Secretions of the GI Tract and Pancreas Lecture (TEST 2)

Question 1

Saliva is Produced by Salivary Glands

Answer 1

• 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

Question 2

Salivary Gland

Answer 2

• 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

Question 3

Structure of Salivary Glands

Answer 3

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

Question 4

Saliva is not a Simple Ultra-Filtrate of Plasma

Answer 4

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

Question 5

Two Main Steps in Formation of Saliva

Answer 5

1) Formation of ISOTONIC, Plasma-like, Solution by ACINAR CELLS
2) Modification of the ISOTONIC Solution by the DUCTAL CELLS

Question 6

Mechanism of Salivary Secretion

Answer 6

• 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!!!!!!!

Question 7

Mechanism of Salivary Secretion Cont

Answer 7

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)

Question 8

How does Saliva become Hypotonic as it flows through the Ducts?

Answer 8

• DUCTAL CELLS are H2O IMPERMEABLE!!!!!

Question 9

Ionic Composition of Saliva Depends upon Rate of Secretion

Answer 9

• 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

Question 10

Innervation of Salivary Glands

Answer 10

• 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

Question 11

Regulation of Salivation Secretion by the ANS

Answer 11

• 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

Question 12

Two Unusual Features in the Regulation of Salivary Secretion

Answer 12

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

Question 13

Cells of the Gastric Mucosa secrete Gastric Juice

Main Components of Gastric Juice:

Answer 13

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

Question 14

The Gastric Mucosa is divided into the OXYNTIC Gland area and the Pyloric Gland Area

Answer 14

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

Question 15

Major Function of the Parietal Cells in the Secretion of HCL

Answer 15

• 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

Question 16

Cellular Mechanism of HCL Secretion by Gastric Parietal Cells

Answer 16

• Result: Net Secretion of HCL and Net Absorption of HCO3-

- OMEPRAZOLE inhibits the H+/K+ Exchanger that sends the H+ into the Lumen!!!!!!!!

Question 17

Regulation of HCL Secretion

HISTAMINE (A Paracrine)

Answer 17

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

Question 18

Regulation of HCL Secretion

ACH (A Neurotransmitter)

Answer 18

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

Question 19

Regulation of HCL Secretion

Gastrin (A Hormone)

Answer 19

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

Question 20

Regulation of HCL Secretion

Somatostatin (A Paracrine)

Answer 20

• 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

Question 21

The Rate of Secretion of HCL is also regulated by Interactions among Histamine, ACh, and Gastrin

Answer 21

• 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

Question 22

Summary of the Agents that Stimulate and Inhibit H+ Secretion by Gastric Parietal Cells

Answer 22

• 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!!!!

Question 23

The Role of the Vagus Nerve on HCL Secretion from Parietal Cells is TWOFOLD

Answer 23

• 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!!!!!!!!!

Question 24

Gastric HCL Secretion is divided into Three Phase

Answer 24

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

Question 25

Cephalic Phase

Answer 25

• 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!!!!!!**

Question 26

Gastric Phase

Answer 26

• 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!!!!!!!!!****

Question 27

Intestine Phase

Answer 27

• 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

Question 28

Gastric Juice composition depends on Secretion Rate

Answer 28

• 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

Question 29

Two Component Model of Gastric Secretion

Answer 29

• 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!!!!!

Question 30

Regulation of Gastrin Release

Answer 30

• 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

Question 31

Pepsinogen is Secreted ONLY when the Gastric pH is ACIDIC enough to Convert it to Pepsin

Answer 31

• 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

Question 32

Pepsin Degrades Food Proteins into Peptides

Answer 32

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

Question 33

Intrinsic Factor is required for Absorption of Vitamin B12 in the Ileum

Answer 33

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!

Question 34

Growth of Gastric Mucosa

Answer 34

• 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

Question 35

Peptic Ulcer Diseases

Answer 35

• ~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

Question 36

Gastric Ulcers

Answer 36

• 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!!!!!!!*

Question 37

Duodenal Ulcers

Answer 37

• 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

Question 38

Zollinger-Ellison Syndrome

Answer 38

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

Question 39

Gastric Ulcer Summary

Answer 39

H+ Secretion:
- DECREASES

Gastrin Leves:
- INCREASES (Because of Decreased H+ Secretion)

Other Description:
- Causes damage to Protective Barrier of Gastric Mucosa

Question 40

Duodenal Ulcer

Answer 40

H+ Secretion:
- INCREASES

Gastrin Leves:
- INCREASES (Gastrin response to Ingestion of Food)

Other Description:
- INCREASES Parietal Cell Mass due to INCREASE Gastrin Levels

Question 41

Zollinger-Ellison Syndrome

Answer 41

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

Question 42

Overview of Pancreatic Secretion

Answer 42

• Pancreatic Juice contains HCO3- for the NEUTRALIZATION of H+ from the Stomach, and Enzyme Secretions to Digest Carbohydrates, Proteins, and Lipids into ABSORBABLE MOLECULES!!!!!

Question 43

Exocrine Pancreas

Answer 43

• 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!!!!!!!***

Question 44

Innervations of the Exocrine Pancreas

Answer 44

• 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!!!!!!!**

Question 45

Modification of Initial Pancreatic Secretion by Ductal Cells

Answer 45

• The Net result is the Secretion of HCO3- into Pancreatic Ductal Juice and Net Absorption of H+!!!

Question 46

Ionic Composition of Pancreatic Juice depends upon rate of Secretion

Answer 46

• 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!!!

Question 47

Regulation of Pancreatic Secretions

Answer 47

1) Phenylalanine, Methionine, Tryptophan, Small Peptides, Fatty Acids
2) I Cells
3) CCK
4) ACINAR CELLS: IP3, Ca2+ (ACh Potentiates)
5) Enzymes

Question 48

Regulations of Pancreatic Secretions Cont

Answer 48

1) H+
2) S Cells
3) Secretin
4) DUCTAL CELLS: cAMP (ACh Potentiates)
5) Aqueous Solution (Na, HCO3-)

Question 49

Saliva

Answer 49

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

Question 50

Gastric

Answer 50

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

Question 51

Pancreatic

Answer 51

Characteristics of Secretion:

• High [HCO3-]
• Isotonic
• Pancreatic Lipase, Amylase, Proteases

Factors that Increase Secretion:

• Parasympathetic
• Secretin
• CCK (Potentitates Secretion)

Factors that Decrease Secretion:
- None

Question 52

Bile

Answer 52

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

Question 53

Formation of Pancreatic Secretion

Answer 53

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!!!!!!!!!

Question 54

Like Gastric Secretion, Pancreatic Secretion is divided into CEPHALIC, GASTRIC, and INTESTINAL Phases

Answer 54

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!!!!!!!!!

Question 55

How Acute Pancreatitis occurs

Answer 55

• 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!!!!!!!