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Pharmacology > Gastrointestinal Disorders (Exam 3) > Flashcards

Gastrointestinal Disorders (Exam 3) Flashcards

1
Q

Most common GI disorder in the US

A

GERD

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2
Q

major GI disorders in the US

A

GERD
IBS
Gallstones
Celiac disease
Crohn’s disease
Ulcerative colitis
Hemorrhoids
Diverticulosis
Colon cancer

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3
Q

cells in the GI tract

A

pit cell
stem cell
neck cell
parietal cell
chief cell
endocrine cell

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4
Q

which layer of the stomach wall does drugs typically act?

A

mucosa

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5
Q

types of enzymes in the small intestine

A

pancreatic enzymes
brush border enzymes

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6
Q

pancreatic enzymes

A

lipases, amylases, exopeptidase, nucleases

secreted into the intestine, in intestinal lumen

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7
Q

brush border enzymes

A

embedded in the absorptive cell membranes
carry digestive work, not in lumen

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8
Q

intestinal cells can absorb only

A

monosaccarhides

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9
Q

digestion of proteins begins in the

A

stomach

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10
Q

digestion and absorption of lipids

A

bile salts must emulsify the lipid droplets into smaller ones

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11
Q

micelle

A

cholesterol
monoglyceride
fatty acid

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12
Q

how does components of a micelle cross the membrane?

A

cholesterol - carrier protein
monoglycerides and fatty acids - simple diffusion

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13
Q

what happens when the components of a micelle cross the membrane?

A

triglycerides reform
cholesterol, TG, proteins form chylomicrons
chylomicrons released into lacteal

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14
Q

what types of drugs are used to treat GI disorders?

A

drugs that neutralize acids
drugs that decrease acid output
drugs that affect GI motility

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15
Q

histamine

A

produced in enterochromaffin-like cells, mast cells, basophils and neurons

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16
Q

histamine has an important role in

A

gastric secretion

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17
Q

site of histamine storage is mainly in

A

mast cells

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18
Q

serotonin

A

modulation of platelet function and neurotransmission
important role in the gut

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19
Q

serotonin is produced in

A

enterochromaffin cells, neurons

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20
Q

serotonin is not produced in _____________, only stored there

A

platelets

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21
Q

precursor of serotonin

A

tryptophan

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22
Q

5HT1 subtypes and where they act

A

A-F - brain
P - enteric NS

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23
Q

5HT2 subtypes and where they act

A

2A - platelets, smooth muscle
2B - stomach

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24
Q

where does 5HT3 act?

A

vomiting centers - CNS
stomach

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25
Q

what stimulates gastric acid secretion?

A

acetylcholine, histamine, gastrin

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26
Q

G cells are

A

gastrin producers

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27
Q

D cells are

A

somatostatin producers

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28
Q

somatostatins role

A

inhibits G cell
inhibits gastrin secretion

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29
Q

nerve involved in gastric acid secretion

A

vagus preganglionic nerve

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30
Q

acetylcholine is present in

A

D cells
ECL cells
Parietal cells

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31
Q

where is the proton pump located and what is its official name?

A

in parietal cells

H+K+ ATPase

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32
Q

drugs that neutralize acids

A

systemic antacids
nonsystematic antacids

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33
Q

systemic antacids

A

are soluble and reabsorbable
cause systemic alkalosis

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34
Q

example of systemic antacids

A

sodium bicarbonate

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35
Q

nonsystematic antacids

A

not absorbed into systemic circulation
do not produce systemic alkalosis

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36
Q

examples of nonsystematic antacids

A

aluminum containing antacids
calcium containing antacids
magnesium containing antacids
combination antacids

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37
Q

magaldrate

A

use to treat variety of conditions such as esophagitis, duodenal and gastric ulcers and GERD

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38
Q

mechanism of systemic antacids

A

in stomach: instantaneous interaction with HCl –> NaCl, water and CO2
in intestines: NaCl + HCO3 to Na+ HCO3

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39
Q

side effects of systemic antacids

A

hypernatremia
fluid retention
metabolic alkalosis

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40
Q

where part of the MOA of systemic antacids does absorption occur?

