Secretions of the GI Tract and Pancreas Lecture (TEST 2) Flashcards
Saliva is Produced by Salivary Glands
- Saliva is produced at a rate of 1L/ day
Function:
- Initial Digestion of Starches and Lipids
- Dilution and buffering of Ingested Food
- Lubrication of Ingested Food with Mucus
Three Major Salivary Glands:
1) PAROTID GLAND
- Largest of the Salivary Structure
- Located near the angle of the Jaw and ear
- Composed of SEROUS CELLS
- Secrete fluid composed of Water, Ions, and Enzymes (Rich in AMYLASE)
- Secrete 25% of daily output of Saliva
2 and 3) SUBMAXILLARY and SUBLINGUAL GLANDS (Mixed Glands)
- Composed of SEROUS and MUCOUS CELLS
- Secrete aqueous Fluid and MUCIN Glycoprotein for Lubrication
- Secrete most of the remaining 75% of daily output of Saliva
Salivary Gland
- ECTODERMAL in Origin
- Has the appearance of “Bunch of Grapes”
- Similar features as the EXOCRINE PANCREAS
- The Blood supplied to the Salivary Glands is distributed by Branches of the EXTERNAL CAROTID ARTERY
Structure of Salivary Glands
1) ACRINUS: Blind End
- Acinar Cells secrete INITIAL Saliva
2) MYOEPITHELIAL CELLS
- Rest of the Basement Membrane of ACINAR Cells
- Contain ACTINOMYCIN
- Have MOTILE Extensions
- When stimulated by Neural Input, contract to EJECT Saliva into the Mouth
3) INTERCALATED DUCTS
- Contains MYOEPITHELIAL CELLS
- Saliva in the INTERCALATED DUCTS is Similar in Ionic Composition to Plasma
4) STRIATED DUCT
- Lined by COLUMNAR EPITHELIAL CELLS (Ductal Cells)
- DUCTAL CELLS Modify the Initial Saliva to produce the FINAL SALIVA (HYPOTONIC)
- Ductal Cells ALTER the Concentration of various Electrolytes
Saliva is not a Simple Ultra-Filtrate of Plasma
1) Saliva is composed of H2O, Electrolytes, Alpha-Amylase, Lingual Lipase, Killikrein, and Mucose
a) ALPHA AMYLASE: Begins Initial Digestion of Carbohydrates
b) LINGUAL LIPASE: Begins Initial Digestion of Lipids
c) KILLIKREIN: PROTEASE involved in the production of BRADYKININ (Vasodilation)
2) Saliva is HYPOTONIC (Compared to Plasma)
a) INCREASE K+ and HCO3- Concentrations
b) DECREASE Na+ and CL- Concentration
Two Main Steps in Formation of Saliva
1) Formation of ISOTONIC, Plasma-like, Solution by ACINAR CELLS
2) Modification of the ISOTONIC Solution by the DUCTAL CELLS
Mechanism of Salivary Secretion
- Combined action is ABSORPTION of Na+ and Cl- and SECRETION of K+ and HCO3-
- There is a NET ABSORPTION of Solute!
- More NaCL is ABSORBED that KHCO3 SECRETION!!!!!!!
Mechanism of Salivary Secretion Cont
1) HCO3- leaves the cell either through the cAMP-activated CFTR (Cystic Fibrosis Transmembrane Regulator) Cl- Channel or via the Cl-/ HCO3- EXCHANGER, both at the Apical membrane
2) CYSTIC FIBROSIS Patients LACK the Cl- Transporter (CFTR)
- Therefore Salivary Ca2+, Na+, and Protein are ELEVATED (Also true for Bronchial Secretions, Pancreatic Juice, and Sweat)
How does Saliva become Hypotonic as it flows through the Ducts?
- DUCTAL CELLS are H2O IMPERMEABLE!!!!!
