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PMCOL 344 > GI 2 - acid > Flashcards

GI 2 - acid Flashcards

1
Q

how much gastric juice does a human secrete per day

A

2.5 litres

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2
Q

what do peptic/ chief cells release

A

pro enzymes like prorennin and pepsinogen

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3
Q

what do parietal cells secrete

A

HCl

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4
Q

what are 3 reasons that gastric secretions are so acidic?

A

to promote proteolysis (convert pepsinogen to pepsin)
kill pathogens
aids in iron absorption

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5
Q

which form of iron is better to be absorbed, which is favoured in acidic?

A

Fe2+ is better absorbed than Fe3+

Fe2+ is made in acidic environment

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6
Q

what is the main protective mechanism of the stomach wall from acid

A

mucosal cells that secrete prostaglandins

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7
Q

what are the 2 main prostaglandins that mucosal cells secrete

A

PGE2 and PGI2

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8
Q

what do mucosal cells secrete

A

PGE2 and PGI2 (prostaglandins), also mucus and bicarbonate

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9
Q

what are the targets for PGE2 and PGI2

A

EP1, EP2, EP3, EP4

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10
Q

where do prostaglandins act to stimulate mucous secretion

A

EP4 receptors on mucosal cells

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11
Q

where do prostaglandins act to stimulate bicarbonate ion secretion

A

EP1/2 receptors on mucosal cells

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12
Q

what happens when EP4 receptors on mucosal cells are activated

A

release mucus

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13
Q

what happens when EP1/2 receptors on mucosal cells are activated

A

stimulate bicarbonate ion secretion

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14
Q

what is the pH of the stomach lumen

A

1-2

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15
Q

how is the stomach wall physically protected from mucous? What is the ph of this?

A

mucosal surface forms gel-like protective surface, pH 6-7

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16
Q

what kind of prostaglandins receptors are on enterochromaffin like cells

A

EP2/3

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17
Q

what happens when EP2/3 on enterochromaffin like cells are activated

A

inhibits release of histamine

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18
Q

what does histamine do and how

A

stimulates acid production via H2 receptors

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19
Q

what kind of prostaglandins receptors are on vascular cells

A

EP2/4

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20
Q

what happens when prostaglandins act on vascular EP2/4 receptors

A

vasodilation, improve blood flow to mucosal layer

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21
Q

what are the 3 cell targets of prostaglandins

A

mucosal cells, enterochromaffin like cells (ECL), vascular cells

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22
Q

what is the concentration of HCL secretion by parietal cells

A

150mM

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23
Q

how is Cl- secreted by parietal cells

A

actively (alongside K+) (on lumen side)

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24
Q

how is K+ secreted by parietal cells

A

actively (alongside Cl-) (on lumen side)

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25
Q

what kind of transporter is the Cl- K+ mechanism in parietal cells

A

it is co transport, 2ary active (on lumen side)

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26
Q

what provides the energy for the Cl- K+ co transport

A

K+ being exchanged in a H+/K+ ATPase (H+ into lumen, K+ back inside)

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27
Q

what is the pH inside the parietal cell

A

7.2

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28
Q

what is the pH inside the stomach lumen

A

1-2

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29
Q

what kind of gradient is the ATPase pumping against in the parietal cell

A

HUGE gradient, 10^5 fold gradient

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30
Q

what is the source of H+ in parietal cells

A

carbonic anhydrase generating H+ and HCO3- from H2O and CO2

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31
Q

what is the source of Cl- in parietal cells

A

HCO3- exchanges for Cl- (on blood side)

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32
Q

what is the pH of the HCl secreted by parietal cells

A

less than 1!

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33
Q

where is histamine released (and where in the cell specifically)

A

basally released from ECL cells

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34
Q

which cell releases histamine

A

ECL cells

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35
Q

where does histamine from ECL cells act

A

on parietal cell H2 receptors

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36
Q

what happens once histamine acts on parietal H2 receptors

A

activates Gs, cAMP –> proton pump

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37
Q

which cells release gastrin

A

G cells

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38
Q

what causes the release of gastrin by G cells

A

nerve stimulation and stomach contents

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39
Q

what are 2 example of stomch contents that stimulate HCl release

A

amino acids, Ca++

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40
Q

what does gastrin do? where does it act?

