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Pharmacotherapy > orthopedics/pain management > Flashcards

orthopedics/pain management Flashcards

1
Q

what are the factors to consider when evaluating a web source?

A

determine what information is needed, critically evaluate the site

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2
Q

what should you consider with credibility of a site?

A

is there a publishing or sponsoring organization? is the org an authority on the subject? is the author listed? is the author an authority on the subject? are there spelling errors, etc?

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3
Q

what should you consider when determine accuracy of a site?

A

does the info agree with other sources? does the site contradict itself? what is the date of publication?

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4
Q

what should you consider when determining reasonableness of site?

A

does the author, etc have a bias? what is the motivation or purpose for creating the site?

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5
Q

what should you consider when determining support of a site?

A

are the sources listed? can they be checked? is there a way to contact the author or orgnaization?

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6
Q

what are some good medication sites?

A

prescribersletter.com, micromedex, medline plus drug information

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7
Q

what are good resources for herbal info?

A

natural medicines database, national center for complementary and alternative medicine

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8
Q

what senses pain?

A

nociceptors sense many kinds of tissue injury

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9
Q

nociceptive pain

A

transient pain in response to a noxious stimulus at nociceptors in cutaneous tissue, bone, muscle, CT, vessels, viscera. prevents further damage via withdrawal reflex

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10
Q

inflammatory pain

A

contributes to pain hypersensitivity to prevent contact or movement of injured part until healing is complete

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11
Q

neuropathic pain

A

sponteanous and hypersensitivity to pain associated with damage or pathologic changes in PNS

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12
Q

functional pain

A

pain sensitivity due to an abnormal processing or functioning of CNS in response to normal stimuli

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13
Q

how long does pain have to last beyond normal healing period to be classified as chronic nonmalignant?

A

6 months

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14
Q

under tx of pain is a big problem. why is it under txd?

A

incorrect assumptions: about amount of pain someone should feel for a given injury, assumption that people always get addicted to narcotics (if pain adequately tx’d there’s a smaller chance they’ll become addicted), incorrect attitudes: pain builds character, or pain meds show weak character, complexity of pain assessment: prn dosing is based on pt’s reported need, difficult to assess in young children and elderly with dementia. research and training inadequacy: limited info on pain management

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15
Q

what are the 4 predictors of poor pain management?

A

age, non-caucasian (discrepancy between race of provider and pt), low cognitive performance, multiple meds (providers hesitant to put them on another)

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16
Q

what are the PQRSTs of pain assessment?

A

palliative/provocative, quality, radiation/location, severity, timing

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17
Q

T or F: always use physiologic measures of pain (diaphoreses, BP, HR) before self reporting measures

A

F: chronic pain usu does not have the physiologic response.

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18
Q

what are the physiologic and behavioral characteristics of pain?

A

physiologic: HR, RR, BP, diaphoresis
behavioral: cry, facial expressio, objective pain scale

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19
Q

pain scale

A

0-10

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20
Q

what are non pharm methods to tx acute and chronic pain?

A

acute: psych interventions: controlled mental imagery, controlled attention or distraction; PT: heat/cold/water, uS therapy, TENS, massage, therapeutic exercise
chronic: psych: relaxation training, biofeedback, CBT, psychotherapy, support groups, spiritual counseling

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21
Q

acetaminophen: indication, MOA, usual dose, AE

A

indication: treatment of mild to moderate pain; analgesic effect  ASA
 MOA: Analgesic: inhibits pg (prvents pigs from stimulating nociceptors) synthesis in CNS and peripherally blocks pain impulse generation;
(antipyretic: inhibits hypothalamic heat-regulating center)
 Usual Dose: 325-650 mg q4-6 hours
Maximum Daily Dose: Maximum Geriatric Dose: Recent dosing changes:
All Rx APAP combination analgesics contain 325 mg max by 1/14/14 per FDA
OTC maximum dose lowered to 3000 mg/day
 Adverse effects: usually well tolerated; may cause hepatotoxicity, analgesic nephropathy, anemia, blood dyscrasias, rare skin rxns; overdose can  serious or fatal hepatotoxicity

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22
Q

T or F: ASA is an NSAID

A

T

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23
Q

T or F: tylenol has anti-inflammatory properties

A

F

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24
Q

T or F: acetaminophen should be written as APAP on a rx because its the generic name

A

F: use acetaminophen. if you write APAP it may go on the label and confuse patients. they may not think its acetaminophen and take other products at home with acetaminophen in it not knowing they are exceeding the rec’d dose

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25
Q

what are the differences in the MOAs of acetaminophen and aspirin?

