gastric function: git hormones Flashcards

(22 cards)

1
Q

hormones and communication:
- Digestive motility and secretion are carefully regulated to — digestion and absorption of ingested food.
- GI tract is the largest — organ in the body - produces < — substances that have a diverse range of roles: gastrointestinal motility, absorption, and growth; control of glucose homeostasis, appetite, and metabolism
-Hormones are stored in specific — storage granules cells, which are subsequently released by —

❑ AUTOCRINE– communicate within the — cell
▪ Some cells possess — for their own messengers
❑ PARACRINE– communicate with — cells
❑ ENDOCRINE – communicate with — cells
▪ Secreted into —

A

maximise
endocrine
20
peptide
exocytosis
same
cell surface receptors
nearby
distant
bloodstream

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2
Q

HORMONES AND THE GASTROINTESTIONAL TRACT
❑ Major GIT Hormones:
▪ — and — (CCK)
▪ –
▪ Various others

❑ Non-gastric actions
▪ Pancreatic — cells and —
▪ — glands

❑ Regulation of —

A

gastrin and cholecystokinin
secretion
pancreatic acinar and bile
duodenal brunners
food intake

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3
Q

GASTRIN AND CHOLECYSTOKININ (CCK)
❑ Structurally-related — hormones
▪ Share a — aa — terminal sequence essential for receptor— - both act on — receptors
▪ CCK1 (CCKA) — specific receptor
▪ CCK2 (CCKB) — and — are CCK2R ligands with similar — and —

A

peptide
four aa
c terminal
receptor activation
CCK receptors
CCK
CCK and gastrin
affinity and potency

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4
Q

GASTRIN
RELEASE
❑— in the — of the stomach, some in —
1- Stimuli that increase gastrin secretion:
▪ — and —
▪ Gastric —
▪ — stimulation
▪ Presence of —

2- Stimuli that inhibit
gastrin secretion
▪ Accumulation of — in
stomach ( — pH)
▪ —
▪ — , — , — , —

A

g cells
pyloric antrum
duodenum
peptides and amino acids
gastric distension
vagal
gastrin-releasing peptides GRP
acid
decreasing
somatostatin
secretin , GIP , VIP , glucagon

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5
Q

GASTRIN
FUNCTIONS
❑ Acts to — secretion of — from — cells
➢ directly binding to — receptors on — cells
➢ Indirectly stimulating release of — from — cells ( — effect)
- Increased H+ feeds back to — of the antrum to release — to turn off — release
❑ Enhances gastric —
❑ Stimulates the — of stomach mucosa ( —- effects) - helps maintain well-developed,
functionally viable digestive tract lining

A

increase
acid
oxyntic
CCK2
parietal cells
histamine
ECL
paracrine
d cells
somatostatin
gastrin
motility
growth
proliferative

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6
Q

GASTROINTESTINAL HORMONES
CHOLECYSTOKININ (CCK):

RELEASE
❑ From— in — ( — , — )
❑ Stimulated by increased levels of — / — & — (fats & protein) in —
FUNCTIONS:
❑ Most actions are on — and —
▪ Stimulates — of the — with simultaneous — of the — of — (allows bile and —- to flow between the pancreas and the small intestine)
▪ Stimulates secretion of— enzymes: lipases, amylase, and proteases
▪ Secretion of —- from the —
❑ Inhibits —-

❑ Effects on oxyntic cells:
▪ Indirectly — secretion of acid – binding to — receptors on D cells, stimulating release of —
▪ Some action at CCK2 (very – effect on acid secretion)

A

I cells
small intestine ( duodenum and jejunum )
FA , monoglycerides , aa
duodenum
pancreas and gallbladder
contraction of gallbladder
relaxation
sphincter of oddi
pancreatic juices
pancreatic enzymes
bicarbonate
pancrease
gastric emptying
decreases
CCK1
somatostatin
weak

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7
Q

GASTROINTESTINAL HORMONES
SECRETIN
RELEASE
❑ Released from — mostly in the — .
❑ Stimulated in response to the presence of — in duodenum and to a lesser extent, — .

