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Pharmacology Exam 2 > GI medications > Flashcards

GI medications Flashcards

1
Q

When is early PONV?

A

within 6 hours

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2
Q

When is late PONV?

A

6-24 hours

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3
Q

What is the ASA’s recommendation for PONV?

A

treat only high risk groups but not routine use; use patient’s risk to guide prophylactic therapy

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4
Q

What are some patient factors that increase risk for PONV?

A

women, non-smokers, hx motion sickness, previous incidence of PONV

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5
Q

What are some surgical factors that increase risk for PONV?

A

length of procedure, laparotomies, gyn surgery, lap surgery, ENT, breast, ortho

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6
Q

What are some anesthesia factors that increase risk for PONV?

A

inhalation agents, N20, Neo, narcs, etomidate

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7
Q

Where is the vomiting center located?

A

medulla oblongata

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8
Q

What are the 4 areas that trigger the vomiting zone?

A

CTZ, vestibular apparatus (muscarinic 1 receptor), thalamus/cerebral cortex (CNS), and neurons in GI tract

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9
Q

Describe how the vomiting center is triggered.

A

NT regulate activity in vomiting center. Once activated, efferent signal sent via cranial nerves to vagal parasympathetic fibers and sympathetic chain

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10
Q

What NTs are associated with PONV?

A

dopamine, serotonin, acetylcholine, histamine, substance P

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11
Q

What NTs act at CTZ?

A

dopamine, serotonin

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12
Q

What NTs are intrinsic within vomiting center?

A

substance P, acetylcholine, and histamine

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13
Q

What NTs are in CNS within vomiting center?

A

???

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14
Q

What NTs are at the vestibular apparatus within the vomiting center?

A

acetylcholine, histamine (H1 and M1 receptors)

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15
Q

What NTs act on GI tract within vomiting center?

A

acetylcholine, histamine, serotonin, substance P, and mechanoreceptors.

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16
Q

What are the drug classes used to treat PONV?

A

anticholinergics, benzamines, benzodiazepines, butrophenones, cannabinoids, glucocorticoids, 5-HT3 antagonists, NK1 antagonists, phenothiazines

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17
Q

What anti-emetics are anticholinergics?

A

atropine, hyoscine, scopolamine

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18
Q

What antiemetics are benzamines?

A

metoclopramide

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19
Q

What antiemetics are benzodiapezines?

A

midazolam

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20
Q

What antiemetics are butrophenones?

A

droperidol, haloperidol

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21
Q

What antiemetics are cannabinoids?

A

dronabinol, nabilone

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22
Q

What antiemetics are glucocorticoids?

A

dexamethasone

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23
Q

What antiemetics are 5-HT3 antagonists?

A

dolasetron, granisetron, ondansetron, palonosetron, ramosetron, tropisetron

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24
Q

What antiemetics are NK-1 antagonists?

A

Aprepitant, Fosprepitant

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25
Q

What antiemetics are phenothiazines?

A

prochlorperazine, promethazine, chlorpromazine

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26
Q

What is the MOA of Scopolamine?

A

block transmission of impulses from vestibular apparatus to the medulla. can cross BBB.

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27
Q

What is the dose of scopolamine?

A

5mcg/hr for 72 hours (best 4 hours before stimulus) transdermal provides sustained effect and avoids anticholinergic side effects. If given IV can cause anticholinergic syndrome

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28
Q

What are the uses for scopolamine?

A

motion sickness, middle ear surgery, N/V with PCA or epidural morphine

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29
Q

True/False: Narcotics increase the sensitivity of vestibular apparatus to motion.

A

True

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30
Q

What are the side effects of scopolamine?

A

possible visual disturbances.

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31
Q

What is the MOA of metoclopramide?

A

stimulate GI tract via cholinergic mechanism and an anti-dopaminergic effect: contraction of lower esoph sphincter and gastric fundus, increased gastric and SI motility, decreased muscle activity in pylorus and duodenum with stomach contraction

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32
Q

Who should you use caution in with metoclopramide?

A

parkinsons and RLS in high doses due to antidopamine effects

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33
Q

What is the MOA of midazolam?

