Week 5 - NV Flashcards
define nausea
- a feeling of discomfort in the epigastrium with a conscious desire to vomit
- the sensation
define vomiting
- the forceful ejection of partially digested food & secretions from the upper GI tract
- aka emesis
what controls the sensation of nausea and action of vomitting?
- the emetic center in the medulla
what happens once the emetic center receives enough stimulation
- it will become active & you will get the sensation of nausea & action of vomitting
where does the emetic center receive input from? (4)
- the chemoreceptor trigger zone
- the vestibular system
- vagal & enteric nervous system
- the CNS
what is the chemoreceptor trigger zone (CTZ)?
- an area of the medulla center that lies outside the blood brain barrier
- it detects chemical stimuli in the blood such as hormones & drugs
what does the CTZ have receptors for? (5)
- dopamine
- serotonin
- opiates
- acetylcholine
- substance P
what is the vestibular system
- system inside the ear that helps maintain our posture, sense of balance
- sends info to the brain via crnial nerve VIII (auditory nerve)
what kind of receptors are present in the vestibular system
- muscarinic receptors (acetylcholine receptors) and histamine
what does the vestibular system play a major role in?
motion sickeness
describe how motion sickness occurs? provide an example with sea sickness
- due to a mismatch between vestibular and visual info
ex. with sea sickness you look at the deck and it doesn’t look like your moving but your vestibular system detects movement
what does the vagal and enteric system receive info about?
- it inputs transmit info regarding the state of the GI system
what kinda receptors are present in the vagal & enteric nervous system?
- serotonin
what activates the serotonin receptors in the vagal & enteric nervous system (4)
irritation of the GI by:
- chemo
- radiation
- distension
- acute infectious gastroenteritis
the CNS mediates vomitting that arises from? provide 3 examples
things from higher brain centers:
- psychiatric disorders
- stress
- when we see & smell someone else vomitting
what are 5 causes of vomitting
- causes in the digestive tract
- sensory system & brain
- pregnancy
- drug reaction
- illness
what are some examples of causes in the GI tract that cause vomiting (3)
- gastritis
- overeating
- food poisoning
what are some examples of how the sensory system & brain cause vomiting? (3)
- motion sickness
- concussion
- cerebral hemorrhage
what are some examples of how drug reactions can cause vomiting (4)
- alcohol
- opioids
- selective serotonin reuptake inhibitors
- chemo
what is an example of an illness that causes vomitting
- the stomach flu (gastric irritation caused by viruses or bacteria)
list 3 complications of vomiting
- aspiration
- mallory-weiss tear
- fluids & electrolytes abnormalities
what is aspiration r/t vomiting
- passage of gastric contents into the airways
list 2 reasons someone is at an increased risk of aspiration when vomiting
- decreased LOC
- if vomiting for prolonged periods
what is the mallory-weiss tear
- a tear in the esophageal lining which causes GI bleeding
what causes the mallory-weiss tear
- retching or dryheaving
list 4 fluids & electrolytes that vomiting effects
- loss of HCl
- loss of K+
- increased production of HCO3-
- dehydration
what is the alkaline tide
- when we lose HCl through vomiting, the body tries to restore the acid and HCO3- is made as a biproduct
what does the changes in fluid & electrolytes lead to (3)
- hypochloremia
- hypokalemia
- metabolic alkalosis
how is the metabolic alkalosis compensated
- decreased RR (to try to accumulate CO2)
what is metabolic alkalosis
- loss of H+ ions > excessive production of bicarb ions
= high pH, high HCO3-
what does prolonged vomiting result in
- switch from metabolic alkalosis to metabolic acidosi
what does the switch to metabolic acidosis indicate?
- even with continued loss of H+ ions, we are now getting more HCO3- losses than H+ losses
what are 2 causes of the switch to metabolic acidosis
- physical losses of HCO3-
2. chemical consumption of HCO3-
what is meant by physical losses of HCO3
- with prolonged vomiting, the place where secretions are lost digs deeper each time (start with stomach contents, then pylorus, then duodenom)
- so, with prolonged vomiting we lose duodenal secretions which are rich in HCO3-
what is included as duodenal secretion
- pancreatic & small intestine secretions
what is chemical consumption of HCO3-
- hypovolemia & increased muscle activity associated with comiting results in lactic acid production
- in addition, depletion of liver glucose stores & loss of ingested carbs could cause ketoacidosis
- the bicarb is then used to buffer these acids & is “chemically consumed”
what are drugs that work for nausea & vomitting called
- antiemetics
- antinausea
what are 6 types of antiemetics?