Ionic Composition of Saliva Depends upon Rate of Secretion
- At INCREASED FLOW RATE, Final Saliva resembles Plasma and Initial Saliva
- At DECREASED FLOW RATE Saliva has LOWER Concentration of Na+ and Cl- Higher Concentration of K+
- Amount of Time that Saliva is in Contact with DUCTAL CELLS Influences the Ionic Composition (“CONTACT TIME” Dependent Mechanism)
- At INCREASED FLOW RATES, Ductal Cells have LESS TIME to MODIFY Saliva; At DECREASED FLOW RATES, they have MORE TIME to MODIFY Saliva
- The “Contact Time” explanation DOES NOT apply to HCO3-
- HCO3- Secretion is SELECTIVELY Stimulated when Saliva Production is Stimulated
Innervation of Salivary Glands
- ANS not only has effects on Secretion, but also on Blood Flow, Ductular Smooth Muscle Activity, Growth, and Metabolism of the Salivary Glands
1) PARASYMPATHETIC:
- Presynaptic Nerves originated at FACIAL and GLOSSOPHARYNGEAL Nerves, Postsynaptic Fibers in the Autonomic Ganglia Innervate INDIVIDUAL Glands
2) SYMPATHETIC:
- Preganglionic Nerves originate at the CERVICAL Ganlgion, whose Postglanglionic Fibers extend to the Glands in the PERIARTERIAL SPACES
Regulation of Salivation Secretion by the ANS
- Parasympathetic effects DOMINATE
- VASOPRESSIN and ALDOSTERONE modify the Composition of Saliva by DECREASING its Na+ Concentration and INCREASING its K+ Concentration
- Stimulation of Salivary Cells results in:
a) INCREASED Saliva Production
b) INCREASED HCO3- and Enzyme Secretions
c) Contraction of MYOEPITHELIAL Cells
Two Unusual Features in the Regulation of Salivary Secretion
1) Salivary is EXCLUSIVELY under the Control of the ANS!!!!
- Other GI Secretions are under BOTH Neural and Hormonal Control
2) Salivary Secretion is INCREASED by BOTH Parasympathetic and Sympathetic Stimulation
- generally, PNS and SNS have OPPOSITE Actions
Cells of the Gastric Mucosa secrete Gastric Juice
Main Components of Gastric Juice:
Main Components of Gastric Juice:
1) HCL (H+):
- Together with Pepsin, it INITIATES the Process of PROTEIN Digestion
- However, in their Absence, PANCREATIC ENZYMES HYDROLYZE all Ingested Proteins
- Necessary for the CONVERSION of PEPSINOGEN to the Enzyme PEPSIN
- Kills a LARGE NUMBER of Bacteria that enter the cell
2) PEPSINOGEN:
- Inactive Precursor of Pepsin
3) MUCUS
- Lines the Wall of the Stomach and PROTECTS it from Damage
- Acts as LUBRICANT
- Together with HCO3-, it Neutralizes Acid and maintains the Surface of the Mucosa at a NEUTRAL pH
4) INTRINSIC FACTOR
- Required for the Absorption of VITAMIN B12 in the ILEUM
- Indispensable Component
5) H2O
- Medium for the action of HCL and Enzymes
- Solubilizes much of the Ingested Material
The Gastric Mucosa is divided into the OXYNTIC Gland area and the Pyloric Gland Area
OXYNTIC Gland:
- Located in the PROXIMAL 80% of the STOMACH (Body and Fundus)
- Secretes ACID!!!!!
PYLORIC GLAND:
- Located in the DISTAL 20% of the Stomach (Antrum)
- Synthesizes and release GASTRIN
Major Function of the Parietal Cells in the Secretion of HCL
- Stomach contains ~1 Billion parietal Cells
- The Number of Parietal Cells determine the Maximal SECRETORY RATE
- The Stomach Secretes 1 to 2 L of Gastric Juices
- The Function of the LOW GASTRIC pH (1 to 2) is to CONVERT Pepsinogen to Pepsin
- HCL is formed at the VILLUS-Like Membranes of the Canaliculi which are continuous with the Lumen
Cellular Mechanism of HCL Secretion by Gastric Parietal Cells
- Result: Net Secretion of HCL and Net Absorption of HCO3-
- OMEPRAZOLE inhibits the H+/K+ Exchanger that sends the H+ into the Lumen!!!!!!!!
