ch 16 anti-inflammatory drugs Flashcards

1
Q

salicylates

A

used in managing conditions from headache to MI

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2
Q

NSAIDs

A

used primarily as anti-inflammatory drugs but are also used as analgesic

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3
Q

acetylsalicylic acid (aspirin) indications

A

mild to moderate pain
fever
prevents platelet aggregation

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4
Q

acetylsalicylic acid (aspirin) pharmacokinetics

A

absorbed in stomach/small intestine

highly protein bound

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5
Q

acetylsalicylic acid (aspirin) pharmacodynamics

A

fever: inhibits PGE2 synthesis in hypothalamus
inflammation: peripheral inhibition of prostaglandin
antiplatelet: irreversible inhibition of thromboxane A2

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6
Q

acetylsalicylic acid (aspirin) contraindications

A
hypersensitivity
peptic ulcer disease
bleeding disorders
"children with illness"
last trimester of pregnancy
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7
Q

acetylsalicylic acid (aspirin) adverse effects

A
renal failure
abnormal bleeding
GI upset
drowsiness
confusion
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8
Q

acetylsalicylic acid (aspirin) interactions

A

coumadin/heparin (may icnrease r/o bleeding)
beta blockers (may decrease antihypertensive effect)
anti-diabetic drugs (may increase hypoglycemic effect)
corticosteroids (may decrease aspirin effects)
other drugs that are highly protein bound

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9
Q

acetylsalicylic acid (aspirin) nursing dx

A

acute or chronic pain r/t ineffectiveness of aspirin

risk for injury (GI bleed, hepatic/renal toxicity) r/t drug therapy

disturbed sensory perception r/t blurred vision or tinnitus

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10
Q

acetylsalicylic acid (aspirin) interventions

A

max therapeutic effects: give with milk/food to avoid GI upset, use uncoated aspirin for cardiac, use coated aspirin in stomach ulcer pts

min adverse effects: stop drug 5-7 days before elective surgery to allow time for production and release of new platelets

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11
Q

acetylsalicylic acid (aspirin) assessments

A

during prolonged therapy: assess hematocrit, Hb level, PT, INR, renal function

monitor for tinnitus

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12
Q

acetylsalicylic acid (aspirin) pt education

A

do not crush enteric coated tabs
discard if strong vinegar odor
ibuprofen may decrease low dose aspirin therapy effects

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13
Q

aspirin is contraindicated in

A

children with varicella

can cause Reye syndrome (rapid worsening brain disease with flu-like symptoms, vomiting, seizures)

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14
Q

NSAIDs

A

inhibit COX and prostaglandin synthesis

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15
Q

NSAID black box warning

A

may increase risk of MI or stroke
may cause GI bleed
may cause aseptic meningitis

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16
Q

ibuprofen indications

A
arthritis
mild to moderate pain
dysmenorrhea
migraine
fever
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17
Q

ibuprofen pharmacokinetics

A

absorbed from GI
peak 1-2 hrs
highly protein bound

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18
Q

ibuprofen pharmacodynamics

A

inhibited synthesis or release of prostaglandins

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19
Q

ibuprofen contraindications

A

GI disease

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20
Q

ibuprofen adverse effects

A
GI upset/bleeding
hepatotoxicity, acute renal failure
increased risk of CVA/MI
fluid/electrolyte imbalances
skin rash
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21
Q

ibuprofen interactions

A

digoxin (increase risk of dig toxicity)
blood thinners (increased risk for bleeding)
cyclosporine (nephrotoxicity)

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22
Q

ibuprofen nursing dx

A

acute/chronic pain r/t ineffectiveness of ibuprofen therapy

increased risk for injury r/t incorrect self admin OR drug induced GI bleeding OR hepatic/renal toxicity

ineffective protection r/t blood dyscrasias

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23
Q

ibuprofen interventions

A

max therapeutic effect: give with food or milk to decrease GI distress

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24
Q

ibuprofen pt education

A

medication has CV risk
monitor BP; drug can cause HTN
avoid alcohol use
avoid excessive exposure to sunlight and wear sunscreen

25
Q

ibuprofen nursing interventions

A

monitor renal/hepatic function
(BUN, Cr, liver enzymes, Hg, Hct)
monitor and report vision changes in pt

