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Gastrointestinal > 7. Stomach Function > Flashcards

7. Stomach Function Flashcards

1
Q

how does the STOMACH accomodate a LARGE MEAL

A

RECEPTIVE RELAXATION of the CORPUS (BODY) of the STOMACH

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2
Q

what causes a SIGNAL to be sent via the VAGAL AFFERENT FIBRE (nodose ganglion) to the BRAIN STEM to accommodate a large meal

A

DISTENSION of the STOMACH

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3
Q

how do VAGAL EFFERENT FIBRES from the BRAIN STEM cause RELAXATION of the CORPUS to accommodate food

A
  • VAGAL EXCITORY fibres switched OFF,
    INHIBIT ACH release
  • VAGAL INHIBITORY fibres switched ON,
    relaxing factors VIP and NO release
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4
Q

how do VAGAL EFFERENT FIBRES from the BRAIN STEM cause RELAXATION of the CORPUS to accommodate food

A
  • VAGAL EXCITORY fibres switched OFF,
    INHIBIT ACH release
  • VAGAL INHIBITORY fibres switched ON,
    relaxing factors VIP and NO released
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5
Q

RELEASE of what HORMONE tells us we have eaten enough and so LOWERS FOOD INTAKE (SATIETY EFFECTS) and DECREASES GASTRIC MOTILITY

A

CKK - CHOLECYSTOKININ

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6
Q

what MOLECULES cause CKK RELEASE to DECREASE FOOD INTAKE and GASTRIC MOTILITY

A

FATTY ACIDS
PROTEIN

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7
Q

FATTY ACIDS and PROTEIN are RECOGNISED BY … which causes CKK RELEASE

A

ICC CELLS in intestines

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8
Q

what type of MEALS DELAY GASTRIC EMPTYING by RELEASING CKK from DUODENUM and how

A

FATTY MEALS

  • fats sit on top of gastric contents and empty last, therefore signal END of meal
    -> turn off gastric motility
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9
Q

what does CKK tell the brain (VAGAL AFFERENT) and what does it CAUSE of the STOMACH (via VAGAL EFFERENT)

A

tells the brain the MEAL is NEARLY OVER,
SATIETY EFFECTS (feelings of FULLNESS)

-> RELAXATION of CORPUS of stomach to TURN OFF GASTRIC MOTILITY

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10
Q

why type of FOODS EMPTY FROM STOMACH into intestines MORE RAPIDLY

A

LIQUIDS (more rapid than solids)

ie GLUCOSE

  • in a form more READY for ABSORPTION, don’t need more time for digestion/break-down)
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11
Q

what other TYPES of MEALS DELAY GASTRIC EMPTYING

A
  • FAT-RICH
  • HYPERTONIC (high solute conc.)
  • ACIDIC
  • HIGH VISCOSITY
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12
Q

RATE of GASTRIC EMPTYING is CONTROLLED BY

A

DUODENUM - duodenal sensing mechanisms
(for neural or hormonal activation)

and FORM food is in

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13
Q

MAJOR CELL TYPE of the FUNDUS of the STOMACH and FUNCTIONS

A

SURFACE EPITHELIAL

-> MUCOUS, HCO3- release (barrier)
-> GASTRIC LIPASE release

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14
Q

what does SURFACE EPITHELIA RELEASE that has protective effect

A

MUCOUS, HCO3-

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15
Q

what can be DIGESTED in the FUNDUS of the STOMACH

A

FAT by GASTRIC LIPASE

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16
Q

MAJOR CELL TYPES in the CORPUS of the STOMACH and their FUNCTIONS

A
  • SURFACE EPITHELIA -> mucous, HCO3-
  • CHIEF CELLS (ZYMOGEN) –> PEPSINOGEN (needs activation by acid into pepsin)
  • PARIETAL CELLS –> HCL (optimum environment for pepsin), INTRINSIC FACTOR (glycoprotein for VIT B12 absorption in small intestine)
  • ECL (ENTEROCHROMAFFIN-LIKE) CELLS –> HISTAMINE (controls acid and pepsinogen secretions)
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17
Q

what is the role of CHIEF CELLS in the STOMACH (CORPUS, ANTRUM)