Regulation of HCL Secretion
HISTAMINE (A Paracrine)
1) HISTAMINE (A Paracrine)
- STIMULATES HCL Secretion
- Released from the ENTEROCHROMAFFIN-LIKE (ECL) Cells in the Gastric Mucosa
- Gastrin and ACh stimulate Histamine RELEASE
- Binds to H2 Receptors on Parietal Cells (CIMETIDINE BLOCKS THESE RECEPTORS)
- Binding of histamine to H2 Receptors leads to a SECOND MESSENGER CASCADE (cAMP) that ultimately results in the Secretion of H+ through the H+/K+ ATPase
Regulation of HCL Secretion
ACH (A Neurotransmitter)
ACH (A Neurotransmitter):
- STIMUALES HCL Secretion
- Released from VAGUS NERVE Innervating the Gastric Mucosa
- Binds to M3 mAChR on PARIETAL CELLS (Atropine blocks these Receptors)
- Binding to ACh to M3 mAChRs leads to a SECOND MESSENGER CASCADE (IP3/ Ca2+) that ultimately results i the Secretion of H+ through the H+/K+ ATPase
- Has also INDIRECT Effects on HCL Secretion through the stimulation of ECL Cells, which release HISTAMINE
Regulation of HCL Secretion
Gastrin (A Hormone)
Gastrin (A Hormone)
- STIMUALTES HCL Secretion
- Secreted into the Circulation of G Cells in the Antrum and delivered back to the Stomach via the Circulation
- Binds to CCKb Receptors on PAREITAL CELLS (Atropine Blocks these receptors)
- CCKb Receptor has EQUAL AFFINITY for Gastrin and CCK
- CCKa Receptor is SPECIFIC for CCK
- Binding to CCKb Receptors leads to a Second Messenger Cascade (IP3/ Ca2+) that ultimately results in the Secretion of H+ through the H+/ K+ ATPase
- Stimulated by Gastric Distension, presence of Small Peptides and Amino Acids, and stimulation of the VAGUS NERVE
- Like ACh, it has also INDIRECT EFFECTS on HCL Secretion through the Stimulation of ECL Cells, which release Histmaine
Regulation of HCL Secretion
Somatostatin (A Paracrine)
- INHIBITS HCL Secretion
- Released for DELTA (D) Cells, which are mostly licked in the ANTRUM
- Binds to SOMATOSTATIN Receptors (Somatostatin Receptor Type 2, SSTR2) on PARIETAL CELLS
- Bidns to SOMATOSTATIN to its Receptor INHIBITS ADENYLATE CYCLASE that ultimately results in the Inhibition of Secretion of H= (DIRECT PATHWAY)
- In the INDIRECT PATHWAY, Somatostatin INHIBITS BOTH Histamine release from ECL Cells and Gastrin Release from G Cells
- Also INHIBITS other GI Hormones
The Rate of Secretion of HCL is also regulated by Interactions among Histamine, ACh, and Gastrin
- Potentiation occurs when the combined response to Two Stimulants EXCEEDS the SUM of their INDIVIDUAL Responses
- ** Requires the presence of Separate Receptors on the Target Cell for EACH Stimulant
- Examples of Potentiation Include:
a) HISTAMINE Potentiates the actions of ACh and Gastrin
b) ACh potentiates the actions of HISTAMINE and GASTRIN - Due to Potentiation Phenomena:
a) ANTAGONISTS of H2 Receptors (Ex: Cimetidine) blocks the DIRECT Action of Histamine and also BLOCK POTENTIATED Effects of ACh and Gastrin
b) ANTAGONIST of mAChRs (Ex: Atropine) block the DIRECT EFFECTS of ACh and the ACh-Potentiated effects of HISTAMINE and GASTRIN
Summary of the Agents that Stimulate and Inhibit H+ Secretion by Gastric Parietal Cells
- OMEPRAZOLE: Inhibits the H+/K+ ATPase, used in the Treatment of ULCERS to REDUCE H+ Secretion
- CIMETIDINE: Antagonist of H2 Receptors, used to read DUODENAL and GASTRIC ULCERS, Gastroesophageal Reflex Disease
***There is a PASSIVE FEEDBACK MECHANISM regulating HCL Secretion! As the pH FALLS, Gastrin Release is INHIBITED; DECREASED HCL Secretion!!!!
