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Pharm 3 Module 2: GI > anti-emetics, laxatives > Flashcards

anti-emetics, laxatives Flashcards

1
Q

Where is the vomiting/emesis center

A

group of cells in the medulla oblongata

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2
Q

How is the vomiting/emesis centers activated

A

several mechanisms:
-afferent fibers in the gut
-chemoreceptor trigger zone
-cerebral cortex
vestibular aparatus

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3
Q

What is the CTZ

A

area postrema response to blood-born substances
serotonin 5-HT3
dopamine D2
Muscarinic M1 receptors

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4
Q

what is vestibular apparatus activation

A

fibers into cerebellum
triggers release of Ach/histamine

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5
Q

what is gut activation of vomiting center

A

vagal afferent pathways to solitary tract nucleus to vomiting center
nerve stimulation of CTZ
D2, 5-HT3, and neurokinin 1 (NK1) receptors

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6
Q

what are the drug categories for nausea and vomiting

A

cholinergic/muscarinic antagonists
dopamine receptor antagonists
serotonin receptor antagonists
cannabinoids
histamine antagonists

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7
Q

what is the cholinergic antagonists for N/v

A

scopolamine (hyoscine)
patch/injectables

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8
Q

what is the MOA for scopolamine

A

blocks ach at parasympathetic sites (smooth muscle, secretory glands, CNS)
reduces histamine and serotonin activity

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9
Q

what is the PK for scopolamine

A

Onset: 6-8hours
Duration: 72 hours
Metabolism: hepatic
T1/2: 9.5 hours
peak: 24 hours
Excretion: less than 10% in urine

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10
Q

what are the SE of scopolamine

A

similar to atropine (Bradycardia (initially) - tachy, flushing, orthostatic hypotension)
cognitive impairement (drowiness/blurred vision)
psychosis and hallucinations

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11
Q

what are contraindications with scopolamine

A

contraindicated in narrow-angle glaucoma or with other agents containing belladonna
anticholinergic agents, other CNS depressants (hydrocodone), magnesium sulfate, nitroglycerin, potassium citrate, SSRIs, thiazide

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12
Q

What are the dopamine receptor antagonists medications for N/V

A

phenothiazines - prochlorperazine
Butyrophenones - haloperidol, droperidol
Benzamides - metoclopramide, trimethobenzamide

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13
Q

What is the MOA of dopamine receptor antagonist medications

A

acts primarily on CTZ and afferent pathway in the gut
antagonize D2 dopamine receptors in area postrema (midbrain) and peripheral sites
M1-muscarinic and H1-histamine blocking effects
metocloperamide has weake 5-HT3 blockage at higher doses

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14
Q

what are the SE of dopamine receptor antagonists medications

A

extrapyramidal reactions (dystonia), tardive dyskinesia, hypotension, EKG abnormaliteis, CNS effects, psychological effects, hyperprolactinemia

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15
Q

what are the major interactions with Dopamine receptor antagonists

A

TCAs, SSRIs, Antipsychotics, opioids, anticholinergics, anti-parkinson drugs, alcohol, potassium

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16
Q

what are the PK of Dopamine receptor antagonists

A

onset:
PO: 30-40 min
rectal: approx 60 minutes
duration: 3-4 hours for oral, 3-12 hours for rectal

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17
Q

what is the PK for metoclopramide

A

duration: 1-2 hours
T1/2: 5-6 hours in adults
excretion in urine
CYP2D6

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18
Q

what are the serotonin receptor antagonists

A

ondansetron (zofran)
granisetron

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19
Q

what is the MOA for ondansetron

A

blocks serotonin centrally (chemoreceptor trigger zone) and peripherally (vagal nerve terminals0

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20
Q

what is the PK for ondansetron

A

onset: aprox 30 min
metabolism: CYP pathways
T1/2: aprox 3-6 hours in adults
peaks: 1-2 hours
excretion in urine and feces

