Gastric Function

Question 1

Stomach Functions

Answer 1

• short term storage
• intrinsic factor secretion
• chemical/enzymatic digestion initiated (proteins)
• liquifys food
• slowly releases to SI

Question 2

Ouabain

Answer 2

“arrow poison” plant derived toxin used in eastern Africa

• Na+/K+ pump - ATPase blocker
• in turn increases intracellular Ca++
• higher cardiac contractility increases cardiac vagal tone
• Cardiac glycoside - treats hypotension/arrhythmias in LOW doses

Question 3

Atropine

Answer 3

• blocks Ach from binding muscarinic gastric gland (directly secretes HCl-)
• blocks gastrin release
• inhibits parasympathetic nervous system

Question 4

Gastric Secretions

Answer 4

2 Glands
1) Gastric (oxyntic) 
HCl 
pepsinogen
intrinsic factor
mucus
rennin (chymosin) 
2) Pyloric 
gastrin
mucus
(some pepsinogen)

Question 5

Antrum

Answer 5

NO ACID SECRETION

part of pylorus in stomach

Question 6

Gastric Gland - Oxyntic (upper 80%)

Answer 6

3 cells
1) Mucous neck cells (mucus)
2) Chief Cells (peptic)
pepsinogen –> activated

Question 7

Pyloric Gland (lower 20%)

Answer 7

2 cells
1) G cells
2) mucus neck cells
mucus and some pepsinogen

Question 8

Acid Secretion

Answer 8

H+/K+ pump required!!!
In mitochondria, requires ALOT of ATP!!! (surface area is active)

Most secretion is salt = Na+ and H+ trade positions (Na+ decreases and H+ increases with Cl-)

increased acid = decreased gastrin

Mechanism? –> H+ into lumen of canaliculus and K+ into parietal cell (requires Mg+)

Calcium Calmodulin Kinase phosphorylates H+/K+ pump to open

Question 9

Gastric Acid

Answer 9

3 functions

1) bacteriostatic
2) converts pepsinogen –> pepsin
3) begins protein digestion (with pepsin)

Question 10

Gastric Secretion

Answer 10

Stimulated by neural, paracrine AND endocrine! (G coupled rec)
1) Ach: (from ENS)
HCl secretion, mucus, pepsinogen and gastrin
2) Histamine: direct
HCl secretion (H2 receptor)
3) Gastrin: (direct or indirect)
HCl secretion (1500x more powerful than histamine)

regulation?
+ peptides, aa bind gastrin cell to stimulate gastrin
- protons bind somatostatin cell to inhibit

Question 11

Vagus Nerve Role

Answer 11

inhibits somatostatin and activates gastrin!!!

vagus binds ENS which

1) DIRECTLY sends signal to gastric gland to produce HCl - atropine blocks
2) INDIRECTLY sends signal to pyloric gland to produce Gastrin - atropine does NOT block

Question 12

Histamine

Answer 12

Gastrin and ACh stimulate histamine release from ECL cells

which indirectly releases HCl (paracrine)

Question 13

ECL Cell

Answer 13

entero-chromaffin-like cell

• specialized endocrine cell in gastric mucosa
• proliferation of ECL cells with LOTS of gastrin from tumor or long term therapy from drugs that block acid secretion

Question 14

Parietal Cell

Answer 14

Does the acid secretion!!!

Question 15

Phases of Digestion

Answer 15

1) Cephalic (NaCl to HCl when see food!!!)
parasympathetic excites pepsin and acid production
2) Gastric (stomach distention)
local nervous secretary reflexes, vagal reflexes, gastrin-histamine stimulation
3) Intestinal
nervous mechanisms, hormonal mechanisms (enzymes and zygomens)

Question 16

Somatostatin

Answer 16

D cells secrete

• tells histamine to STOP releasing gastrin
• enters blood via basolateral cell and acts on corpus to inhibit gastric acid secretion

Question 17

Gastrin Types

Answer 17

Little Gastrin - 17 aa in stomach
BIG Gastrin - duodenum
CCK = gastrin + sulfate + tyrosine

Question 18

CCK

Answer 18

type of gastrin!!!

gastrin + sulfate + tyrosine

Question 19

Chief Cell

Answer 19

secrete pepsinogen which is activated by pH

Question 20

Pepsin

Answer 20

ACTIVE form of pepsinogen (less than 3.5 pH)

Question 21

Mucosal Barrier

Answer 21

strengthened by:
mucus, bicarb, gastrin, epidermal growth factor
weakened by:
H. pylori, aspirin, ethanol, NSAIDS, bile salts

Question 22

Gastric Releasing Peptide

Answer 22

required for ACh release