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Pharmacology > Nausea and vomiting > Flashcards

Nausea and vomiting Flashcards

1
Q

Chemical transmitters involved in vomiting

A

Dopamine: D2 receptors
ACh: MR in vomiting center
Histamine: H1 receptors
Serotonin: 5HT3 receptors

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2
Q

Indications of H1 R antagonists

A

N&V induced by any stimuli.
Vomiting produced by substance acting directly on CTZ
Motion sickness, substances acting on stomach

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3
Q

H1 R antagonist drugs are

A

Cyclizine
Cinnarizine
Buclizine
Doxylamine
Promethazine

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4
Q

Sedation in H1 R antagonist

A

Promethazine and Doxylamine
Cyclizine
Cinnarizine

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5
Q

MOA of Cyclizine

A

inhibits H1 R in VC
also has antimuscarinic activity

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6
Q

I of Cyclizine

A

for all types of vomiting including motion sickness

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7
Q

DOA of cyclizine

A

4-6 hrs

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8
Q

AE of Cyclizine

A

Drowsiness
Xerostomia

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9
Q

CI of Cyclizine

A

Closed angle Glaucoma
Urinary retention
Prostatic hypertrophy
Chronic pulmonary disease
acute asthma

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10
Q

DI of Cyclizine

A

CNS depressants
Anti-cholinergics: incr. their effects

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11
Q

MOA of Cinnarizine

A

inhibits H1 R in VC and vestibular system
also has antimuscarinic activity

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12
Q

I of Cinnarizine

A

motion sickness
Vestibular disorders (meniere’s)

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13
Q

Half-life of Cinnarizine

A

3-6 hrs

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14
Q

AE of Cinnarizine

A

Extrapyramidal symptoms
Depressive feeling (with prolonged therapy)
Hypotension (high doses)

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15
Q

CI of Cinnarizine

A

Hypersenstivity to drug

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16
Q

DI of Cinnarizine

A

CNS depressants
Anti cholinergics
Anti histamines
MAOi
TC antidepressants

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17
Q

MOA of Doxylamine

A

competes for H1 R sites on target cells
has anti-cholinergic effects= depresses labyrinthine function, blocks CTZ, diminishes vestibular stimulation

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18
Q

Doxyalmine can be used

A

alone or with Pyridoxine and dicyclomine

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19
Q

Half-life of doxylamine

A

10-12 hrs

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20
Q

AE of Doxylamine

A

Tachycardia
urinary retention
constipation
drowsiness
blurred vision

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21
Q

CI of doxylamine

A

children <12 years

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22
Q

DI of doxylamine

A

CNS depressants
Anti-cholinergics= incr. their effects

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23
Q

MOA of Buclizine

A

inhibits H1 R in VC and vestibular system
also has anti-cholinergic properties

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24
Q

I of Buclizine

A

Motion sicness
radio/chemo induced NV

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25
Q

AE of Buclizine

A

sedation
dizziness
headache
anxiety
hypotension
dry mouth-xerostomia
tight chest
urinary retention

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26
Q

CI of Buclizine

A

Asthma
Pulmonary disease
bladder neck obstruction
Closed angle Glaucoma

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27
Q

DI of Buclizine

A

CNS depressants

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28
Q

MOA of Promethazine HCL

A

inhibits D2 R, MR and H1 R
crosses BBB

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29
Q

I of Promethazine HCL

A

all types of vomiting including:
severe morning sickness (only if essential)
Prevention of motion sickness

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30
Q

HAlf-life of Promethazine HCL

A

10-14hrs

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31
Q

AE of Promethazine HCL

A

strong sedative effect
dizziness
fatigue
incoordination
Extrapyramidal symptoms

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32
Q

CI of Promethazine HCL

A

children <2years

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33
Q

DI of Promethzine HCL

A

CNS depressants
ANti-cholinergic agents

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34
Q

MR antagonists are

A

Hyoscine

35
Q

MOA of hyoscine

A

inhibits MR
blocks impulses from CTZ to vomiting center (acts direct in VC)

36
Q

I of Hyoscine

A

motion sickness
nausea as a result of labyrinthine disturbances

37
Q

AE of Hyoscine

A

Drowsiness
Xerostomia
Dry skin
blurred vision
Urinary retention (high doses)
Constipation
dementia

38
Q

CI of Hyoscine

A

Glaucome
GI obstruction
Prophyra

39
Q

DI of Hyoscine

A

TCA
Antihistamines
Antipsychotics

40
Q

Indictations of D2 R antagonists

A

NV caused by nausea/labyrinthine disturbances
Chemo-induced NV
Post-op NV
Radiation-induced NV

41
Q

D2 R antagonist drugs are

A

Domperidone (CTZ: peripheral actions)
Droperidol (butyrophenone, inhibits GIT)
Metocloopramide (inhibits CTZ and GIT)
Prochlorperazine (phenothiazine, inhibits CTZ