A

in intestines

NaHCO3 –> Na+ and HCO3

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41
Q

Nonsystemic antacids CaCO3 MOA

A

in stomach: CaCO3 + 2HCl –> CaCl2, water and CO2
in intestines: CaCl2 + HCO3 –> CaCO3 and HCl

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42
Q

CaCO3 reacts slower than

A

Na+ bicarbonate

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43
Q

side effects of CaCO3

A

hypercalcemia can trigger gastrin release –> acid rebound

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44
Q

how much of CaCO3 is absorbed (nonsystemic antacid)

A

about 10%

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45
Q

nonsystematic acids Mg(OH)2 and Al(OH)3 MOA

A

in stomach: reacts slowly with HCl –> MgCl2 and water
in intestines: MgCl2 and HCO3 –> Mg(OH)2 and HCl

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46
Q

Mg(OH)2 and Al(OH)3 are relatively

A

insoluble and slow neutralize acid
retention in stomach

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47
Q

side effects of Mg(OH)2

A

cathartic
can induce N/V
diarrhea

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48
Q

side effects of Al(OH)3

A

constipation
can bind to antibiotics, antifungals, iron supplements and prevent absorption
toxicity in renal insufficiency

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49
Q

nonsystemic antacids can be combined with

A

anticholinergic drugs to delay gastric emptying

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50
Q

common anticholinergics combined with nonsystemic antacids

A

pirenzepine, propantheline and mepenzolate

all act as M1 receptor antagonists

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51
Q

side effects of nonsystemic antacids with anticholinergics

A

blurry vision
contraindicated with glaucoma

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52
Q

potency of H2 receptor antagonists (from greatest to least)

A

famotidine > nizatidine = ranitidine > cimetidine

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53
Q

H2 receptor antagonists examples

A

cimetidine
nizatidine
famotidine
ranitidine (discontinued)

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54
Q

H2 receptor antagonists MOA

A

competitive H2 receptor antagonist
permissive and transmissive role of histamine

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55
Q

permissive role of histamine

A

presence of histamine permits action of acetylcholine and gastrin

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56
Q

transmissive role of histamine

A

histamine is basic and final requirement for acetylcholine and gastrin

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57
Q

how are H2 receptor antagonists metabolized?

A

hepatic metabolism
glomerular filtration
tubular secretion

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58
Q

H2 receptor antagonists are very effective at

A

inhibiting nocturnal H+ secretion

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59
Q

which H2 receptor antagonists has little first pass hepatic metabolism?

A

nizatidine

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60
Q

cimetidine inhibits

A

CYP450 hepatic drug metabolism

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61
Q

toxicity of H2 receptor antagonists from greatest to least

A

cimetidine > nizatidine > famotidine > ranitidine

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62
Q

toxicity of H2 receptor antagonists

A

inhibits dihydrotestosterone binding to androgen receptors
inhibits estradiol metabolism
increase serum prolactin levels
inhibition of hepatic alcohol metabolism

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63
Q

toxicity of H2 receptor antagonists can lead to

A

Gynecomastia in men
Galactorrhea in women

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64
Q

proton pump inhibitors examples

A

omeprazole
esomeprazole
rabeprazole
lansoprazole
pantoprazole

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65
Q

MOA of PPIs

A

non competitive inhibitors of the H+K+ ATPase

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66
Q

PPIs are _____________ and are activated in an _________ environment

A

prodrugs

acidic

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67
Q

PPIs must pass through the

A

stomach to be effectively absorbed

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68
Q

PPIs are absorbed in the _______ into ________________ and converted into the __________

A

intestine

PC vesicles

active form

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69
Q

omeprazole

A

Prilosec

metabolized in the liver by CYP2C19 and CYP3A4

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70
Q

CYP3A4 converts ___-omeprazole to _________________

A

S

3-hydroxyomeprazole

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71
Q

__ isomer of omeprazole is the conversion to _________________ by CYP______

A

R

5-hydroxyomperazole

CYP2C19

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72
Q

metabolites of R-omeprazole

A

5-hydroxyomeprazole
omeprazole sulfone
5’-O-desmethylomeprazole
3-hydroxyomeprazole

73
Q

The S-isomer of omeprazole is converted primarily to

A

5’-O-desmethylomeprazole via CYP2C19

74
Q

proton pump encodes for which 2 genes?

