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SUM '20 - Pharm II > week 2 Antiemetics and GI motility 2 of 4 > Flashcards

week 2 Antiemetics and GI motility 2 of 4 Flashcards

1
Q

2 examples of Macrolides

A

Erythromycin, Azithromycin (macrolide antibiotics)

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2
Q

GI effects of Macrolide antibiotics

A

Increase lower esophageal sphincter tone, enhances intraduodenal coordination and promotes gastric emptying of liquids and solids

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3
Q

what types of patients are more susceptible to effects of Macrolide antibiotics

A

pts with diabetic gastroparesis; pts awaiting emergent surgery; normal pts; ICU pts with food intolerance

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4
Q

properties of macrolide antibiotics

A

prokinetic properties attributed to thier binding to motilin receptors in the stomach and duodenum

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5
Q

when are macrolides used

A

used only when other prokinetic agents have failed

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6
Q

name 2 5HT4 receptor agonist

A

Cisapride and Mosapride

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7
Q

5HT4 receptor agonist: use/effect

A

Decreases GERD; Increases lower esophageal sphincter tone; improves gastric motility and increases motility in small and large intestine

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8
Q

how do 5HT4 receptor angonist decrease GERD and improve gastric motility

A

by enhancing the release of acetylcholine from nerve endings in the myenteric plexus of the gastrointestinal mucosa.

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9
Q

what drug is used to reverse opioid induced gastric stasis

A

Cisapride (5HT4 agonist)

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10
Q

what is a negative side effect of 5HT4 receptor agonist cisapride and mosapride

A

prolongation of QT interval due to non selectivity

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11
Q

what are the 2 distinct entities of PONV (classifications)

A

Early & Late

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12
Q

what defines “early” PONV

A

within 6 hours of emergence from anesthesia

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13
Q

what defines “late” PONV

A

6-24 hours after the procedure

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14
Q

what are the most important complaints patients make

A

pain and PONV

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15
Q

what is the leading cause of unanticipated hospital admission following outpatient surgery

A

PONV

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16
Q

6 things that PONV cause that are associated with morbidity

A

Dehydration Electrolyte Abnormalities Wound Dehiscence Bleeding Esophageal rupture (Boerhaave’s Syndrome) Airway Compromise

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17
Q

pathophysiology of PONV: how the process begins

A

begins with antiperistalsis of muscular contractions within the ileum and jejunum, moving contents backwards toward the stomach

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18
Q

pathophysiology of PONV: the expelling contents phase (MOA of emesis)

A

closure of the glottis and contraction of the diaphragm, creating negative intrathoracic pressure at the same time that pharyngeal sphincters relax. Near simultaneously abdominal muscles contract creating increased intraabdominal pressure, the stomach contents follow the path of least resistance and emesis occurs

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19
Q

definition of regurgitation: how it differs form emesis

A

Regurgitation is acidic gastric material passively reflexes into the esophagus because of the incompetent esophageal sphincter and elevated abdominal pressure

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20
Q

Sequence of events causing emesis are controlled by the _______?

A

vomiting center in the brain

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21
Q

where is the vomiting center

A

lies in the medullas oblongata and consists of the nucleus of the tractus solitarius and parts of reticular formation

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22
Q

6 pharmacological systems that interact with the vomiting center figure 34-1 pg 693

A

dopamine serotonin substance P acetylcholine gamma-aminobutyric acid cannabinoids

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23
Q

Chemoreceptor Trigger Zone (CRTZ) location/function

A

Slightly cephalad to vomiting center. Detects noxious chemicals in the bloodstream. Ex: ethanol

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24
Q

MOA of (CRTZ) Chemoreceptor Trigger Zone

A

The detection of noxious chemicals sends signals via neural networks which activate vomiting center.

25
Q

anatomic sites that activate the vomiting center (other than CRTZ)

A

vestibular apparatus, thalamus, cerebral cortex, Neurons in the GIT

26
Q

MOA of Neurons in GIT activating the vomiting center

A

ex: if a SBO triggered antiperistalsis, and as small intestinal contents were forced backwards filling the stomach, afferent signals would be transmitted to the vomiting center

27
Q

once the vomiting center is activated what happens? MOA: what type of signal does it send

A

vomiting center sends efferent signals via the cranial nerves V, VII, IX, X, and XII through the vagal parasympathetic fibers and sympathetic chain and to skeletal muscle through alpha motor neurons.

Signals from the vomiting center trigger the complex motor process resulting in emesis

28
Q

vomiting center sends what type of signal?

