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NSG 318 - Pharm > Topic 7 > Flashcards

Topic 7 Flashcards

1
Q

inflammation patho

A

protective response top tissue injury and infection
a vascular reactions occurs causing fluid, blood elements, leukocytes and chemical mediators (prostaglandins) to accumulate at the injured site

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2
Q

what do prostaglandins do?

A

help dilate blood vessels to get more blood flow

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3
Q

what are the inflammatory phases

A

vascular phase
delayed phase

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4
Q

vascular phase

A

occurs 10-15 minuses after injury
vasodilation and increased capillary permeability
fluid and blood substances move to injured site

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5
Q

delayed phase

A

leukocytes infiltrate the inflamed tissue

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6
Q

what does the cyclooxygenase (COX) gene do?

A

converts arachidonic acid into prostaglandins

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7
Q

what are the two forms of cyclooxygenase

A

COX-1 and COX-2

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8
Q

COX-1

A

protects stomach lining and regulates blood platelets

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9
Q

COX-2

A

triggers inflammation and pain

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10
Q

what are the cardinal signs of inflammation

A

redness
swelling (edema)
heat
pain
loss of function

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11
Q

what are the anti-inflammatory drug groups

A

non steroidal inflammatory drugs (NSAIDs)
coticosteroids
disease modifying anti rheumatic drugs (DMARDS)
antigout drugs

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12
Q

what are the action of NSAIDs

A

INHIBIT biosynthesis of prostaglandins
analgesic effects
antipyretic effects
inhibit platelet aggregation
mimic effect of corticosteroid but are not chemically similar
inhibit COX enzyme

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13
Q

analgesic effet

A

pain relief

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14
Q

antipyretic effect

A

reduces fever

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15
Q

inhibit platelet aggregation

A

inhibit clotting

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16
Q

what are the first generation NSAIDs

A

salicylate (aspirin)
parachlorobenzoic acid derivatives
phenylacetic acids
propionic acid derivatives (ibuprofen)
fenamates
oxicams
INHIBIT BOT COX 1&2

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17
Q

what are second generation NSAIDs

A

SELECTIVE COX 2 inhibitor

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18
Q

action of salicylates (aspirin)

A

antiinflammaroty, antiplatelet, antipyretic

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19
Q

what is the therapeutic aspirin (salicylate) level

A

15-30 mg/dL

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20
Q

what is the mild toxicity level of aspirin

A

greater than 30 mg/dL

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21
Q

what is the severe toxicity level of aspirin

A

greater than 50mg/dL

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22
Q

what is a MAJOR sign of toxicity for aspirin

A

TINNITUS

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23
Q

Reye’s syndrome

A

Syndrome which is an acute inflammation of the brain, N/V, confusion. Usually follows a viral illness & linked to intake of aspirin. Use acetaminophen (not aspirin) to reduce fever with child with a communicable disease (virus) to prevent this.

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24
Q

what is the most widely used NSAID

A

Ibuprofen

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25
Q

what is the max amount of ibuprofen that can be taken

A

3200 mg/day

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26
Q

ibuprofen has _____ GI distress but is also ______ protein bound

A

Lower
very high

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27
Q

what is the action of corticosteroid

A

control inflammation by suppressing for preventing ,any of the components of the inflammatory process at the injured site

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28
Q

What is the use of corticosteroids?

A

arthritic flare-up
BUT NOT the drug of choice for arthritis because of the NUMEROUS side effects

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29
Q

what is important about the discontinuation of corticosteroids

A

taper off over 5-10 days

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30
Q

what is important about taking NSAIDS before menses?

A

avoid NSAIDs 1-2 days before menses to avoid excessive bleeding

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31
Q

what are the types of Disease Modifying Antirheumatic drugs

A

immunosuppressive agents
immunomodulators
antimalarials

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32
Q

what is the use fro DMARDS

A

alleviate symptoms of RA when other treatments fail
osteoarthritis, ankylosing spondylitis
psoriatic arthritis, sever psoriasis
chrons and UC

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33
Q

action of immunosuppressive agents

A

suppress inflammatory process caused by the immune system

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34
Q

what is the use of immunosuppressive agents

A

refractory RA unresponsive to antiinfalmmaotry drugs

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35
Q

what are the classifications of immunodmodulators

A

interleukin I (IL-I) receptor antagonistst
Tumor necrosis factor (TNF)

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36
Q

what is the action of immunomodulators

A

disrupt inflammatory process
delayed disease progression
neutralize TNF

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37
Q

what is the use for immunomodulators

A

RA, psoriatic arthritis, psoriasis, spondylitis, UC, chrons

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38
Q

what is important about immunomodulators

A

puts the patient at increases risk for infection becausse it suppresses the immune system
no live vaccines

