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NURS 3510 - Supportive and Palliative Care > Week 10 > Flashcards

Week 10 Flashcards

1
Q

what are some impacts of nausea and vomiting (8)

A
  • dehydration & hypovolemia
  • electrolyte abnormalities
  • esophageal tears/bleeds (d/t straining w retching)
  • decreased QOL
  • weight loss/anorexia
  • psychological distress
  • refusal of beneficial therapy (ex. chemo)
  • risk of aspiration pneumonia (d/t weakness, decreased gag reflex at end of life)
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2
Q

where does the emetic center receive info from (4)

A
  • the chemoreceptor trigger zone (CTZ)
  • the vestibular system
  • the CNS
  • the vagal and enteric nervous system = GI system
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3
Q

chemical disturbances impact what area?

A
  • the CTZ
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4
Q

what receptors are activated in the CTZ by chemical disturbances (2)

A
  • dopamine (D2)

- serotonin (5HT3)

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5
Q

what are some examples of stimuli that trigger NV at the CTZ (3)

A
  • opioids
  • electrolyte disorders
  • hypercalcemia
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6
Q

what are 3 meds of choice if the receptor impacted in the CTZ is dopamine (3)

A
  • stemitil
  • haldol
  • maxeran (low dose)
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7
Q

what are 2 meds of choice if the receptor impacted in the CTZ is serotonin

A
  • maxeran (high dose)

- ondansetron

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8
Q

what area is impacted in NV center by visceral disturbances

A
  • abdominal organs/gut
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9
Q

what receptors are activated w visceral disturbances (2)

A
  • dopamine (D2)
  • serotonin (5HT3)

meds = same as CTZ

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10
Q

what area is affected in NV center by vestibular disturbances

A
  • vestibular nuclei
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11
Q

what receptors are activated in vestibular nuclei (2)

A
  • histamine (H1)

- muscarinic (M)

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12
Q

NV caused by vestibular disturbances may be seen in pts with…

A

acoustic neuroma (ear tumour)

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13
Q

what are 2 meds of choice for histamine receptors

A
  • gravol

- phenergan

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14
Q

what is a med of choice if the receptor if muscarinic

A
  • scopolamine
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15
Q

what area is affected w NV caused by CNS disturbances

A

cerebral cortex

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16
Q

what receptor is activated in the cerebral cortex w CNS disturbances

A
  • histamine (H1)

* same meds as before*

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17
Q

what are the 2 principles of therapy for NV

A
  • identify the underlying cause

- antiemetic use

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18
Q

what are some principles regarding antiemetic therapy (5)

A
  • anticipate need
  • use adequate, regular doses
  • aim at receptor involved
  • combos if necessary
  • anticipate need for alternate routes (ex. enviro measures)
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19
Q

what are some environmental measures that can help w NV (7)

A
  • limit exposure to food smells
  • bland foods
  • small, freq meals/snacks
  • good oral hygiene
  • fresh air
  • calming enviro
  • sitting upright post meal
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20
Q

what should you consider if the NV continues

A
  • reassess
  • all causes identified?
  • correct med used?
  • adequate dosing?
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21
Q

true or false: chemical disturbances affect emetic receptors in the CTZ

A

true

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22
Q

true or false: there are muscarinic receptors in the CTZ

A

false

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23
Q

T or F: the med Stemitil blocks emetic stimuli that trigger dopamine receptors

A

true

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24
Q

T or F: the med Ondansetron blocks emetic stimuli that trigger serotonin receptors

A

T

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25
Q

T or F: the med Phenergan blocks emetic stimuli that trigger histamine receptors

A

T

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26
Q

T or F: there are serotonin receptors in the inner ear

A

false

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27
Q

T or F: there are histamine receptors in the abdominal oragans and gut

A

False

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28
Q

T or F: there are histamine receptors in the cerebral cortex

A

true

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29
Q

what is CACS

A
  • cancer anorexia cachexia syndrome

- cluster of symptoms

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30
Q

what symptoms are included w CACS (5)

A
  • cachexia
  • anorexia
  • early satiety
  • chronic nausea
  • asthenia
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31
Q

what is anorexia

A
  • “without appetite”