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21
Q

what are the SE of ondansetron

A

QT prolongation, dizzinness, confusion, SOB, constipation

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22
Q

what are the considerations for ondansetron

A

EKG monitoring, potassium and magensium elvels
watch for serotinin syndrome with serotoninergic drugs

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23
Q

what are the contraindications with ondansetron

A

amiodarone
cyp3a4 inducers
QT prolonging agents

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24
Q

what is the Canabinoid

A

Dronabinol

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25
Q

what is the MOA of Dronabinol

A

activates cannabinoid receptors

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26
Q

what is the PK of Dronabinol

A

Onset: 30-60 min
Peak 2-4 hours
duration: 4-6 hours
metabolism: hepatic
T1/2: 4-5/25-36 hours

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27
Q

what are the SE of Cannabinoids

A

euphoria, CNS changes, abdominal pain, vomiting, flushing, palpitations, hypotension, xerostonia, vertgo

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28
Q

what are the special considerations of cannabinoids

A

monitor HR and BP
psychiatric changes/CNS effects
worsening N/V/abd pain
may contain propylene glycol
subastance use hx

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29
Q

what are contraindicatiosn of cannabinoids

A

alcohol
anticholinergics
CNS depresssants
CYP3A4 inhibitors/inducers
metronidazole
disulfiram
warfarin

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30
Q

what are the histmaine antagonist meds for N/v

A

promethazine
mecizine
dimenhydrinate

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31
Q

what is the MOA for promethazine

A

blocks mesolimbic dopaminergic receptors in postsynaptic sites. blocks release of hromones from the hypothalamus. blocks histmaine 1 receptors in brainstem

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32
Q

what are the PK of promethazine

A

ONset: IV: 5 min,PO/IM: 20 min
duration: 4-6 hours
metabolism: CYP
T1/2: IM approx 10 hours, IV 9-15, supp 16-19 hours

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33
Q

what are the SE of promethazine

A

EKG changes
anticholinergic effets
CNS depressionm extrapyramidal efffects orthostatic hypotension photosensitivity

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34
Q

what is the MOA of meclizine

A

blocks H1 histamine receptor and prevents vasodilation, increased capillary permeability, bronchoconstriction, and spasmodic contraction of gastriintestinal smooth muscle.
also depress labyrinth excitability and vesticular stimulation, and may affect the medullary chemoreceptors trigger zone

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35
Q

what is the PK of meclizine

A

onset; aprox 1 hour
duration: approx 24 hours
metabolism: hepatic
T1.2”: aprox 5-6 hours
excretion: urine and feces

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36
Q

what are the SE of meclizine

A

sedation, headaches, vommiting, blurred vision

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37
Q

what is the MOA of dimenhydrinate

A

binds to H1 receptor sites in peripheral sites including GI tract, respiratory tracts and blood vessels. blocks chemoreceptor trigger zones
dpresses layrthinine function and vestibular stimulation.
central anticholinergic activity

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38
Q

what are the PK of dimnhydrinate

A

onset: up to 30 min for IM and oral
duration: 4-6 hours
metabolism: hepatic
T1/2: 5-8 hours
excretion: renal

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39
Q

what are the SE of dimenhydrinate

A

tachy, sedation, dizziness, xerostimia, anorexia, epigastric distress, blurred vision, thickened brochial secretion

40
Q

what are the types of drugs for diarrhea and IBS-D

A

opioid agonists
serotinin receptor modulators
bile acid sequestriants
anti-spasmodics
antimicrobial agents

41
Q

what is the MOA of opioid agnoists

A

activation of opioid receptors in the smooth msucle of the GI tract, alters periostalis by preventing smooth msucle contraciton and relaxation.
reduced stool volume and can prevent electroylte depletion.