26
Q

para-aminophenol derivatives

A

analgesic/antipyretic

prototype acetaminophen

27
Q

acetaminophen indications

A

fever

mild pain

28
Q

acetaminophen pharmacokinetics

A

given PO, absorbed GI
peak 60 min
half life 1-3.5 hrs

29
Q

acetaminophen action

A

primarily centrally acting

inhibits prostaglandin synthesis in CNS

30
Q

acetaminophen contraindications

A

hepatic disease
viral hepatitis
alcoholism
warfarin/heparin

31
Q

acetaminophen adverse effects

A

overdose can be fatal

hypoxia, dyspnea, atelectasis, pleural effusion, pulmonary edema, stridor

32
Q

acetaminophen interactions

A
activated charcoal
antacids
ethanol (alcohol) (liver damage)
hydantoins
warfarin
sulfinpyrazone (risk for liver damage)
33
Q

acetaminophen pregnancy category

A

category B

34
Q

acetaminophen nursing dx

A

acute/chronic pain r/t ineffectiveness of acetaminophen

risk for injury r/t drug induced hepatic and renal toxicity

ineffective protection r/t potential blood dyscrasias

35
Q

acetaminophen interventions

A

max therapeutic effect: given without regard to meals

min adverse effect: periodic CBC, platelet count, liver and renal function tests for pts on long term therapy, monitor IV infusions closely

36
Q

acetaminophen pt education

A

pay attention to dose limit

seek medical attention if rash or other reactions occur

37
Q

acetaminophen in children

A

use with children under 2 should be checked with provider first

appears in breastmilk in low levels

38
Q

tylenol is contraindicated in

A

pt with hepatitis

39
Q

serotonin-selective drugs

A

used to relieve pain and inflammation r/t migraine headaches
not useful for other headaches or other pain/inflammation
-triptans

40
Q

sumatriptan (Imitrex) indications

A

migraine headache, cluster headache

41
Q

sumatriptan (Imitrex) pharmacokinetics

A

given PO, intranasally, subQ

met in liver, excreted by kidneys

42
Q

sumatriptan (Imitrex) action

A

selective for 5-HT1B/1D receptors located on cranial blood vessels and sensory nerves of trigeminovascular system

stimulation of receptors results in vasoconstriction

43
Q

sumatriptan (Imitrex) contraindications

A

CAD

ischemic cardiac diseases

44
Q

sumatriptan (Imitrex) adverse effects

A
coronary artery vasospasm
cardiac dysrhythmias
angina
myocardial ischemia
dizziness
45
Q

sumatriptan (Imitrex) interactions

A

SSRIs: risk for serotonin syndrome
MAOIs: may reduce Imitrex clearance and use within 2 weeks of MAOI is contraindicated

46
Q

sumatriptan (Imitrex) pregnancy category

A

category C

47
Q

sumatriptan (Imitrex) nursing dx

A

risk for impaired tissue perfusion r/t cardiovascular or cerebrovascular events

risk for injury r/t weakness, dizziness, lightheadedness

48
Q

sumatriptan (Imitrex) interventions

A

max therapeutic effect: confirm diagnosis of migraine, administer as soon as headache begins

min adverse effect: assess for CV history, monitor for s/s allergy or vasospasm

monitor for seizures

49
Q

sumatriptan (Imitrex) pt education

A

identify migraine triggers

drug will only treat migraines and will not prevent them

50
Q

fever

A

temperature reg = hypothalamus
pyrogens: substances that cause fever
fever causes activation of monocytes/macrophages that secrete cytokines
cytokines increase synthesis and secretion of prostaglandins in hypothalamus

51
Q

inflammation

A

local: warmth. swelling, redness, pain, LOF

acute inflammation is divided into cellular and vascular responses

52
Q

cellular inflammation response

A
  1. margination of WBC to periphery of blood vessels
  2. emigration of WBC to tissue spaces
  3. chemotaxis; cellular debris becomes more “attractive” to WBC
  4. phagocytosis; neutrophils and macrophages engulf cellular debris
53
Q

prostaglandin

A

modulates some components of inflammation, body temp, pain transmission, platelet aggregation

derived from arachidonic acid and covnerted by cyclooxygenase (COX)

54
Q

COX-1

A

synthesizes prostaglandins that are involved in the regulation of normal cell activity

55
Q

COX-2

A

appears to produce prostaglandins mainly at sites of inflammation

56
Q

platelet aggregation

A

first temp in sequence of events that leads to a thrombus (clot)

platelet aggregation is increased in smokers and hypercholesterolemia

57
Q

migraine headache

A

2 types:

migraine with aura: sensory disturbances like light flashes and blind spots
migraine without aura

58
Q

migraine pathology

A

it is postulated that migraine begins when intracranial blood vessels dilate

this dilation stimulates the trigeminovascular system resulting in abnormally excitable neurons that send pain impulses to the brain’s pain receptors