A

it acts on CCK2 receptors on ECL cells, elevates [Ca++]i to stimulate release of histamine

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41
Q

what do G cells release

A

gastrin

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42
Q

what do ECL cells release

A

histamine

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43
Q

where is ACh released

A

postganglionic cholinergic neurons

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44
Q

where does ACh act (2)

A

on parietal M3 receptors AND D cells

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45
Q

what happens when ACh acts on M3 receptors (where are they)

A

parietal cell, stimulates proton pump via elevation of [Ca++]i

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46
Q

what does ACh do to D cells

A

inhibits somatostatin release

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47
Q

what does ACh do to somatostatin release and how

A

inhibits its release from D cells

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48
Q

what do prostaglandins do in the HCl pathway (3)

A

inhibit histamine production, increase HCO3- and mucous secretion, vasodilation

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49
Q

where is somatostatin released (and what cell types)

A

from D cell in stomach

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50
Q

where does somatostatin act

A

SST2 receptors on G cells, ECL cells, parietal cells

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51
Q

what does somatostatin do to G cells

A

acts on SST2 receptors on G cells to inhibit gastrin release

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52
Q

what does somatostatin do to ECL cells

A

inhibit histamine release

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53
Q

what does somatostatin do to parietal cells cells

A

inhibit acid secretion

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54
Q

what are stomach ulcers and how can they be serious?

A

bleeding, perforation leading to stomach contents entering body cavity and causing peritonitis

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55
Q

what is GERD and how can it be serious?

A

damage to esophageal epithelium can lead to barretts esophagus (damaged, precancerous)

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56
Q

what are 3 examples of these GI diseases

A

ulcer, GERD, hiatal hernia

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57
Q

what is the problem with Hiatal hernia

A

similar with GERD and esophageal acid reflux, similar treatment

(dw too much bout this one)

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58
Q

what are 3 main causes of ulcers

A

stress, cyclooxygenase, helicobacter pylori infection

59
Q

how does stress cause ulcers

A

vagal stimulation increases ACh release

60
Q

how can NSAIDs cause ulcers

A

they decrease production of protective mucosal prostaglandins

61
Q

what does COX-1 do

A

basal prostaglandin production

62
Q

when is COX-2 induced

A

inflammation and growth

63
Q

what % of gastric ulcers has helicobacter pylori infection

A

80-90%

64
Q

what % of duodenal ulcers has helicobacter pylori infection

A

95%

65
Q

what usually protects the duodenum from stomach acid

A

high levels of bicarbonate secretion there

66
Q

what are the 3 main treatment goals with ulcers

A

relieve symptoms, allow damaged tissue to heal, eliminate cause

67
Q

which gram is helicobacter pylori

A

negative

68
Q

what % of population has helicobacter pylori in their stomach lining

A

50%

69
Q

what % of population gets peptic ulcer disease in helicobacter pylori affected population

A

20%

70
Q

how does helicobacter pylori cause ulcers (general)

A

asymptomatic inflammation of stomach lining, eventually causes ulcers and is linked to cancer

71
Q

what class carcinogen is having helicobacter pylori

A

apparently WHO says class 1

72
Q

what are 4 main ways that H. pylori survives in stomach acid

A
  • burrowing into stomach lining
  • urease (helps them neutralize acid)
  • produces toxins
  • local inflammation
73
Q

what happens once helicobacter pylori burrows into stomach lining

A

the damage permits acid and pepsin to reach stomach epithelium

74
Q

how does urease work (helicobacter pylori)