The Role of the Vagus Nerve on HCL Secretion from Parietal Cells is TWOFOLD
- Vagus Nerve stimulation of HCL Secretion by Parietal Cells:
1) DIRECT PATHWAY
2) INDIRECT PATHWAY - Atropine BLOCK the DIRECT PATHWAY of Vagal Stimulation
- Atropine WILL NOT BLOCK the Vagal Effects go Gastrin Secretion because the Neurotransmitter at the Synapse of G Cells is GRP!!!!!!!!!
Gastric HCL Secretion is divided into Three Phase
1) CEPHALIC PHASE via Vagus
- Parasympathetic EXCITE Pepsin and Acid Production
2) GASTRIC PHASE
- Local Nervous Secretory Reflexes
- Vagal Reflexes
- Gastrin-Histamine Stimualtion
3) INTESTINAL PHASE
- Nervous Mechanism
- Hormonal Mechanism
Cephalic Phase
- Accounts for ~30% of Total HCL Secreted in response to a Meal
- Brain tells stomach to prepare for receipt of Meal
STIMULI:
- Smelling and Tasting, Chewing, Swallowing, and Conditioned Reflexes
MECHANISMS:
1) Vagus Nerve —> Parietal Cell
- Innervation releasing ACh to Parietal Cells
- ACh Stimulate Secretion of HCL from parietal Cells
2) Vagus Nerve —> Gastrin —> Periatal Cells
- Innervation releasing Gastrin-Releasing Peptide (GRP) to G Cells
- G Cells release GASTRIN into the Circulation
- Gastrin is delivered back to the Stomach to STIMULATE HCL Secretion fro Parietal Cells
VAGOMTOMY ABOLISHED this PHASE!!!!!!**
Gastric Phase
- Account for ~60% of the total HCL Secreted in response to a meal
STIMULI:
- Distension of the Stomach and presence of Breakdown of Proteins, Amino Acids, and Small Peptides
MECHANISMS:
- Distention (Activates Mechanoreceptors in the Mucosa of both OXYNTIC and PYLORIC Gland)
1) Vagus Nerve —> Parietal Cell - Innervation releasing ACh to parietal Cells
- ACh stimulate Secretion of HCL from Parietal Cell
2) Vagus nerve —> Gastrin —> Parietal Cell
- Innervation released Gastrin-Releasing Peptide (GRP) to G Cells
- G Cells release Gastrin into Circulation
- Gastrin is delivered back to the Stomach to stimulate HCL Secretion from Parietal Cells
3) Distension of Antrum
- Local Reflex (Pyloropyloric Reflex) —> Gastrin —> Parietal Cells
4) Amino Acids and Small Peptides
- Gastrin —> Parietal Cells
Coffee (Caffeinated and Decaffeinated) also stimulate gastric HCL Secretion!!!!!!!!!****
Intestine Phase
- Accounts for > 10% of the total HCL Secreted in Response to Meals
1) Distention of Small Intestine
- Stimulates ACID Secretion
2) Digested Protein (Amino Acids)
- Stimulate Acid Secretion via DIRECT Effect on Pareital Cell: Gastrin (Intestinal G Cells) —> Parietal Cells
Gastric Juice composition depends on Secretion Rate
- At LOW Secretion Rates, the Final Juice is essentially a Solution of NaCl
- At HIGHER Secretion Rates, the Concentration of Na+ DECREASES and that go H+ INCREASES
- At PEAK RATES, Gastric Juice is PRIMARILY HCL
- Gastric Juice and Plasma are approximately ISOTONIC
Two Component Model of Gastric Secretion
- Gastric Juice can be seen as a Mixture of two separate Secretions:
1) NON PARIETAL: - Basal Alkaline Secretion of Constant and Low Volue
- Its Primary constituents are Na+ and Cl-, K+ is present at the same Concentration as in Plasma
- HCO3- is Secreted at a Concentration of approximately 30 mEq/L
2) PARIETAL:
- Is Slimly HYPEROSMOTIC
- Contains 150 to 160 mEq H+/L and 10 to 20 mEq K+/L
- Cl- is the ONLY ANION Present
- At the Secretion Rate iNCREASES, the Concentrations of Electrolytes begin to approach those of pURE PARIETAL CELL SECRETION
***Knowledge of the Composition of Gastric Juice is required in the Treatment of Patients suffering from Vomiting or Patients maintained with IV!!!!!
