week 2 Antiemetics and GI motility 2 of 4 Flashcards
2 examples of Macrolides
Erythromycin, Azithromycin (macrolide antibiotics)
GI effects of Macrolide antibiotics
Increase lower esophageal sphincter tone, enhances intraduodenal coordination and promotes gastric emptying of liquids and solids
what types of patients are more susceptible to effects of Macrolide antibiotics
pts with diabetic gastroparesis; pts awaiting emergent surgery; normal pts; ICU pts with food intolerance
properties of macrolide antibiotics
prokinetic properties attributed to thier binding to motilin receptors in the stomach and duodenum
when are macrolides used
used only when other prokinetic agents have failed
name 2 5HT4 receptor agonist
Cisapride and Mosapride
5HT4 receptor agonist: use/effect
Decreases GERD; Increases lower esophageal sphincter tone; improves gastric motility and increases motility in small and large intestine
how do 5HT4 receptor angonist decrease GERD and improve gastric motility
by enhancing the release of acetylcholine from nerve endings in the myenteric plexus of the gastrointestinal mucosa.
what drug is used to reverse opioid induced gastric stasis
Cisapride (5HT4 agonist)
what is a negative side effect of 5HT4 receptor agonist cisapride and mosapride
prolongation of QT interval due to non selectivity
what are the 2 distinct entities of PONV (classifications)
Early & Late
what defines “early” PONV
within 6 hours of emergence from anesthesia
what defines “late” PONV
6-24 hours after the procedure
what are the most important complaints patients make
pain and PONV
what is the leading cause of unanticipated hospital admission following outpatient surgery
PONV
6 things that PONV cause that are associated with morbidity
Dehydration Electrolyte Abnormalities Wound Dehiscence Bleeding Esophageal rupture (Boerhaave’s Syndrome) Airway Compromise
pathophysiology of PONV: how the process begins
begins with antiperistalsis of muscular contractions within the ileum and jejunum, moving contents backwards toward the stomach
pathophysiology of PONV: the expelling contents phase (MOA of emesis)
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
definition of regurgitation: how it differs form emesis
Regurgitation is acidic gastric material passively reflexes into the esophagus because of the incompetent esophageal sphincter and elevated abdominal pressure
Sequence of events causing emesis are controlled by the _______?
vomiting center in the brain
where is the vomiting center
lies in the medullas oblongata and consists of the nucleus of the tractus solitarius and parts of reticular formation
6 pharmacological systems that interact with the vomiting center figure 34-1 pg 693
dopamine serotonin substance P acetylcholine gamma-aminobutyric acid cannabinoids
Chemoreceptor Trigger Zone (CRTZ) location/function
Slightly cephalad to vomiting center. Detects noxious chemicals in the bloodstream. Ex: ethanol
MOA of (CRTZ) Chemoreceptor Trigger Zone
The detection of noxious chemicals sends signals via neural networks which activate vomiting center.
anatomic sites that activate the vomiting center (other than CRTZ)
vestibular apparatus, thalamus, cerebral cortex, Neurons in the GIT
MOA of Neurons in GIT activating the vomiting center
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
once the vomiting center is activated what happens? MOA: what type of signal does it send
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
vomiting center sends what type of signal?
efferent
what cranial nerves does the vomiting center send signals through
CN V, VII, IX, X, and XII
what pathway is used (MOA) to activate vomiting center:
smell, sight, taste, fear, emotions, memory
slide 28 image
cortical afferent pathway = nausea
what pathway is used (MOA) to activate vomiting center:
pharynx (gag)
slide 28 image
midbrain afferent pathway: nuleus tractus solitarius (SHt3, D2, M1, H1): vomiting center
what pathway is used (MOA) to activate vomiting center:
emetogenic drugs and toxins, catecholamines (nitrous oxide, opioids, cyclopropane, ether, ketamine)
slide 28 image
chemoreceptor trigger zone (5HT3,D2, M, H1): triggers nucleus tractus solitarius: triggers vomiting center
what pathway is used (MOA) to activate vomiting center:
positional changes, ear surgery, motion sickness (Nitrous Oxide)
slide 28 image
vestibular Afferent pathway (H1, M): triggers cerebellum: triggers vomiting center
what pathway is used (MOA) to activate vomiting center:
Local irritants, surgery, pain, toxins (nitrous oxide, cytotoxic drugs, levodopa, bromocriptine, ipecac)
slide 28 image
vagal mucosal afferent pathway (5HT3, M3, H3): triggers vomiting center
slide 28 image:
vomiting center triggers what?
visceral, comatic and motor pathways: trigger the vomiting reflex: result in vomiting
drug class of Odansetron & Dolasetron
Serotonin Receptor Blockers (5HT3): antiemetic drugs
Dopamine receptor site blockers (D2)
name 3
droperidol, haloperidol, metoclopramide
side effect of droperidol
(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
which dopamine receptor blocker has a long half life
haloperidol
antiemetic: histamine blocker
list 2
promethazine (H1)
Diphenhydramine
antiemetics: Muscarinic receptor blockers: name two
glycopyrrolate & scopolamine
side effect of transdermal scopolamine
mydriasis
sedation, cycloplegia, drying of secretions
what is commonly given in conjunction with a 5HT3 or with droperidol for antiemetic effect
dexamethasone
substance P: what family of neurotransmitters does it belong to:
neurokinin family: affinity for neurokinin 1 (NK-1) receptors
only neurokinin antagonist in use
“aprepitant” or Emend: PO used prophylactically
how is Ephedrine used for PONV
Ephedrine used to maintain BP minimizing cerebral ischemia thereby preventing PONV
Patient risk factors for PONV
Women
nonsmokers
hx of motion sickness
previous PONV
Surgical risk factors for PONV
´Length of Surgery
´Laparotomies
´Gynecologic surgeries
´Laparoscopic procedures
´ENT
´Breast
´Plastic
´Ortho
Risk factors for PONV Pediatrics
´Age: Weak Association
´Herniorrhaphy
´T&A
´Strabismus Surgery
´Male Genitalia Surgeries: Highest Risk
´Risk reduced in adults as they age
Risk factors for PONV anesthetics
´Inhalation Agents
´Nitrous Oxide
´Neostigmine
´Opioids
´Correlation is limited with these factors and PONV
Scopolamine
transdermal use/dose/location
- transdermal: motion inducted nausea
- loction: post auricular (behind ear) delivers 5mcg/hr for 72 horus (less than 0.5mg)
why we dont use oral or IV scopolamine
they require large doses and have undesirable side effects and poor pt acceptance
when to place a transdermal scopolamine patch
4 hours before noxious stimuli: less effective after symptoms start
MOA of Scopolamine
blocks transmission to the medulla of impulses arising from over stimulation of the vestibular apparatus of the inner ear
what causes motion sickness
stimulation of the vestibular apparatus
effect of morphine and synthetic opioids on motion sickness
increase vestibular sensitivity to motion
what protects against N/V after middle ear surgery
transdermal scopolamine
most common side effect of transdermal scopolamine and when to expect it to happen
unilateral dilated pupil
visual disturances at 24-48 hours post surgery
(on the same side as the patch)
