pharm exam 3 pt 1

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Last updated 5:01 PM on 4/8/26
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148 Terms

1
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Is acetaminophen appropriate for rhematoid arthiritis flare why or why not

no it is not good for inflammation

2
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what is inflamamtion

reaction to tissue injury to neutralize harmful agents

3
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what is prostoglandins

cause vadodilation anf sensitixe nerve cells to pain

4
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what is cyclooxygenase enzyme (cox)

converts arachidonic acid into prostoglandins

the reason we get pain and inflammation

5
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function of cox 1

produces prostaglandins that protect gastric lining and help with renal blood flow and regulated platelets

found in many tissues

mild/moderate pain, fever, inflammation

usually for arthritis or musculoskeletal injury

produces prostaglandins that protect gastric lining and help with renal blood flow

6
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function of cox 2

trigger inflammation and pain at the injury site

7
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5 signs of inflmaation

redness

swelling

heat

pain

loss of function

8
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Inflammation is __ as infections

Example of non infectious cause of inflammationa noninfectious

not the same as

trauma, surgery , heat or cold

9
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2 key cns substances that modulate pain

serotonin and norepinephrine

10
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acetamionophen BLANK (IS OR IS NOT) an NSAID so BLANK IS OR IS NOT appropriate for treating inflammation

IS NOT

NOT

11
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mechanism for acetaminophen

inhibit prostaglandin synthesis, which decreases pain sensation

12
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max adult dose of acetaminophen

4g/day

13
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max adult dose of acetaminophen for alchol users

2 g/day

14
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antidote for acetaminophen overdose

NAC (N-acetylcysteine)

15
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early sign of acetaminophen toxicity

nasuea vomiting diarrhea abdominal pain

16
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Is acetaminophen appropriate for fever why or why not

yes

It acts directly on thermoregulatory cells in hypothalamus to cause sweating and vasodilation. This causes release of heat and lowers fever.

17
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Is acetaminophen appropriate for mild post op pain why or why not

yes it is good for moderate pain

18
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Is acetaminophen appropriate for osteoarthiritis pain why or why not

yes it is appropriate for pain - if NSAID not available

19
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what generation is apsirin (asa) and its drug class/subtype

first generation

NSAID

Salycilic acid

20
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what generation is ibuprofen (advil.motrin) and its drug class/subtype

first generation

what generation is ibuprofen (advil.motrin) and its drug class/subtype

Propionic acid

21
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what generation is naproxen (Naprosyn) and its drug class/subtype

First generation

NSAID

22
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what generation is indomethacin (indocin) and its drug class/subtype

first generation

NSAID

Acetic acid

23
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what generation is meloxicam (mobic) and its drug class/subtype

1st generation

NSAID

24
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what generation is celecoxib (celebrex)) and its drug class/subtype

second generation

NSAID

25
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clincial trade off between cox 1 and cox 2 inhibition

Cox-1 protects against pain and inflammation but lose stomach lining protection, leading to ulcers.

cox 2- cardiovascular events but proetecting stomach lining protecting

26
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why do first-gen NSAIDs cause GI upset and ulcers with chronic use? Be specific about what enzyme is used

COX-1 produces a prostaglandin that protects stomach lining. When this is inhibited, ulcers can form.

Inhibits COX-1 and COX-2.

27
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cox enxyme inhibited in aspirin

irreversibly inhibit COX-2 and COX-2

28
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affects of aspirin

anti-inflammatory , antiplatelet analgesic, antipyretic

29
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do not give aspirin to children with viral illness because

can lead to Reye's syndrome, which is swelling of the liver and brain, leading to neurological impact.

30
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avoid aspirin during 3rd semester because

risk of premature closing of ductus arteriosus of the fetus

31
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Salicylism: toxicity sign of apsirin

tinnitus vertigo acidosis vomit diarrhea nausea confusion fatigue (lassitude)

32
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concurrent nsaid use concern of aspirin

Tinnitus, GI bleeding, renal impairment, hypersensitivity

33
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mechanism of ibuprofen

Inhibit COX-1 and COX-2 enzymes by blocking arachidonate binding.

34
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key side effects ibuprifen

CNS— drowsy, dizzy, headachey, confused, insomnia, blurred-vision, tinnitus, and edematous state

GI-gi upset ulcer bleeding

35
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timing rule between apirin anf ibuprofen

take ibuprofen 8 hours before or 30 minutes after aspirin.

36
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dangeorus combo of ibuprofen and warfarin is

increase bleeding risk

37
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avoid combing inuprofen with BLANK inhibitors and dieuretics in patients with BLANK dyscfunction

ACE INHIBITORS

renal

can reduce efficacy in ACE inhibitors and have renal risk

38
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what makes oxicams better suited for chronic inflammatory conditions than other first-generation NSAIDs?

they have a long half-life, meaning they can be taken once a day and have less GI upset.

