pharm-ponv Flashcards
who is high risk for ponv?
- females
- Fatties (obese)
- full stomach/ fatty foods
- history of PONV
- motion sickness, migraine
- anxiety
- use of post op opiates
who is least at risk for PONV
smokers
young,girls, non smoker, use of post op opiates has a___% chance of ponv
50%
what procedures have higher risk?
- craniotomy
- strabismus repair
- ENT/ T&A
- orthopedic shoulder repair
- certain cosmetic procedures (chest augmentation)
- intra-abdominal
- Laparoscopic procedures
- heria repair (especially under spinal) .
- GYN procedures
- orchiopexy
what does surgery length do to incidence of PONV
longer=more risk
rank the iatrogenic PONV causers (in order of highest incidence to lowest)
- regional
- gas/opiates
- SAB
- general (gas and opiates)
- SAB
- regional
what drugs increase chance of PONV
- opiates (balanced anesthesia)
- nitrous
- ketamine
- anticholinesterases
- what conditons increase PONV
2. how does the treatment of this cause PONV
- pain can cause PONV
2. opiates to treat pain trigger the CRTZ in the brain and cause nausea (very important fact)
what 5 other conditions cause PONV?
- hypotension (including orthostatic) /dehydraton
- hypoxia
- hypoglycemia
- movement (thru vestibular stimulation)
- oral intake too soon after procedure
what are the 3 acts of vomiting?
nausea
retching
vomiting
nausea
typically associated with decreased gastric motility and increased small intestine tone and reverse peristalsis in small intestine
retching:
“dry heaves”, spasmodic respiratory movements conducted with closed glottis causing herination of abdominal esophagus into thoracid cavity due to negative pressure (due to resp effort with glottis closed)
vomiting (phase 1)
when gastric and small intestinal contents are expelled
1. deep breath; glottis closes; larynx raises and opens upper esophageal sphincter; soft palate raises to close off posterior nares
vomiting phase 2
diaphragm contracts sharply downward; creates neg pressure in thorax which opens esophagus and distal esophageal sphincter
vomiting (phase 3)
simultaneous downward movement of diaphragm and contraction of abdomen walls squeezes the stomach elevating intragastric pressure. pylorus is closed and esophagus is open, vomit is expelled.
who is at risk for PONV?
- children and adolescents
- women (d/t gonadotropin and estrogen)
- history of PONV
- non smokers
- anxious persons/ anxiety
- obesity (d/t larger gastrc volume, higher chance of reflux, amount of fat soluble drugs accumulated, and gall bladder/gi disease
- Oral Intake: excess fatty foods (slows peristalsis), full stomach, currently intoxicated
- use of post op opiates
- history of motion sickness
can nauser be triggered from multiple things at once?
yes
what can stimulation of pharynx cause
N/V (ilicits emetic resopnse)
why does car/ motion sickness occur
labyrinthine (vestibular) apparats and auricular branch of the tympanum of the ear detects motion stimulus from histhamine or ACH receptors
- what is the name of the receptors that detect overdistention and altered gastric motility which can lead to N/V?
- In what organs of the abdomen are they located?
- mechanoreceptors
2. bladder, gall bladder, uterus
- where are chemical stimulus detectors located in the abdomen?
- what do they sense?
- hepatic portal vein detectors
2. cheicals in the venous drainage of gut
gastric and duodenal chemoreceptors detect what?
irritation from toxins such as serotonin
what nerve sends signals regarding nausea to the brain?
vagus
- vagus nerve from gut sends signal to ___,___ & ___ receptors in brain?
- what is the name of these areas of the brain?
- histhamine, cholinergic or enkephalin receptors
2. nucleus tractus solitarius; area postrema and subpostrema
what parts of the brain are affected by emotions, sights, smells or thoughts?
higher brain centers in the cortex and limbic system
- where is the chemoreceptor trigger zone (CRTZ , CTZ),
2. what does it do?