A

converts urea to HCO3 and ammonia (forms ammonium) to neutralize the acid

75
Q

where does the urea come from for helicobacter pylori

A

the breakdown of amino acids from food

76
Q

what happens once helicobacter pylori prouces toxins

A

it kills epithelial cells

77
Q

how does helicobacter pylori cause local inflammation

A

immune cells spill destructive agents (like superoxide radicals) on stomach lining cells, leading to sores and ulcers

78
Q

how can you test for helicobacter pylori? (Simple, name of test)

A

urea breath test

79
Q

how does the urea breath test work

A

-drink solution containing urea labelled with 13C or 14C, collect exhaled breath and analyze for labelled CO2

80
Q

what are 3 pros of the urea breath test

A

it is a quick, cheap and non invasive way to test for helicobacter pylori

81
Q

what are 4 therapeutic strategies for ulcers/GERD/hiatal hernia

A

antibiotics, decrease acid secretion, neutralize secreted acid, protect mucosa

82
Q

what is the point in using antibiotics for ulcers/GERD/hiatal hernia

A

to eliminate H. pylori

83
Q

how can you decrease gastric acid secretion for ulcers/GERD/hiatal hernia

A

proton pump inhibitors or H2 receptor antagonists

84
Q

how can you neutralize gastric acid for ulcers/GERD/hiatal hernia

A

antacids

85
Q

what is the only cure for ulcers/GERD/hiatal hernia

A

antibiotics for H. pylori infection

86
Q

what is Triple Therapy

A

proton pump inhibitor
+
antibacterial drugs (2 of them)

87
Q

what are 2 mechanisms antibiotics used in triple therapy

A

a macrolide that inhibits bacterial protein synthesis + broad spectrum penicillin to inhibit bacterial wall synthesis

88
Q

what are 2 antibiotic drugs used in triple therapy

A

clarithromycin and amoxicillin

89
Q

what is an example of a proton pump inhibitor

A

omeprazole

90
Q

how does clarithromycin work

A

a macrolide that inhibits bacterial protein synthesis

91
Q

how does amoxicillin work

A

broad spectrum penicillin to inhibit bacterial wall synthesis

92
Q

is triple therapy always useful

A

maybe, 2 week treatments is usually effective, but re infection can occur

93
Q

what is the last step in the gastric acid secretion pathway

A

H+/K+ ATPase

94
Q

what is first line therapy for reducing acid secretion

A

proton pump inhibitors

95
Q

what is the mechanism of action of proton pump inhibitors (omeprazole)

A

a prodrug, when activated it binds covalently with cysteines in active site on outside of cell

-inhibits both basal and stimulated acid secretion

96
Q

do proton pump inhibitors (omeprazole) inhibits basal or stimulated acid secretion

A

both

97
Q

how long does omeprazole last and why

A

2-3 days because it is irreversible (but half life is only 1 hour)

98
Q

what kind of pKa for omeprazole and what is its significance

A

around 8, so weak base/ ionized form accumulates on outside of cell in acid environment (perfect targeting, promotes conversion of prodrug)

99
Q

what is the lipid solubility of omeprazole

A

low (BH+ B + H+

100
Q

why may omeprazole have some drug interactions

A

because it inhibits some cytochrome P450 enzymes, potentiates actions of other drugs

101
Q

what other drugs does omeprazole potentiate the action of

A

warfarin (anticoagulant) clodipogrel (antiplatelet), anti-epileptic phenytoin, benzos, TCAs

102
Q

what kind of bad side effect may happen with omeprazole (2)

A

osteoporosis, cardio issues

103
Q

what is cimetidine

A

H2 receptor antagonist (selective, competitive)

104
Q

what is omeprazole

A

proton pump inhibitor

105
Q

where are the H2 receptors that cimetidine targets

A

parietal cells

106
Q

what kind of secretion does cimetidine reduce

A

histamine and gastrin stimulated acid secretion

107
Q

what decrease in acid level happens?