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39
Q

what is gout

A

inflammatory disease of joints tendons and other tissues

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40
Q

what is the patho of gout

A

caused by build up of uric acid crystals
usually occurs in the great toe
DEFECT in purine metabolism leads to uric acid accumulation

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41
Q

patients with gout should avoid which foods

A

foods containing purine (organ meats, sarsdines, salmon, gravy, herring, liver, meat soups, alcohol especially beer) avoid deli meat

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42
Q

what is the difference between colchicine and allopurinol

A

colchicine is an anti inflammatory drug for gout, but DOES NOT inhibit uric acid synthesis
allopurinol is NOT an anti inflammatory, but rather inhibits the final steps of uric acid biosynthesis, preventing the gout attack

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43
Q

when should colchicine NOT be given

A

when the patient has severe renal, cardiac, or GI issues

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44
Q

fifth vital sign

A

pain

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45
Q

pain threshold

A

amount of stimulation required before a person experiences the sensation of pain

46
Q

pain tolerance

A

the amount of pain a patient can endure without its interfering with normal function

47
Q

analgesics

A

pain relievers (opiod and non opioid)

48
Q

opioid

A

narcotic

49
Q

nonopioid

A

nonnarcotic

50
Q

Nociceptors

A

sensory receptors for pain

51
Q

neuropathic pain

A

unusual sensory disturbance that often involves neural super sensitivity, this pain is due to PNS or CNS injury ir disease
often burning, tingling, electric shock sensations

52
Q

gate-control theory

A

the theory is hat tissue injury activates nociceptors and causes release of chemical mediators such s substance P, prostaglandins, etc and these substances initiate an action potential along a sensory nerve fiber and sensitize pain receptors

53
Q

acute pain

A

pain that is felt suddenly from injury, disease, trauma, or surgery (less than 3 months)

54
Q

chronic pain

A

pain persists for more than 3 months and is difficult to treat or control

55
Q

cancer pain

A

pain occurs from pressure on nerves and organs, blockage to blood supply or metastasis to bone

56
Q

somatic pain

A

pain is in skeletal muscle ligaments and joints

57
Q

superficial pain

A

pain is from surface ares such s skin and mucous membranes

58
Q

vascular pain

A

pain occurs from vascular or perivascular tissues contributing to headaches or migraines

59
Q

visceral pain

A

pain is from smooth muscle and organs

60
Q

up to _____ of patients have unrelieved pain

A

75%

61
Q

reasons fro under-treatment of pain

A

pt. may not be able to explain pain
fear of addiction
nurses ability to measure pain/lack of regular pain assessment
unwillingness to believe pt. report of pain
inadequate pain dose

62
Q

effects of under-treatment of pain

A

increases in RR and HR
hypertension
increased stress response
urinary retention, fluid overload, electrolyte imbalance
glucose intolerance, hyperglycemia, pneumonia
atelectasis, anorexia, paralytic ileus
constipation, weakness, confusion, infection

63
Q

use of nonopiod analgesics

A

less potent than opiod analgesics
use for mild to moderate pain (dull throbbing pain of HA, dysmenorrhea, inflammation, muscluar aches, ect)

64
Q

action site of nonopiod analgesics

A

PNS at pain receptors sites

65
Q

what is used for assessment of pain

A

pain scale

66
Q

what are the types of NSAIDs

A

aspirin (salicylate)
ibuprofen (Motrin)
indomethacin (indocin)
ketotolac (Toradol)

67
Q

effects of NSAIDs

A

analgesic
antipyretic
anti-inflammatory

68
Q

use of opioid analgesics

A

moderate to severe pain

69
Q

many opioids have _______ effects

A

antidiarrheal
(induce constipation)

70
Q

many opioids have _______ effects

A

antidiarrheal
(induce constipation)

71
Q

Action of Opioid Analgesics

A

acts on CNS to suppress pain impulses
suppress respiration and coughing by acting on respiratory and cough centers in the medulla

72
Q

contraindications of opioid analgesics

A

head injury, respiratory disorders, hypotension

73
Q

disposal of fentanyl patch

A

in locked box

74
Q

use of fentanyl

A

moderate to severe pain, anesthesia induction and maintenance

75
Q

Fentanyl is ____ times more potent than morphine, and has longer duration

A

100

76
Q

Fentanyl is available as:

A

transdermal patchy IM IV

77
Q

what is a major concern of opioids

A

withdrawal and dependence

78
Q

use for hydromorphone (Dilaudid)

A

moderate to severe pain

79
Q

hydromorphone is ___ more potent than morphine and has ___ onset and ___ duration

A

6x
faster
shorter

80
Q

hydromorphone is available as

A

PO, rectal, SQ, IM, IV

81
Q

oxycodone use

A

moderate to severe pain

82
Q

oxycodone is ____ stronger than morphine and can be used when morphone does not provide relief

A

1.5-2x

83
Q

oxycodone should be taken w food to..