42
Q

what are the opioid agonist medicatiosn

A

loperamide (imodium)
diphenoxylate/atropine
octreotide
eluxadoline

43
Q

what is the MOA of loperamide

A

also incresase IAS and EAS tone

44
Q

what is the PK of loperamide

A

metabolism: hepatic
t1/2: 9-14 hours
excretion feces

45
Q

what are the SE of loperamide

A

CONSTIPATION, dizziness, abdominal pain and cramping

46
Q

what is the MOA of diphenoxylate/atropine

A

contains small amount of atropine to prevent abuse

47
Q

what ist eh PK of diphenoxylate/atropine

A

onset: aprox 45 min
metab: hepatic
T1/2: 2.5 hours
Excretion: feces and urine

48
Q

what are the SE of diphenoxylate/atropine

A

flushing, tachy, CNS effects, xeroderma, vomiting, toxic megacolon, urinary retetnion

49
Q

what is the MOA of Octreotide

A

inhibits serotonin release. inhibits secretion of gastrin, VIP, insulin, glucagon, secretin, motilin, and pancreatic polypeptide

50
Q

what is the PK of octreotide

A

duration: 6-12 hours
metab: hepatic
t1/2: aprox 2 hours
excretion: urine

51
Q

what are the SE of octreotide

A

bradycardia, fatigue, HA, dizziness, pruruits, hyperglycemia, hypothyroidism, cholelithiasis, abdominal pain, diarrhea, constipation, biliary obstruction, URI, cardiac arrhythmias, depression

52
Q

what is the MOA of eluxadoline

A

binds to mu, kappa, and delta opioid receptors in the intestinal lumen. decreases intestinal motility without causing constipation

53
Q

what is the PK of eluxadoline

A

metab?
t1/2: 4-6 hours
peak 1.5 hours
excretion: feces and urine

54
Q

what are the SE of eluxadoline

A

dizziness, drowsiness, constipation, nausea, abodminal pian, vomiting, elevated LFTs, URI

55
Q

what are the serotonin receptor modulators

A

alosetron and tegaserod

56
Q

what is the MOA of alosetron

A

selective 5-HT3 agonist. acts on receptors in the enteric neurons in addition to receptors in other location centrally and peripherally. affects visceral pain, colonic transit and alters secretions in the GI tract

57
Q

what is the PK of alosetron

A

metab: CYP
t1/2: 1.5 hours
peak 1 hour
excretion: urine and feces

58
Q

what are the SE of alosetron

A

constipation, fatigue, HA, abodminal pain, nausea

59
Q

what is the MOA for bile acid sequestrants

A

bind to bile salts in the intestine. inhbiits reuptake of bile salts, increases fecal loss of bile salt bound on LDL cholesterol as well

60
Q

what is the PK of bile acid sequestrants

A

onset: peak effect 21 days
no absorption
excreted in feces

61
Q

what are the SE of bile acid sequestrants

A

abodminal pain, bloaitng, biliary colic, gallbladder calcifcation, melena, vomiting, dental erosion/discoloration, abnromal LFTs, tinnitus, bleeding issues

62
Q

what are the antimicrobials

A

rifaximin
metronidazole
ciprofloxacin
amoxicillin
neomycin

63
Q

what is the MOA of Rifaximin

A

binds to bacterial DNA dependent RNA polymerase, thus inhbiting RNA synthesis

64
Q

what are the PK of Rifaximin

A

metabolism: CYP
T1/2: 5-6 hours
excretion in feces

65
Q

what are the SE of rifaximin

A

peripheral edema, dizziness, fatigue, ascites, nausea, HA prurutis

66
Q

what are the anti-spasmodics

A

hyoscyamine
dicyclomine

67
Q

what is the MOA of anti-spasmodics

A

blocks ach at parasympathetic receptors. antagonist of histamine and serotonin

68
Q

what is the PK of anti-spasmodics

A

onset: 2-3 minutes
duration: 4-6 hours
metab: hepatic
T1/2: 3.5 hours or 7 hours for longer acting
excretion in urine

