Week 5 - NV Flashcards
(72 cards)
1
Q
define nausea
A
- a feeling of discomfort in the epigastrium with a conscious desire to vomit
- the sensation
2
Q
define vomiting
A
- the forceful ejection of partially digested food & secretions from the upper GI tract
- aka emesis
3
Q
what controls the sensation of nausea and action of vomitting?
A
- the emetic center in the medulla
4
Q
what happens once the emetic center receives enough stimulation
A
- it will become active & you will get the sensation of nausea & action of vomitting
5
Q
where does the emetic center receive input from? (4)
A
- the chemoreceptor trigger zone
- the vestibular system
- vagal & enteric nervous system
- the CNS
6
Q
what is the chemoreceptor trigger zone (CTZ)?
A
- an area of the medulla center that lies outside the blood brain barrier
- it detects chemical stimuli in the blood such as hormones & drugs
7
Q
what does the CTZ have receptors for? (5)
A
- dopamine
- serotonin
- opiates
- acetylcholine
- substance P
8
Q
what is the vestibular system
A
- system inside the ear that helps maintain our posture, sense of balance
- sends info to the brain via crnial nerve VIII (auditory nerve)
9
Q
what kind of receptors are present in the vestibular system
A
- muscarinic receptors (acetylcholine receptors) and histamine
10
Q
what does the vestibular system play a major role in?
A
motion sickeness
11
Q
describe how motion sickness occurs? provide an example with sea sickness
A
- 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
12
Q
what does the vagal and enteric system receive info about?
A
- it inputs transmit info regarding the state of the GI system
13
Q
what kinda receptors are present in the vagal & enteric nervous system?
A
- serotonin
14
Q
what activates the serotonin receptors in the vagal & enteric nervous system (4)
A
irritation of the GI by:
- chemo
- radiation
- distension
- acute infectious gastroenteritis
15
Q
the CNS mediates vomitting that arises from? provide 3 examples
A
things from higher brain centers:
- psychiatric disorders
- stress
- when we see & smell someone else vomitting
16
Q
what are 5 causes of vomitting
A
- causes in the digestive tract
- sensory system & brain
- pregnancy
- drug reaction
- illness
17
Q
what are some examples of causes in the GI tract that cause vomiting (3)
A
- gastritis
- overeating
- food poisoning
18
Q
what are some examples of how the sensory system & brain cause vomiting? (3)
A
- motion sickness
- concussion
- cerebral hemorrhage
19
Q
what are some examples of how drug reactions can cause vomiting (4)
A
- alcohol
- opioids
- selective serotonin reuptake inhibitors
- chemo
20
Q
what is an example of an illness that causes vomitting
A
- the stomach flu (gastric irritation caused by viruses or bacteria)
21
Q
list 3 complications of vomiting
A
- aspiration
- mallory-weiss tear
- fluids & electrolytes abnormalities
22
Q
what is aspiration r/t vomiting
A
- passage of gastric contents into the airways
23
Q
list 2 reasons someone is at an increased risk of aspiration when vomiting
A
- decreased LOC
- if vomiting for prolonged periods
24
Q
what is the mallory-weiss tear
A
- a tear in the esophageal lining which causes GI bleeding
25
what causes the mallory-weiss tear
- retching or dryheaving
26
list 4 fluids & electrolytes that vomiting effects
- loss of HCl
- loss of K+
- increased production of HCO3-
- dehydration
27
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
28
what does the changes in fluid & electrolytes lead to (3)
- hypochloremia
- hypokalemia
- metabolic alkalosis
29
how is the metabolic alkalosis compensated
- decreased RR (to try to accumulate CO2)
30
what is metabolic alkalosis
- loss of H+ ions > excessive production of bicarb ions
| = high pH, high HCO3-
31
what does prolonged vomiting result in
- switch from metabolic alkalosis to metabolic acidosi
32
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
33
what are 2 causes of the switch to metabolic acidosis
1. physical losses of HCO3-
| 2. chemical consumption of HCO3-
34
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-
35
what is included as duodenal secretion
- pancreatic & small intestine secretions
36
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"
37
what are drugs that work for nausea & vomitting called
- antiemetics
| - antinausea
38
what are 6 types of antiemetics?
- anticholinergics
- antihistamines
- cannabinoids
- glucocorticoids
- phenothiazides
- serotonin receptor antagonists
39
how do antiemetics & antinausea drugs work
- many different MOAs
| - most work by blocking one of the vomitting pathways = blocks the stimulus that induces vomiting
40
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)
41
what is the prototype of anticholinergics
- scopolamine (buscopan)
42
what specifically is scopoalimine good for?
- motion sickness (transdermal patch)
43
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
44
what are the 4 uses of antihistamines
- motion sickness
- nonproductive cough
- allergy symptoms
- sedation
45
what are 2 examples of antihistamines
- dimenhydrinate (gravol, dramamine)
| - diphenhydramine (benadryl)
46
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)
47
what is the use of glucocorticoids r/t NV
- treat NV associated with chemo drugs
48
what is an example of glucocorticoids for NV
- dexamethasone (dexasone)
49
what is tetrahydrocannabinoids (TCH)
- major psychoactive substance in marijuana
50
describe the use of TCH (4)
- for NV associated with chemo
- for anorexia associated with weight loss in AIDS pts
- increases appetite
- nerve pain
51
what is a herbal product used for NV
ginger
52
describe the use of ginger (3)
for NV caused by:
- chemo
- motion sickness
- morning sickness
53
what are the adverse effects of ginger (3)
- anorexia
- NV
- skin reactions
54
what are the drug interactions associated w ginger (2)
- increase absorption of oral meds
| - increase bleeding risk w anticoagulants
55
what is the MOA of serotonin blockers (3)
- blocks serotonin receptors in:
1. GI tract
2. CTZ
3. emetic center
56
describe the use of serotonin blockers (2)
NV r/t
1. chemo
2. postop
57
list 2 examples of serotonin blockers
- dolasetron (anzemet)
| - ondansetron (zofran)
58
what is the MOA of phenothiazines
- dopamine antagonists --> block dopamine receptors in the CTZ
59
list 2 examples of phenothiazines
- metoclopramide (maxeran)
| - prochlorperazine (stemitil)
60
describe the use of phenothiazines (3)
reduce emesis r/t
1. surgery (postop)
2. cancer chemo
3. toxins
61
list adverse effects of phenothiazines (4)
- anticholinergic rxn
- hypotension
- sedation
- extrapyramidial rxn
62
what is the main side effect r/t histamine blocking
- sedation
63
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)
64
what adverse effects will be seen with anticholinergics & antihistamines
- both will see s/e r/t to blocking Ach
| + sedation for antihistamine
65
describe side effects for glucocorticoids
- minimal with short term use
66
describe side effects for serotonin antagonists (4)
- HA
- diarrhea
- dizziness
- increased QT interval
67
list 2 examples of cannibinoids
- cannadibiol
| - nabilone
68
list side effects of cannibinoids (3)
- subjective
- tachy
- hypotension
69
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
70
who can metoclopramide not be used in
- bowel obstruction
- perforation
- GI hemorrhage
71
list 3 common s/e of metoclorpramide
- sedation
- diarrhea (due to increased motility)
- tardive dyskinesia (irrevresible twitching)
72
what should be present prior to giving metoclorpramide
- BS