A

RELEASE PEPSINOGEN

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18
Q

what is PEPSINOGEN from STOMACH CHIEF CELLS ACTIVATED by

A

ACID

-> PEPSIN (protein breakdown)

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19
Q

what is the ROLE of PARIETAL CELLS in the STOMACH (CORPUS)

A

HCL acid secretion
- activated pepsinogen and creates optimum environment for pepsin

INTRINSIC FACTOR release
- glycoprotein for VITAMIN B12 ABSORPTION in small intestines (for rbc synthesis)

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20
Q

ROLE of ECL CELLS in CORPUS of STOMACH

A

RELEASES HISTAMINE

  • REGULATORY CELLS for control of ACID and PEPSINOGEN RELEASE

(endocrine cells)

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21
Q

ACID is SECRETED BY

A

PARIETAL CELLS in CORPUS of STOMACH
(HCL)

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22
Q

CELL TYPES in ANTRUM of STOMACH and their FUNCTIONS

A
  • SURFACE EPITHELIA –> Mucous, HCO3-
  • CHIEF (ZYMOGEN) CELLS –> PEPSINOGEN
  • G-CELLS –> GASTRIN (regulates acid, pepsinogen and mucus secretion)
  • D-CELLS –> SOMATOSTATIN (Inhibitor, switches everything off)
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23
Q

which CELLS in the STOMACH SECRETE GASTRIN and where are they found

A

G-CELLS in ANTRUM

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24
Q

which HORMONE from the STOMACH switches everything OFF and where

A

SOMATOSTATIN

  • ANTRUM
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25
Q

which CELLS of the STOMACH allow VITAMIN B12 ABSORPTION

A

PARIETAL CELLS (CORPUS)

-> secretes INTRINSIC FACTOR

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26
Q

which CELLS of the STOMACH RELEASE PEPSINOGEN

A

CHIEF CELLS

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27
Q

which CELLS of the STOMACH RELEASE HISTAMINE and where are they

A

ECL

  • CORPUS
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28
Q

GASTRIC (CORPUS) GLAND STRUCTURE
which CELLS are at the BOTTOM

A

CHIEF CELLS

Pepsinogen moves up to be activated by acid

29
Q

GASTRIC (CORPUS) GLAND STRUCTURE
which CELLS are at the TOP

A

SURFACE EPITHELIA
- PROTECTIVE role (mucus, HCO3-)

30
Q

GASTRIC (CORPUS) GLAND STRUCTURE
ORDER of the CELLS from TOP to BOTTOM

A
  • SURFACE EPITHELIA
  • PROLIFERATING CELLS
  • PARIETAL CELLS (acid)
  • ECL (ENTEROCHROMAFFIN-LIKE) (histamine)
  • CHIEF CELLS (pepsinogen)
31
Q

which CELLS are BETWEEN CHIEF and PARIETAL CELLS of the GASTRIC (CORPUS) GLAND

A

ECL

  • REGULATORY FUNCTION,
    HISTAMINE CONTROLS acid and pepsinogen release
32
Q

GASTRIC (CORPUS) GLAND STRUCTURE
which CELLS are at the MID-POINT

A

PARIETAL CELLS (ACID)

33
Q

what happens to ACID-SECRETING PARIETAL CELLS when they are STIMULATED by FOOD ENTERING the stomach

A

undergo MORPHOLOGICAL TRANSFORMATION
(more food, more change)

