Transcript Document

Anatomy and Physiology, Seventh Edition
Rod R. Seeley
Idaho State University
Trent D. Stephens
Idaho State University
Philip Tate
Phoenix College
Chapter 24
Lecture Outline*
*See PowerPoint Image Slides for all figures and tables pre-inserted into PowerPoint without notes.
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Digestive
Process
Figure 23.2
GI Tract
• External environment for the digestive
process
• Regulation of digestion involves:
– Mechanical and chemical stimuli – stretch
receptors, osmolarity, and presence of
substrate in the lumen
– Extrinsic control by CNS centers
– Intrinsic control by local centers
Receptors of the GI Tract
• Mechano- and chemoreceptors respond
to:
– Stretch, osmolarity, and pH
– Presence of substrate, and end products of
digestion
• They initiate reflexes that:
– Activate or inhibit digestive glands
– Mix lumen contents and move them along
Nervous Control of the GI
Tract
• Intrinsic controls
– Nerve plexuses near the GI tract initiate short
reflexes
– Short reflexes are mediated by local enteric
plexuses (gut brain)
• Extrinsic controls
– Long reflexes arising within or outside the GI tract
– Involve CNS centers and extrinsic autonomic
nerves
Nervous
Control
of the GI
Tract
Figure 23.4
Secretions of the Stomach
• Chyme: ingested food plus stomach secretions
• Mucus: surface and neck mucous cells
– Viscous and alkaline
– Protects from acidic chyme and enzyme pepsin
– Irritation of stomach mucosa causes greater mucus
• Intrinsic factor: parietal cells. Binds with vitamin B12 and helps it to
be absorbed. B12 necessary for DNA synthesis
• HCl: parietal cells
– Kills bacteria
– Stops carbohydrate digestion by inactivating salivary amylase
– Denatures proteins
– Helps convert pepsinogen to pepsin
• Pepsinogen: chief cells. Packaged in zymogen granules released
by exocytosis. Pepsin catalyzes breaking of covalent bonds in
proteins.
• G-cells: secrete the hormone gastrin which stimulates HCl secretion
from parietal cells
Hydrochloric Acid Production
1. CO2 and Cl- diffuse from the
blood into the stomach cell.
2. CO2 combines with H2O
to form H2CO3.
3. H2CO3 dissociates into
bicarbonate (HCO3-) and H+.
4. H+ combines with Cl- in duct
of gastric gland to form HCl-.
5. An ATP pump is necessary to
pump the HCl- into the duct
since the concentration of
HCl- is about a million times
more concentrated in the
duct than in the cytosol of the
cell.
Regulation of Gastric Secretion
• Neural and hormonal mechanisms regulate
the release of gastric juice
• Stimulatory and inhibitory events occur in
three phases
– Cephalic (reflex) phase: prior to food entry
– Gastric phase: once food enters the stomach
– Intestinal phase: as partially digested food enters
the duodenum
Release of Gastric Juice
Figure 23.16
Cephalic Phase
• The taste or smell of food, tactile
sensations of food in the mouth, or
even thoughts of food stimulate the
medulla oblongata.
• Parasympathetic action potentials
are carried by the vagus nerves to
the stomach.
• Preganglionic parasympathetic
vagus nerve fibers stimulate
postganglionic neurons in the
enteric plexus of the stomach.
• Postganglionic neurons stimulate
secretion by parietal and chief cells
(HCl and pepsin) and stimulate the
secretion of the hormone gastrin.
• Gastrin is carried through the
circulation back to the stomach
where it stimulates further secretion
of HCl and pepsin.
Gastric Phase
• Distention of the stomach
activates a parasympathetic
reflex. Action potentials are
carried by the vagus nerves
to the medulla oblongata.
• Medulla oblongata
stimulates further secretions
of the stomach.
• Distention also stimulates
local reflexes that amplify
stomach secretions.
Intestinal Phase
•
1.
2.
3.
Chyme in the duodenum with a
pH less than 2 or containing lipids
inhibits gastric secretions by three
mechanisms
Sensory input to the medulla from
the duodenum inhibits the motor
input from the medulla to the
stomach. Stops secretion of
pepsin and HCl.
