Gastric Function Flashcards

1
Q

Stomach Functions

A
  • short term storage
  • intrinsic factor secretion
  • chemical/enzymatic digestion initiated (proteins)
  • liquifys food
  • slowly releases to SI
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2
Q

Ouabain

A

“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
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3
Q

Atropine

A
  • blocks Ach from binding muscarinic gastric gland (directly secretes HCl-)
  • blocks gastrin release
  • inhibits parasympathetic nervous system
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4
Q

Gastric Secretions

A
2 Glands
1) Gastric (oxyntic) 
HCl 
pepsinogen
intrinsic factor
mucus
rennin (chymosin) 
2) Pyloric 
gastrin
mucus
(some pepsinogen)
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5
Q

Antrum

A

NO ACID SECRETION

part of pylorus in stomach

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6
Q

Gastric Gland - Oxyntic (upper 80%)

A

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

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7
Q

Pyloric Gland (lower 20%)

A

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

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8
Q

Acid Secretion

A

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

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9
Q

Gastric Acid

A

3 functions

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

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10
Q

Gastric Secretion

A

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

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11
Q

Vagus Nerve Role

A

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

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12
Q

Histamine

A

Gastrin and ACh stimulate histamine release from ECL cells

which indirectly releases HCl (paracrine)

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13
Q

ECL Cell

A

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
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14
Q

Parietal Cell

A

Does the acid secretion!!!

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15
Q

Phases of Digestion

A

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)

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16
Q

Somatostatin

A

D cells secrete

  • tells histamine to STOP releasing gastrin
  • enters blood via basolateral cell and acts on corpus to inhibit gastric acid secretion
17
Q

Gastrin Types

A

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

18
Q

CCK

A

type of gastrin!!!

gastrin + sulfate + tyrosine

19
Q

Chief Cell

A

secrete pepsinogen which is activated by pH

20
Q

Pepsin

A

ACTIVE form of pepsinogen (less than 3.5 pH)

21
Q

Mucosal Barrier

A

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

22
Q

Gastric Releasing Peptide

A

required for ACh release