  • TUBULOVASCULAR MEMBRANE and INTRACELLULAR CANALICULUS MERGE to INCREASE SURFACE AREA
  • INCREASED EXPOSURE of PROTON PUMPS (in tubulovascular membrane)
34
Q

in ACID-SECRETING PARIETAL CELLS, where are PROTON (H+) PUMPS FOUND

A

TUBULOMUSCULAR MEMBRANES

which MERGE with INTRACELLULAR CANALICULUS
upon stimulation

for increased SURFACE AREA and exposure of proton pumps

35
Q

why do ACID-SECRETING PARIETAL CELLS have LOTS of MITOCHONDRIA

A
  • most acid secretion is from Cellular RESPIRATION
  • ATP to PUMP ACID AGAINST ELECTROCHEMICAL GRADIENT (already high acid environment)
36
Q

what ION CHANNELS are used for HCL SECRETION from PARIETAL CELLS
on APICAL SIDE:

A
  • PROTON PUMP H+/K+ ATPase (H+ out, K+ In)
  • K+ CHANNELS OPEN (K+ out)
  • CL- CHANNELS OPEN (Cl- out)
37
Q

what ION CHANNELS are used for HCL SECRETION from PARIETAL CELLS
on BASOLATERAL SIDE:

A
  • SODIUM PUMP - NA+/K+ ATPase
    K+ in
    Na+ exchanged out
  • CL-/HCO3- EXCHANGER
    removes HCO3- so cell does not alkalinize, into blood
    Cl- exchanged in (lost at apical end)
  • K+ CHANNEL OPEN
    (K+ out)
38
Q

how do we get H+ from CELLULAR RESPIRATION

A

H20 + CO2 converted by CARBONIC ANHYDRASE into CARBONIC ACID H2CO3

DISSOCIATES into HCO3- and H+

39
Q

when does the CEPHALIC PHASE of GASTRIC ACID SECRETION occur

A

in PREPARATION for incoming food

triggered by THOUGHT, SIGHT, SMELL, TASTE

40
Q

what NEUROTRANSMITTERS are RELEASED in CEPHALIC PHASE of GASTRIC ACID SECRETION

A

ACH - for release of HISTAMINE from ECL
(PARACRINE)

GRP (GASTRIN RELEASING PEPTIDE) - for release of GASTRIN from G-CELLS
(ENDOCRINE)

41
Q

what is the ROLE of GASTRIN

A

INCREASE GASTRIC ACID SECRETIONS

42
Q

what is the ROLE of HISTAMINE

A

activates H2 RECEPTORS of PARIETAL and CHIEF CELLS for ACID and PEPSINOGEN SECRETION

43
Q

when does GASTRIC PHASE of GASTRIC ACID SECRETIONS occur

A

when FOOD ENTERS STOMACH
- DISTENSION

44
Q

RELEASE OF … in GASTRIC PHASE of GASTRIC ACID SECRETIONS

A

ACH –> HISTAMINE (PARACRINE)
(& NEURAL)

GASTRIN from antrum G-CELLS –> HISTAMINE (PARACRINE)
(& ENDOCRINE)

45
Q

what is released in INTESTINAL PHASE of GASTRIC ACID SECRETIONS, EARLY PHASE

A

GASTRIN from DUODENAL G-CELLS
(ENDOCRINE)
GASTRIN –> HISTAMINE (PARACRINE)

ACH –> HISTAMINE

GASTRIC ACID SECRETIONS

46
Q

what is released in INTESTINAL PHASE of GASTRIC ACID SECRETIONS, LATE PHASE

A

ACID SECRETION TURNED OFF

  • SOMATOSTATIN
  • CKK (ICC stimulated as fats empty last)
  • VIP
  • GIP
47
Q

ACH STIMULATES … in CONTROL of ACID SECRETION

A

PARIETAL CELLS (ckk2 receptor) - ACID
CHIEF CELLS - PEPSINOGEN
ECL CELLS - HISTAMINE (on H2 receptors)

48
Q

SOMATOSTATIN is RELEASED FROM… to do what?

