Physiology 4.3

Front 1

True or False

Acinar cells synthesize and secrete proteins and isotonic fluid.

Back 1

True

Front 2

True or False

Duct cells transport fluid and electrolytes.

Back 2

True

Front 3

? stimulate basolateral membrane receptors.

Back 3

Secretagogues

Front 4

Make sure to go over TABLE 2-1

Back 4

Make sure to go over TABLE 2-1

Front 5

The parietal cell has receptors for what 3 things?


--therefore 3 different pathways to stimulate HCl secretion!!!

Back 5

CCK-B ==> Gastrin

M3 ==> ACh

H2 ==> Histamine

Front 6

? inhibits acid secretion by a PARACRINE mechanism whereby histamine release by the ECL cells is blocked.

Back 6

Somatostatin (SST)

Front 7

Histamine is secreted by the ? cells.

Back 7

Enterochromaffine-Like Cells

(ECL)

Front 8

? in the gastric antrum inhibits G Cell secretion of gastrin and stimulates secretion of ? by the ? cells.

Back 8

Excess H+ (pH < 3)

Somatostatin (SST) by D cells

Front 9

Fine tuning of control of the ECL cell is mediated through receptors for ? , ? , and ?

Back 9

ACh

Gastrin

SST

Front 10

REMEMBER

inhibition of HCl secretion can also be done by

secretin
CCK
GIP
Prostaglandin E2

Back 10

REMEMBER

inhibition of HCl secretion can also be done by

secretin
CCK
GIP
Prostaglandin E2

Front 11

What are the 4 phases of Gastric Acid Secretion?

Back 11

Basal (interdigestive) Phase

Cephalic Phase

Gastric Phase

Intestinal Phase

Front 12

Describe what happens in the Basal Phase.

Back 12

Rate of acid secretion is LOW but the luminal [H+] is HIGH because of the absence of the buffering effect of food in the stomach.

Front 13

Describe the Cephalic Phase


**this phase accounts for 30% of TOTAL ACID SECRETION

Back 13

sight, smell, taste, and thought stimulate the DORSAL MOTOR NUCLEUS of the VAGUS NERVE.

ACh stimulates Parietal cells, ECL cells, release of GRP and INHIBIT D cells

Front 14

Describe the Gastric Phase


**this phase accounts for about 60% of the TOTAL ACID

Back 14

Distention activates release of ACh locally via Vago-Vagal Reflex

Hydrolyzed proteins and amino acids stimulate G CELLS to secrete GASTRIN

low pH stimulates D cells to release SST

Front 15

Describe the Intestinal Phase


**this phase accounts for about 10% of TOTAL ACID

Back 15

hydrolyzed protein in the duodenum stimulate duodenal G Cells ---> Gastrin

unknown mechanism -- absorption of amino acids in duodenum stimulates GASTRIC secretion of acid

Fat, acid, and hyperosmolar contents ==> inhibit acid secretion via SECRETIN and SST, GIP, CCK, Prostaglandins

Front 16

List the stimulus and mediator for the given site in regards to mechanisms for controlling gastric acid secretion:

Duodenum (2)

Duodenum and Jejenum

Gastric Antrum

Back 16

protein products ==> Gastrin

Acid pH < 4.5 ==> Secretin // Enterogastric Reflex


Fatty acids, glucose, amino acids ==> GIP and CCK


Acid pH < 3 ==> Somatostatin

Front 17

Pepsinogens are from ? cells and are active at pH ?

Back 17

Chief Cells

pH < 5

Front 18

? from parietal cells is critical to the absorption of Vitamin ?

Back 18

Intrinsic Factor

Vitamin B-12

Front 19

? are potent stimulators of mucus secretion.

Back 19

Prostaglandins

Front 20

What are the consequences of a damaged gastric mucosal barrier?

figure 3-3

Back 20

What are the consequences of a damaged gastric mucosal barrier?

figure 3-3

Front 21

A patient has Zollinger-Ellison Syndrome and has symptoms of ulcers, diarrhea, malabsorption, possible vitamin deficiencies, and steatorrhea.

What is the cause ?

Back 21

Gastrinoma secretes GASTRIN

==> causes excess HCl

gastric glands proliferate

Front 22

A patient has increased NH3 production, increased Gastrin, decreased SST, and increased HCl.

What is a possible reason for this?

Back 22

H. Pylori infection

colonizes under the gastric mucus layer

risk for gastritis, ulcers, and gastric adenocarcinoma

Front 23

REMEMBER

use of NSAID results in

decrease mucus
decrease HCO3-
decrease prostaglandin E2

increase Gastrin

Back 23

REMEMBER

use of NSAID results in

decrease mucus
decrease HCO3-
decrease prostaglandin E2

increase Gastrin

Front 24

Pancreas acinar cells have basolateral membranes that possess receptors for ? and ? that stimulate phosphorylation of structures proteins via cAMP.


via Ca2+ second messenger?

Back 24

VIP (cAMP)
Secretin (cAMP)



ACh (Ca2+)
CCK (Ca2+)

Front 25

MAKE SURE TO COVER FIGURE 4-1 and 4-2 and TABLE 4-1 IN LECTURE

pH osmolarity and electrolyte concentration changes in pancreatic fluid

Back 25

MAKE SURE TO COVER FIGURE 4-1 and 4-2 and TABLE 4-1 IN LECTURE

pH osmolarity and electrolyte concentration changes in pancreatic fluid

Front 26

Pancreatic Acinar cells secrete what type of products?