Local reflexes inhibit gastric
secretion
Secretin, gastric inhibitory
polypeptide, and cholecystokinin
produced by the duodenum inhibit
gastric secretions in the stomach.
Regulation of Gastric Emptying
• Gastric emptying is regulated by:
– The neural enterogastric reflex
– Hormonal (enterogastrone) mechanisms
• These mechanisms inhibit gastric secretion
and duodenal filling
• Carbohydrate-rich chyme quickly moves
through the duodenum
• Fat-laden chyme is digested more slowly
causing food to remain in the stomach longer
Regulation
of Gastric
Emptying
Figure 23.19
Microscopic Anatomy of the Liver
Figure 23.24c, d
•
Histology of
the Liver
Connective tissue septa branch
from the porta into the interior
– Divides liver into lobules
– Nerves, vessels and ducts follow
the septa
•
Lobules: portal triad at each corner
– Three vessels: hepatic portal vein,
hepatic artery, bile duct (hepatic
duct in diagram)
– Central vein in center of lobule
•
Central veins unite to form hepatic
veins that exit liver and empty into
inferior vena cava
• Hepatic cords: radiate out from
central vein. Composed of
hepatocytes
• Hepatic sinusoids: between
cords, lined with endothelial
cells and hepatic phagocytic
(Kupffer) cells
• Bile canaliculus: between cells
within cords
Functions of the Liver
• Bile production: 600-1000 mL/day. Bile salts (bilirubin), cholesterol,
fats, fat-soluble hormones, lecithin
– Neutralizes and dilutes stomach acid
– Bile salts emulsify fats. Most are reabsorbed in the ileum.
– Secretin (from the duodenum) stimulates bile secretions,
increasing water and bicarbonate ion content of the bile
• Storage
– Glycogen, fat, vitamins, copper and iron. Hepatic portal blood
comes to liver from small intestine.
• Nutrient interconversion
– Amino acids to energy producing compounds
– Hydroxylation of vitamin D. Vitamin D then travels to kidney
where it is hydroxylated again into its active form
• Detoxification
– Hepatocytes remove ammonia and convert to urea
• Phagocytosis
– Kupffer cells phagocytize worn-out and dying red and white blood
cells, some bacteria
• Synthesis
– Albumins, fibrinogen, globulins, heparin, clotting factors
Composition of Bile
• A yellow-green, alkaline solution containing
bile salts, bile pigments, cholesterol, neutral
fats, phospholipids, and electrolytes
• Bile salts are cholesterol derivatives that:
– Emulsify fat
– Facilitate fat and cholesterol absorption
– Help solubilize cholesterol
• Enterohepatic circulation recycles bile salts
• The chief bile pigment is bilirubin, a waste
product of heme
Regulation of
Bile Release
Figure 23.25
Blood and
Bile Flow
Through the
Liver
•
•
•
•
•
•
Pancreas both endocrine and
exocrine
Head, body and tail
Endocrine: pancreatic islets.
Produce insulin, glucose, and
somatostatin
Exocrine: groups acini (grape-like
cluster) form lobules separated by
septa.
Intercalated ducts lead to
intralobular ducts lead to
interlobular ducts lead to the
pancreatic duct.
Pancreatic duct joins common bile
duct and enters duodenum at the
hepatopancreatic ampulla controlled
by the hepatopancreatic ampullar
sphincter
Pancreas
Pancreatic Secretions: Pancreatic Juice
• Aqueous. Produced by columnar epithelium lining smaller ducts. Na+,
K+, HCO3-, water. Bicarbonate lowers pH inhibiting pepsin and
providing proper pH for enzymes
• Enzymatic portion:
– Trypsinogen
– Chymotrypsinogen
– Procarboxypeptidase
– Pancreatic amylase
– Pancreatic lipases
– Deoxyribonucleases and ribonucleases
• Interaction of duodenal and pancreatic enzymes.
– Enterokinase from the duodenal mucosa and attached to the
brush border activates trypsinogen to trypsin.
– Trypsin activates chymotrypsinogen to chymotrypsin
– Trypsin activates procarboxypeptidase to carboxypeptidase.
• Trypsin, chymotrypsin and carboxypeptidase digest proteins:
proteolytic.