A

ATP4A and ATP4B

75
Q

the binding of the PPI to the ATP4A/ATP4B complex prevents

A

acid secretion

76
Q

PPIs enter through

PPIs exit through

A

diffusion

ATP4A/B transporter

77
Q

omeprazole brand name and bioavailability

A

prilosec

40-65%

78
Q

esomeprazole brand name and bioavailability

A

Nexium

> 80%

79
Q

lansoprazole brand name and bioavailability

A

Prevacid

> 80%

80
Q

pantoprazole brand name and bioavailability

A

protonix

77%

81
Q

rabeprazole brand name and bioavailability

A

aciphex

52%

82
Q

dexlansoprazole brand name

A

dexilant

83
Q

what is the difference in effects of H2 receptor antagonists and PPIs?

A

H2 receptor antagonists have a marked effect on nocturnal acid but only a modest effect on meal stimulated acid
PPIs have a markedly suppress both

84
Q

Adverse effects of PPIs

A

diarrhea
headache
abdominal pain (1-5%)
increased gastric biota in chronic use

85
Q

Prostaglandin analogues

A

misoprostol

86
Q

misoprostol

A

PGE1 analogue
EP agonist

87
Q

Prostaglandin E2 is the most widely

A

produced prostanoid in the human body

88
Q

MOA of misoprostol

A

protects mucus lining in two ways

increases gastric pH and enhances the mucosal barrier that protects the stomach

89
Q

prostaglandin E receptors

A

found on parietal cells
when stimulated, have an inhibitory effect on the proton pump

90
Q

PGE2 acts as a __________ on _____ receptors on parietal cells and __________ activity of the proton pump

A

agonist
EP3
reduces

91
Q

PGE2 contributes to the maintenance of

A

the mucosal barrier, stimulating secretion of mucin and bicarbonate –> enhances mucosal blood flow

92
Q

PGE2 is synthesized in the

A

COX pathway

93
Q

NSAIDs effect on PGE2

A

NSAIDs inhibit COX enzymes –> reduce amount of PGE2
reduce the amount of protective mucus in the stomach

94
Q

Misoprostol is typically given as an

A

adjunct in patents undergoing NSAID therapy, substituting for PGE lost by NSAID use

95
Q

misoprostol enhances

A

epithelial mucus and bicarbonate secretion

96
Q

misoprostol inhibits

A

histamine induced H release
gastrin release

97
Q

adverse effects of misoprostol

A

diarrhea
abortive

98
Q

bismuth compounds

A

non rx: bismuth subsalicylate
rx: bismuth substrate potassium

99
Q

what is included in the formulation of bismuth substrate potassium?

A

metronidazole

tetracycline

100
Q

mechanism of bismuth compounds

A

not clear
coats and protects stomach
antibacterial effect

101
Q

adverse effects of bismuth compounds

A

blackening of the stool

102
Q

types of laxatives

A

bulk
osmotic
stimulants
stool softeners

103
Q

bulk laxatives

A

insoluble and non absorbable
not digestible

104
Q

examples of bulk laxatives

A

psyllium
bran
methylcellulose

105
Q

why do bulk laxatives need to be taken with lots of water?

A

if they don’t constipation will get worse

106
Q

bulk laxatives MOA

A

increase in bowel content volume triggers stretch receptors in intestinal wall
causes reflux contraction and propels contents forward

107
Q

types of saline and osmotic laxatives

A

non-digestible sugars and alcohols (lactulose)
salts (milk of magnesia, epsom salt, Glauber’s salt, sodium phosphates and citrate)
polyethylene glycol

108
Q

lactulose is broken down by

A

bacteria to acetic and lactic acid which causes the osmotic effect

109
Q

mechanism of polyethylene glycol

A

fluid is drawn into the bowel by osmotic force –> increased volume triggers peristalsis –> used to purge intestine