A

acetaminophen blocks synthesis of prostaglandins centrally and initiation of pain signals peripherally; NSAIDS block cox-1 and cox-2 which are upstream of prostaglandins

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26
Q

what is the mechanism of acetaminophens hepatotoxicity?

A

1 of the 3 things that tylenol is metabolized to is a toxic metabolite that is normally conjugated immediately to glutathione. but if the dose is so much that glutathione can’t bind to it=hepatotoxicity

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27
Q

what’s the term for the way NSAIDS dose efficacy levels out at some point?

A

ceiling effect

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28
Q

do NSAIDS produce a tolerance or dependence?

A

no

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29
Q

NSAIDS: MOA, AE (not in detail)

A

mOA: Nonselective NSAIDs inhibit
both COX-1 and COX-2 (N-NSAID)
 Partially selective NSAIDs inhibit COX-2 > COX-1 (P-NSAID)
 Selective COX-2 inhibitors inhibit only COX-2

ae: Gastrointestinal: dyspepsia  mucosal lesions  serious GI complications  Renal
 Hematologic
 Cardiovascular
 Hepatic
 CNS: High doses can cause sedation and decreased cognition in older adults  Skin: Rare serious skin reactions, e.g. Stevens-Johnson or TEN

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30
Q

NSAID risk factors for ulcers and GI complications related to NSAID use

A 
Age>60years
 Concomitantanticoagulantuse
 Preexistingcoagulopathy
 ConcomitantcorticosteroidorSSRItherapy  PreviousPUDorPUDcomplications
 CVdiseaseandothercomorbidconditions
 MultipleNSAIDuse
 DurationofNSAIDuse(>1month)  High-doseNSAIDuse
 NSAID-relateddyspepsia
 Cigarettesmokers
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31
Q

NSAID efficacy T or F: EFFICACY:  1. At single full doses, most nonselective NSAIDs are more effective than full dose ASA or APAP 
2. Some have ≥ analgesic effect of oral opioid combinations

  1. Some patients respond better to one NSAID than another

    Celecoxib single 100-200 mg dose is more effective than ibuprofen 400 mg or naproxen 550 mg
A
  1. T
  2. T
  3. T
  4. F
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32
Q

which NSAIDS are salicylates?

A

acetylated: aspirin, non acetylated: salsalate trisalicylate

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33
Q

which NSAIDS are non salicylates?

A

non selective, partially selective and selective cox-2 inhibitors

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34
Q

which NSAIDS are non selective NSAIDS?

A

indomethacin, piroxicam, ibuprofen, naproxen, sulindac, ketoprofen, flurbiprofen, diclofenac

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35
Q

which NSAIDS are partially selective NSAIDS?

A

etodolac, nabumetone, meloxicam

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36
Q

which NSAIDS are selective NSAIDS?

A

cox-2 inhibitors: celecoxib

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37
Q

which NSAID has the lowest GI toxicity?

A

celecoxib

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38
Q

which NSAIDS have low GI toxicity?

A

meloxicam, ibuprofen, nabumetone, salsalte, etodolac

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39
Q

which NSAIDS have the highest r/o GI toxicity?

A

flurbiprofen, ketorolac, piroxicam

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40
Q

which NSAIDs have moderate-high GI toxicity?

A

naproxen, indomethacin

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41
Q

how can NSAIDS have nephrotoxic effects? what are RFs for it?

A

they prevent renal prostaglandins which normally increase renal blood flow, therefore they decrease renal blood flow. more pronounced in people with renal dz. they can cause interstitial nephritis, hyperkalemia, hyponatremia, and papillary necrosis
RFs: older age, HF, renal insufficiency, ascites, volume depletion, diuretic therapy

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42
Q

how can NSAIDS have hematology toxicity?

A

May prolong bleeding times due to anti-platelet effects
 ASA inhibits platelet aggregation for the lifetime of the platelet (7-10 days)
 Other nonselective NSAIDs affect platelet aggregation to a lesser degree & only when the drug is “on
board” (COX-2 and NAS do not affect platelet aggregation)
 Do not affect INR but do increase bleeding risk when used with anticoagulants

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43
Q

how can NSAIDS cause cardiovascular toxicity?

