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

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1
Q

Saliva is Produced by Salivary Glands

A
  • 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
2
Q

Salivary Gland

A
  • 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
3
Q

Structure of Salivary Glands

A

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

4
Q

Saliva is not a Simple Ultra-Filtrate of Plasma

A

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

5
Q

Two Main Steps in Formation of Saliva

A

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

6
Q

Mechanism of Salivary Secretion

A
  • 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!!!!!!!
7
Q

Mechanism of Salivary Secretion Cont

A

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)

8
Q

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

A
  • DUCTAL CELLS are H2O IMPERMEABLE!!!!!
9
Q

Ionic Composition of Saliva Depends upon Rate of Secretion

A
  • 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
10
Q

Innervation of Salivary Glands

A
  • 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

11
Q

Regulation of Salivation Secretion by the ANS

A
  • 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
12
Q

Two Unusual Features in the Regulation of Salivary Secretion

A

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

13
Q

Cells of the Gastric Mucosa secrete Gastric Juice

Main Components of Gastric Juice:

A

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

14
Q

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

A

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
15
Q

Major Function of the Parietal Cells in the Secretion of HCL

A
  • 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
16
Q

Cellular Mechanism of HCL Secretion by Gastric Parietal Cells

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

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

17
Q

Regulation of HCL Secretion

HISTAMINE (A Paracrine)

A

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
18
Q

Regulation of HCL Secretion

ACH (A Neurotransmitter)

A

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
19
Q

Regulation of HCL Secretion

Gastrin (A Hormone)

A

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
20
Q

Regulation of HCL Secretion

Somatostatin (A Paracrine)

A
  • 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
21
Q

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

A
  • 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

22
Q

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

A
  • 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!!!!

23
Q

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

A
  • 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!!!!!!!!!
24
Q

Gastric HCL Secretion is divided into Three Phase

A

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

25
Q

Cephalic Phase

A
  • 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!!!!!!**

26
Q

Gastric Phase

A
  • 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!!!!!!!!!****

27
Q

Intestine Phase

A
  • 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

28
Q

Gastric Juice composition depends on Secretion Rate

A
  • 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
29
Q

Two Component Model of Gastric Secretion

A
  • 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!!!!!

30
Q

Regulation of Gastrin Release

A
  • 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
31
Q

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

A
  • 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
32
Q

Pepsin Degrades Food Proteins into Peptides

A

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
33
Q

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

A

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!
34
Q

Growth of Gastric Mucosa

A
  • 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

35
Q

Peptic Ulcer Diseases

A
  • ~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

36
Q

Gastric Ulcers

A
  • 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!!!!!!!*

37
Q

Duodenal Ulcers

A
  • 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

38
Q

Zollinger-Ellison Syndrome

A

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
39
Q

Gastric Ulcer Summary

A

H+ Secretion:
- DECREASES

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

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

40
Q

Duodenal Ulcer

A

H+ Secretion:
- INCREASES

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

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

41
Q

Zollinger-Ellison Syndrome

A

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
42
Q

Overview of Pancreatic Secretion

A
  • Pancreatic Juice contains HCO3- for the NEUTRALIZATION of H+ from the Stomach, and Enzyme Secretions to Digest Carbohydrates, Proteins, and Lipids into ABSORBABLE MOLECULES!!!!!
43
Q

Exocrine Pancreas

A
  • 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!!!!!!!***

44
Q

Innervations of the Exocrine Pancreas

A
  • 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!!!!!!!**

45
Q

Modification of Initial Pancreatic Secretion by Ductal Cells

A
  • The Net result is the Secretion of HCO3- into Pancreatic Ductal Juice and Net Absorption of H+!!!
46
Q

Ionic Composition of Pancreatic Juice depends upon rate of Secretion

A
  • 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!!!
47
Q

Regulation of Pancreatic Secretions

A

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

48
Q

Regulations of Pancreatic Secretions Cont

A

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

49
Q

Saliva

A

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
50
Q

Gastric

A

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
51
Q

Pancreatic

A

Characteristics of Secretion:

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

Factors that Increase Secretion:

  • Parasympathetic
  • Secretin
  • CCK (Potentitates Secretion)

Factors that Decrease Secretion:
- None

52
Q

Bile

A

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

53
Q

Formation of Pancreatic Secretion

A

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!!!!!!!!!
54
Q

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

A

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!!!!!!!!!

55
Q

How Acute Pancreatitis occurs

A
  • 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!!!!!!!