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Gastrointestinal > 7. Stomach Function > Flashcards

7. Stomach Function Flashcards

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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
which CELLS of the STOMACH allow VITAMIN B12 ABSORPTION
PARIETAL CELLS (CORPUS) -> secretes INTRINSIC FACTOR
26
which CELLS of the STOMACH RELEASE PEPSINOGEN
CHIEF CELLS
27
which CELLS of the STOMACH RELEASE HISTAMINE and where are they
ECL - CORPUS
28
GASTRIC (CORPUS) GLAND STRUCTURE which CELLS are at the BOTTOM
CHIEF CELLS Pepsinogen moves up to be activated by acid
29
GASTRIC (CORPUS) GLAND STRUCTURE which CELLS are at the TOP
SURFACE EPITHELIA - PROTECTIVE role (mucus, HCO3-)
30
GASTRIC (CORPUS) GLAND STRUCTURE ORDER of the CELLS from TOP to BOTTOM
- SURFACE EPITHELIA - PROLIFERATING CELLS - PARIETAL CELLS (acid) - ECL (ENTEROCHROMAFFIN-LIKE) (histamine) - CHIEF CELLS (pepsinogen)
31
which CELLS are BETWEEN CHIEF and PARIETAL CELLS of the GASTRIC (CORPUS) GLAND
ECL - REGULATORY FUNCTION, HISTAMINE CONTROLS acid and pepsinogen release
32
GASTRIC (CORPUS) GLAND STRUCTURE which CELLS are at the MID-POINT
PARIETAL CELLS (ACID)
33
what happens to ACID-SECRETING PARIETAL CELLS when they are STIMULATED by FOOD ENTERING the stomach
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
in ACID-SECRETING PARIETAL CELLS, where are PROTON (H+) PUMPS FOUND
TUBULOMUSCULAR MEMBRANES which MERGE with INTRACELLULAR CANALICULUS upon stimulation for increased SURFACE AREA and exposure of proton pumps
35
why do ACID-SECRETING PARIETAL CELLS have LOTS of MITOCHONDRIA
- most acid secretion is from Cellular RESPIRATION - ATP to PUMP ACID AGAINST ELECTROCHEMICAL GRADIENT (already high acid environment)
36
what ION CHANNELS are used for HCL SECRETION from PARIETAL CELLS on APICAL SIDE:
- PROTON PUMP H+/K+ ATPase (H+ out, K+ In) - K+ CHANNELS OPEN (K+ out) - CL- CHANNELS OPEN (Cl- out)
37
what ION CHANNELS are used for HCL SECRETION from PARIETAL CELLS on BASOLATERAL SIDE:
- 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
how do we get H+ from CELLULAR RESPIRATION
H20 + CO2 converted by CARBONIC ANHYDRASE into CARBONIC ACID H2CO3 DISSOCIATES into HCO3- and H+
39
when does the CEPHALIC PHASE of GASTRIC ACID SECRETION occur
in PREPARATION for incoming food triggered by THOUGHT, SIGHT, SMELL, TASTE
40
what NEUROTRANSMITTERS are RELEASED in CEPHALIC PHASE of GASTRIC ACID SECRETION
ACH - for release of HISTAMINE from ECL (PARACRINE) GRP (GASTRIN RELEASING PEPTIDE) - for release of GASTRIN from G-CELLS (ENDOCRINE)
41
what is the ROLE of GASTRIN
INCREASE GASTRIC ACID SECRETIONS
42
what is the ROLE of HISTAMINE
activates H2 RECEPTORS of PARIETAL and CHIEF CELLS for ACID and PEPSINOGEN SECRETION
43
when does GASTRIC PHASE of GASTRIC ACID SECRETIONS occur
when FOOD ENTERS STOMACH - DISTENSION
44
RELEASE OF ... in GASTRIC PHASE of GASTRIC ACID SECRETIONS
ACH --> HISTAMINE (PARACRINE) (& NEURAL) GASTRIN from antrum G-CELLS --> HISTAMINE (PARACRINE) (& ENDOCRINE)
45
