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SF4 Exam I > Regulation of Gastric Secretion Emesis > Flashcards

Regulation of Gastric Secretion Emesis Flashcards

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1
Q

stimulants of acid secretion (name them)

A

ACh
Histamine
Gastrin

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2
Q

how does ACh stimulate acid sectretion

A

binds muscarinic receptors on parietal cell membrane
activates phospholipase C (PLC)
that catalyses formation of IP3
IP3 causes release of Ca2+

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3
Q

how does histamine stimulate acid secretion?

A

binds to H2 receptors on parietal cell membrane

activates adenylate cyclase to form cAMP

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4
Q

how does gastrin stimulate acid secretion?

A

binds gastrin/CCK-B receptors on parietal cell membrane
activates phospholipase C (PLC)
that catalyses formation of IP3
IP3 causes release of Ca2+

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5
Q

what type of receptor does ACh bind in a parietal cell

A

muscarinic

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6
Q

what type of receptor does histamine bind in a parietal cell

A

H2

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7
Q

what type of receptor does gastrin bind in a parietal cell

A

gastrin/CCK-B

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8
Q

what do Ca2+ and cAMP do inside of a parietal cell

A

increase concentration of (H+,K+)Atlases and CL- channels in apical membrane

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9
Q

potentiation (when does it occur)

A

when response to simultaneous administration of two stimulants greater than sum of responses to either agent given alone

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10
Q

potentiation (what does it allow for)

A

small amounts of endogenous stimuli to produce near maximal effects

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11
Q

histamine potentiates what

A

gastrin

ACh

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12
Q

why are H2 blocker effective in inhibiting acid secretion

A

block not only action of histamine but histamines potentiating effects on ACH and gastrin

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13
Q

ACh potentiates what?

A

histamine and gastrin

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14
Q

ECL (enterochromaffin-like) cell has receptors for what

A

gastrin and ACh

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15
Q

gastrin stimulates what in ECL (enterochromaffin-like) cells

A

release and synthesis of histamine

proliferation of cells

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16
Q

ACh stimulates what in ECL (enterochromaffin-like) cells

A

release and synthesis of histamine (not as much as gastrin)

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17
Q

what is best at stimulating the release and synthesis of histamine from ECL (enterochromaffin-like) cells

A

gastrin

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18
Q

inhibitors of acid section (name them)

A

low pH in stomach

chyme in duodenum

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19
Q

how does low pH in stomach inhibit acid secretion

A

somatostatin released (inhibits acid secretion by parietal cells and gastrin secretion by G cells)

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20
Q

somatostatin

A

inhibits acid secretion (after a meal) by parietal cells and gastrin secretion by G cells
when stomach pH less than 3

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21
Q

after a meal is ingested what happens to pH of stomach and what odes this cause?

A

pH of stomach rises

leads to secretion of acid

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22
Q

an increase of pH in stomach leads to what

A

secretion of acid

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23
Q

once meal is digested and stomach empties what happens to pH in stomach

A

drops

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24
Q

what happens when the pH in the stomach is below 3.0

A

gastrin release inhibited (negative feedback mechanism)