FUNCTIONS
❑ Main function is to — acid in the intestine by effects on secretions from the pancreas and gallbladder
▪ Secretion of large volumes of —- from the pancreas
▪ Stimulates — to secrete bicarbonate-rich bile which assists in —- process.
❑ inhibit gastrin, gastric motility & acid secretion (via — )
▪ Inhibits — in order to prevent further acid from entering
duodenum until acid already present is —
▪ Inhibits gastrin secretion to reduce amount of acid being —

A

s cells
duodenum
acid
fatty acids
neautralise acid
aqueous bicarbonate
liver
neautralization
somatostatin
gastric emptying
neutralise
produced
check slide 12 for summary

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8
Q

GASTROINTESTINAL HORMONES
SOMATOSTATIN
RELEASE
❑ — cells of the — , — and —
▪ CCK ( — receptor) and — (muscarinic receptor) stimulate release in response to presence of — in duodenum, —- blood glucose/amino acids
FUNCTIONS
❑ Mainly — actions: —- all the activities of the gastrointestinal tract,decreases motility and gastric secretion, suppresses hormone release.
❑ In response to increased acid (decreasing pH), D cells to secrete — and reduce the amount of acid being produced:
▪ Directly: inhibitory effects on — cells (decreased cAMP production → — H+ secretion)
▪ Indirectly via inhibition of — and — release. D cells in close
proximity to gastrin-producing cells secrete somatostatin and inhibit gastrin release by a — effect.
▪ Inhibits gastric emptying in order to prevent further acid from entering duodenum until acid already present is neutralized.

A

delta cells
stomach , dududeum , pancreatic islets
CCK1
ACh
acid
increased
inhibitory
suppresses
somatostatin
oxyntic
decreased
gastric anf histamine
paracrine

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9
Q

MOTILIN
❑ Peptide released from — cells of the mucosa during — to stimulate gastrointestinal —
▪ During the fasting state, plasma levels of motilin fluctuate, released in ~ — min cycles and increases gastrointestinal motility by stimulating the migrating — complex in the absence of food that moves through the fasting stomach and small intestines (‘ —-’).
▪ This — release and action get inhibited by the — of food requires — presence of food
▪ — role → helps clear intestine of — & residual — material.

A

endocrine cells
fasting
gastrointestinal motility
90 min
migrating motor complex
rumbling
cyclical
ingestion
physical
housekeeping role
forge in bodies and residual indigested

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10
Q

SEROTONIN (5-HT)
❑ Released from — cells in response to mechanical or chemical — of GI tract- e.g.
presence of — and —
▪ Increased — activity e.g. emptying of a noxious substance from the GIT
❑ Excessive activation of — sensory afferent 5-HT3 receptors in — trigger zone induces — and —
▪ Blocking of 5-HT-3 receptors is very effective as an —

A

enterochromaffin
irritation
drugs or toxins
contractile
vagal
chemoreceptors
nausea and vomitting
anti emetic

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11
Q

GASTRIC INHIBITORY POLYPEPTIDE (GIP)
❑ Released from — ( —mucosa) in response to the presence of food in the — small
intestine.
❑ Also known as —-dependent insulinotropic polypeptide
▪ Major action is the stimulation of — secretion (insulinotrophic peptide).
▪ Lesser (weak) roles: Inhibits gastric acid secretion and motility – slows gastric emptying when
the upper small intestine is full of food products – requires higher than normal physiological
levels.

A

k cells
duodenal
upper small intestine
glucose
insulin

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12
Q

VASOACTIVE INTESTINAL PEPTIDE (VIP)
❑ Vasoactive peptide hormone
❑ Induces smooth muscle — (lower esophageal sphincter, stomach, sphincter of Oddi) –
mediates —-induced reflexes
❑ — of gastric acid secretion
❑ Stimulates pancreatic — secretion

A

relaxation
smooth
distention
inhibition
bicarbonate

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13
Q

exocrine pancreatic secretions:
PANCREATIC SECRETIONS

Pancreas has both — and — secretions
❑ Endocrine secretions (in the —): — and —
❑ Exocrine (into — ): can be thought of as an —-
component and a —/— component

EXOCRINE SECRETIONS
❑ — — cells
▪ Produce – volumes of — solution, mainly — , —

❑ Acinar cells
▪ Produce – volumes of —-rich “juice”
▪ Inactive precursors of the digestive enzymes, — , — etc.

A

endocrine and exocrine
blood
glucagon anf insulin
ducts
aqueous
proteinaceous/enzymatic
ductal epithelial cells
large
aqueous
Na+ and HCO3-
smaller
protein rich
tryspisnogen anf chymotrypsinogen

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14
Q

stimulation of exocrine pancreatic secretions:
Cephalic (Reflex) and Gastric Phases

1- Cephalic phase
Sight, taste, or smell of food ( — nerve)
❑ Stimulates pancreatic — cells to release — enzymes
❑ Stimulates —- cells to secrete —- and —

2-Gastric phase
Presence of food in the — ( — and — ) stimulates — secretions—primarily from the — cells—through two routes:
❑ Distention of the stomach activates a —- reflex
❑ Protein digestion products (—) stimulate —in the antrum of the stomach to release—.