Regulation of Gastrin Release
- GRP stimulate GASTRIN Release
- SOMATOSTATIN acts on G Cells to INHIBIT Gastrin Release
- VAGAL Activation Stimulates Gastrin release by Releasing GRP and INHIBITING the release of SOMATOSTATIN
- NEGATIVE FEEDBACK Regulation by Gastrin
(Gastrin itself INCREASES Somatostatin) - H+ in the Lumen of the Stomach stimulate release of Somatostatin
Pepsinogen is Secreted ONLY when the Gastric pH is ACIDIC enough to Convert it to Pepsin
- PEPSINOGEN is Secreted by CHIEF CELLS and by MUCUS Cells in the OXYNTIC GLANDS
- In order to begin the process of PROTEIN DIGESTION, Pepsinogen need to be converted to Pepsin
- ** This require H+ Secretion from Parietal Cells to lower pH of Gastric Contents (pH > 5)
- VAGUS NERVE stimulation is the MOST IMPORTANT Stimulus for PEPSINOGEN Secretion
- H+ Triggers LOCAL CHOLINERGIC Reflexes that stimulate Chief Cells to secrete PEPSINOGEN
Pepsin Degrades Food Proteins into Peptides
PEPSIN Converts More Pepsinogen to Pepsin
- Proteolytic Enzyme (Splits Interior Peptide Linkages)
- Optimal pH is between 1.8 to 3.5
- REVERSIBLE Inactivated at > pH 5.0
- IRREVERSIBLE Inactivated > pH 7 to 8
Intrinsic Factor is required for Absorption of Vitamin B12 in the Ileum
INTRINSIC FACTOR:
a) Is a MUCOPROTEIN that is Secreted by PARIETAL CELLS
b) Combines with Vitamin B12 to form a Complex that is REQUIRED for Vitamin B12 ABSORPTION
c) Is the ONLY Secretion by the Stomach that is REQUIRED (ESSENTIAL)
- Failure to Secrete Intrinsic Factor leads to PERNICIOUS ANEMIA
- ** A common underlying Cause is Destruction of Gastric Parietal Cells (As in Atrophic Gastritis)
- Liver stores enough Vitamin B12 to last for several Years!
Growth of Gastric Mucosa
- The Gastric Epithelium secretes HCO3- and Mucus to form the Gel-Liek MUCOSAL BARRIER
a) Mucous neck cells SECRETE MUCUS
b) Gastric Epithelial cells SECRETE HCO3-
- The Mucosal Barrier PROTECTS the Gastric Mucosal Epithelium against the HCL and PEPSIN
- HCO3- and Mucus, Prostaglandins, Mucosal Blood Flow, and Growth Factor PROTECT the Gastric Mucosa
- Acid, Pepsin, NSAIDs, Helicobacter pylori, Aspirin, Alcohol, Bile, and Stress DAMAGE the Gastric Mucosa
Peptic Ulcer Diseases
- ~500 people develop PEPTIC ULCER DISEASE in the US each year
- In the US, H. pylori infection and the use of Nonsterodal Anti-Infalmmatoruy Drugs (NSAIDS) are the PREDOMINANT CAUSE (48% and 24% of cases, respectively)
Peptic Ulcer is created when:
a) Loss of PROTECTIVE Mucosal Barrier
b) EXCESSIVE H+ and PEPSIN Secretion
c) Combination of the Above mentioned
TWO TYPES:
1) GASTRIC Ulcers
2) DUODENAL Ulcers
Gastric Ulcers
- Forms PRIMARILY because the MUCOSAL BARRIER is DEFECTIVE
- Major causative agent is Helicobacter pylori
Helicobacter pylori:
- Release CYTOTOXINS that breakdown the Mucosal Barrier and underlying Cells
- The enzyme UREASE allows the Bacteria to Colonize the Gastric Mucosa
- UREASE converts the Urea to NH3, which ALKALIZES the Local Environment