A

thought to decrease the synthesis and release of dopamine within the CTZ. give at END OF CASE

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34
Q

What is the MOA of droperidol?

A

competitive dopamine antagonist, receptor is D2 and ligands are dopamine and GABA

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35
Q

What is the dose of prophylactic droperidol?

A

(prophylactic)0.625-1.25mg(rescue)

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36
Q

When should you use caution with droperidol?

A

parkinsons, RLS, high doses black box warning for prolonged QTc

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37
Q

What is the MOA of dexamethasone?

A

centrally inhibits prostaglandin synthesis and controls endorphin release

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38
Q

What is the dose of dexamethasone?

A

4mg

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39
Q

When should you use caution with dexamethasone?

A

obese patients, patients with DM

40
Q

Describe 5-HT3 serotonin receptor.

A

ligand-gated Na and K cation channel. depolarizes plasma membrane, excitatory. stimulated by serotonin..

41
Q

Where is serotonin found?

A

intestines: regulates intestinal movement, raphe nucleus in the brainstem projecting to other regions of brain to affect mood, cognition, and sleep.

42
Q

What does stimulation of the 5-HT3 serotonin receptor cause?

A

nausea

43
Q

What are other effects of serotonin?

A

addiction, aggression, vasoconstriction, increased intestinal motility, learning and memory consolidation

44
Q

When are 5-HT3 antagonists used?

A

N/V related to chemo/PONV. NOT useful for motion sickness and vestibular stimulation related nausea–there’s no 5-HT3 receptors in the vestibular apparatus.

45
Q

Does ondansetron cross the BBB?

A

No, little CNS side effects

46
Q

What is the dose and onset of ondansetron?

A

4mg, 30-60 min

47
Q

What are the side effects of ondansetron?

A

headache, diarrhea, QTc prolongation

48
Q

What is tropisetron used for?

A

treat symptoms with carcinoid syndrome

49
Q

What is the dose and DOA of granisetron?

A

dose 0.1mg, lasts 24h

50
Q

What is the only 5-HT3 antagonist that has an active metabolite?

A

dolasetron

51
Q

What is substance P’s claim to fame?

A

primary NT produced by pain/temperature afferent peripheral neurons

52
Q

What are the receptors for substance p?

A

neurokinin receptors (NK1, NK2, NK3)

53
Q

Where are substance P and its receptors located?

A

gut and N/V pathways

54
Q

What is the MOA of Aprepitant/Fosaprepitant?

A

competitive antagonist at the NK1 receptors, inhibiting substance P from binding to this protein coupled receptor.

55
Q

What is Aprepitant/fosaprepitant used for?

A

chemo induced N/V.

56
Q

What is an important side effect of aprepitant/fosaprepitant?

A

can inhibit steroidal contraceptives for 7-10 days.

57
Q

What is the MOA of phenothiazines?

A

antagonizes H1 (stimulated by histamine) and M1 (stimulated by ACh) receptors

58
Q

What is histamine synthesized from?

A

histadine

59
Q

Where is histamine?

A

CNS (wakefulness), immune cells (basophils/mast cells), GI tract (mast cells in stomach wall)

60
Q

Where are H1 receptors and what do they do?

A

vascular smooth muscle (dilation), bronchial smooth muscle (contraction), and in CNS

61
Q

What are the H1 receptor antagonists?

A

diphenhydramine, loratadine (treat allergic reactions); hydroxyzine, phenergan, meclizine, dimenhydrinate

62
Q

Where are H2 receptors and what do they do?

A

stomach, increase acid secretion

63
Q

What is an H2 antagonists?

A

famotidine

64
Q

What do H3 receptors do?

A

presynaptic reduction in further histamine release

65
Q

What is the dose, onset, duration of benadryl?

A

25-50mg IV, onset 3 min, DOA 1-7h

66
Q

What does dimenhydrinate do?

A

antagonizes H1 and M1 receptors, used for motion sickness and sleep aid (crosses BBB)

67
Q

What are the clinical uses for H1 receptor antagonists?

A

allergic reactions, motion sickness and vestibular disturbances, N/V of pregnancy.

68
Q

What effects of H1 antagonists are NOT due to H1 blockade?