A

Selective inhibition of COX-2 may ↓ endothelial production of prostacyclin
 This leaves platelet thromboxane A2 mediated by COX-1 relatively unopposed, which may 
vasoconstriction, platelet aggregation and thrombosis
 Risk usually  with higher doses, longer duration, and degree of COX-2 selectivity
NSAIDs may also increase blood pressure (Pharmacist’s Letter 2011;27(1):2701033; see table in Appendix) (via decreased renal flow and increase in sodium and water retention)
 Avoid NSAIDs after MI indefinitely

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44
Q

which NSAIDS have the highest and lowest CV risk?

A

Highest CV risk with celecoxib ≥ 400 mg/day and diclofenac 100 mg/day, followed by meloxicam,
etodolac, and most others; aspirin, naproxen, and piroxicam lowest risk (Pharmacist’s Letter 2010, 2015)

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45
Q

how should NSAIDS be taken to avoid anti platelet effect?

A

Certain NSAIDs may inhibit ASA’s antiplatelet effect; take non-enteric coated ASA 1 hour before
ibuprofen or naproxen (so it can bind to platelets first); all NSAIDs have this potential unless proven
otherwise

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46
Q

how can NSAIDS can hepatotoxicity?

A

Overall incidence is 300 hospitalizations/year  No clear link between chemical structure and risk
 Histologic type of injury varies within/between chemical classes
 No consistent mechanism for liver injury from NSAIDs

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47
Q

what are some adverse effects of salicylates?

A 
ASA sensitivity (asthma, bronchospasm, angioedema, urticaria) related to COX-1 inhibition, which   PgE2 production   in leukotriene production &  in H release
 Reye’s syndrome
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48
Q

what are some NSAID combos? what are they combined with?

A

combined with a PPI or misoprostol b/c these are the only drugs that protect stomach: diclofenac/misoprostol and lansoprazole/naproxen

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49
Q

which NSAID has a max dose of 5 days?

A

ketorolac, which was also the first injectable NSAID

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50
Q

can injectable NSAIDS still cause GI bleeds?

A

yes, though the upside is they have a slower onset and longer duration

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51
Q

which non opioids have highest GI risk?lowest?

A

highest: nonselective NSAIDS, acetylated salicylates; lowest: acetaminophen

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52
Q

which non opioids have highest CV risk?

A

highest: selective cox-; lowest: acetaminophen and acetylated salicylates

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53
Q

which non opiods have highest renal risk? lowest?

A

all are the same

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54
Q

which non opioids have highest hepatic risk? lowest/

A

highest: acetaminophen; lowest: the rest

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55
Q

which non opiod has no r/o CNS problems?

A

acetaminophen

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56
Q

which non opioids have cross sensitivity with allergies?

A

all except acetaminophen: if allergic to one, could be allergic to all

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57
Q

which non opiod has a CI of sulfa allergy and 3rd tri pre?

A

celecoxib

58
Q

which non opioids are 3rd trim preg class c/d? (b/c of risk to baby–dont want them on it near labor)

A

non selective, partially selective. CI in celecoxib. risk in salicylates. none in tylenol.

59
Q

what kind of NSAID should you give to someone with a low GI risk and low CV risk?

A

ibuprofen or other low-GI NSAID

60
Q

what kind of NSAID should you give to someone with a low GI risk and high CV risk?

A

naproxen

61
Q

what kind of NSAID should you give to someone with a moderate GI risk and low CV risk?

A

celecoxib alone or NSAID + PPI or misoprostol or nSAID + double dose H2 blocker (2nd line)

62
Q

what kind of NSAID should you give to someone with a moderate GI risk and high CV risk?

A

Naproxen + PPI or misoprostol or naproxen + double dose H2 blocker (2nd line)

63
Q

what kind of NSAID should you give to someone with a high GI risk and low CV risk?

A

avoid NSAIDS if possible or celecoxib + PPI or misoprostol

64
Q

what kind of NSAID should you give to someone with a high GI risk and high CV risk?

A

avoid nsaids

65
Q

opioids: MOA, AE

A

MOA: stimulate opioid receptors (, , and ) in the CNS
Mood changes
Dysphoria, euphoria
Somnolence
Lethargy, drowsiness, apathy, inability to concentrate
Stimulation of CTZ
Nausea, vomiting
Respiratory depression
Decreased respiratory rate
Decreased GI motility
Constipation
Increase in sphincter tone
Biliary spasm, urinary retention (varies among agents)
Histamine release
Urticaria, pruritus, rare exacerbation of asthma (varies among agents)
Tolerance
Larger doses for same effect
Dependence
Withdrawal symptoms upon abrupt discontinuation

66
Q

in what patients should you be especially cautious of using opioids b/c of respiratory depression?