**A DiagnosticTest is based on UREASE ACTIVITY!!!!!!!*
Duodenal Ulcers
- MORE COMMON than Gastric Ulcers
- Forms because H+ Secretory Rates are HIGHER than Normal
- Role fo H. pylori is INDIRECT
a) Inhibits SOMATOSTATIN Secretion from D Cells: INHIBITION OF INHIBITION
b) Gastric H+> Pylori Infection spread to the Duodenum and INHIBITS Duodenal HCO3- Secretion
- When excessive H+ arrives to the Duodenum, it overwhelms the Buffer Capacity to HCO3- in Pancreatic Juice
Zollinger-Ellison Syndrome
DUODENAL ULCERS
- H+ Secretory Rates are the HIGHEST
- Tumor, usually in the Pacreas, Secretes ALRGE QUANTITIES of GASTRIN
a) INCREASES H+ Secretion by Parietal Cells
b) INCREASES parietal Cell Mass (Trophic Effects) - When excessive H+ arrives to the Duodenum, it overwhelms the Buffer Capacity of HCO3- in Pancreatic Juice, creating an ULCER
- Low Duodenal pH INACTIVATES PANCREATIC LIPASES, resulting in STEATORRHEA
- Treatment options include Cimetidine, Omeprazole, and Surgical Removal of the Tumor
Gastric Ulcer Summary
H+ Secretion:
- DECREASES
Gastrin Leves:
- INCREASES (Because of Decreased H+ Secretion)
Other Description:
- Causes damage to Protective Barrier of Gastric Mucosa
Duodenal Ulcer
H+ Secretion:
- INCREASES
Gastrin Leves:
- INCREASES (Gastrin response to Ingestion of Food)
Other Description:
- INCREASES Parietal Cell Mass due to INCREASE Gastrin Levels
Zollinger-Ellison Syndrome
H+ Secretion:
- INCREASE GREATLY
Gastrin Leves:
- INCREASES GREATLY
Other Description:
- Gastrin is Secreted by Pancreatic Tumor
- INCREASES parietal Cell Mass due to Trophic effect of INCREASED Gastrin levels
Overview of Pancreatic Secretion
- Pancreatic Juice contains HCO3- for the NEUTRALIZATION of H+ from the Stomach, and Enzyme Secretions to Digest Carbohydrates, Proteins, and Lipids into ABSORBABLE MOLECULES!!!!!
Exocrine Pancreas
- Constitutes ~90% of the Pancreas
- Secrete ~1L/ day of Fluid into the Lumen
Two Main Components of its Secretion:
1) Aqueous Solution CONTAINING HCO3-
2) ENZYMATIC SECRETION
Anatomically, it is Organized like Salivary Glands
1) ACINUS:
- Lined by ACinar Cells that Secrete the Enzymatic Portion
2) DUCTS:
- Lined by Ductal Epithelial Cells, which extend to the region of the Acinus contains CENTROACINAR CELLS
* **Ductal and Centroacinar cells secrete the Aqueous Solution containing HCO3-
PANCRETIC SECRETION is ISOTONIC!!!!!!!***
Innervations of the Exocrine Pancreas
- Innervated by PARASYMPATHETIC and SYMPATHETIC Nervous System
Sympathetic NS:
- Postganglionic nerves from the Celiac and Superior Mesenteric plexus
Parasympathetic NS:
- Vagus Nerves
- PREGanglionic Fibers synapse in the ENS
- POSTGanglionic Fibers synapse on the EXOCRINE PANCREASE
In Contrast to the Salivary Glands, Parasympathetic activity STIMULATES PANCREATIC SECRETION and Sympathetic activity INHIBITS PANCREATIC SECRETION!!!!!!!**
Modification of Initial Pancreatic Secretion by Ductal Cells
- The Net result is the Secretion of HCO3- into Pancreatic Ductal Juice and Net Absorption of H+!!!
