non opiates 2 Flashcards

(52 cards)

1
Q

what neurotransmitters are involved in the neuropathic pain pathway?

A

serotonin (inhibits and promotes pain perception) and norepinephrine (primarily inhibitory)

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2
Q

SNRIs

A

serotonin-norepinephrine reuptake inhibitors

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3
Q

antidepressant drugs that are used as analgesics

A

doxepin, milnacipran (fibromyalgia), amitrityline, duloxetine

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4
Q

antiseizure drugs used as analgesics

A

phenytoin, carbamazepine, pregabalin

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5
Q

which is better for pain: antiseizure drugs, antidepressants

A

antidepressants - antiseizure drugs focus on Na channels

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6
Q

what did carbamazepine begin treating?

A

trigeminal neuralgia (better for pain)

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7
Q

do SSRIs help relieve pain?

A

not as well as SNRIs

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8
Q

how do antiseizure drugs decrease pain experienced?

A

decrease excitatory transmission, inactivate Na channels (not a class effect)

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9
Q

which antiseizure/antidepressant drugs are albeled for use to decrease pain?

A

minacipran, gabapentin, duloxetine, carbamazepine, pregabalin

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10
Q

MOA of pregabalin

A

effect on presynaptic N-type channels, sits in GAMA receptor sites (doesn’t mimic it)

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11
Q

ADRs of pregabalin

A

dizziness, sleepiness, peripheral edema, weight gain, suicide risk warning (screen for this!), slow taper when d/c

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12
Q

max dose of pregabalin?

A

450mg/day

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13
Q

Duloxetine MOA

A

serotonin and NE reuptake

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14
Q

ADR of duloxetine

A

CNS sxs like sleepiness, fatigue, eadache, nausea, xerostomia, suicide risk warning

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15
Q

Goals of treating osteoarthritis

A

control pain/swelling, minimize disability, improve QOL, educate on disease mgmt (lifestyle)

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16
Q

what is osteoarthritis AKA?

A

degenerative joint disease

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17
Q

What is osteoarthritis?

A

involves cartilage and bone destruction accompanied by osteophyte formation and other changes to the joint that result in pain and limited mobility

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18
Q

Compare/contrast osteoarthritis and RA in terms of site affected

A

OA: joint localization, RA: articular, systemic and extra-articular manifestations

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19
Q

Compare/contrast OA and RA in terms of pathogenesis

A

OA: biomechanical; leads to loss of cartilage matrix, RA: autoimmune response and extra-articular manifestations

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20
Q

compare/contrast OA and RA in terms of sxs

A

OA: pain, stiffness > 20mins, limited motion, RA: pain, joint swelling, stiffness >1 hours, limited motion

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21
Q

Can you use RA drugs for OA?

22
Q

compare/contrast RA and OA in terms of inflammation

A

OA: usually limited, may be present in advanced disease; RA: chronic

23
Q

compare/contrast RA and OA in terms of osteophytes

A

OA: present, RA: absent

24
Q

compare/contrast Oa and rA in terms of rheumatoid factors

A

OA: absent, RA: usually present

25
non-pharmacologic treatment of OA
weight loss, exercise, patient education
26
Pharmacologic treatment of OA
analgesic (acetaminophen), NSAIDs, intraarticular corticosteroids
27
Step 1 of progressive therapy of OA
Acetaminophen: no inflammation = prn, routine dosing if inflammation
28
Step 2 of progressive therapy of OA
NSAID: if inflammation or tylenol is inadequate
29
Step 3 of progressive therapy of OA
intraarticular corticosteroids: persistent sxs in one or a few joints (don?t use chronically - more than 2 yrs)
30
what should you monitor with acetaminophen use?
hepatotoxicity
31
how should NSAIDs be prescribed at first?
titrate up to effect and adverse event monitoring, naproxen or ibuprofen? Try either - can switch
32
NSAIDs are a bad choice for pts with
upper GI issues, Asa for cardioprotection, warfarin users, increased CVD risk, renal insufficiency
33
labs for NSAID chronic use monitoring
yearly CBC, BUN, serum creatinine, AST
34
effects of NSAIDs on warfarin
blunt warfarin, increase antiplatelets - could bleed out!
35
If oral agents are contraindicated, what are substitutes for NSAID therapy?
topical NSAID, capsaicin
36
problems with topical NSAIDs?
variable length of effectiveness, local skin reactions (diclofenac)
37
uses for capsaicin
mild to moderate effect for hands and knees
38
who should get intraarticular corticosteroids?
pts with one or a few joints involved not adequately controlled, NSAIDs contraindicated
39
how are itnraarticular steroids dosed?
depending on joint size (20, 40, 60mg)
40
what joints are most effected by intraarticular steroids?
hips and knees
41
what is glucosamine?
isolate of chitin or synthetic used in synthesis of articular cartilage
42
what is chondroitin?
cow trachea or synthetic, this is glycosaminoglycan
43
watch out for this with glucoasmin use?
increased insulin resistance
44
watch out for this with chondroitin use?
looks like heparin, careful with hemodynamically touchy pts
45
true or false: glucosamine or chondroitin alone may reduce risk of OA
TRUE
46
True or false: glucosamine and chondroitin are safe to use and well tolerated
TRUE
47
true or false: chondroitin alone may reduce pain in OA
TRUE
48
true or false: glucosamine alone may reduce pain in OA
TRUE
49
MOA of capsacin
activates TRPV1 cation channels on nociceptive nerve fibers, increases release of substance P and then levels dramatically drop
50
ADR of capsaicin
burning of skin!
51
Is capsaicin useful on larger joints?
no
52
What are salonpas and bengay based off of?
methyl salicylate or oil of wintergreen - all products have diff ingredients