1
Q
pt experiences vomiting w/out nausea and shows sign of papilledema
A
tumor
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2
Q
drug used for testicular cancer w/ SE of N/V
A
Cisplatin
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3
Q
feeling of a need to vomit; involves cerebral cortex
A
nausea
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4
Q
emesis
A
vomiting
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5
Q
effortless passage of gastric contents into mouth
A
regurgitation
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6
Q
repeated regurgitation of food residue; may be rechewed and reswallowed
A
rumination
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7
Q
uses antiperstalsis
A
emesis
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8
Q
controller of all emesis info. in brainstem and sends for action
A
emesis center
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9
Q
area in brainstem that regulates both appetite and emesis
A
area postrema
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10
Q
CTZ (chemoreceptor trigger zone) located where
A
area postrema
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11
Q
area in brainstem that receives peripheral neural input
A
NTS
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12
Q
area in brainstem that receives input from sympathetic afferents and vagal afferents about N/V
A
NTS
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13
Q
area in brainstem that receives peripheral humoral input
A
area postrema
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14
Q
drugs in the blood reach emesis center through what
A
area postrema
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15
Q
areas in brainstem that receives central neural input
A
vestibular nuclei and emesis center
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16
Q
nausea develops as a result of activation of the ______ from emesis center info.
A
cerebral cortex
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17
Q
retroperistalsis
pyloric constriction
abd and thoracic wall contraction
A
effectors for emesis
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18
Q
2 routes to cause vomiting from emesis center
A
straight to effectors
to dorsal nucleus then vagus
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19
Q
A
vestibular nuclei
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20
Q
A
NTS
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21
Q
A
area postrema
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22
Q
A
emesis center
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23
Q
drugs that bind what 2 receptors are most effective (b/c the receptors are in the 3 main centers for N/V in brainstem)
A
5-HT3 and D2
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24
Q
_____ receptor found in vestibular nuclei, NTS, and emesis center
A
H1
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24
Q
Anti-5-HT3 drugs
A
-setrons
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24
Q
anti-H1 and anti-M drugs
A
Diphenhydramine
Dimenhydrinate
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25
Q
corticosteroid that binds GR in NTS
A
Dexamethasone
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26
Q
Anti-D2 drugs
A
Metoclopramide
Domperidone
27
Q
A
anti-psychotics that act as anti-D2 too
28
Q
Meclizine
Cyclizine
A
Anti-H1
29
Q
Anti-H1 drug that is used in pregnancy
A
Doxylamine
30
Q
emesis Gq receptors
A
H1
NK1
a1
M1
M3
31
Q
emesis Gi receptors
A
u, D2, CB1
32
Q
-setron used for IBS-D that is not antiemetic drug
A
Alosetron
33
Q
A
-setrons not including Alosetron
34
Q
anti-emetic effects______ long after 5-HT3 blockers disappear from circulation
A
persist
35
Q
use this type of drug w/ chemo, radiation and pre and post op; safe in pregnancy
A
-setrons
36
Q
SE of -setrons
A
constipation (blocks 5-HT3 effect on Ach (M3)
37
Q
A
Anti-D2 Metoclopramide
38
Q
use this Anti-D2 drug in N/V and gastroparesis
A
Anti-D2 Metoclopramide
38
Q
acute adverse effects of this drug include acute dystonia (muscle spasms) and akathisia (restlessness)
A
Anti-D2 metoclopramide
39
Q
____blocks prolactin
A
dopamine
40
Q
SE of this drug is hyperprolactinemia
A
anti-D2 metoclopramide
41
Q
CI in Achalasia
A
anti-D2 metoclopramide
42
Q
this anti-D2 drug does not cross BBB
A
Domperidone
43
Q
antiemetic D2 block in area postrema and D2 block in stomach
A
Anti-D2 domperidone
44
Q
this Anti-D2 drug is used in GERD and postsurgical gastroparesis and diabetic gastroparesis
A
Anti-D2 Domperidone
45
Q
1st generation cross BBB and also block M1
A
anti-H1 drugs
46
Q
M1 blocker (which would mainly target M1 in brain)
A
SCOPOLAMINE
47
Q
blocks NK1 (receptor for substance P) in CTZ
A
anti-NK1 APREPITANT
48
Q
what drug to use in Cisplatin-induced emesis in early phase
A
Ondansetron
49
Q
Anti-NK1 drugs to use in late phase Cisplatin induced emesis
A
APREPITANT and FOSAPREPITANT
50
Q
why is there morning sickness in the first 1/2 of pregnancy
A
elevated hCG
51
Q
an elevation in this causes stimulation of gastric CCK receptors
A
hCG
52
Q
A
to treat emesis in first 1/2 of pregnancy
53
Q
main drug that is now used in morning sickness during first 1/2 of pregnancy
A
Doxylamine
54
Q
when is hyperemesis most common in the 1st and 2nd trimesters
A
multiple gestation
55
Q
to Rx hyperemesis in pregnancy
A
hospitalize and antiemetics
56
Q
explain effect of protracted emesis (metabolic alkalosis)
A
lose HCl- when vomiting
HCO3-/Cl- exchanger activated
increase in serum HCO3-
57
Q
____required to breakdown food after a meal and leads to postprandial alkalosis
A
HCl (turns on exchanger and increase in HCO3- in blood)
58
Q
what maintains Cl- depleted alkalosis
A
pendrin in beta-intercalated cells of collecting duct
59
Q
decreased delivery of Cl- to beta-intercalated cells does what to Cl-/HCO3- exchanger (pendrin)
A
turns it off
60
Q
how to treat Cl- depletion alkalosis
A
NaCl (brings Cl- to beta-intercalated cells and brings it in and secretes HCO3-)
61
Q
Pendrin exchanger brings what into cell and secretes what into urine (lumen)
A
brings Cl- in and secretes HCO3-
62
Q
no nausea + VOMITING=
A
intestinal obstruction (peripheral neural input)
63
Q
morning vomiting + no nausea=
A
increased intracranial pressure (ICP) (central neural input)
64
Q
morning vomiting + nausea=
A
pregnancy (peripheral neuro-humoral input)
65
Q
nausea + vomiting=
A
metabolic toxins/drugs (peripheral humoral input)
66
Q
newborn + persistent, non-bilious projectile
A
hypertrophic pyloric stenosis (peripheral neural input)
