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Physiology Unit 7 > Salvation and gastric Function > Flashcards

Salvation and gastric Function Flashcards

1
Q

pathway of GI hormones

A

produced in GI endocrine cells, portal circulation, pass through liver, systemic circulation to target cells

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2
Q

target cells of gastrin

A

parietal cells in stomach

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3
Q

3 main GI paracrines

A

somatostatin,
histamine,
serotonin

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4
Q

act locally on same tissue that secretes them

A

paracrines

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5
Q

produced by enterochromaffic cells in intestine in response to distension; excites ENS to increase motility and secretions

A

serotinin (paracrine)

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6
Q

produced by D cells; inhibits pancreatic and gastric secretions/motility; endocrine and paracrine

A

somatostatin

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7
Q

released by EC-like cells in the stomach; stimulates HCl secretion via H2 receptors

A

histamine

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8
Q

synthesized in neurons in GI tract; released following AP

A

neurocrines

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9
Q

ACh, norepi, VIP, GRP (gastrin releasing peptide), substance P

A

neurocrines

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10
Q

released from G-cells in stomach in response to food, distension, vagus; increases HCl secretion by parietal cells; stimulates growth of gastric mucosa

A

Gastrin

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11
Q

secreted by I-cells in mucosa of duodenum and jejunum in response to facts and proteins/peptides/amino acids; increases gall bladder contraction; increases pancreatic enzymes (trypsin, chymotrypsin, lipases, amylases) and bicarb; inhibits gastric emptying

A

CCK

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12
Q

secreted by S cells in mucosa of duodenum in response to acidic chyme from stomach; increases bicarb and fluid secretion by pancreas; decreases gastrin and gastric acid secretion; inhibits gastric emptying

A

Secretin

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13
Q

trypsin, chymotrypsin, lipases, amylases

A

pancreatic enzymes

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14
Q

secreted by M cells in mucosa of duodenum and jejunum during fasting period; promotes contraction of distal stomach and intestines to clear

A

Motilin

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15
Q

secreted by K cells in mucosa of duodenum and jejunum in response to fat and carbs; act on pancreas to stimulate insulin secretion; inhibits HCl secretion by parietal cells

A

GIP (glucose-dependent insulinomic peptide)

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16
Q

digestion starts in mouth

A

carbs, fats

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17
Q

digestions starts in stomach

A

proteins

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18
Q

what are and are not digested in stomach

A

are: proteins, lipids

are not: carbs

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19
Q

pancreatic enzyme; digestion of proteins in intestine

A

chymotrypsin

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20
Q

pancreatic enzyme; digestion of lipids in intestine

A

lipase

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21
Q

pancreatic enzyme; digestion of carbs in intestine

A

amylase

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22
Q

brush border disaccharidases and dipeptidases complete digestion of carbs and proteins respectively

A

membrane digestion

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23
Q

lysozyme, IgA-binding protein

A

in saliva to reduce bacterial growth

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24
Q

ptyalin; denatured below pH 4

A

salivary amylase

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25
Q

progressive, chronic autoimmune disease which destroys salivary and lacrimal glands

A

Sjogren syndrome

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26
Q

dry mouth; dental caries and halitosis due to bacterial overgrowth

A

Xerostromia

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27
Q

secrete serous (watery) substance rich in a-amylase; secrete 25% of saliva each day

A

acinar cells of parotid gland

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28
Q

produce sero-mucous product rich in mucin glycoproteins; produce 75% of daily saliva

A

acinar cells of submandibular (70%) and sublingual (5%) glands

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29
Q

high flow rates - saliva is

A

like plasma

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30
Q

low flow rates - saliva is

A

hypotonic

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31
Q

flow in duct cells for saliva

A

Na and Cl out, K and HCO3 into saliva

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32
Q

only humoral agent to affect salivation; stimulates Na reabsorption and K secretion by salivary glands

A

aldosterone

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33
Q

are salivary duct cells permeable to water

A

no - tight junctions

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34
Q

what cells secrete lingual lipase

A

von ebner’s cells

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35
Q

otic and submandibular ganglia

A

stimulated by parasympathetics via salivary nucleus of medulla

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36
Q

otic ganglion stimulates

A

parotid gland via Ach

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37
Q

submandibular ganglion stimnulates

A

submandibular gland via Ach

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38
Q

parotid and submandibular glands cause increased

A

salivary secretion via effects on acinar secretion and vasodilation

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39
Q

parotid and submandibular glands increase salivation via

A

acinar secretion, vasodilation

40
Q

activated by salivary glands; causes production of bradykinin for vasodilation

A

kallikrein

41
Q

how does bradykinin cause vasodilation

A

increased capillary hydrostatic P,
increased capillary filtration,
supplies fluid for secretion

42
Q

PNS vs SNS effect on salivary flow

A

PNS - sustained increase

SNS - transient, smaller increase

43
Q

where is the appetite area of brain

A

near parasym centers of anterior hypothalamus

44
Q

where does appetite area of brain get its signals from

A

cerebral cortex or amygdala

45
Q

mucous neck cells of oxyntic glands

A

secrete mucous

46
Q

peptic/chief cells of oxyntic glands

A

secrete pepsinogen and gastric lipase

47
Q

parietal/oxyntic cells of oxyntic glands

A

secrete HCl and intrinsic factor

48
Q

what happens when parietal cells are destroyed

A

achlorhydria - lack of stomach acid secretion, pernicious anemia from lack of intrinsic factor