what is released in INTESTINAL PHASE of GASTRIC ACID SECRETIONS, EARLY PHASE
GASTRIN from DUODENAL G-CELLS (ENDOCRINE) GASTRIN --> HISTAMINE (PARACRINE) ACH --> HISTAMINE GASTRIC ACID SECRETIONS
46
what is released in INTESTINAL PHASE of GASTRIC ACID SECRETIONS, LATE PHASE
ACID SECRETION TURNED OFF - SOMATOSTATIN - CKK (ICC stimulated as fats empty last) - VIP - GIP
47
ACH STIMULATES ... in CONTROL of ACID SECRETION
PARIETAL CELLS (ckk2 receptor) - ACID CHIEF CELLS - PEPSINOGEN ECL CELLS - HISTAMINE (on H2 receptors)
48
SOMATOSTATIN is RELEASED FROM... to do what?
D-CELLS INHIBITS GASTRIC MOTILITY INHIBITS ACID, PEPSINOGEN, HISTAMINE SECRETION (inhibits parietal, chief and ECL cells)
49
how are D-CELLS ACTIVATED to SECRETE SOMATOSTATIN
when NO FOOD IN STOMACH: HIGH ACID LEVELS - sense LOW PH
50
What other factors/molecules ACTIVATE SOMATOSTATIN RELEASE / INHIBIT GASTRIC MOTILITY and SECRETIONS
CKK VIP NORADRENALINE (sympathetic nerves) CGRP (calcitonin gene related peptide)
51
what affect does CKK have on ACID SECRETIONS in stomach
INHIBITS
52
what do G-CELLS RELEASE
GASTRIN
53
what STIMULATES G-CELLS to SECRETE GASTRIN
PROTEIN/PEPTIDES/AMINO ACIDS or GASTRIN RELEASING PEPTIDE (GRP)
54
what INHIBITS GASTRIN RELEASE from G-CELLS
SOMATOSTATIN (from D-CELLS)
55
2 ACID INHIBITORY MECHANISMS when gastric acid is too HIGH, is by USING...
- PROTON PUMP INHIBITORS : make H+/K+ ATPase dysfunctional - H2 RECEPTOR ANTAGONISTS: BLOCK HISTAMINE BINDING to H2 receptors on PARIETAL CELLS - OUTCOMPETE
56
HISTAMINE BINDS to which RECEPTORS on PARIETAL and CHIEF CELLS
H2 RECEPTORS
57
H2 RECEPTOR ANTAGONISTS BLOCK the action of...
HISTAMINE
58
examples of H2 RECEPTOR ANTAGONISTS in ACID INHIBITORY THERAPY
TAGAMENT ZANTAC PEPCID AC
59
EXAMPLE of a PROTEIN PUMP INHIBITOR in ACID INHIBITORY THERAPY
OMEPRAZOLE
60
what does ZANTAC do for ACID SECRETIONS
DECREASES by acting as a H2 RECEPTOR ANTAGONIST
61
what does OMEPRAZOLE do for ACID SECRETIONS
DECREASES by acting as a PROTON (H+) PUMP INHIBITOR
62
name of the BACTERIA that COLONISES the STOMACH and AFFECTS ACID SECRETIONS
HELICOBACTER PYLORI (GRAM NEGATIVE) (adapted to survive in high acid environment of stomach)
63
is HELICOBACTER PYLORI GRAM positive or negative
GRAM NEGATIVE
64
if HELICOBACTER PYLORI is in the ANTRUM of stomach what does it cause
- BLOCKS SOMATOSTATIN SECRETIONS (D-CELLS) -> HIGH GASTRIN (HYPERGASTRINAEMIA) -> HIGH ACID SECRETION can cause Duodenal and Peptic ULCERS
65
if HELICOBACTER PYLORI is in the ANTRUM AND CORPUS of stomach what does it cause
- 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
when can HELICOBACTER PYLORI CAUSE LOW ACID LEVELS
when IN ANTRUM AND STOMACH
67
in ANTRUM ONLY, ACID SECRETIONS are ... with HELICOBACTER PYLORI
HIGH
68
how are there LOW ACID SECRETIONS with HELICOBACTER PYLORI in the ANTRUM AND CORPUS
LOSS of PARIETAL CELLS
69
discovery of HELICOBACTER PYLORI and gastritis and ulcers by
Barry J Marshall, J. Robin Warren

Gastrointestinal (19 decks)

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