- anticholinergics
- antihistamines
- cannabinoids
- glucocorticoids
- phenothiazides
- serotonin receptor antagonists
how do antiemetics & antinausea drugs work
- many different MOAs
- most work by blocking one of the vomitting pathways = blocks the stimulus that induces vomiting
what are the 3 MOAs of anticholinergics
- bind to & block acetylcholine receptors in the inner ear labyrinth = vestibular pathway
- block transmission of nauseating stimuli to CTZ
- block transmission of nauseating stimuli to emetic center
(bc each of these contain muscurinic/Ach receptors)
what is the prototype of anticholinergics
- scopolamine (buscopan)
what specifically is scopoalimine good for?
- motion sickness (transdermal patch)
what is the MOA of antihistamine drugs (H1 receptor blockers) (2)
- block action of histamine at the H1 receptor
- indirectly inhibit ACh by binding to muscurinic receptors = prevent cholinergic stimulation = prevent NV
what are the 4 uses of antihistamines
- motion sickness
- nonproductive cough
- allergy symptoms
- sedation
what are 2 examples of antihistamines
- dimenhydrinate (gravol, dramamine)
- diphenhydramine (benadryl)
how do glucocorticoids work to prevent NV (2)
- anti-inflammatory –> inflammation of gut can cause NV
- can increase the antiemetic effect of serotonin blockers (ondansetron)
what is the use of glucocorticoids r/t NV
- treat NV associated with chemo drugs
what is an example of glucocorticoids for NV
- dexamethasone (dexasone)
what is tetrahydrocannabinoids (TCH)
- major psychoactive substance in marijuana
describe the use of TCH (4)
- for NV associated with chemo
- for anorexia associated with weight loss in AIDS pts
- increases appetite
- nerve pain
what is a herbal product used for NV
ginger
describe the use of ginger (3)
for NV caused by:
- chemo
- motion sickness
- morning sickness
what are the adverse effects of ginger (3)
- anorexia
- NV
- skin reactions
what are the drug interactions associated w ginger (2)
- increase absorption of oral meds
- increase bleeding risk w anticoagulants
what is the MOA of serotonin blockers (3)
- blocks serotonin receptors in:
1. GI tract
2. CTZ
3. emetic center
describe the use of serotonin blockers (2)
NV r/t
- chemo
- postop
list 2 examples of serotonin blockers
- dolasetron (anzemet)
- ondansetron (zofran)
what is the MOA of phenothiazines
- dopamine antagonists –> block dopamine receptors in the CTZ
list 2 examples of phenothiazines
- metoclopramide (maxeran)
- prochlorperazine (stemitil)
describe the use of phenothiazines (3)
reduce emesis r/t
- surgery (postop)
- cancer chemo
- toxins
list adverse effects of phenothiazines (4)
- anticholinergic rxn
- hypotension
- sedation
- extrapyramidial rxn
what is the main side effect r/t histamine blocking
- sedation
what are side effects r/t blocking Ach
- mad as a hatter (delirium)
- blind as a bat (blurred vision)
- dry as a bone (dry mouth and skin)
- hot as a hare (fever)
- red as a beet (vasodilation)
- bowel & the bladder lose their tone (urinary retention & constipation)
- heart runs alone (tachy)
what adverse effects will be seen with anticholinergics & antihistamines
- both will see s/e r/t to blocking Ach
+ sedation for antihistamine
describe side effects for glucocorticoids
- minimal with short term use
describe side effects for serotonin antagonists (4)
- HA
- diarrhea
- dizziness
- increased QT interval
list 2 examples of cannibinoids
- cannadibiol
- nabilone
list side effects of cannibinoids (3)
- subjective
- tachy
- hypotension
what is the MOA of metoclopramide (2)
prokinetic drug:
- suppresses emesis by blocking dopamine receptors
- increases upper GI motility by enhancing the effects of Ach
who can metoclopramide not be used in
- bowel obstruction
- perforation
- GI hemorrhage
list 3 common s/e of metoclorpramide
- sedation
- diarrhea (due to increased motility)
- tardive dyskinesia (irrevresible twitching)
what should be present prior to giving metoclorpramide
- BS