110
Q

stool softeners examples

A

docusate sodium
liquid paraffin
glycerin suppositories

111
Q

docusate MOA

A

decreases surface tension of fecal matter and allows for water to penetrate feces

112
Q

adverse effects of stool softeners

A

excessive use disrupts GI epithelial cells

113
Q

stimulants examples

A

Senna
bisacodyl
lubiprostone

114
Q

lubiprostone

A

prostanoic acid derivative
stimulates epithelial chloride channel
increases intestinal motility
irritates GI mucosa and pulls water into lumen

115
Q

lubiprostone is indicated for

A

severe constipation where rapid effect is required

116
Q

dopamine D2 receptor antagonists examples

A

metoclopramide
chlorpromazine
Prochlorperazine
promethazine
haloperidol
droperidol

117
Q

dopamine receptor antagonists MOA

A

block dopamine induced attenuation of pro kinetic effects of Ach
inhibition of D2-R in CTZ –> antiemetic effect

118
Q

dopamine decreases _____________

decreases _________ release from myenteric motor neurons

A

peristalsis

acetylcholine

119
Q

metoclopramide pharmacodynamics

A

primarily D2-R antagonist
5-HT4-R agonist
5-HT3-R antagonist

120
Q

metoclopramide pharmacokinetics

A

absorbed rapidly after oral ingestion
undergoes sulfaten and glucuronidation by the liver

121
Q

metoclopramide adverse effects

A

crosses BBB
extrapyramidal effects (movement disorders)
tardive dyskinesia (unusual movements of muscles of face)

122
Q

chemoreceptor trigger zone

A

induces emesis
sensitive to chemical stimuli

123
Q

emetics

A

agents to induce vomiting

124
Q

emetics examples

A

emetine
dehydroemetine
apomorphine

125
Q

emetine and dehydrometine are used as

A

second or third line of antiprotozoal therapy

126
Q

dehydroemetine

A

induces emesis
direct stimulation of CTZ

127
Q

side effects of dehydroemetine

A

drowsiness
diarrhea
stomach ache

128
Q

apomorphine

A

dopaminergic agonist
treats off episodes in Parkinson’s

129
Q

antihistamines and anticholinergics examples

A

dimenhydrinates
hydroxyzine
cyclizine
meclizine
scopolamine
trimethobenzamide

130
Q

5HT3 receptor antagonist examples

A

ondansetron
granisetron
dolasetron
ramosetron
tropisetron
alosetron

131
Q

neurokinin-1 receptor antagonists

A

aprepitant
fosaprepitant
rolapitant

132
Q

other anti emetic examples

A

cannabinoids
nabilone
dronabinol
nabiximol
dexamethasone
netupitant / palonosetron

133
Q

5HT3 antagonists MOA

A

5HT3-R antagonism in both peripheral and CNS

134
Q

ondansetron PK

A

metabolized in liver –> glucoronide/sulfate conjugation

135
Q

patents with hepatic dysfunction have reduced plasma clearance of

A

ondansetron

136
Q

granisetron PK

A

metabolized by CYP3A
inhibited by ketoconazole

137
Q

dolasetron PK

A

converted by plasma enzymes to active metabolite hydrodolasetron

138
Q

where is hydrodolasetron metabolized?

A

2/3 - liver
1/3 - excreted unchanged in urine

139
Q

palonosetron PK

A

metabolized 1/2 in liver and 1/2 excreted unchanged in urine

140
Q

adverse effects of 5HT3 antagonists

A

headache
dizziness
constipation

141
Q

Irritable bowel disease

A

bowel inflammation
no causative agent
systemic manifestations (axial arthritis, eye inflammation, skin lesions)

142
Q

Crohn disease

A

inflammation skips lesions
mostly in SI and colon
genetic susceptibility, distinct HLA associations

143
Q

ulcerative colitis

A

continuous involvement of colon and rectum
HLA associations likely

144
Q

what is a risk factor for IBD?