- not a willful choice, simply no desire to eat at all

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32
Q

what is cachexia

A
  • “bad condition”
  • “wasting” disorder that causes extreme weight loss and muscle wasting
  • wasting of lean muscle & adipose tissue
33
Q

cachexia is a …

A
  • symptom of disease progression

- occurs on a continuum

34
Q

what is defined as pre-cachexia (3)

A
  • weight loss < or equal to 5%
  • anorexia
  • metabolic change
35
Q

what is defined as cachexia (5)

A
  • weight loss >5%
  • or BMI < 20 kg/m2 and weight loss >2%
  • or sacropenia (breakdown of lean muscle mass) and weight loss >2%
  • reduced food intake
  • systemic inflammation
36
Q

what is refractory cachexia (5)

A
  • variable degree of cachexia
  • applies to individuals w cancer
  • cancer disease both procatabolic & not responsive to anticancer treatment
  • low performance score
  • <3 month expected survival
37
Q

what is meant by low performance score w refractory cachexia

A
  • independence
  • mobility
  • ability to ADLs

all massively decreased

38
Q

what is early satiety

A
  • feeling full quickly when eating (ex. after a couple bites)
39
Q

what is the cause of early satiety

A
  • delayed gastric emptying (meals can sit in stomach for 8-12 hr)
40
Q

what is asthenia

A
  • extreme muscle weakness and lack of energy

- unusual fatigue without or before any effort

41
Q

what can impact the amt of weight lost in pts w cancer

A
  • tumour site

ex. pancreas & gastric = higher % incidence than breast

42
Q

CACS can also be seen in pts w:

A
  • end stage COPD & HF

- other chronic illnesses

43
Q

the amt of weight loss associated w CACS depends on

A
  • location of the tumour

ex. pancreas, gastric, esophagus, and head & neck cause more than breast cancer

44
Q

describe the mechanisms that cause CACS

A

cancer —-> tumour products & endocrine alterations & systemic inflammatory response (cytokines) —> metabolic abnormalitiess (body cannot use carbs, fat, proteins in food properly) —> lipolysis & protein loss & anorexia —> cachexia

45
Q

describe the relationship between anorexia & metabolic alterations

A
  • anorexia, lipolysis, protein loss, & cachexia = result of metabolic alterations
  • anorexia is not the cause of weight loss and cachexia
    = eating more does not cause less weight loss bc the body cannot use the nutrients properly d/t metabolic abnormalities
46
Q

describe the effectiveness of nutritional and pharmacological interventions (ex. TPN, tube feeds, IV therapy) to manage CACS

A
  • it is intuitive for people push more food on pts experiencing anorexia & weight loss in order to prevent weight loss but since it is due to metabolic disturbances (and not anorexia), it is not an effective intervention since the body cannot use the nutrients properly
  • may actually be more harmful
  • parental nutrition = net harm
  • voluntary supplements = no effect on mortality
47
Q

what are risks associated w TPN (3)

A

increased risk of:

  • thrombus
  • infection
  • increased BG
48
Q

what are risks associated w tube feeds (2)

A
  • chronic nausea

- diarrhea

49
Q

at what point might nutritional interventions be helpful for pts w cancer

A
  • only w early stage tumors where the issue is not CACS, but an inability to swallow
  • otherwise cause more harm than good
50
Q

what investigational interventions may be used for the increased lvls of proinflammatory cytokines associated w tumour-host interaction? (4)

A
  • thalidomide
  • interleukin inhibitors
  • NSAIDs
  • fish oils
51
Q

what investigational interventions may be used for the poor appetite d/t tumour host interactions?

A
  • ghrelin
  • ghrelin mimetic

= increased cals. ingested, increased hunger

52
Q

what investigational interventions may be used for the endocrine dysfunction associated w tumour-host interaction? (2)

A
  • androgens

- androgen receptor modulators

53
Q

what investigational interventions may be used for the elevated resting energy expenditure d/t tumour-host interactions?