42
Q

MOA of Domperidone

A

Inhibits D2 R in CTZ, to prevent circulation action of emetic drugs

43
Q

I of Domperidone

A

Post-op NV
NV of central/peripheral origin

44
Q

Half-life of Domperidone

A

7-8hrs

45
Q

AE of Domperidone

A

Extrapyramidal symptoms (decr)
Drowsiness
Headache
Reversible Galactorrhoea

46
Q

CI of Domperidone

A

Hepatic impairment
GI obstruction/Perforation
CVS disease

47
Q

DI of Domperidone

A

CYP34A inhibitors
K-depleting agents
Macrolides
Antacids
Anticholinergics
Protease inhibitors

48
Q

MOA pf Droperidol

A

inhibits D2 R at CTZ

49
Q

I of Droperidol

A

Prevention of Post-op NV where other treatments are ineffective/inappropriate

50
Q

Half-life of Droperidol

A

2-3hrs

51
Q

AE of Droperidol

A

EXtrapyramidal symptoms
Drowsiness
Hypotension
Blurred vision
anxiety

52
Q

CI of Droperidol

A

Electrolyte imbalance
Parkinson’s
severe depression
pregnancy

53
Q

DI of Droperidol

A

alcohol
K-depleting diuretics
Glucocorticoids
CNS depressants
Opioids
Bromocriptine
Levodopa
CYP34A/1A2 inhibitors: incr. risk of QT prolongation

54
Q

MOA of Metoclopramide

A

Inhibtis D2 R in CTZ and VC
Has stimulant effect on GIT (facilitates emptying of stomach, relaxes pylorus and incr. GI motility)

55
Q

I of Metoclopramide

A

V caused by:
uraemia
radiation
GIT disorders
Drug-related NV(cytotoxic drugs)
Post-op NV

56
Q

CI of Metoclopramide

A

Epilepsy
Pheochromocytma
Mechanical bowel obstruction
Intestine perforation

57
Q

Half-life of Metoclopramide

A

4-6 hrs

58
Q

AE of Metoclopramide

A

Extrapyramidal symptoms
Light sedation
Constipaion
Incr. prolactin release=galactorrhoea

59
Q

DI of Metoclopramide

A

Antipsychotic agents
CNS depressants
Digoxin
Paracetamol
Ampicillin
Tetracyclines

60
Q

MOA of Prochlorperazine

A

inhibits D2 R in CTZ
inhibits Cholinergic and a adrenergic R
=sedation, muscle relaxation, hypotension

61
Q

I of Prochlorperazine

A

V due to:
uraemia
Radiation
Oncotherapy
Viral gastroenteritis
severe morning sickness(if essential only)

62
Q

DOA of Prochlorperazine

A

3-4hrs

63
Q

AE of Prochlorperazine

A

Extrapyramidal symptoms
Constipation
dry mouth
Hypotension
Reflex tachycardia
blurred vision
drowsiness

64
Q

DI of Prochlorperazine

A

CNS depressants
Anti-Parkinsons’s agents
Metoclopramide (Incr. extrapyramidal SEs)

65
Q

I of 5HT3 R anatgonists

A

V caused by:
Cytotoxic anti-cancer drugs
Post-op NV
Radiation-induced NV (oncotherapy)

66
Q

AE of 5HT3 R antagonists

A

Headache
dizziness
muscle pain
GIT upsets
Constipation

67
Q

Which are the 5HT3 R antagonists

A

Granisetron
Ondansetron
Palonosetron

68
Q

MOA of Granisetron

A

inhibits 5HT3 in vagal n. terminal and centrally in CTZ (selective)=antiemesis

69
Q

I of Granisetron

A

Post-cytotoxic chemo/radi NV
Post-op NV

70
Q

CI of Granisetron

A

Hypersenstivity to any of ingredients

71
Q

Half-life of Granisetron

A

9 hrs

72
Q

DI of Granisetron

A

QT prolonging agents
Serotonergic agents
Cardiotoxic drugs
Phenobarbital

73
Q

MOA of Ondansetron

A

inhibits 5HT3 in vagal n. terminal and centrally in CTZ (selective)=antiemesis

74
Q

I of Ondansetron

A

Post-cytotoxic chemo/radio NV
Post-op NV

75
Q

AE of Ondansetron

A

headache
flushing
constipation
dry mouth
sedation
Hypersensitivity rxns
Seizures
CVS effects: arrythmia, bradycardia, hypotension
Fatigue

76
Q

CI of Ondansetron

A

Congenital long QT syndrome
Concomitant use of Apomorphine

77
Q

DI of Ondansetron

A

Tramadol
Rifampicin
Carbamazepine
Phenytoin

78
Q

MOA of Palonosetron

A

selectively inhibits 5HT3 R both in peripheral and CNS with primary effects in GIT

79
Q

I of Palonosetron

A

Post-cytotoxic chemo/radio NV
Post-op NV

80
Q

Half-life of Palonosetron

A

40hrs

81
Q

AE of Palonosetron

A

Anxiety
dizziness
headache
weakness
constipation
pruritus
Hyperkalemia

82
Q

CI of Palonosetron

A

Hypersensitivity to drug
Coadministration with ampomorphine= prolonged hypotension and loss of consiousness

83
Q

DI of Palonosetron

A

Serotonergic agents
SSRIs
SSNRis
anti-arrythmic agents
QT-prolonging agents
agents resulting in electrolyte abnormalities

84
Q

Which are the Substance P (NK1) antagonists

A

Aprepitant/Fosaprepitant

Pharmacology (50 decks)

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