A

Respiratory depression is of greater concern in the following situations: COPD, cor pulmonale,  decreased respiratory reserve, pre-existing resp. depression, general anesthetics, phenothiazines, benzodiazepines, barbituates, TCAs, CNS depressants

67
Q

what are the opiod withdrawal sx?

A

minor: Rhinorrhea
 Lacrimation
 Excessive yawning
 Mild irritability or restlessness  Mild nausea or vomiting
moderate: ncreasing restlessness or irritability  Tremors
 Abdominal cramps
 Anxiety
 Persistent nausea or vomiting
 Increased HR, BP, hot or cold flashes, fever

68
Q

what is the difference in opioids between agonists, partial agonists, agonists/antagonists and antagonists? what are examples of each?

A

Agonists: Maximal biologic response through binding to the opioid -receptor i.e. codeine, methadone, hydromorphone, morphine
Partial agonists: Submaximal response at the receptor even at high doses i.e. buprenorphine
Agonist/antagonists: Divergent activities at different receptors ( agonist,  antagonist)  Analgesia ceiling
 Ceiling effect on respiratory depression
 Lower abuse potential
 Can precipitate withdrawal in patients who are dependent on full agonists i.e. butorphanol
Antagonist: Reverse or inhibit the effects of agonists by preventing receptor access i.e. naloxone

69
Q

what are some things to keep in mind when dosing opioids?

A 
Severity and type of pain
 Duration of expected treatment
 Duration of action necessary
 Route of administration
 Patient adherence/ability to self dose  Allergies or intolerances
 Concomitant medications
 Cost
 Others...
70
Q

drug: codeine
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A

drug: codeine
trade name: tylenol #3
indication: moderate pain
related to morphine? y
AE/notes: Codeinealoneinusualdoses≈efficacyto ASA/APAP
 Combocommon(codeiene/APAP class III, cough syrup class Iv)
 Gastritisfrequent
 Metabolizedtomorphine;ultrarapidCYP2D6
metabolizers -  risk of toxicity (also hydro, oxy, tram)
class controlled substance:II

71
Q

drug: hydrocodone
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A

drug: hydrocodone
indication: moderate pain
trade name: vicodin
related to morphine? y
AE/notes: Combocommon(vicodin + APAP)
 Alsoantitussive
 Maycauselessgastritisthancodeine  CYP3A4substrate: metabolized to hydromorphone
e;ultrarapidCYP2D6
metabolizers -  risk of toxicity (also hydro, oxy, tram)
class controlled substance:II

72
Q

drug: oxycodone
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A

drug: oxycodone
trade name: oxycontin
indication: moderate pain
related to morphine? y
AE/notes: Combocommon (oxycodone+ APAP=percocet)
 Maycauselesshallucinationsthanmorphine  -cet=APAP
 CYP3A4substrate(blackboxwarning): metabolized to oxymorphone, pt on a CYP3A4 inhibitor can get toxicity.  ;ultrarapidCYP2D6
metabolizers -  risk of toxicity (also hydro, oxy, tram)
class controlled substance:II

73
Q

drug: meperidine
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A 
drug: meperidine
trade name; demerol
indication: moderate pain
related to morphine? n
AE/notes: can be given IM, IV; Metabolite(normeperidine)isadirectCNSirritant that → sz. only one dose. Use discouraged (only short term tx of acute pain)  DonotusewithMAOI
class controlled substance:II
74
Q

drug: tramadol
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A

drug: tramadol
indication: moderate pain
trade name: ultram
related to morphine? n
AE/notes: Similarefficacytocodeine/APAP
1/3 mu, 2/3 NE&5-HTreuptake
 Riskfordependence/addiction;sz(espwithsz
disorder, anti-depressant or antipsychotic use),
death due to OD or suicide, hypoglycemia
 Slowonsetofaction
 CYP3A4substrate;activemetabolitevia2D6
class controlled substance: IV

75
Q

drug: tapentadol
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A

drug: tapentadol
indication: moderate pain
trade name: nucynta
related to morphine? n
AE/notes: Slight,moreactionsonNEand5-HTreuptake  Similarefficacytooxycodone15mg
 LessN,V,constipationthanoxycodone
class controlled substance:II