• Pancreatic amylase continues digestion of starch
• Pancreatic lipase digests lipids
• Deoxyribonucleases and ribonucleases digest DNA and ribonucleic
acid, respectively
Bicarbonate Ion Production in
Pancreas
Regulation of Pancreatic Secretion
Figure 23.28
Secretions of Large Intestine
• Mucus provides protection
– Parasympathetic stimulation increases rate of goblet cell secretion
• Pumps: bacteria produce acid and the following remove
acid from the epithelial cells that line the large intestine
– Exchange of bicarbonate ions for chloride ions
– Exchange of sodium ions for hydrogen ions
• Bacterial actions produce gases (flatus) from particular
kinds of carbohydrates found in legumes and in artificial
sugars like sorbitol
• Bacteria produce vitamin K which is then absorbed
• Feces consists of water, undigested food (cellulose),
microorganisms, sloughed-off epithelial cells
Digestion, Absorption,
Transport
• Digestion
– Breakdown of food molecules for absorption into
circulation
• Mechanical: breaks large food particles to small
• Chemical: breaking of covalent bonds by digestive
enzymes
• Absorption and transport
– Molecules are moved out of digestive tract and into
circulation for distribution throughout body
Carbohydrates: Hydrolyzed into
Monosaccharides
• Glucose is transported to cells requiring energy; insulin
influences rate of transport
Lipids
•
•
•
•
Include triglycerides, phospholipids,
steroids, fat-soluble vitamins
Bile salts surround fatty acid and glycerol to
form micelles
Chylomicrons are 90% triglyceride, 5%
cholesterol, 4% phospholipid, 1% protein.
Chylomicrons enter blood stream and travel
to adipose tissue. In blood, triglycerides
converted back into fatty acids and glycerol
where they are transported into the adipose
cells, then converted back into triglycerides.
Transport of Lipids Across Intestinal
Epithelium
Fatty Acid
Absorption
Figure 23.36
Lipoproteins
•
•
•
•
•
•
•
All lipids carried in the blood are done so
in combination with protein to make them
soluble in plasma.
Cholesterol: 15% ingested; 85%
manufactured in liver and intestinal
mucosa
Lipids are lower density than water;
proteins are higher density than water
Chylomicrons: 99% lipid and 1% protein
(extremely low density); enter lymph
VLDL: 92% lipid, 8% protein
– Form in which lipids leave the liver
– Triglycerides removed from VLDL
and stored in adipose cells. VLDL
has been converted to LDL.
LDL: 75% lipid, 25% protein
– Transports cholesterol to cells
– Cells have LDL receptors
– # of LDL receptors become less once
cell’s lipid/cholesterol needs are met.
HDL: 55% lipid, 45% protein
– Transports excess cholesterol from
cells to liver
Transport of LDL into Cells
Proteins
• Pepsin breaks proteins into smaller
polypeptide chains
• Proteolytic enzymes produce small
peptide chains
– Dipeptides, tripeptides, amino acids
• After absorption, amino acids are are
carried through the hepatic portal vein
to the liver.
Amino Acid Transport
Chemical Digestion: Nucleic Acids
• Absorption: active transport via
membrane carriers
• Absorbed in villi and transported to liver
via hepatic portal vein
• Enzymes used: pancreatic
ribonucleases and deoxyribonuclease in
the small intestines
Electrolyte Absorption
• Most ions are actively absorbed along the length of
small intestine
– Na+ is coupled with absorption of glucose and amino
acids
– Ionic iron is transported into mucosal cells where it binds
to ferritin
• Anions passively follow the electrical potential
established by Na+
• K+ diffuses across the intestinal mucosa in
response to osmotic gradients
• Ca2+ absorption:
– Is related to blood levels of ionic calcium
– Is regulated by vitamin D and parathyroid hormone
(PTH)
Water Absorption
• 95% of water is absorbed in the small
intestines by osmosis
• Water moves in both directions across
intestinal mucosa
• Net osmosis occurs whenever a concentration
gradient is established by active transport of
solutes into the mucosal cells
• Water uptake is coupled with solute uptake,
and as water moves into mucosal cells,
substances follow along their concentration
gradients
Water and Ions
• Water: can move in
either direction
across wall of small
intestine depending
on osmotic
gradients
• Ions: sodium,
potassium, calcium,
magnesium,
phosphate are
actively transported