49
Q

in body of stomach; empty secretory products via ducts into lumen; duct openings are called pits; contain parietal and chief cells

A

oxyntic glands

50
Q

in antrum of stomach; deeper pits than oxyntic glands; contain G cells and mucous cells

A

pyloric glands

51
Q

contain G cells (secrete gastrin) and D cells (secrete somatostatin)

A

pyloric glands

52
Q

what do cardiac glands secrete

A

mucous

53
Q

lack pepsin

A

digest meats poorly - can’t digest collagen

54
Q

condition for spontaneous conversion of pepsinogen to pepsin

A

pH < 3-5

55
Q

HCO3-, mucous, prostaglandins, mucosal blood flow, GFs

A

protective of gastric mucosa

56
Q

H+, pepsin, H. pylori, NSAIDs, stress, smoking, alcohol

A

damaging factors of gastric mucosa

57
Q

if H+ penetrates into gastric epithelium

A
  • damages mast cells which release histamine, inflammatory response
  • if severe blood flow decreases and cells are damaged
58
Q

erosive gastritis

A

NSAIDs inhibit prostaglandin synthesis

59
Q

stimulates HCO3- release in stomach

A

prostaglandin

60
Q

enzyme for CO2 combining with H2O

A

carbonic anhydrase

61
Q

where does a strong solution of HCl form in HCl secretion

A

canaliculus

62
Q

driving force for HCl secretion

A

H+-K+ ATPase in lumenal membrane of stomach

63
Q

alkaline tide

A

HCO3- is absorbed form the cell into the blood at the basolateral membrane via a Cl/HCO3 exchanger

64
Q

target of drugs for GERD or ulcers

A

H+/K+ ATPase

65
Q

vomiting center

A

medulla oblongata

66
Q

where is the chemoreceptor which can stimulate vomiting

A

4th ventricle of brain

67
Q

how does histamine stimulate acid secretion

A

acts on adjacent parietal cells

68
Q

how does the vagus stimulate acid secretion

A

directly and indirectly

69
Q

how does gastrin stimulate acid secretion

A

acts directly on parietal cells,

also acts indirectly via stimulation of histamine release

70
Q

how does insulin stimulate acid secretion

A

acts directly on parietal cells to stimulate histamine secretion

71
Q

how does somatostatin inhibit acid secretion

A

paracrine manner on parietal cells and G cells (inhibits gastrin)

72
Q

how does GIP inhibit acid secretion

A

acts directly on parietal cells

73
Q

how does secretin inhibit acid secretion

A

acts on G cells to suppress gastrin

74
Q

atropine

A

inhibits Ach

75
Q

Cimetidine

A

H2 receptor antagonist,

inhibits histamine

76
Q

omeprazole, prilosec

A

proton pump inhibitors

77
Q

direct and indirect stimulation of HCl secretion

A

direct - vagus (via Ach receptors)

indirect - gastrin

78
Q

how does the vagus stimulate gastrin release

A

vagus releases gastrin releasing peptide (GRP) onto G cells

79
Q

the vagus has direct stimulation in the cephalic phase on HCl release via

A

Ach receptor on parietal cells

80
Q

the vagus has indirect stimulation in the cephalic phase on HCl release via

A

GRP on G cells which then release Gastrin

81
Q

cephalic phase stimuli

A

smell, taste, conditioning

82
Q

gastrin phase stimuli

A

distention, distention of antrum, amino acids/peptides

83
Q

major inhibitiory mech of HCl secretion (factor; direct/indirect)

A

somatostatin - direct and indirect

84
Q

HCl is needed for activation of

A

pepsinogen

85
Q

histamine is released from

A

ECL cells

86
Q

in the stomach, the vagus directly stimulates

A
  • parietal cells (via Ach) = direct
  • ECL cells (increased histamine)
  • D cells (decreased somatostatin)
87
Q

lumenal H+ directly stimulates D cells, somatostatin inhibits gastrin, reduce acid secretion

A

negative feedback

88
Q

products of protein digestion directly stimulate G cells, gastrin stimulates acid secretion

A

positive feedback

89
Q

pepsinogen is secreted from

A

oxyntic glands of the stomach

90
Q

xerostomia, or antichonlinergics, would cause what change in Cl and K content in saliva

A

deacreased flow rate - more time to diffuse

  • Cl decreases
  • K increases
91
Q

is gastrin inhibitory peptide (GIP) found in the lumen of the stomach?

A

no - intestines only

92
Q

HCl, lipase, mucous, and intrinsic factor are all secreted

A

directly into lumen of stomach

93
Q

where does most carb digestion occur

A

duodenum

94
Q

RLS in acid secretion

A

proton pump

95
Q

effect of vagotomy on cephalic phase acid secretion

A

wipes it out

96
Q

Digestion of ___ is impaired to the greatest extent in patients with achlorhydria (failure of HCl secretion by stomach)

A

protein

Physiology Unit 7 (3 decks)

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