A

tobacco smoke

145
Q

IBD is an exaggerated

A

immune response against normal flora

146
Q

treatment for Crohn’s disease and ulcerative colitis

A

coticosteroids
immunomodulators
biologis: HUMIRA

147
Q

anti TNF antibodies used in IBD

A

infliximab
adlimumab
certolizumab
golimumab

148
Q

what do anti-TNF antibodies do?

A

neutralize soluble TNF (tumor necrosis factor)

149
Q

release of serotonin by enterochromaffin cells from _________________ stimulates ________________

A

gut distension

submucosal intrinsic primary afferent neurons

150
Q

submucosal IPANs activate

A

the enteric neurons responsible for peristaltic and secretory reflex activity

151
Q

stimulation of 5HT4 receptors of IPANs enhances

A

release of Ach and calcitonin gene related peptide, promoting reflex activity

152
Q

5HT4 partial agonist example

A

tegaserod

153
Q

azo compounds include

A

balsalazide
olsalazine
sulfsalazine

154
Q

azo compounds are converted by _________________ to ____________________ which is the active therapeutic moiety

A

bacterial azoreductase

5-aminosalicylic acid (mesalamine)

155
Q

sites of 5-ASA release from different formulations in the small and large intestine include the

A

jejunum (SI) - DR C
ileum (SI) - pH dependent release
proximal - sulfasalazine/balsalazide
colon distal - enema
rectum - suppository

156
Q

anti emetic examples

A

promethazine
prochlorperazine
chlorperazine

157
Q

anti emetics MOA

A

D2 receptor antagonism at the CTZ

158
Q

anti emetics are of value in

A

motion sickness

159
Q

anti emetics are weak ______________ without _______________ activity

A

DA antagonists

antiphsychotic activity

160
Q

adverse effects of anti emetics

A

extra-pyramidal symptoms or other movement disorders

161
Q

cannabinoids examples

A

cannabis sativa
cannabis indica
cannabis ruderalis

162
Q

endocannabinoids examples

A

anandamide
2-arachidonyl glycerol (2-AG)

163
Q

active compound that produces the most pharmacological effects of smoked marajuana

A

delta-9-tetrahydrocannabinol

164
Q

cannabinoid receptors that have been identified and cloned

A

CB1 and CB2

165
Q

the endocannabinoids for the cannabinoid receptors are

A

arachidonic acid derivatives

166
Q

cannabis has been used for its

A

physcotropic effects (sensory perception, elation, euphoria)

medicinal properties (pain relief, nausea and vomiting)

167
Q

the clinical potential of delta-9 THC against

A

chemotherapy induced nausea and vomiting (CINV)

168
Q

synthesis of anandamide

A

N-arachidonyl phosphotidylethenolamine –> (PLD2) –> Anandamide

169
Q

synthesis of 2-AG

A

membrane phospholipid –> PLC to Diacylglycerol (DAG) –> DAG lipase to 2-AG

170
Q

when anandamide acts on CB1 receptor it inhibits _______________ which acts on ________________

A

adenylate cyclase

CNS, leukocytes, and testis

171
Q

when anandamide acts of CB2 receptor it inhibits ________________ which acts on _______________

A

adenylate cyclase

spleen, tonsils, bone marrow, peripheral blood leukocytes

172
Q

delta-9-THC anti emetic examples

A

dronabinol
marinol

173
Q

pharmacodynamics of delta-9-THC

A

stimulation of CB1 receptors on neurons in and around the vomiting center in the brainstem

174
Q

pharmacokinetics of delta-9-THC

A

highly soluble lipid compound
absorbed readily after oral administration
onset = 1 hour

175
Q

delta-9-THC undergoes extensive _____________________ with limited ________________

A

first pass metabolism

systemic bioavailability

176
Q

principle active metabolite of delta-9-THC

A

11-OH-delta-9-tetrahydrocannabinol

177
Q

delta-9-THC is excreted via

A

biliary fecal route

178
Q

only ____________ delta-9-THC is excreted in the ____________ and it is highly bound to _____________

A

10-15%

urine

plasma proteins

179
Q

adverse effects of delta-9-THC

A

complex effects on the CNS
can displace other plasma protein bound drugs

Pharmacology (18 decks)

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