A

efferent

29
Q

what cranial nerves does the vomiting center send signals through

A

CN V, VII, IX, X, and XII

30
Q

what pathway is used (MOA) to activate vomiting center:

smell, sight, taste, fear, emotions, memory

slide 28 image

A

cortical afferent pathway = nausea

31
Q

what pathway is used (MOA) to activate vomiting center:

pharynx (gag)

slide 28 image

A

midbrain afferent pathway: nuleus tractus solitarius (SHt3, D2, M1, H1): vomiting center

32
Q

what pathway is used (MOA) to activate vomiting center:

emetogenic drugs and toxins, catecholamines (nitrous oxide, opioids, cyclopropane, ether, ketamine)

slide 28 image

A

chemoreceptor trigger zone (5HT3,D2, M, H1): triggers nucleus tractus solitarius: triggers vomiting center

33
Q

what pathway is used (MOA) to activate vomiting center:

positional changes, ear surgery, motion sickness (Nitrous Oxide)

slide 28 image

A

vestibular Afferent pathway (H1, M): triggers cerebellum: triggers vomiting center

34
Q

what pathway is used (MOA) to activate vomiting center:

Local irritants, surgery, pain, toxins (nitrous oxide, cytotoxic drugs, levodopa, bromocriptine, ipecac)

slide 28 image

A

vagal mucosal afferent pathway (5HT3, M3, H3): triggers vomiting center

35
Q

slide 28 image:

vomiting center triggers what?

A

visceral, comatic and motor pathways: trigger the vomiting reflex: result in vomiting

36
Q

drug class of Odansetron & Dolasetron

A

Serotonin Receptor Blockers (5HT3): antiemetic drugs

37
Q

Dopamine receptor site blockers (D2)

name 3

A

droperidol, haloperidol, metoclopramide

38
Q

side effect of droperidol

A

(Q-T Prolongation): Sudden death can happen in doses > 25 mg in patients at risk for dysrhythmias. Historically doses for adult range 0.624 to 2.5 mg IV

39
Q

which dopamine receptor blocker has a long half life

A

haloperidol

40
Q

antiemetic: histamine blocker

list 2

A

promethazine (H1)

Diphenhydramine

41
Q

antiemetics: Muscarinic receptor blockers: name two

A

glycopyrrolate & scopolamine

42
Q

side effect of transdermal scopolamine

A

mydriasis

sedation, cycloplegia, drying of secretions

43
Q

what is commonly given in conjunction with a 5HT3 or with droperidol for antiemetic effect

A

dexamethasone

44
Q

substance P: what family of neurotransmitters does it belong to:

A

neurokinin family: affinity for neurokinin 1 (NK-1) receptors

45
Q

only neurokinin antagonist in use

A

“aprepitant” or Emend: PO used prophylactically

46
Q

how is Ephedrine used for PONV

A

Ephedrine used to maintain BP minimizing cerebral ischemia thereby preventing PONV

47
Q

Patient risk factors for PONV

A

Women

nonsmokers

hx of motion sickness

previous PONV

48
Q

Surgical risk factors for PONV

A

´Length of Surgery

´Laparotomies

´Gynecologic surgeries

´Laparoscopic procedures

´ENT

´Breast

´Plastic

´Ortho

49
Q

Risk factors for PONV Pediatrics

A

´Age: Weak Association

´Herniorrhaphy

´T&A

´Strabismus Surgery

´Male Genitalia Surgeries: Highest Risk

´Risk reduced in adults as they age

50
Q

Risk factors for PONV anesthetics

A

´Inhalation Agents

´Nitrous Oxide

´Neostigmine

´Opioids

´Correlation is limited with these factors and PONV

51
Q

Scopolamine

transdermal use/dose/location

A
  • transdermal: motion inducted nausea
  • loction: post auricular (behind ear) delivers 5mcg/hr for 72 horus (less than 0.5mg)
52
Q

why we dont use oral or IV scopolamine

A

they require large doses and have undesirable side effects and poor pt acceptance

53
Q

when to place a transdermal scopolamine patch

A

4 hours before noxious stimuli: less effective after symptoms start

54
Q

MOA of Scopolamine

A

blocks transmission to the medulla of impulses arising from over stimulation of the vestibular apparatus of the inner ear

55
Q

what causes motion sickness

A

stimulation of the vestibular apparatus

56
Q

effect of morphine and synthetic opioids on motion sickness

A

increase vestibular sensitivity to motion

57
Q

what protects against N/V after middle ear surgery

A

transdermal scopolamine

58
Q

most common side effect of transdermal scopolamine and when to expect it to happen

A

unilateral dilated pupil

visual disturances at 24-48 hours post surgery

(on the same side as the patch)

SUM '20 - Pharm II (30 decks)

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