39
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2 important drug interactions with oxicams

reduce effectiveness of a lot of BP medicine—causing sodium and water retention.

ACE inhibitor, beta-blocker, diuretic, ARB—reduce efficacy and renal risk

lithium and methotrexate (psychiatric medicine)—reduces clearance, causing buildup

SSRI/SSNRI - increased bleeding risk

Cyclosporine-kidney issues

Corticosteroids: GI risk, bleeding, and stomach ulcer

40
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2 drug interactions specific to celecoxib nurse must monitor

Fluconazole increases celecoxib levels—it inhibits the body's ability to eliminate celecoxib.

corticosteroid - increased GI side effects

Lithium toxicity in blood

SSRI and SNRIs increase gi bleeding

Warfarin—increase bleeding risk

NSAIDs and aspirin—GI ulcer and bleeding risk

41
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cox enzyme inhibited in first gen NSAIDS

cox 1 and cox 2

42
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cox enzyme inhibited in celecoxib (celebrix)

selectively inhibit only COX-2

43
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gi ulcer/bleed risk in first gen NSAIDS

yes because protective stomach lining is inhibited

44
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gi ulcer/bleed risk in celecoxib (celebrex)

No because stomach lining is protected; COX-2 is NOT inhibited.

45
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antiplatelet effect in first gen NSAIDS

exert an antiplatelet effect by inhibiting platelet aggregation

46
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antiplatelet effect in celecoxib (celebrex)

No antiplatelet effect because cox 1 is not inhibited

47
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cardiovascular risk of first gen NSAIDS

none

48
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cardiovascular risk of celexoib (celebrix)

increase risk because it is a selective COX-2 inhibitor

49
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best patient candidate for first gen NSAIDS

rheumatoid arthritis

mild to moderate pain

osteoarthritis

fever reduction

primary dysmenorrhea

50
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best patient candidate for celecoxib (celebrix)

patient with severe arthritis that needs high dose of anti-inflammatory or history of GI bleed

PROTECT GASTRIC AND LESS GI BLEEDING

51
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TNF blockers work by

are biologic

bind to cytokines that initiate proinflammatory activities

SLOWS THE INFLAMMATORY RESPONSE AND DAMAGE ; DOES NOT STOP

52
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3 indications of DMARDS

Rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis (spine inflammation), Crohn's disease, ulcerative colitis, plaque psoriasis

53
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3 contraindications of DMARDS

active infection, cancer, sepsis, TB, hepatitis, myelosuppression, demyelinating disorders, BC DMARD BLOCKS BODY’S IMMUNE RESPONSE

ALSO renal and hepatic dirosde heart failure, and latex allergies

54
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should patients on DMARDS recieve live vaccines why or why not

no

immune system is weak to fight virus

55
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Nurses' priority assessment before administering a tnf blocker

Evaluate for active infection and screening for TB

56
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why must corticosteroids not be stopped abruptly. what is the correct discontinuation approach?

taper off over 5-10 days

If not, it can cause withdrawal syndrome—the adrenal gland produces steroids; if you take oral steroids and abruptly stop, you can cause fatigue, body weakness, and aches

57
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a patient using corticosteroids for asthma develops white patches in their mouth. what is this called and how is it prevented

thrush

Rinse your mouth with water.

58
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Allopurinol and azathioprine are a dangerous combo. why and what should the nurse do

inhibits xanthine oxidase enzyme, which breaks down azathioprine, leading to toxic accumulation (decreased urine output)

increase fluid intake

59
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a pateint is started on allopurinol. what lifstyle or fluid modification should the nurse teach and why

increase fluid intake to promote diuresis (production of urine).

60
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what is pain threshold

level of stimulus needed to create painful sensation

61
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what is pain tolerance

amount of pain able to endure without interfering with normal function

62
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what is nociceptors

Sensory receptors activated by noxious stimuli

63
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what is neuropathic pain, the sensation and quality

pain due to injury of the PNS or CNS

very sensitive—burning, tingling, shocking feeling *involuntary and aggressive

64
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what is opioid mu receptors, where are they found and what do they regulate

Responses to naturally occurring peptides (chemical) endorphins and enkephalins in the CNS

CNS (brain stem)

Suppress paon impulses, respiration, and cough.

A lot of mu receptors mean reduced pain sensitivity (high pain threshold).

vary in each person.

65
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Serotonin and norepinephrine modulate pain, which is why some BLANK medications can be used as adjunctive pain treatment.

antidepressants

66
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4 classic side effects of all opiod agonists

neurological and sensory effect

cardiovascular and integumentary

affect multiple body systems—life-threatening

gi effects

67
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highest prioirty adverse effect to monitor in opioid

Respiratory depression: *monitor respirations and o2 sats*

, euphoria, sedation, analgesia

68
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fastest route to theraputic levevl in opioid

IV

69
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route with most variable absorption in opioid

IM and SUBQ - females have higher fat content.

