucose and fructose
Maltase digests maltose to glucose and glucose
Lactase digests lactose to glucose and galactose
What are the resulting monosaccharides from breaking down disaccharides
Sucrase digest sucrose to glucose and fructose
Maltase digests maltose to glucose and glucose
Lactase digests lactose to glucose and galactose
How are fats absorbed from the GI into the blood?
Forms absorbed: Monoglycerides, glycerol, and free fatty acids
Absorption and Transport: Inside intestinal epithelial cells (enterocytes), lipids are reassembled into triglycerides and packaged with proteins into chylomicrons
Chylomicrons enter lacteals (lymphatic capillaries) → travel via the thoracic duct → enter systemic venous circulation, bypassing the liver initially
In Circulation: Lipoprotein lipase (LPL) – an enzyme on capillary endothelium – hydrolyzes chylomicron triglycerides into free fatty acids (FFA) and glycerol. FFA are taken up by cells (especially adipose and muscle)
Primary fates:
Immediate energy use – FFAs oxidized in mitochondria via β-oxidation → acetyl-CoA → ATP
Storage – When cellular ATP and glucose levels are high, FFAs are re-esterified into triglycerides and stored in adipose tissue
Structural roles – Used in cell membrane phospholipids and steroid synthesis.
How are carbohydrates absorbed from the GI into the blood?
Monosaccharides are able to cross the epithelial cells surface for absorption
Glucose and galactose enter the apical surface via a SGLT symporter (co-transport with Na+)
Fructose enters by facilitated diffusion using a GLUT 5 transporter
Glucose, galactose and fructose all leave the basolateral surface of the cell via a GLUT 2 transporter In the liver fructose and galactose are converted to glucose
Primary fates:
Immediate energy use – Glucose is oxidized through glycolysis and the citric acid cycle to produce ATP
Storage as muscle glycogen – Stored locally in skeletal muscle for energy use during contraction
Storage as liver glycogen – Stored in hepatocytes and released during fasting to maintain blood glucose levels
Conversion to fat (lipogenesis) – When glycogen stores are full and energy needs are met, excess glucose is converted to triglycerides for storage in adipose tissue
How are proteins absorbed from the GI into the blood?
Digestion and Absorption:
In the intestinal lumen
Endopeptidases (e.g., trypsin, chymotrypsin) break proteins into smaller peptides
Exopeptidases (e.g., carboxypeptidase, aminopeptidase) release individual amino acids
Peptides and amino acids are absorbed across the luminal membrane of enterocytes:
As dipeptides, tripeptides, or amino acids
Inside the cell, peptides are further hydrolyzed to amino acids
Amino acids enter capillary blood and travel via the hepatic portal vein to the liver
Note: Some larger peptides can cross the enterocyte intact via transcytosis (especially in infants, allowing passive immunity from maternal antibodies)
Primary fates:
Protein synthesis – Taken up by hepatocytes and other body cells for synthesis of enzymes, contractile proteins, and plasma proteins
Energy production – Deamination removes the amino group, leaving a keto acid that enters the citric acid cycle for ATP production
Conversion to fat or glucose – Keto acids can be converted to fatty acids or used in gluconeogenesis when energy demands require
What are the primary functions of the liver
CHO metabolism
Glycogenesis: conversion of glucose to glycogen when blood sugar is high
if glycogen stores are full then glucose is converted into triglycerides
Glycogenolysis: Breakdown of glycogen to glucose, when blood glucose is low
Gluconeogenesis: Synthesis of glucose from non-carbohydrate sources such as lactic acid and amino acids
Lipid metabolism
β-Oxidation: Fatty acids are broken down into acetyl-CoA, which enters the citric acid cycle for ATP production
Lipid synthesis: Hepatocytes synthesize cholesterol, phospholipids, and lipoproteins (VLDL, HDL) for transport
Ketogenesis: During fasting, acetyl-CoA is converted to ketone bodies as an alternate energy source
Protein metabolism
Deamination: Removal of the amine (–NH₂) group from amino acids, producing ammonia (NH₃)
Ammonia is converted to urea in the urea cycle and excreted by the kidneys
Protein synthesis: Hepatic cells produce most plasma proteins, including
Albumin – maintains oncotic pressure
Fibrinogen and clotting factors (II, VII, IX, X) – essential for coagulation
Transport proteins for hormones, lipids, and metals
Exception: The liver does not synthesize γ-globulins (antibodies)
Detoxification of Drugs and Hormones
Cytochrome P450 enzymes chemically modify and inactivate drugs and toxins
Steroid and thyroid hormones (e.g., aldosterone, estrogen, cortisol) are metabolized and excreted after conjugation
Alcohol and ammonia are detoxified via specific hepatic pathways
Excretion of bile pigments:
Bilirubin (from breakdown of heme in worn-out RBCs) is absorbed, conjugated, and excreted in bile
Conjugated bilirubin gives bile its yellow-green color
Synthesis: Bile salts used for emulsification and absorption of dietary fats
Phagocytosis: Kupffer cells destroy aged erythrocytes and microbes
Storage: Glycogen, Vitamins A, B12, D, E, K; minerals copper and iron
What is the primary function of the gallbladder
Stores and concentrates bile up to 10-fold (until it is needed in the small intestine)
H2O and ions reabsorbed by gallbladder mucosa during concentration
CCK stimulates smooth muscle in wall of gallbladder to contract forcing bile into cystic duct → common bile duct → small intestine
Bile flow: Canaliculi empty into small bile ductulus → empty into the R and L hepatic duct → unite to form the common hepatic duct
The common hepatic duct joins with the cystic duct from the gallbladder to form the common bile duct
The common bile duct and pancreatic duct enter the duodenum via the hepatopancreatic ampulla
Bile: Consists of H2O; bile salts; bile acids; cholesterol; lecithin; bile pigment; several ions
Bile salts
sodium and potassium salts of bile acids play a role in emulsification
breakdown of large fat globules into small fat droplets so that pancreatic lipase can act quickly on it
Principle bile pigment is bilirubin derived from the heme of worn-out RBC's