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25
chyme in duodenum (how does it inhibit acid secretion)
both neutral and humoral mechanisms triggered by acidity, osmolarity, and fat content of chyme inhibit gastrin release by G cell and or acid secretion by parietal cell
26
what type of acid secretion occurs in absence of all gastrin stimulation
basal secretion
27
what type of acid secretion shows circadian rhythm in humans (thus having highest output in evening and lowest in morning)
basal secretion
28
between meals, pH of gastric juice is low, causing what?
acidification of mucosa
29
cephalic phase of acid secretion of initiated by what?
thought, sight, taste, or smell of food (depends on food) | chewing swallowing
30
cephalic phase of acid secretion (what triggers afferents and pathway)
chemoreceptors and central pathways trigger afferent impulses that are relayed to vagal nucleus then vagal efferent nerves carry impulses to stomach
31
the vagus nerve increases acid section by what two mechanisms during cephalic phase of acid secretion?
ACh directly stimulates parietal cell | ACh causes release of GRP
32
the gastric phase of acid secretion is initiated by what?
entry of food into stomach
33
gastric phase of acid secretion (what does it do)
buffers acid, raising pH from about 2 to as high as 6
34
what does the rise in pH during the gastric phase of acid secretion permit?
vagal stimulation from cephalic phase to initiate, and stimuli fro gastric phase to maintain, gastrin release
35
during gastric phase of acid secretion distention of stomach actives what?
mechanoreceptors
36
activation of mechanoreceptors during gastric phase of acid secretion initiates what?
local and vasovagal reflexes | which stimulate gastrin release via GRP and acid secretion via ACh
37
during gastric phase what is the only major nutrient that can stimulate gastric secretion
digested protein (must be broken down into peptides and amino acids- direct chemical release of gastrin from G cells)
38
caffeine has what effect on stomach acid secretion
stimulates it
39
intestinal phase of stomach acid secretion is initiated by what
presence of protein digestion products in duodenum (gastrin) | distention (hormonal/nervous mechanisms)
40
what part of duodenum secretes gastrin and thus stimulates acid secretion
proximal
41
what are the two types of peptic ulcers
gastric | duodenal
42
gastric ulcers are caused by what?
proactive barrier of stomach breaks down, leading to injury of gastric mucosa by acid and pepsin
43
where are gastric ulcers usually found
distal stomach
44
in gastric ulcers what occurs the H+ secretion into the stomach
reduced because some acid leaks into gastric mucosa
45
what type of peptic ulcer is most common
duodenal
46
in duodenal ulcers patients tend to have increased levels of what?
acid, gastrin, and pepsin
47
in some patients with duodenal ulcers pepsin can do what?
potentiates ulcer formation initiated by acid
48
patients with duodenal cancers may have high levels of acid and pepsin, this would do what?
damage cells lining duodenum
49
patients with duodenal ulcers may have defects in what mechanism?
defense mechanism against acid
50
in some patients with duodenal ulcers there bicarbonate secretion is what compared to normal
lower
51
what are the cause of damage in peptic ulcers (name them
Helicobacter pylori infection NSAIDs alcohol
52
Helicobacter pylori infection does what
breaks down gastric epithelial barrier | in duodenum- inhibits secretion of somatostatin, allowing increased gastrin release and acid production
53
almost all ulcer patients have what type of infection
helicobacter pylori
54
helicobacter pylori thrives in stomach because it can produce large quantities of what?
urease
55
urease (what is it)
produces by H pylori | an enzyme that generates ammonia to neutralize the acid that quickly kills other bacteria
56
H. pylori contributes to ulcers how?
thinning the protective mucus layer poisoning nearby cells with ammonia or other toxins or even byincreasing acid production
57
treatment for ulcers include
antibiotics (H. pylori) proton-pump inhibitors (block (H+,K+) ATPase usually two antibiotics and proton-ump inhibitor; may add Pepto-Bismol
58
what is another term for emesis
vomiting
59
vomiting (emises) what is it?
forceful expulsion of gastric and intestinal contents through mouth
60
emises (vomiting) is a protective mechanism for what?
to rid body of noxious or toxic substances
61
is vomiting always accompanied with nausea
no
62
is nausea always accompanied with vomiting
no
63
where do the waves of contractions begin during emesis (and what does this do)
distal small intestine, moving GI contents toward stomach
64
retching (what is it)
involves all of involuntary motions f vomiting without production of vomitus`
65
before or during emesis discharge of autonomic nervous system leads to what?
increased salivation and sweating rapid breathing irregular heartbeat
66
where is the vomiting center located
medulla
67
the vomiting center is activated by afferent impulses triggered by?
``` ticking back of through (via NTS) distention of stomach or duodenum vestibular stimulation (motion sickness) intense pain sights and smells ```
68
direct activation of the vomiting center causes what?
vomiting without nausea or retching
69
what leads to retching without vomiting
stimulating of second separate medullary area
70
chemoreceptor trigger zone (CTZ) | (where is it and what activates itP
in area postrema | activated by emetics, radiation, and motion sickness
71
vomiting center ahs receptors present where?
duodenum and, to lesser extent, stomach
72
morning sickness (why does it happen)
believed to have evolved to protect fees early in development when toxins can cause most damage
73
"hyperemesis of pregnancy" (what is it)
about 5/1000 pregnant women have severe nausea and vomiting that causes them to lose weight
74
nausea affects about what percentage of pregnant woman
70-85%
75
vomiting affects about what percentage of pregnant women
50%
76
what are the effects of protracted vomiting
metabolic alkalosis due to loss of gastric acid hypokalemia due to loss of K+ in vomitus and decreased K+ uptake hyponatremia due to loss of Na+ in vomitus dehydration

SF4 Exam I (16 decks)

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