A

sedation, anti-nausea/anti-emetic actions (especially motion sickness), adrenoreceptor blocking actions (especially in phenothiazine group (phenergan) may cause orthostatic hypotension.

69
Q

What is the incidence of aspiration in adults? kids?

A

1:8500 adults; 1:4400 in kids <16yo

70
Q

How do you prevent aspiration?

A

antacids (increase pH of gastric contents); prokinetic drugs (decrease gastric fluid volume)

71
Q

Who is at increased risk for aspiration?

A

pregnancy, DM (delayed gastric emptying), mask induction, emergency cases

72
Q

What salts are oral antacids usually?

A

aluminum, magnesium, calcium

73
Q

True/False: Oral antacids increase gastric volume.

A

True

74
Q

True/False: Oral antacids do not change the metabolism of other drugs.

A

False, they can.

75
Q

What is the main oral antacid used before surgery?

A

Bicitra, liquid, 15-30mL given right before induction, used in c-sections

76
Q

What is the most frequently prescribed type of drug in USA?

A

H2 antagonists: Tagamet (cimetidine), zantac, pepcid, axid (nizatidine)

77
Q

How do H2 antagonists work?

A

Selectively and reversibly compete with histamine at H2 sites.

78
Q

What are the clinical uses of H2 receptor antagonists?

A

treatment/prevention of peptic duodenal ulcers, gastric ulcers, erosive esophagitis, hypersecretory conditions.

79
Q

What are the toxicity effects of H2 antagonists?

A

CNS dysfunction–slurred speech, delirium, confused states in elderly (most often with tagamet); liver toxicity; pregnancy (DO cross placenta and into breastmilk

80
Q

What are some common drug interactions with H2 antagonists–specifically Tagamet?

A

Dilantin, Propranolol, metoprolol, labetalol, diazepam, calcium channel blockers, also warfarin, quinidine, caffeine, lidocaine, theophylline, aprazolam, flurazepam, triazolam, carbamazepine, ethanol, TCAs

81
Q

Why does Tagamet interact with many drugs?

A

reduces hepatic blood flow and inhibits P450 system so can have increased risk of toxicity if given with several drugs.

82
Q

What are some proton pump inhibitors?

A

omeprazole, pantoprazole, esomerprazole, lansoprazole

83
Q

What are gastrointestinal prokinetics?

A

dopamine blockers–metoclopramide, domperidone

84
Q

What are prokinetic drugs used for?

A

treating esophagitis, treating GERD, prescribed less due to increased expense.

85
Q

How do PPI’s work?

A

increase gastric pH, decrease gastric volume

86
Q

Does omeprazole cross the BBB?

A

yes

87
Q

What are side effects of omeprazole?

A

headache, agitation, confusion

88
Q

What ailment is omeprazole used for?

A

zollinger-ellison syndrome

89
Q

How do gastrointestinal prokinetic drugs work?

A

modulate motility by increasing lower esophageal sphincter tone, enhancing peristaltic contractions, and accelerating rate of gastric emptying.

90
Q

What is the MOA of metoclopramide?

A

competitive dopamine antagonist, stimulates GI tract via cholinergic mechanisms; contraction of LES and gastric fundus; increase gastric and SI motility, decrease muscle activity in pylorus and duodenum

91
Q

Does metoclopramide cross the BBB?

A

yes and affect CTZ

92
Q

What is the dose of metoclopramide?

A

10-30mg IV over 3-5 min

93
Q

What are some cautions with metoclopramide?

A

parkinsons, RLS, patients on MAOI, tricyclic antidepressants, GI surgery, patients taking phenothiazines or butrophenones

94
Q

Does metoclopramide change gastric pH?

A

NO

95
Q

What is metoclopramide used for?

A

diabetic gastroparesis, preop to decrease gastric fluid volume, antiemetic, GERD, assist with enteral feeding in chronically ill

96
Q

What are some side effects of metoclopramide?

A

placental transfer, abdominal cramping if given fast, extrapyramidal reactions–related to antidopamine effects, prolonged Succs–inhibits plasma cholinesterase activity, c

Pharmacology Exam 2 (5 decks)

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