Back 26

Proteases
Amylolytic Enzyme
Lipases
Nucleases

Front 27

Pancreatic Duct cell functions in the fed state are ---?

Back 27

secrete isotonic NaHCO3-

via Cl- / HCO3- exchange channel

=>linked to apical Cl- channel (CFTR) and Cl- recycling


source of HCO3- from Basolateral Na / HCO3 co-transport and CO2 + OH- catalyzed by Carbonic Anhydrase

Front 28

Describe the regulation of pancreatic secretions during fasting

Back 28

Cephalic phase I = secretion lowest

Gastric phase II = increase

Intestinal phase III = secretion highest

Front 29

Describe the regulation of pancreatic secretion in the Fed Period.

Cephalic Phase?

Gastric Phase?

Intestinal Phase?

Back 29

Cephalic phase - initiated by sight, taste, smell and chewing via VAGAL EFFERENTS --20% total response

Gastric Phase - food in stomach and is via VAGO-VAGAL REFLEX --minor significance

Intestinal Phase - CHYME entering duodenum --80% total secretion.

Front 30

Chyme stimulates the release of ? , ? and ? during the Intestinal Phase of the pancreas.

Back 30

Secretin
CCK
ACh (vagovagal response)

Front 31

in regards to the pancreas...

? is a potent stimulator of water and bicarbonate secretions.

The stimulus for ? is long-carbon chain fatty acids and amino acids.

Back 31

Secretin


CCK

Front 32

What is the role of CCK in the pancreas--

what cell does it affect?

Released by ?

Regulated by ?

Back 32

binds to CCK-A receptors on Basolateral Membranes of ACINAR Cells

I cells of the duodenal mucosa

CCK-RP => response to fatty acids and amino acids

Monitor Peptide => acinar cells

Front 33

Describe the role of SECRETIN in pancreas.

Back 33

binds to basolateral receptor

=> G protein to Adenyl Cyclase

=> cAMP targets PKA

=> PKA phosphorylates CFTR channel in APICAL MEMBRANE of DUCT CELLS

Front 34

Hepatocytes synthesize primary bile acids from ? and conjugate them with ? or ?

Back 34

Cholesterol


conjugate with GLYCINE or TAURINE

Front 35

How is Canalicular Bile formed?

Back 35

bile acids are actively secreted across the canalicular membrane.

pulls water and solutes and absorbs them passively

Front 36

What is Ductule Bile?

Back 36

product of CHOLANGIOCYTES (columnar epithelial cells) that line the ductules.

Hepatic Bile emerges from the ductules prior to entering the Gallbladder

Front 37

? from hepatocyte membranes combine with Bile Acids form mixed ?

Back 37

Phosphatidylcholine

Micelles

Front 38

Active absorption of bile acids occurs in the ?

Absorbed bile acids return via portal circulation to the liver bound to ? where hepatocytes extract them.

Back 38

ILEUM


Albumin

Front 39

The volume of bile secreted in response to recycling of bile acids is called the ?

Back 39

Bile Acid - Dependent Fraction

Front 40

Bile acid synthesis is regulated by negative feedback control by ? which is the RATE LIMITING STEP.

Back 40

7 α-hydroxylase

Front 41

How are bile acids extracted from portal blood?

What is this dependent upon ?

Back 41

via co-transport with Na+
(basolateral surface)


dependent on Na+ / K+ pump

Front 42

Secretion of bile is accomplished by WATER TRANSPORT coupled to TRANSPORT OF Na+.

What hormones help with this process?

Back 42

Bile Acid-Independent


Secretin --stimulates secretion of water and HCO3-

CCK --potentiates this activity

Front 43

Make sure to go over Hepatocyte Transporters

Table 5-1

Back 43

Make sure to go over Hepatocyte Transporters

Table 5-1

Front 44

CONTRACTIONS of gallbladder begin within an hour of eating due to ? and ?

Back 44

CCK binding to CCK-A receptors in gallbladder Smooth Muscle.

CCK --> Activation of the Vago-Vagal Reflex releases ACh

Front 45

What causes Gallstones?

Back 45

hypersecretion of Cholesterol

or

diminished Bile Acid Pool

Front 46

Summary of regulation of Bile Flow

for each stimulus given list the TARGET and EFFECT

Bile Acids

Secretin

CCK

Vagus Nerve

Back 46

bile acids --> HEPATOCYTES --> increase bile flow, inhibit bile acid SYNTHESIS

Secretin --> Bile Ducts (liver) --> stimulates secretion of water and HCO3-

CCK --> Gallbladder --> stimulates CONTRACTION
CCK --> Sphincter of Oddi --> stimulates RELAXATION

Vagus N. --> Gallbladder --> stimulates Contractions (minor)

Front 47

How does Cl- enter the enterocytes from the basolateral membrane?

How does Cl- leave the cell and enter the lumen?

Back 47

Na+ / K+ / 2 Cl- cotransporter


CFTR channel

Front 48

What activates the CFTR channel?

Back 48

increase cAMP

increase cytosolic Ca2+

Front 49

Cl- moving through the CFTR channel will cause ? and ? to enter the lumen paracellularly.

Back 49

Water and Na+

enter into the lumen paracellularly

Front 50

What primarily controls the CFTR and Na+/K+/2Cl- cotransporter

Back 50

Submucosal Plexus

Front 51

Where does the HCO3- secretion by the duodenum come from?

Back 51

Comes from the ALKALINE TIDE and from the actions of CARBONIC ANHYDRASE

Na+ / HCO3- Cotransporter from plasma into cell

Cl- / HCO3- Exchanger for lumen