76
Q

drug: morphine
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A

drug: morphine
indication: severe pain
trade name:MS contin
related to morphine? y
AE/notes: Goldstandardforpotentopioids
 Histaminereleaseandgastritisnotuncommon
class controlled substance:II

77
Q

drug: hydromorphone
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A

drug: hydromorphone
indication: severe pain
trade name:dilaudid
related to morphine? y
AE/notes: Highpotency/solubility,usefulforterminalpain syndromes
 Antitussiveinlowerdoses
 Maycauselessgastritisthanmorphine
class controlled substance:II

78
Q

drug: oxymorphone
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A

drug: oxymorphone
indication: severe pain
trade name:opana
related to morphine? y
AE/notes: Take on an empty stomach; taking with food can lead to excessive peak levels
 Alcoholcanoxymorphonelevelsleadingto potential for OD
class controlled substance:II

79
Q

drug: levorphanol
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A

drug: levorphanol
indication: severe pain
trade name:levo-dromoran
related to morphine? y
AE/notes n/a
class controlled substance:II

80
Q

drug: fentanyl
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A

drug: fentanyl
indication: severe pain
trade name: sublimaze
related to morphine? n
AE/notes: Patchforchronicpainonly
 Oral(lollipop)forbreakthroughpain(rarelyused)  Oralassociatedwithemesiswhenusedpre-op
 CYP3A4substrate
class controlled substance:II

81
Q

drug: methadone
indication:
trade name:
related to morphine?
AE/notes
class controlled substance:

A

drug: methadone
indication: severe pain
trade name:
related to morphine? n
AE/notes: Commonlyusedinnarcoticmaintenanceprograms or weaning protocols
 Longhalf-life,suitableforchronicuse
 Caution: elderly 2◦ accumulation; QT prolongation
class controlled substance:II

82
Q

which mixed agonist/antagonist is 2nd line opioid often used for migraine tx in a nasal spray form?

A

butorphanol

83
Q

besides methadone, which other substance is used to treat opiod dependence with naloxone to block high if crushed and injected?

A

buprenorphine

84
Q

which drug is used for reversal of respiratory depression in opioid ODs?

A

naloxone (narcan)

85
Q

which drug is used for tx of alcohol dependence and to prevent relapse in opioiid depedent pts?

A

naltrexone(depade)

86
Q

for which drug should opioid conversion be done only by an expert?

A

methadone

87
Q

what are your options for pseudo allergy of an opioid? (flushing, itching, sweating, mild hypotension)

A

use a non opioid like APAP or NSAID, switch to higher potency with less chances of causing rxn (most likely to cause rxns are morphine, codeine, and meperidine), decrease dose if possible, give with benadryl

88
Q

which acute pain adjuvant analgesic may enhance analgesic effect of APAP, ASA or ibuprofen?

A

caffeine

89
Q

which acute pain adjuvant may add to analgesic effect of opioids in post op and cancer pts while reducng incidence of nausea and vomiting?

A

hydoxyzine

90
Q

which pharm combo is rec’d for acute, mild pain (1-3)

A

always non pharm, then non opioids +/- adjuvant (caffeine or corticosteroids)

91
Q

which pharm combo is rec’d for acute, moderate pain (4-6)

A

always non pharm, and weak opioids plus non opioids +/- adjuvant (caffeine, corticosteroids)

92
Q

which pharm combo is rec’d for acute, moderate pain (7-10)

A

always non pharm, then strong opioids and a non opioid +/- adjuvant

93
Q

what classifies as strong opioids?

A

Morphine

Fentanyl Hydromorphone Methadone Levorphanol Oxymorphone

94
Q

what classifies as weak opioids?

A

Codeine

Hydrocodone Oxycodone Tramadol

95
Q

T or F: you should never put someone on a regularly scheduled pain pill because they may become tolerant

A

F

96
Q

how should tolerance be effectively tx’d?

A

increase dose

97
Q

how should withdrawal be prevented if taking off an opioid?

A

Beawareofthedevelopmentofphysicaldependenceand
preventwithdrawal.Taperdailydose
by 10% q1-2 weeks.

98
Q

T or F: do not Labelthepatientas
“addicted”(psychologicallydependent)if you
reallymeanphysically dependent on or tolerant to opioids.

A

T

99
Q

what are some signs and sx of persistent pain?

