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SF4 Exam I > Regulation of Gastric Secretion Emesis > Flashcards

Regulation of Gastric Secretion Emesis Flashcards

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
Q

chyme in duodenum (how does it inhibit acid secretion)

A

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

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26
Q

what type of acid secretion occurs in absence of all gastrin stimulation

A

basal secretion

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27
Q

what type of acid secretion shows circadian rhythm in humans (thus having highest output in evening and lowest in morning)

A

basal secretion

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28
Q

between meals, pH of gastric juice is low, causing what?

A

acidification of mucosa

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29
Q

cephalic phase of acid secretion of initiated by what?

A

thought, sight, taste, or smell of food (depends on food)

chewing swallowing

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30
Q

cephalic phase of acid secretion (what triggers afferents and pathway)

A

chemoreceptors and central pathways trigger afferent impulses that are relayed to vagal nucleus
then vagal efferent nerves carry impulses to stomach

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31
Q

the vagus nerve increases acid section by what two mechanisms during cephalic phase of acid secretion?

A

ACh directly stimulates parietal cell

ACh causes release of GRP

32
Q

the gastric phase of acid secretion is initiated by what?

A

entry of food into stomach

33
Q

gastric phase of acid secretion (what does it do)

A

buffers acid, raising pH from about 2 to as high as 6

34
Q

what does the rise in pH during the gastric phase of acid secretion permit?

A

vagal stimulation from cephalic phase to initiate, and stimuli fro gastric phase to maintain, gastrin release

35
Q

during gastric phase of acid secretion distention of stomach actives what?

A

mechanoreceptors

36
Q

activation of mechanoreceptors during gastric phase of acid secretion initiates what?

A

local and vasovagal reflexes

which stimulate gastrin release via GRP and acid secretion via ACh

37
Q

during gastric phase what is the only major nutrient that can stimulate gastric secretion

A

digested protein (must be broken down into peptides and amino acids- direct chemical release of gastrin from G cells)

38
Q

caffeine has what effect on stomach acid secretion

A

stimulates it

39
Q

intestinal phase of stomach acid secretion is initiated by what

A

presence of protein digestion products in duodenum (gastrin)

distention (hormonal/nervous mechanisms)

40
Q

what part of duodenum secretes gastrin and thus stimulates acid secretion

A

proximal

41
Q

what are the two types of peptic ulcers

A

gastric

duodenal

42
Q

gastric ulcers are caused by what?

A

proactive barrier of stomach breaks down, leading to injury of gastric mucosa by acid and pepsin

43
Q

where are gastric ulcers usually found

A

distal stomach

44
Q

in gastric ulcers what occurs the H+ secretion into the stomach

A

reduced because some acid leaks into gastric mucosa

45
Q

what type of peptic ulcer is most common

A

duodenal

46
Q

in duodenal ulcers patients tend to have increased levels of what?

A

acid, gastrin, and pepsin

47
Q

in some patients with duodenal ulcers pepsin can do what?

A

potentiates ulcer formation initiated by acid

48
Q

patients with duodenal cancers may have high levels of acid and pepsin, this would do what?

A

damage cells lining duodenum

49
Q

patients with duodenal ulcers may have defects in what mechanism?

A

defense mechanism against acid

50
Q

in some patients with duodenal ulcers there bicarbonate secretion is what compared to normal

A

lower

51
Q

what are the cause of damage in peptic ulcers (name them

A

Helicobacter pylori infection
NSAIDs
alcohol

52
Q

Helicobacter pylori infection does what

A

breaks down gastric epithelial barrier

in duodenum- inhibits secretion of somatostatin, allowing increased gastrin release and acid production

53
Q

almost all ulcer patients have what type of infection

A

helicobacter pylori

54
Q

helicobacter pylori thrives in stomach because it can produce large quantities of what?

A

urease

55
Q

urease (what is it)

A

produces by H pylori

an enzyme that generates ammonia to neutralize the acid that quickly kills other bacteria

56
Q

H. pylori contributes to ulcers how?

A

thinning the protective mucus layer
poisoning nearby cells with ammonia or other toxins
or even byincreasing acid production

57
Q

treatment for ulcers include

A

antibiotics (H. pylori)
proton-pump inhibitors (block (H+,K+) ATPase
usually two antibiotics and proton-ump inhibitor; may add Pepto-Bismol

58
Q

what is another term for emesis

A

vomiting

59
Q

vomiting (emises) what is it?

A

forceful expulsion of gastric and intestinal contents through mouth

60
Q

emises (vomiting) is a protective mechanism for what?

A

to rid body of noxious or toxic substances

61
Q

is vomiting always accompanied with nausea

A

no

62
Q

is nausea always accompanied with vomiting

A

no

63
Q

where do the waves of contractions begin during emesis (and what does this do)

A

distal small intestine, moving GI contents toward stomach

64
Q

retching (what is it)

A

involves all of involuntary motions f vomiting without production of vomitus`

65
Q

before or during emesis discharge of autonomic nervous system leads to what?

A

increased salivation and sweating
rapid breathing
irregular heartbeat

66
Q

where is the vomiting center located

A

medulla

67
Q

the vomiting center is activated by afferent impulses triggered by?

A 
ticking back of through (via NTS)
distention of stomach or duodenum
vestibular stimulation (motion sickness)
intense pain
sights and smells
68
Q

direct activation of the vomiting center causes what?

A

vomiting without nausea or retching

69
Q

what leads to retching without vomiting

A

stimulating of second separate medullary area

70
Q

chemoreceptor trigger zone (CTZ)

(where is it and what activates itP

A

in area postrema

activated by emetics, radiation, and motion sickness

71
Q

vomiting center ahs receptors present where?

A

duodenum and, to lesser extent, stomach

72
Q

morning sickness (why does it happen)

A

believed to have evolved to protect fees early in development when toxins can cause most damage

73
Q

“hyperemesis of pregnancy” (what is it)

A

about 5/1000 pregnant women have severe nausea and vomiting that causes them to lose weight

74
Q

nausea affects about what percentage of pregnant woman

A

70-85%

75
Q

vomiting affects about what percentage of pregnant women

A

50%

76
Q

what are the effects of protracted vomiting

A

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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