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NURS 2514 > Week 5 - NV > Flashcards

Week 5 - NV Flashcards

1
Q

define nausea

A
  • a feeling of discomfort in the epigastrium with a conscious desire to vomit
  • the sensation
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2
Q

define vomiting

A
  • the forceful ejection of partially digested food & secretions from the upper GI tract
  • aka emesis
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3
Q

what controls the sensation of nausea and action of vomitting?

A
  • the emetic center in the medulla
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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
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5
Q

where does the emetic center receive input from? (4)

A
  1. the chemoreceptor trigger zone
  2. the vestibular system
  3. vagal & enteric nervous system
  4. the CNS
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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
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7
Q

what does the CTZ have receptors for? (5)

A
  • dopamine
  • serotonin
  • opiates
  • acetylcholine
  • substance P
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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)
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9
Q

what kind of receptors are present in the vestibular system

A
  • muscarinic receptors (acetylcholine receptors) and histamine
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10
Q

what does the vestibular system play a major role in?

A

motion sickeness

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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
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12
Q

what does the vagal and enteric system receive info about?

A
  • it inputs transmit info regarding the state of the GI system
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13
Q

what kinda receptors are present in the vagal & enteric nervous system?

A
  • serotonin
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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
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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
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16
Q

what are 5 causes of vomitting

A
  • causes in the digestive tract
  • sensory system & brain
  • pregnancy
  • drug reaction
  • illness
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17
Q

what are some examples of causes in the GI tract that cause vomiting (3)

A
  • gastritis
  • overeating
  • food poisoning
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18
Q

what are some examples of how the sensory system & brain cause vomiting? (3)

A
  • motion sickness
  • concussion
  • cerebral hemorrhage
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19
Q

what are some examples of how drug reactions can cause vomiting (4)

A
  • alcohol
  • opioids
  • selective serotonin reuptake inhibitors
  • chemo
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20
Q

what is an example of an illness that causes vomitting

A
  • the stomach flu (gastric irritation caused by viruses or bacteria)
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21
Q

list 3 complications of vomiting

A
  • aspiration
  • mallory-weiss tear
  • fluids & electrolytes abnormalities
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22
Q

what is aspiration r/t vomiting

A
  • passage of gastric contents into the airways
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23
Q

list 2 reasons someone is at an increased risk of aspiration when vomiting

A
  • decreased LOC

- if vomiting for prolonged periods

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24
Q

what is the mallory-weiss tear

A
  • a tear in the esophageal lining which causes GI bleeding
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25
Q

what causes the mallory-weiss tear

A
  • retching or dryheaving
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26
Q

list 4 fluids & electrolytes that vomiting effects

A
  • loss of HCl
  • loss of K+
  • increased production of HCO3-
  • dehydration
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27
Q

what is the alkaline tide

A
  • when we lose HCl through vomiting, the body tries to restore the acid and HCO3- is made as a biproduct
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28
Q

what does the changes in fluid & electrolytes lead to (3)

A
  • hypochloremia
  • hypokalemia
  • metabolic alkalosis
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29
Q

how is the metabolic alkalosis compensated

A
  • decreased RR (to try to accumulate CO2)
30
Q

what is metabolic alkalosis

A
  • loss of H+ ions > excessive production of bicarb ions

= high pH, high HCO3-

31
Q

what does prolonged vomiting result in

A
  • switch from metabolic alkalosis to metabolic acidosi
32
Q

what does the switch to metabolic acidosis indicate?

A
  • even with continued loss of H+ ions, we are now getting more HCO3- losses than H+ losses
33
Q

what are 2 causes of the switch to metabolic acidosis

A
  1. physical losses of HCO3-

2. chemical consumption of HCO3-

34
Q

what is meant by physical losses of HCO3

A
  • 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
Q

what is included as duodenal secretion

A
  • pancreatic & small intestine secretions
36
Q

what is chemical consumption of HCO3-

A
  • 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
Q

what are drugs that work for nausea & vomitting called

A
  • antiemetics

- antinausea

38
Q

what are 6 types of antiemetics?