A 
Depression
decreased   libido
 Anxiety
 Work issues
 Sleep disturbances
 Inactivity
 Frustration
 Altered family dynamics
 Anger
 Frequent use of meds
decreased   self-esteem
 Legal issues
  involvement in social activities
increased  number of health care visits
 Financial stresses and concerns
100
Q

what is important for pt ed in tx’ing persistent pain?

A

Simultaneouslyaddressthevariouscomponentsoftheproblem
 Taperuseofinappropriatemedswhileinitiatingappropriatetherapy
 Provideeducationaboutchronicpain;correctanymisconceptions (we may not be able to get rid of it entirely)
 Focusonfunctionandphysicalactivity
 Establishatimeframeforachievingspecificgoals (it may take a while)
 Remindyourpatientandyourselfthatchronicpainisnotthe
sameasacutepain (it may respond differently to meds)
 Emphasizethemultifactorialnatureofchronicpainandavoidthe
distinctionbetweenphysicalandpsychological causes

101
Q

which pain killer is good for bone pain?

A

NSAIDS

102
Q

what are 1st line tx’s for persistent pain?

A

non pharm: TENS, biofeedbac, PT if appropriate. pharm: non opioids, tramadol/tapendtadol. reserve opioids for chronic non cancer pain and for severe pain unresponsive to other options)

103
Q

if starting an opioid, what should you do?

A

start a scheduled and PRN dose, titrate scheduled so less pRN is needed, then go on extended release to decrease number of doses needed. also start on bowel program stat.

104
Q

what are some adjuvant analgesics to consider in persistent pain?

A

Tricyclic antidepressants (TCAs)
 Antiepileptic drugs (AEDs)
 Serotonin norepinephrine reuptake inhibitor (SNRI)
 Local anesthetics (lidocaine)

105
Q 
drug: TCA: amitriptyline
moa
indication: 
trade name:
AE/notes
A

drug: amitriptyline
mOA: Inhibit NE & 5- HT reuptake (like tramadol)
indication: persistent pain, adjuvant
trade name: alluvial
AE/notes: Amitriptyline: anticholinergic effects (2° amines less)
 Sedation
 Onset is weeks

106
Q 
drug: antiepileptic: carbamazepine, gabapentin, valproic acid, and pregabalin
moa
indication: 
trade name:
AE/notes
A

indication:
moa:  synaptic transmission Inhibits neuronal activity and  GABA
???
 release of glutamate, NE, substance P
trade name: carbamazepine (tegretol) , gabapentin (neurontin) , valproic acid (depakote) , and pregabalin (lyrica)
AE/notes: CBZ: CNS SE, CYP450 inducer
 GBP: CNS, GI SE
 VPA: GI, CNS,  LFTs,  plts
 PGB: dizziness, sedation, dry mouth, peripheral edema, blurred vision, wt gain

107
Q 
drug: SNRI 
moa
indication: 
trade name:
AE/notes
A

drug: SNRI
moa: Potent inhibition of NE, 5-HT reuptake
indication: Indicated for tx of pain associated with diabetic neuropathy & chronic MS pain due to low back pain & OA
trade name: duloxetine
AE/notes

108
Q 
drug: local anesthetic: lidocaine patches
moa
indication: 
trade name:
AE/notes
A 
drug: local anesthetic
moa Stabilizes neuronal membrane
indication: persistent pain adjuvant
trade name: lidoderm
AE/notes: 12 hours on; 12 hours off
 Potential option for bridging
109
Q

what’s the best tx for persistent chronic low back pain?

A

acetaminophen first, tramadol or opioids in selected pts. reserve opioids for flare ups.

110
Q

what’s the best tx for persistent fibromyalgia?

A

acetaminophen first, then TCAs, AEDs, SNRIs (stronger evidence), tramadol better than opioids. NSAIDs only with other agents

111
Q

what’s the best tx for persistent neuropathic pain?

A

TCAS, SNRI, AEDs or lidocaine patch. nsaids rarely effecive. tramadol and opiods 2nd line. then capsaicains.

112
Q

what is the timeline for an adequate drug trial?

A

start at low end of dosing range and increase periodically q3-7 days; increase dose if not achieved therapeutic effect and AE are tolerable

113
Q

tx goals of RA:

A

reduce or eliminate pain
 Protect articular structures
 Control systemic complications
Prevent loss of joint function  Improve or maintain QOL

114
Q

non pharm for Ra

A 
Rest
 Occupational therapy
 Physical therapy
 Patient education
Use of assistive devices
 Weight reduction
 Surgery
 Patient support group involvement
115
Q

what effects tx of RA?