A

avoid GI distress

84
Q

what is important about the discontinuation of oxycodone

A

DO NOT stop abruptly , taper off

85
Q

Percocet

A

oxycodone+acetaminophen

86
Q

Percocet use

A

moderate to severe pain, take w food

87
Q

what CAMS should not be taken with opioids and what do they do

A

kava kava, valerian and st johns wort increase sedation
st johns wort can also decrease effects of morphine

88
Q

what is patient controlled analgesia (PCA)

A

Method of drug delivery that permits the client to self-administer opioids on an “As needed basis”.

PCA device has a timing control, limits the total dose that can be administered each hour.

**Patient controlled, NOT FAMILY!!

89
Q

what medication is most often used for PCA

A

morphine
(sometimes fentanyl and hydromorphone)

90
Q

PCA loading dose

A

predetermines safety limits

91
Q

PCA lockouts mechanism

A

near-constant analgesic level

92
Q

transdermal route

A

provide continuous pain control, helpful for chronic pain

93
Q

Analgesics in children

A

use “ouch scale”
give meds before pain becomes severe
oral liquid medication is generally more acceptable
use drawings or pictures related to area of pain with smiling faces

94
Q

analgesics in older adults

A

require dosage adjustments to avoid sever side effects
nurse must monitor pt. closely
tend to have fears about opioids as they think pain is inevitable or fear of addiction
don’t want to report pain in fear of being an burden

95
Q

analgesics in cognitively impaired

A

may be unable to adequately report pain
physical signs of pain may be moaning, grimacing clenched teeth, noisy respirations restlessness

96
Q

analgesics in oncology patient

A

pain is managed my WHO ladder
step1- mild pain (Nonopioids)
step2- moderate pain (nonopioid and mils opioids)
step3- severe pain (stronger opioids)
opioids are titrated until pain relief is achieved

97
Q

analgesics in individuals w substance abuse HX

A

still require pain meds, shouldn’t be denied pain control
larger dosing may be requires
opioid agonist-antagonists should be avoided as I can cause withdrawal syndrome

98
Q

adjuvant therapy

A

used alongside with nonopioid and opioid analgesics; not direct pain meds, but aid in relieving pain and assisting primary tx

99
Q

adjuvant analgesics

A

effective for pain relief in neuropathy
ex: anticonvulsants, antidepressants, corticosteroids, antidysrhythmics, local anesthetics

100
Q

Opioid agonist-antagonist

A

opioid antagontist is added to an opioid agonist (may help decrease opioid abuse)
-NOT given for cancer pain
-safe for use during labor
-safety during early pregnancy has not been established

101
Q

action of opioid antagonists

A

blocks receptor and displaces opioid

102
Q

Uses for opioid antagonists

A

antidote for opiate overdose
reverse effects of opiates including respiratory depression, sedation, hypotension

103
Q

side/adverse effects of opioid antagonist

A

reversal of analgesis
agitation, GI effects
hypo/hypertension, tachycardia
elevated PTT, bleeding

104
Q

nursing implications of opioid antagonist

A

monitor VS (especially BP) and bleeding continuously

105
Q

characteristics of a migraine HA

A

unilateral throbbing pain
N/V photophobia

106
Q

triggers of migraine headaches

A

cheese chocolate, red wine, aspartame, fatigue,stress, monosodium glutamate, missed meals, odors, light hormone, changes, drugs, weather, toomuch/little sleep

107
Q

patho theory for migraine HA

A

due to neurovascular events in cerebral cortex

108
Q

characteristics of cluster HA

A

severe unilateral, nonthrobbing pain
usually located around the eye
occur in a series of cluster attacks (one or more attacks every day for several weeks)
NOT associated with an aura
DOES NOT cause N/V
more common in males

109
Q

what can be used in the prevention of migraine and cluster HA

A

beta-adrenergic blockers (propranolol, atenolol)
anticonvulsants (valproic acid, gabapentin)
tricyclic antidepressants (amitryptline, imipramine)

110
Q

management of migriane and cluster HA

A

analgesics (aspirin w caffeine, acetaminophen, NSAIDS, ibuprofen, naproxen)
opioid analgesics (meperidine, butorphanol nasal spray)
ergot alkaloids (dihydroerotamine mesylate)
selestive serotonin receptor agonist (sumatriptan, zolmitriptan)

NSG 318 - Pharm (11 decks)

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