A

vagus nerve
pancreatic acing
digestive enzymes
duct cells
HCO3- and fluid
stomach
stretch anf chemoreceptors
pancreatic secretions
acinar cells
vagovegal
peptones
g cells
gastrin

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15
Q

STIMULATION OF EXOCRINE PANCREATIC SECRETIONS
Intestinal Phase
CCK
▪ Increased levels of — & — in duodenum stimulates secretion of CCK
Results in:
▪ Increased — production (by — cells).

Secretin
▪ Increased — in duodenum stimulates secretion of secretin
Results in:
▪ Increased secretion of —
solution (by 000 cells).
▪ Increases — and —

A

fatty and amino acids
enzyme production
acing cells
acid chime
aquaous bicarbonate
ductal cells
volume and pH
check slide 20

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16
Q

regulation of bile secretion:
❑ Bile is secreted by — , stored in
the — and released into —
❑ Crucial for — digestion, consists of — , — , — , — , —

A

hepatocytes
gall bladder
duduemon
fat digestion
water, bilirubin,
cholesterol, bile salts
and other fats

17
Q

brunners gland:
❑ — -secreting glands in the — layer of the —
▪ Secrete — and — that protects the duodenum from — content of the stomach.
❑ Mucus secretion in response to:
▪ Presence of — in the duodenum (distension, irritation)
▪— stimulation.
▪ Also — , — , released by the arrival of food into
the duodenum.
▪ Secretion is decreased by — stimulation

A

mucuous
submucosusal
duodenum
mucus and HCO3-
acidic
food
vagal
cck , secretin
sympathetic

18
Q

CONTROL OF FOOD INTAKE
❑ Central regulation of food intake occurs in the — .
❑ The hypothalamus receives signals from various — pathways, those involved in digestion but
also emotion / behaviour / reward.
❑ Hormones that regulate food intake can be separated into those that act — to influence individual meals, and those that act more slowly to promote the —- of body fat stores.
❑ The two efferent pathways from the hypothalamus are:
▪ Inhibition of food intake and — metabolism
▪ Stimulation of food intake and — of metabolism (— )

A

hypothalamus
neurhumoral
rapidly
stability
increase
inhibition ( orexigenic)

19
Q

control of food intake:
GASTRIC CONTROL
Local gastric stimuli pass information back to the —
▪ — -duration, meal-related ‘satiety’ signals released from the gastrointestinal tract during
eating.
▪ Distension of the stomach stimulates — afferents and inhibition of feeding.
CCK
▪ Released due to presence of food in the — stimulates satiety both by stimulating — afferents and — release.
Peptide YY
▪ Released by — cells by —
products stimulates satiety – direct inhibition of — nerves.

A

hypothalamus
short
bagel
small intestine
vagal and insulin
enteroendocrine cells
digestion products
NYP orxigenic

20
Q

control of food intake:
1- INHIBITORY ( —- ) PATHWAY
▪ Releases melanocortins derived from proopiomelanocortin ( — ), a precursor molecule
that can be cleaved in different ways to produce several — products.
▪ Melanocortins — appetite, thus leading to — food intake and —
2-STIMULATORY ( — ) PATHWAY
▪ Releases —- ( — ) – neurotransmitter leads to — food intake. One of the most potent appetite — ever found.
The two pathways are mutually exclusive – stimulation of
the POMC pathway — NPY and vice versa.

A

MELANOCORTIN
POMC
hormone
suppress
reduced
weight loss
orexigenic
neuropeptide Y (NYP)
increased
stimulators
inhibits

21
Q

control of food intake:
PERIPHERAL CONTROL
Vagus nerve contains numerous — fibres that rely information back to the —
▪ Vagal stimulation induces — and — feeding.
▪ Blocking of the vagal afferent eliminates — .

Insulin
▪ Released from pancreatic — cells — a meal, acts
directly on the — to induce —.

Leptin
▪ Released from — , stimulates the — pathway and inhibits the — pathway.
Insulin and leptin act as —-term — released into
the — in proportion to the amount of body fat and exert
sustained inhibitory effects on food intake while increasing
energy expenditure.

A

afferent
brain
satiety anf inhibits feeding
satiety
pancreatic beta cells
following
hypothalamus
satiety
adipocyte
POMC
NPY
long term regulators
blood

22
Q

control of food intake:
STIMULANTS
❑ Ghrelin ( — hormone)
▪ Released from — glands in the stomach (likely extra-gastric sites too) when the stomach is —
▪ Ghrelin acts — on — neurons.
▪ Ghrelin release is not affected by — intake or — .
❑ — pathways (dopaminergic neurons from the
ventral tegmental area (VTA) of the midbrain) in response to sight, smell taste of food etc.
These can both influence the — but are also
equally affected by — etc.

A

hunger
oxyntic
empty
directly
orexigenic NPY
protein intake or distension
reward
hypothalamus
leptin