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pharmacology quiz 5 > non opiates 2 > Flashcards

non opiates 2 Flashcards

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?

A

NO!

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
Q

non-pharmacologic treatment of OA

A

weight loss, exercise, patient education

26
Q

Pharmacologic treatment of OA

A

analgesic (acetaminophen), NSAIDs, intraarticular corticosteroids

27
Q

Step 1 of progressive therapy of OA

A

Acetaminophen: no inflammation = prn, routine dosing if inflammation

28
Q

Step 2 of progressive therapy of OA

A

NSAID: if inflammation or tylenol is inadequate

29
Q

Step 3 of progressive therapy of OA

A

intraarticular corticosteroids: persistent sxs in one or a few joints (don?t use chronically - more than 2 yrs)

30
Q

what should you monitor with acetaminophen use?

A

hepatotoxicity

31
Q

how should NSAIDs be prescribed at first?

A

titrate up to effect and adverse event monitoring, naproxen or ibuprofen? Try either - can switch

32
Q

NSAIDs are a bad choice for pts with

A

upper GI issues, Asa for cardioprotection, warfarin users, increased CVD risk, renal insufficiency

33
Q

labs for NSAID chronic use monitoring

A

yearly CBC, BUN, serum creatinine, AST

34
Q

effects of NSAIDs on warfarin

A

blunt warfarin, increase antiplatelets - could bleed out!

35
Q

If oral agents are contraindicated, what are substitutes for NSAID therapy?

A

topical NSAID, capsaicin

36
Q

problems with topical NSAIDs?

A

variable length of effectiveness, local skin reactions (diclofenac)

37
Q

uses for capsaicin

A

mild to moderate effect for hands and knees

38
Q

who should get intraarticular corticosteroids?

A

pts with one or a few joints involved not adequately controlled, NSAIDs contraindicated

39
Q

how are itnraarticular steroids dosed?

A

depending on joint size (20, 40, 60mg)

40
Q

what joints are most effected by intraarticular steroids?

A

hips and knees

41
Q

what is glucosamine?

A

isolate of chitin or synthetic used in synthesis of articular cartilage

42
Q

what is chondroitin?

A

cow trachea or synthetic, this is glycosaminoglycan

43
Q

watch out for this with glucoasmin use?

A

increased insulin resistance

44
Q

watch out for this with chondroitin use?

A

looks like heparin, careful with hemodynamically touchy pts

45
Q

true or false: glucosamine or chondroitin alone may reduce risk of OA

A

TRUE

46
Q

True or false: glucosamine and chondroitin are safe to use and well tolerated

A

TRUE

47
Q

true or false: chondroitin alone may reduce pain in OA

A

TRUE

48
Q

true or false: glucosamine alone may reduce pain in OA

A

TRUE

49
Q

MOA of capsacin

A

activates TRPV1 cation channels on nociceptive nerve fibers, increases release of substance P and then levels dramatically drop

50
Q

ADR of capsaicin

A

burning of skin!

51
Q

Is capsaicin useful on larger joints?

A

no

52
Q

What are salonpas and bengay based off of?

A

methyl salicylate or oil of wintergreen - all products have diff ingredients

pharmacology quiz 5 (6 decks)

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