A

D-CELLS

INHIBITS GASTRIC MOTILITY
INHIBITS ACID, PEPSINOGEN, HISTAMINE SECRETION
(inhibits parietal, chief and ECL cells)

49
Q

how are D-CELLS ACTIVATED to SECRETE SOMATOSTATIN

A

when NO FOOD IN STOMACH:

HIGH ACID LEVELS
- sense LOW PH

50
Q

What other factors/molecules ACTIVATE SOMATOSTATIN RELEASE / INHIBIT GASTRIC MOTILITY and SECRETIONS

A

CKK
VIP
NORADRENALINE (sympathetic nerves)
CGRP (calcitonin gene related peptide)

51
Q

what affect does CKK have on ACID SECRETIONS in stomach

A

INHIBITS

52
Q

what do G-CELLS RELEASE

A

GASTRIN

53
Q

what STIMULATES G-CELLS to SECRETE GASTRIN

A

PROTEIN/PEPTIDES/AMINO ACIDS
or
GASTRIN RELEASING PEPTIDE (GRP)

54
Q

what INHIBITS GASTRIN RELEASE from G-CELLS

A

SOMATOSTATIN (from D-CELLS)

55
Q

2 ACID INHIBITORY MECHANISMS when gastric acid is too HIGH, is by USING…

A
  • PROTON PUMP INHIBITORS : make H+/K+ ATPase dysfunctional
  • H2 RECEPTOR ANTAGONISTS: BLOCK HISTAMINE BINDING to H2 receptors on PARIETAL CELLS - OUTCOMPETE
56
Q

HISTAMINE BINDS to which RECEPTORS on PARIETAL and CHIEF CELLS

A

H2 RECEPTORS

57
Q

H2 RECEPTOR ANTAGONISTS BLOCK the action of…

A

HISTAMINE

58
Q

examples of H2 RECEPTOR ANTAGONISTS in ACID INHIBITORY THERAPY

A

TAGAMENT
ZANTAC
PEPCID AC

59
Q

EXAMPLE of a PROTEIN PUMP INHIBITOR in ACID INHIBITORY THERAPY

A

OMEPRAZOLE

60
Q

what does ZANTAC do for ACID SECRETIONS

A

DECREASES by acting as a H2 RECEPTOR ANTAGONIST

61
Q

what does OMEPRAZOLE do for ACID SECRETIONS

A

DECREASES by acting as a PROTON (H+) PUMP INHIBITOR

62
Q

name of the BACTERIA that COLONISES the STOMACH and AFFECTS ACID SECRETIONS

A

HELICOBACTER PYLORI (GRAM NEGATIVE)

(adapted to survive in high acid environment of stomach)

63
Q

is HELICOBACTER PYLORI GRAM positive or negative

A

GRAM NEGATIVE

64
Q

if HELICOBACTER PYLORI is in the ANTRUM of stomach what does it cause

A
  • BLOCKS SOMATOSTATIN SECRETIONS (D-CELLS)

-> HIGH GASTRIN (HYPERGASTRINAEMIA)

-> HIGH ACID SECRETION

can cause Duodenal and Peptic ULCERS

65
Q

if HELICOBACTER PYLORI is in the ANTRUM AND CORPUS of stomach what does it cause

A
  • HIGH GASTRIN (HYPERGASTRINAEMIA)
    BUT
  • LOW ACID SECRETIONS
    as inflammation causes gastric atrophy and so
    LOSE PARIETAL CELLS

can cause atropic Gastritis or gastric Cancer

66
Q

when can HELICOBACTER PYLORI CAUSE LOW ACID LEVELS

A

when IN ANTRUM AND STOMACH

67
Q

in ANTRUM ONLY, ACID SECRETIONS are … with HELICOBACTER PYLORI

A

HIGH

68
Q

how are there LOW ACID SECRETIONS with HELICOBACTER PYLORI in the ANTRUM AND CORPUS

A

LOSS of PARIETAL CELLS

69
Q

discovery of HELICOBACTER PYLORI and gastritis and ulcers by

A

Barry J Marshall, J. Robin Warren

Gastrointestinal (19 decks)

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