A

Disease activity
 Measured using a validated instrument, e.g. Disease Activity Score
 Disease duration
 Early: 24 months
 Prognosis
 Poor = functional limitation, extra-articular disease, +Rh factor and/or anticyclic citrullinated peptide
antibodies and/or bony erosions

116
Q

what is the initial or bridging therapy for RA? what are other options?

A

NSAIDS at inflammatory dose. but should never be used as mono therapy; can do oral corticosteroids

117
Q

if someone with RA is going to be on corticosteroids LT, what’s an appropriate dose?

A
118
Q

AE of oral corticosteroids for RA

A

osteoporosis, PUD, HTN, hyperglycemia, dyslipidemia, weight gain, Cushing’s Syndrome,
mood changes, infection, cataracts

119
Q

why is the risk of osteoporosis from oral corticosteroids in RA patients extra risky? how do you minimize this?

A

Patients with RA have an increased risk of osteoporosis that is independent of the risk due to steroids
 Recommend that patients taking steroids get 1,500 mg of elemental calcium per day (from diet and
supplements) and 400-800 IU of vitamin D per day
 Other options that should be considered are raloxifene (Evista) and antiresorptive agents such as the
bisphosphonates (Fosamax, Actonel, etc.)

120
Q

what’s 1st line tx for RA?

A

non bio DMARDS: methotrexate

121
Q 
methotrexate: 
indication
MOA
AE
relative CI
CI
monitoring
clinical response
A

indication: 1st line for active or severe RA
MOA: inhibits dihydrofolate reductase, which  inhibition of purines and thymidylic acid, and by inhibiting
the production of certain cytokines
AE: stomatitis, nausea, diarrhea, and possibly alopecia (may decrease with concomitant use of folic acid without losing efficacy; folic acid 5 mg po qwk on day after MTX dose is recommended)
elevated LFTs most frequent; liver toxicity risk is low
thrombocytopenia, leukopenia; rare pulmonary and lymphoproliferative toxicity
relative CI: liver disease, kidney impairment, significant lung disease, and alcohol abuse
CI Do not use in pregnant or nursing women
monitoring
LFT monitoring during therapy is necessary; also CBC
PPIs, NSAIDs and ASA may decrease  the renal clearance of MTX and its active metabolites Clinical response: 1-2 mo

122
Q 
leflunomide
indication:
MOA
AE
relative CI
CI
monitoring
clinical response
A

indication: 2nd line if MTX not tolerated or don’t response
MOA: inhibits pyrimidine synthesis, resulting in antiproliferative and antiinflammatory effects
AE: Elevated liver enzymes, especially if combined with methotrexate; hepatotoxicity, rare reports of
severe infx, pancytopenia, agranulocytosis, and thrombocytopenia; may interact with warfarin (↑ INR)
relative CI none
CI: Liver disease, viral hepatitis, severe immunodeficiency, obstructive biliary disease, inadequate birth control, and treatment with rifampin ( leflunomide levels)
monitoring: ALT, platelet, white blood cell count, and hemoglobin or hematocrit monitored
Baseline, monthly for 6 months following initiation of therapy, then every 6 to 8 weeks thereafter
If used with concomitant methotrexate and/or other potential immunosuppressive agents, chronic monitoring should be monthly
Undergoes enterohepatic recirculation; half-life of 14-16 days (cholestyramine for rapid clearance and reversal)
clinical response: 1-3 months

123
Q

what’s a good initial choice of tx for someone with RA with less active or milder dz?

A

hydroxychloroquine (plaquenil)

124
Q 
hydroxychloroquine (plaquenil)
indication:
MOA
AE
monitoring
clinical response
A

indication: reatment with hydroxychloroquine alone does not slow disease progression, but early treatment still has
an impact on long-term patient outcome
• MOA: inhibits locomotion of neutrophils and chemotaxis of eosiniphils; impairs complement-dependent
antigen-antibody reactions
AE: Rash, diarrhea, abdominal cramps infrequently
Increased risk of retinal toxicity if the dose exceeds 6 gm/kg
monitoring: No lab monitoring is necessary
Periodic ophthalmic exams are necessary for early detection of reversible retinal toxicity Clinical response: 2-6 months

125
Q 
sulfasalazine (azulfidine)
indication
MOA
AE
monitoring
clinical response
A

indication: Helps slow disease progression in patients with RA and may work more quickly than hydroxychloroquine
• MOA: a pro-drug cleaved by bacteria in colon to metabolites thought to have anti-RA activity, however
exact mechanism in RA is unknown
AE: Nausea, abdominal discomfort
Mostly occur in the first few months, can lessen by starting with low dose and ↑ dose gradually
monitoring: Periodic monitoring for leukopenia is recommended; tell patients they may notice yellow/orange color of urine and/or skin
clinical response: 1-3 months

126
Q

what are biologic DMARDSs?