69
Q

what are the SE of anti-spasmodics

A

tachy, mental status changes, abdominal pain, impotence, blurred vision, urinary retnetion, increased IOP

70
Q

what are different medication types of constipation

A

stool softeners
bulking laxative
osmotic laxatives
stimulant laxatives
selective opioid antagoonists
guanylate cyclase-c agonists

71
Q

what is docusate sodium

A

stool softener

72
Q

what is the MOA of docusate sodium

A

lowers the surface tension at the oil-water interface of the aeces, allowing water and lipids to penetrate the stool
this helsp to hydrate and soften the fecal materaial, facilitating natural defecation

73
Q

what is the PK of docusate sodium

A

onset: 12-72 hours
excretion in feces

74
Q

what are the SE of docustate sodium

A

throat irritation

75
Q

what are bulking laxatives

A

methycellulose
psyllium husk powder
wheat dextrin
calcium polycarbophil

76
Q

what is the MOA of bulking laxatives

A

absorb and retain water in the intestine, thus increasing the mass of stool. this promotes peristaliss through distension of intestinal lumen

77
Q

what are the SE of bulking laxatives

A

bloating, flatulence, GI distress

78
Q

what are the osmotic laxatimes

A

saline laxatives - magnesium oxide, sodium phosphate
lactulose
polyethylene glycol
glycerin

79
Q

what is the MOA of saline laxatives

A

retain water in intestine, thus increaseing intraluminal pressure and promotion of peristalsis

80
Q

what are the SE of saline laxatives

A

blaoting
abdominal pain
apthous stomatitis
hypokalemia and hypophosphatemia

81
Q

what is the MOA of lactulose

A

disaccharide that promotes fluid retention in intestine, thus increaseing intraluminal pressure and promoting peristalsis

82
Q

what is the PK of lactulose

A

colonic microbiota convert the sugars into lactic and aecitic acid. excreted in feces

83
Q

what are the SE of lactulose

A

dehydration, hypernatremia, hypokalemia, bloaitng, nausea, abdominal cramping, diarrhea

84
Q

what is the SE of polyethrylene glycol

A

diarrhea, faltulene, abdominal pain, nausea

85
Q

what is the PK of glycerin suppository

A

onset 15-30 min. poorly absorbed

86
Q

what are the SE of glycerin suppository

A

abodminal cramping, bloating, diarrhea, irritation, tenesmus

87
Q

what are the stimulant laxatives

A

bisacodyl and sennosides

88
Q

what is the MOA of stimulant laxatives

A

alter fluid excretion by acting directly on the cells of the intestinal mucosa. increase motility by acting on cells

89
Q

what are the opiod antagonists

A

naloxegol
methylnaltrexone

90
Q

what is the MOA of naloxegol

A

Mu opioid receptor antagonists. bound to polyethylene glycol to prevent crossing BBB. blocks the effects of opioids on GI tract, thus decreaseing constipation

91
Q

what is the PK of naloxegol

A

absorbed reapidly
metabolized via YCP
t1/2: 6-11 hours
peaks less than 2 hours
excreted in feces and urine

92
Q

what is the MOA of methylnaloxegol

A

same as naloxegol. derivative of naltrexone

93
Q

what is the pK of methylnaloxegol

A

T1/2: 15 hours
peaks 30 min to 1.5 hours
excreted in urine andfeces

94
Q

what are the IBS-C medications

A

Lubiprostone
Linaclotide

95
Q

what is the MOA of Lubiprostone

A

activates chloride channels and increases fluid secretion by the cells int he intestinal membrane. also counteracts the antisecretory effect of opioids

96
Q

what is the MOA of Linaclotide

A

acts on guanylate cyclase on the epithelium of the intestine, icnreasing cyclinc guanosine monophosphate. the stimuates the chloride and bicarbonate secretion and intraluminal pressure, promoting peristalsis. cGMP is thought to decrease visceral pain

Pharm 3 Module 2: GI (4 decks)

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