- located in the area postrema on the floor of the fourth ventricle of brain;
- identify absorbed toxins, or disturbances (hypotension and metabolic acid-base changes)which is reflected as nausea and vomiting
what must coordinate in order for vomiting to occur?
afferent stimuli detect the need to vomit and coordinate the response in the vomiting center in the lateral reticular formation of the brainstem close to foruth ventricle.
what are the receptors that have a role in receiving emetic impulses?
histhamine, serotonin, opiod, muscarenic, and dopaminergic
how do antihisthamines block nausea?
antagonizes H1 & H2
what does H2 stimulation cause?
increased gastric hydrogen ion concentration
where are H2 receptors found besides the stomach/
in the CNS with some in the heart
how does a H2 blocker work?
blocking histhamine stimulation of H2 receptors prevents increases in cAMP (cAMP activates the proton pump of gastric parietsl cells which secrete H+ ion)
H2 blockers are used to manage ____ reactions?
allergic
what is one concern regarding H2 blockers and the lungs?
H2 blockers leave H1 stimuation unopposed (H1 stimulation potentially causes bronchospasm). (although side effects are uncommon).
other side effects of H2 blockers are…
diarrhea, confusion, and drug interactions (mostly with cimetidine (tagament)
what is the method of elimination for H2 blockers ?
renal and hepatic
H1 blockers
name some of the many uses:
give an example:
1 anti nausea/ anti motion sickness
- serotonin blocking action
- anticholinergic activity
- antiparkinson effect
- local sedation
- benadryl 25-100 mg
antihisthamines (H1 & H2 blockers) can cause what changes in drug absorption?
alter absorption of other PO meds by increasing pH
rantidine
- what class of histhamine blocker?
- uses?
- what doesnt it affect?
- less ___ side effects than cimetidine:
- less hepatic _____ ______ than cimetidine;
- H2 blocker
- gerd, duodenal and stress ulcers, prevention of aspiration
- does NOT affect gastric volume, gastric emptying, or pancreatic secretions
- CNS
- hepatic enzyme induction
Rantidine brand name?
- onset:
- peak:
- durtion:
- dose:
zantac
- onset: 15 minutes IV, 30 min PO
- Peak: 1-2 hours IV, 2-3 hrs PO
- duration: 6-8 hours IV, 8-12 PO
- dose: 50 mg IV; 150 mg bid PO
cimetidine:
onset:
duration:
dose:
tagament
60 min
6 hrs
300 mg IV
famotidine s/e: onset: peak: duration: dose:
pepcid same as zantac, safe profile 30 min IV, 60 min PO 10-12 hrs po and IV 20 mg iv and po
nizatidine
dose:
dose for active ulcer:
Axid
150 mg for gerd
300 mg for active ulcer
phenothiazines 1.class: 2.method of action: 3.side effects: 4.what action causes side effects: common phenothiazines:
- antipsychotics
- dopamine receptors in CRTZ
- dopaminergic side effects: tardive dyskinesia, parkinson effects
- compazine, phenergan
promethiazines: prochlorperazine
1. moa
2. may cause hypotension-how?
3. extrapyramidal side effects treated with ?
4. elimination?
5. onset?
6. peak?
7. duration?
8. dose? daily max?
compazine
- direct effect on CRTZ
- by alpha blockade
- benadryl
- hepatic
- less than 5 min
- 15-30 min
- 2-4 hours
- 2.5-10 mg (max less than 40 mg/day)
Phenthiazines: promethiazine
- class
- side effects
- why not good for not a good H1 blocker
- action:
- onset:
- duration
- dose
phenergan
- phenothiazine derivitive
- no antipsychotic effects at theraputic doses, but EPSs are possible
- H1 antihisthamine effects not enough to be theraputic
- sedative, antiemetic and anticholinergic effects
- 2-5 minutes
- <2 hours
- 12.5-50 mg iv
metoclopramide
- origin:
- what is its action on peristalsis and lower esophageal sphincter?
- what is its action on GI muscle?
- affects on dopamine?…where?
- what is the action on the vomiting reflex and peristalsis?
- dose:
- side effects:
reglan
- derived from procainamide
- speeds gastric emptying by stimulating upper gi tract gastric motility and increases lower esophageal sphincter tone
- sensitizes GI smooth muscle to effects of ACH
- antagonism of central & peripheral dopamine effects in CRTZ
- reverses gastric immobility and cephalad peristalsis during vomiting reflex
- 10 mg
- mask like face, EPSs, depression, agitation, jitters, confusion, irregular heart beat, exacerbates porphyria