A

Genetically engineered protein molecules that affect RA pathophysiology. many kinds: Inhibit tumor necrosis factor-alpha, a key inflammatory factor in RA (TNF-alpha inhibitors)
Inhibit interleukin-1, which is involved in inflammation and joint destruction in RA (IL-1 receptor antagonist)
Deplete peripheral beta cells
Inhibit full T-cell activation (Selective co-stimulation modulator)
Block the action of interleukin-6, an immune system protein that is overabundant in people with RA

127
Q

what are downsides of biologic dramas?

A

expensive, higher risk of infection b/c of altering immune system and parenteral

128
Q

TNF alpha inhibitors
examples:
indication:
ae

A

examples:Etanercept (Enbrel) Infliximab (Remicade) Golimumab (Simponi) Adalimumab (Humira) Certolizumab (Cimzia
indication: Monotherapy
Combo with MTX
Combo with MTX Inadequate response to ≥ 1 DMARD
ae: Etanercept, infliximab and adalimumab may exacerbate or cause CHF
Do not use infliximab in pts with mod- severe HF; use others with caution in patients with pre-existing HF;
Risk of infections and lymphomas

129
Q

what are some less frequently used DMARDS that are just good to know about?

A

azathioprine, cyclosporine, minocycline, gold

130
Q

what’s the rec’d initial tx for early RA?

A

DMARD, regardless of dz actiity

131
Q

treatment goals of OA

A 
Educate the patient, caregivers and relatives (www.arthritis.org)  Relieve pain and stiffness
 Maintain or improve joint mobility
 Limit functional impairment
 Preserve joint integrity
 Maintain or improve QOL
132
Q

what is the cornerstone of OA tx?

A

non pharm

133
Q

non pharm tx for OA

A 
Patient education
 Cardiovascular (aerobic) and/or resistance
land-based exercise
Pharmacologic Therapy
 Aquatic exercise
 Weight loss (if overweight)  Surgery
134
Q

T OR F: OA meds can change the course of the dz

A

false, just sx managment

135
Q

what are some of the conditionally rec’d txs for knee and hip (joints most commonly affected)

A

tyenol, NSAIDS, topical NSAIDS, tramadol

136
Q

what’s 1st line pharm tx for mild to moderate oA?

A

acetaminophen

137
Q

when is ibuprofen indicated in OA?

A

mild to moderate pain; no response, adverse effects, or contraindications to APAP

138
Q

what is a safer pain reliever option for adults >75 with OA?

A

Topical NSAIDs
 Diclofenac gel, cream, solution and patch available
 Most beneficial for joints near the skin

139
Q

intrarticular corticosteroid injections
indications
MOA

A

indications: Conditionally recommended for patients with knee or hip OA
 Alternative to oral agents
MOA: effective for knee, not studied in hip

140
Q

what’s conditionally red’c not to use in OA?

A

glucosamine sulfate +/- chondroitin, topical capsaicin,

141
Q

Intraarticular Hyaluronic Acid (no rec)
 Regimen
Advantages
Disadvantages:

A

Intraarticular Hyaluronic Acid
 Regimen: Hyalgan 20 mg intra-articular qweek x 5, Synvisc 16 mg intra-articular qweek x 3,
Supartz 25 mg intra-articular qweek x 5
 Advantages: duration of relief may last up to 6 months
 Disadvantages:
Delayed onset of action, not approved for hip OA, some clinical trial results similar to placebo, use with caution with allergies to avian proteins, feathers and egg products
 Alternative to oral agents

142
Q

duloxetine (cymbalta)
indication
regigmen

A

 Indicated for chronic musculoskeletal pain 2 low back pain & OA
 Regimen: Start at 30 mg/day x 1 week to  nausea; do not exceed 60 mg/day for pain (higher
doses do not improve efficacy but side effects).
 Consider if analgesics are not sufficient and there is concurrent depression

Pharmacotherapy (9 decks)

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