A
  • beta blockers
54
Q

what evidence-based intervention may be used for the poor appetite d/t tumour-host interactions? (2)

A
  • corticosteroids

- megestrol acetate

55
Q

what impact does corticosteroids have on a pt w CACS (3)

A
  • increase appetite
  • cause weight gain –> not lean muscle mass tho, gain of fat & water retention
  • effects only last a couple weeks
56
Q

what impact does megestrol acetate have on a pt w CACS (2)

A
  • increase appetite

- weight gain (not of lean muscle tho)

57
Q

what general interventions can be used for a pt w CACS (especially early on) (3)

A
  • low intensity exercise
  • nutrition counseling (ex. small, freq meals)
  • control of nutritional impact systems (pain, NV, xerostomia, mouth lesions)
58
Q

cachexia impacts… (3)

A
  • function & strength
  • survival
  • sense of self
59
Q

what medication can help with early satiety & chronic nausea

A
  • metoclopramide (maxeran)
60
Q

describe the impacts of CACS (8)

A
  • loss of body image
  • weight loss experience = psychological harm
  • sense of imminent death
  • family distress as loved one becomes a “skeleton”
  • fatigue
  • pain
  • depression & anxiety
  • taste and/or smell changes
61
Q

provide an example of how you would respond if a family member said “i am rlly afraid if my brother doesn’t eat, that he is not going to get better” (6)

A
  • do not say appetite will come back
  • listen & acknowledge emotion being expressed
  • assess understanding of condition
  • do not say he will die whether he eats or not
  • explore what they have been told
  • not eating is one of the many facets of the dying process and not the cause
62
Q

describe how to respond to “you are starving my father to death, do something” (5)

A
  • do not be reactive ; understand they’re in distress
  • don’t be defensive
  • take step back and acknowledge emotion: “you sound very angry”
  • check understanding of condition
  • explore what “doing something” looks like to them
63
Q

describe the continuum of encouragement

A
  • illustrates how the family may respond to anorexia

- gentle coaxing –> haranguing and harassing –> force-feeding

64
Q

what are the 3 behaviors of family members in relation to the pt nearing EOL ? what are these 3 behaviors aims at?

A
  • fighting back
  • waffling
  • letting nature take its course

= aimed at reducing the potential for future regret, family is afraid that their action or inaction could increase suffering & respond to these fears

65
Q

describe the behavior of “fighting back” by the family

A
  • behaviors in which the family engage in to try to fight or reduce the natural progression of disease
66
Q

describe the behavior of “letting nature take its course” by the family

A
  • includes the family trying to understand disease progression
  • try to help in areas which are beneficial (ex. comfort areas)
67
Q

describe the behavior of waffling by the family

A
  • includes going between the behavior of “fighting back” and “letting nature take its course”
68
Q

describe how to approach decisions where the considered treatments and their goals are achievable & possible (3)

A
  • review hopes & goals of treatment
  • expected course with and without the treatment
  • potential burdens and benefits
69
Q

describe how to approach decisions where the considered treatments and their goals are impossible (3)

A
  • discuss, but do not present as an option only to be withdrawn as such when asked for
  • rather, explain why this will not be pursued or attempted
  • “you might be wondering why we can’t just…”
70
Q

provide an example of how to respond to the goal of getting a patient to eat more calories so they don’t lose weight (4)

A
  • goal = not achievable
  • dont say “we could start tube feedings”
  • say “unfortunately, something like tube feedings isn’t an option for this pt because the pt isn’t processing calories which we give them”
  • “you might be wondering why we can’t offer ____”
71
Q

T or F: promotility agents may stimulate GI peristalsis and reduce early satiety

A

T

72
Q

T or F: metoclopramide is an example of a promotility agent

A

T

73
Q

T or F: a pt taking metoclopramide may be at risk for thromboembolic complications

A

T

74
Q

T or F: corticosteroid medication increases muscle mass in pts w CACS

A

F –> increases adipose and water weight briefly but will wear away

75
Q

primary anorexia and cachexia is a result of: (3)

A
  • complex metabolic abnormalities resulting in muscle wasting and loss of fat
  • neuroendocrine alterations resulting in loss of appetite, early satiety and chronic nausea
  • metabolic modifications resulting in decreased muscle building and asthenia
76
Q

decreased oral intake can be due to: (3)

A
  • stomatitis
  • dysphagia
  • social or financial concerns
77
Q

T or F: CACS is a hypocatabolic state

A

F –> hypercatabolism

78
Q

T or F: cachexia is defined as a lack of appetite

A

F –> lack of appetite = anorexia

79
Q

T or F: asthemia is defined as catabolism of skeletal muscle

A
  • F –> definition = profound weakness in absence of exertion

NURS 3510 - Supportive and Palliative Care (11 decks)

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