A

decrease basal and stimulated by >90%

108
Q

do H2 receptor antagonists (cimetidine) inhibits basal or stimulated acid secretion

A

both

109
Q

what happens to pH when you use cimetidine

A

it increases to above 4

110
Q

what protein gets affected by cimetidine

A

pepsin, less gets activated

111
Q

what does cimetidine do to ulcer healing

A

promotes healing

112
Q

what is the KD for cimetidine with H1, H2 and H3 (what does this mean for affinity)

A

lowest for H2, then H3 then H1

so highest affinity for H2

113
Q

does cimetidine have any drug interactions and why

A

yes because it inhibits some cytochrome P450 enzymes (CYP 2C9, 2D6, 3A4)

114
Q

what are some examples of drug interactions with cimetidine

A

warfarin, felodipine (Ca++ channel antagonist), lovastatin, phenytoin, benzos, TCAs

115
Q

what is an unwanted issue in men caused my cimetidine

A

gynaecomastia

116
Q

how does cimetidine cause gynaecomastia

A

affinity for estrogen receptors and increase prolactin secretion

117
Q

what kind of compounds are most antacids

A

basic inorganic salts

118
Q

how do basic inorganic salts work

A

taken orally to directly neutralize gastric acid and thus inhibit peptide enzymes

119
Q

what pH do peptide enzymes need to work

A

under 5 I think

120
Q

what is the mechanism of action of antacids

A

chemical antagonism

121
Q

Are antacids absorbed?

A

no, just act in the lumen anyways

122
Q

how can antacids help with ulcers

A

sufficient doses for prolonged periods can help heal them

123
Q

what is inside antacids

A

micture of salts (Mg and Al hydroxyde) to help preserve normal bowel function

124
Q

what does magnesium cause generally

A

diarrhea

125
Q

what does aluminium cause generally

A

constipation

126
Q

what is the stomach acid neutralization reaction with aluminum hydroxide

A

Al(OH)3 + 3HCl –> AlCl3 + 3H2O

127
Q

what are alginates

A

negatively charged polysaccharides from algal cell wall

128
Q

how do alginates work (2)

A

absorb water to form a viscous gum, maybe increase viscosity and adherence of mucous to stomach lining

129
Q

what are 3 examples of alginates

A

tums, gaviscon, mylanta

130
Q

what is the active ingredient in tums

A

CaCO3

131
Q

what is the active ingredient in gaviscon

A

MgCO3 + alginic acid

132
Q

what is the active ingredient in mylanta

A

MgCO3 + Al(OH)3

133
Q

what is bismuth chelate

A

a colloid, used with triple therapy to treat H. pyloria

134
Q

how does bismuth chelate work

A

kills bacteria (maybe) and prevents adherence

135
Q

what are 2 ways to protect the mucosa (general, not drugs)

A

enhance endogenous mucosal protective mechanisms and/or provide physical barrier over ulcer

136
Q

what are 2 drugs used to protect the mucosa

A

bismuth chelate, sucralfate

137
Q

how does sucralfate work, what is it (big answer)

A

complex of Al(OH)3 and sulfated sucrose which releases Al in acidic enviro to leave -ve charged complex which binds to proteins and glycoproteins in mucous to form gel

138
Q

what are 4 other things that bismuth chelate and sucralfate do other than mucous protection

A

affect absorption of other drugs, adsorb pepsin, enhance PG synthesis, stimulate HCO3 secretion

139
Q

what is misoprostal

A

a stable PGE1 analog

140
Q

how can misoprostal help protect mucosa (4 general things)

A

inhibit HCl release from parietal cells, enhance mucous production and mucosal blood flow, stimulates HCO3- release

141
Q

what are 3 main targets for misoprostol (cellular targets+what does it cause)

A

EP1/2 on mucosal cells (increase HCO3-), EP4 on mucosal cells (increase mucous), EP2/3 on ECL cells (inhibit histamine)

142
Q

what is the main mechanism of action of misoprostol (1 thing)

A

adenylyl cyclase inhibition

143
Q

which peptic ulcer drug is most likely to cause breast enlargement?

A

cimetidine

PMCOL 344 (27 decks)

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