Ionic Composition of Pancreatic Juice depends upon rate of Secretion
- At HIGH FLOW RATE, Pancreatic Juice HCO3- is HIGHEST and Cl- is LOWEST
- AT LOW FLOW RATE, HCO3- is LOWEST and Cl- is HIGHEST
- There is a Reciprocal Relationship between HCO3- and Cl- Concentrations, which is maintained by the HCO3-/ Cl- EXCHANGER in the Apical Membrane of Ductal Cells!!!
Regulation of Pancreatic Secretions
1) Phenylalanine, Methionine, Tryptophan, Small Peptides, Fatty Acids
2) I Cells
3) CCK
4) ACINAR CELLS: IP3, Ca2+ (ACh Potentiates)
5) Enzymes
Regulations of Pancreatic Secretions Cont
1) H+
2) S Cells
3) Secretin
4) DUCTAL CELLS: cAMP (ACh Potentiates)
5) Aqueous Solution (Na, HCO3-)
Saliva
Characteristics of Secretion:
- High [HCO3-]
- High [K+]
- Hypotonic
- Alpha Amylase and Lingual Lipase
Factors that Increase Secretion:
- Parasympathetic (Prominent)
- Sympathetic
Factors that Decrease Secretion:
- Sleep
- Dehydration
- Atropine
Gastric
Characteristics of Secretion:
- HCL
- Pepsinogen
- Intrinsic Factor
Factors that Increase Secretion:
- Gastrin
- Acetylcholine
- Histamine
Factors that Decrease Secretion:
- H+ int he Stomach
- Cyme in the Duodenum
- Somatostatin
- Atropine
- Cimetidine
- Omeprazole
- Parasympathetic
Pancreatic
Characteristics of Secretion:
- High [HCO3-]
- Isotonic
- Pancreatic Lipase, Amylase, Proteases
Factors that Increase Secretion:
- Parasympathetic
- Secretin
- CCK (Potentitates Secretion)
Factors that Decrease Secretion:
- None
Bile
Characteristics of Secretion:
- Bile Salts
- Bilirubin
- Phospholipids
- Cholesterol
Factors that Increase Secretion:
- CCK (Contraction of the Gallbladder and Relaxation of the Sphincter of Oddi)
- Parasympathetic
Factors that Decrease Secretion:
- Ileal Resection
Formation of Pancreatic Secretion
Two Components:
1) ENZYMATIC SECRETION by ACINAR CELLS:
- Enzymes required for Digestion of Carbohydrates, Proteins, and Lipids are Secreted
- PANCREATIC AMYLASE and LIPASES are SECRETED as ACTIVE ENZYMES
- Pancreatic PROTEASES are SECRETED in INACTIVE FORMS and converted to their ACTIVE FORMS in the LUMEN of the DUODENUM
2) AQUEOUS SECRETION by CENTROACINAR and DUCTAL CELLS
- CENTROACINAR and DUCTAL CELLS produce the INITIAL AQUEOUS Solution which is ISOTONIC and CONTAINS Na+, K+, Cl-, HCO3-
- The initial Secretion is then modified by TRANSPORT PROCESSES in the DUCTAL EPITHELIAL CELLS!!!!!!!!!
Like Gastric Secretion, Pancreatic Secretion is divided into CEPHALIC, GASTRIC, and INTESTINAL Phases
1) CEPHALIC PHASE:
- Initiated by Smell. Taste, and Conditioning
- Mediated by the VAGUS NERVE
- PRODUCES MAINLY AN ENZYMATIC SECRETION!!!!!!!!!
2) GASTRIC PHASE:
- Initiated by DISTENTION of the Stomach
- Mediated by the VAGUS NERVE
- PRODUCES MAINLY AN ENZYMATIC SECRETION!!!!!!!!!
3) INTESTINAL PHASE***:
- MOST IMPORTANT PHASE: Accounts for 80% OF PANCREATIC SECRETION!!!!!!!!!
- BOTH ENZYMATIC and AQUEOUS SECRETIONS ARE STIMULATED!!!!!!!!!
How Acute Pancreatitis occurs
- Acute Pancreatitis occurs when the PANCREATIC ENZYMES are ACTIVATED in Pancreatic Tissue rather than in the LUMEN of the Intestine, resulting in the AUTODIGESTION of PANCREATIC TISSUE!!!!!!!