A
  • anticholinergics
  • antihistamines
  • cannabinoids
  • glucocorticoids
  • phenothiazides
  • serotonin receptor antagonists
39
Q

how do antiemetics & antinausea drugs work

A
  • many different MOAs

- most work by blocking one of the vomitting pathways = blocks the stimulus that induces vomiting

40
Q

what are the 3 MOAs of anticholinergics

A
  • 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
Q

what is the prototype of anticholinergics

A
  • scopolamine (buscopan)
42
Q

what specifically is scopoalimine good for?

A
  • motion sickness (transdermal patch)
43
Q

what is the MOA of antihistamine drugs (H1 receptor blockers) (2)

A
  • block action of histamine at the H1 receptor

- indirectly inhibit ACh by binding to muscurinic receptors = prevent cholinergic stimulation = prevent NV

44
Q

what are the 4 uses of antihistamines

A
  • motion sickness
  • nonproductive cough
  • allergy symptoms
  • sedation
45
Q

what are 2 examples of antihistamines

A
  • dimenhydrinate (gravol, dramamine)

- diphenhydramine (benadryl)

46
Q

how do glucocorticoids work to prevent NV (2)

A
  • anti-inflammatory –> inflammation of gut can cause NV

- can increase the antiemetic effect of serotonin blockers (ondansetron)

47
Q

what is the use of glucocorticoids r/t NV

A
  • treat NV associated with chemo drugs
48
Q

what is an example of glucocorticoids for NV

A
  • dexamethasone (dexasone)
49
Q

what is tetrahydrocannabinoids (TCH)

A
  • major psychoactive substance in marijuana
50
Q

describe the use of TCH (4)

A
  • for NV associated with chemo
  • for anorexia associated with weight loss in AIDS pts
  • increases appetite
  • nerve pain
51
Q

what is a herbal product used for NV

A

ginger

52
Q

describe the use of ginger (3)

A

for NV caused by:

  • chemo
  • motion sickness
  • morning sickness
53
Q

what are the adverse effects of ginger (3)

A
  • anorexia
  • NV
  • skin reactions
54
Q

what are the drug interactions associated w ginger (2)

A
  • increase absorption of oral meds

- increase bleeding risk w anticoagulants

55
Q

what is the MOA of serotonin blockers (3)

A
  • blocks serotonin receptors in:
    1. GI tract
    2. CTZ
    3. emetic center
56
Q

describe the use of serotonin blockers (2)

A

NV r/t

  1. chemo
  2. postop
57
Q

list 2 examples of serotonin blockers

A
  • dolasetron (anzemet)

- ondansetron (zofran)

58
Q

what is the MOA of phenothiazines

A
  • dopamine antagonists –> block dopamine receptors in the CTZ
59
Q

list 2 examples of phenothiazines

A
  • metoclopramide (maxeran)

- prochlorperazine (stemitil)

60
Q

describe the use of phenothiazines (3)

A

reduce emesis r/t

  1. surgery (postop)
  2. cancer chemo
  3. toxins
61
Q

list adverse effects of phenothiazines (4)

A
  • anticholinergic rxn
  • hypotension
  • sedation
  • extrapyramidial rxn
62
Q

what is the main side effect r/t histamine blocking

A
  • sedation
63
Q

what are side effects r/t blocking Ach

A
  • 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
Q

what adverse effects will be seen with anticholinergics & antihistamines

A
  • both will see s/e r/t to blocking Ach

+ sedation for antihistamine

65
Q

describe side effects for glucocorticoids

A
  • minimal with short term use
66
Q

describe side effects for serotonin antagonists (4)

A
  • HA
  • diarrhea
  • dizziness
  • increased QT interval
67
Q

list 2 examples of cannibinoids

A
  • cannadibiol

- nabilone

68
Q

list side effects of cannibinoids (3)

A
  • subjective
  • tachy
  • hypotension
69
Q

what is the MOA of metoclopramide (2)

A

prokinetic drug:

  • suppresses emesis by blocking dopamine receptors
  • increases upper GI motility by enhancing the effects of Ach
70
Q

who can metoclopramide not be used in

A
  • bowel obstruction
  • perforation
  • GI hemorrhage
71
Q

list 3 common s/e of metoclorpramide

A
  • sedation
  • diarrhea (due to increased motility)
  • tardive dyskinesia (irrevresible twitching)
72
Q

what should be present prior to giving metoclorpramide

A
  • BS

NURS 2514 (75 decks)

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