70
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opioid is metabolized in BLNAK and excreted in BLANK

liver

urine

71
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start a BLANK regimen BLANK (BEFORE OR AFTE OR WHEN) starting opioid therapy

bowel

when

72
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3 patient conditions that need caution with opioids

respiratory dysfunction—asthma, emphysema—makes respiratory depression worse.

recent GI/GU surgery, ibd, acute abdomen—exacerbate pain

CNS issues—head injury, CVD, tremors, alcohol use—confusion and hallucinations

liver or renal dysfunction

Pregnancy or lactation withdrawal syndrome for the fetus

allergy

diarrhea from toxins

GI obstruction—sphincter of ofi spasm risk—causes pain, n/v/d

73
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hydromorphone is BLANK times more potent than morphine. why deos this matter for nursing practice

six

drug error can be fatal

74
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what is wooden chest syndrome and which opioid carries the risk and how is it prevented?,

muscle tone is chest and abdomen increasing, leading to hypoxia and hypercarbia (CO₂).

fentanyl

do iv push slowly

75
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what toxic metabolite does meperidine produce, and what nuerological symptoms does it cause

norperidrine

causes nervousness agitation irritability tremors seizures

76
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What is loading dose in a PCA?

initial dose to rapidly get pt to a certain level

77
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what is demand dose in a pca

specific amount of medicine delivered when patient presses button

78
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what is lockout interval in a pca

certain time, the pump must wait to deliver another dose of medicine after pressing the button.

prevent overdose

79
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what is basal (continous) infusion in a pca

continuous amount of medicine delivered whether patient presses button or not

80
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what is a hourly maximum of pca

1-hour limit") safety setting in the pump that limits the total amount of opioid a patient can receive, including both demand doses and any continuous background infusio

81
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who presses pca button

patient only

82
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3 patients not appropriate for pca

patients unable to understand or physically operate the device,

those at high risk for opioid-induced respiratory depression,

patients with significant cognitive impairment

83
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prioitrty monitoring paramter for pca

respiratory status and o2 sats

84
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what scale is used to detect over sedation of pca before repsiratoy depression occurs

sedation scale

85
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basal infusion of pca is avoided in who

opioid-naïve patients

to prevent over-sedation and respiratory depression

obstructive sleep apnea (OSA), obesity, renal or hepatic impairment, and

the elderly due to elevated risks of toxicity

86
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a patient recieves naloxcone for opioid overdose and becomes responsive. why must the nurse continue close monitoring after naloxcone adminitration

Is short acting only last 30-90 minutes

could re overdose as it wears off

87
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how long must a patient be opioid free before starting naltextrone. what happens if it is given too soon

7-10 days

avoid severe precipitated withdrawal.

88
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why should triptans and ergot alkaloids never be combined

both cause cranial constriction and can excess constriction, leading to cardiovascular risk.

89
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which triptans are approved fro pediatric age and what age

rizatriptan- age 6 and up

almotriptan- adolescant

90
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why are ergot alkoloids and triptans contrainidcated in pregnancy

can cross the placenta and breastmilk

Vasoconstriction leads to miscarriage or premature birth.

91
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when is the best time to take migraine medicine and why

soon as symptoms begin

to control symptoms before they worsen

92
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A post-op patient on IV morphine develops rep rate of 8 and O₂ sat of 89 and is minimally responsive. What are 4 nursing action in order?

Stop the IV Morphine/PCA Pump Immediately:

Attempt to Stimulate/Arouse the Patient:

Administer Oxygen:

Administer Naloxone (Narcan) as Prescribed:

93
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Compare colchicine and allopurinol, which is used during an acute gout attack , what are the sceanrios

colchicine

alleviate symptoms by inhibiting leukocyte migration

does not inhibit uric acid production or improve excretion

94
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Compare colchicine and allopurinol and which is used for prevention. What are the scenarios?

allopurinol

increase uric acid excretion, decrease uric acid production.

95
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is the side effect hyperglycemia long term or short term for corticosteroids and what is the nursing impliction

short-term

can give insulin

monitor if diabetic

96
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is the side effects of osteoporosis long-term or short-term for corticosteroids and what is the nursing implication?

short-term

Increase break risk up to 20 % bone loss in 6 months espeically eomen , especially for women.

screen bone density

97
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is the side effect moon face/weight gain long term or short term for corticosteroids and what is the nursing impliction

short term - fluid retention and fat deposits

Monitor weight and sodium intake.

98
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is the side effect adrenal suppression long term or short term for corticosteroids and what is the nursing impliction

long term

Less natural steroid production

withdrawal can happen with an abrupt stop.

taper off over 5-10 days

99
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is the side effect increased infection risk long term or short term for corticosteroids and what is the nursing impliction

Short-term- suppression of the immune system leading to pathogen vulnerability

monitor for infectuiobn sign

100
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is the side effect cataracts/glaucoma long term or short term for corticosteroids and what is the nursing impliction

short term—fromp increased eye pressure

assess vision changes