FIBROMYALGIA_FARM Flashcards

(41 cards)

1
Q

MOA duloxetine

A

SSNRIs antidepressants, no action on receptors/dopamine

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2
Q

duloxetine has more specificity in blocking what receptors?

A

Ser>NE

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3
Q

Duloxetine is metabolized by what CYP enzyme?

A

CYP2D6

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4
Q

what is the must know BBW for duloxetine?

A

suicidal ideation

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5
Q

Both duloxetine & milnacipran are eliminated by what mechanism?

A

urinary

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6
Q

MOA pregabalin

A

works by inhibiting presynaptic alpha-2-delta subunits of L-type Ca2+ channels

  • as a result they inhibit excitatory transmission by glutamate
  • seems to alleviate neuropathic pain
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7
Q

pregabalin is a schedule ___________ drug

A

V

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8
Q

how is pregabalin eliminated?

A

renal elimination unchange (adjust dose in renal failure)

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9
Q

What are the notable cautions of pregabalin?

A

rebound w/ drug withdrawal (may cause depend.)
Additive sedation
Monitor pts for depression, suicidal thoughts
In elderly: dizziness sedation, blurred vision, xerostomia

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10
Q

which side effects should you be looking for in the elderly taking pregabalin?

A

dizziness
sedation
blurred vision
xerostomia

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11
Q

what are the monitoring parameters for pregabalin?

A

serum creatinine (makes sense because it is eliminated by the kidneys)

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12
Q

Cyclobenzaprine MOA

A

central action; possibly at the level of the brain stem (related to amitriptyline)

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13
Q

what are the FDA indications for cyclobenzaprine?

A

muscle spasm

FM (off label use)

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14
Q

how is cyclobenzaprine eliminated?

A

enterohepatic recirculation & extensive hepatic metabolism

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15
Q

cyclobenzaprine has reduced clearance in the __________ population and in pts w/ _____________ dysfunction

A

elderly, liver

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16
Q

Amitriptyline and cyclobenzaprine both have significant _________________ action

A

anticholinergic

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17
Q

describe the anticholinergic effects of cyclobenzaprine

A
drowsiness
xerostomia
dizziness
fatigue
N/V/C
blurred vision
18
Q

which pts taking cylclobenzaprine are at risk for confusion & cardiac effects & may lead to falling?

19
Q

what are some of the cautions for cylcobenzaprine?

A
additive CNS depression (depressants & EtOH)
additive anticholinergics (GI problems)
20
Q

what is the most significant GI problem with pts taking cyclobenzaprine?

A

GI–>paralytic ileus

21
Q

TCAs have been reported to have what CV adverse effect?

A

QT prolongation (caution w/ antiarrhythmics)

22
Q

Tizanidine MOA

A

agonist at pre-synaptic alpha-2 receptor–>decreased activation of polynaptic spinal cord motor neurons w/ concomitant reduction in muscle tone but NOT MUSCLE STRENGTH

23
Q

which drug reduces muscle tone but not muscle strength?

24
Q

how is tizanidine metbolized & excreted?

A

extensive 1st pass metab., short t1/2 w/ extensive renal excretion of long lasting metabolites

25
how would you treat pts w/ tizanidine so as to avoid excessive drug toxicity in elderly and renal pts?
dose should be titrated up to effect
26
what are the monitoring parameters of tizanidine?
LFTs (hepatocellular toxicity is reported) | -remember extensive 1st pass metab. in liver
27
what are the adverse effects of tizanidine?
hepatotoxicity tapered cessation to avoid rebound hypertonicity additive CNS depression additive hypotension common side effects related to MOA of drug: asthenia, xerostomia, dizziness, sedation, hypotension
28
Baclofen MOA
acts as GABAb agonist at multiple levels in spinal cord, producing either inhibitor signals or hyperpolarizing & and so reducing the excitatory (aspartate & glutamate) polysynaptic pathways - pain relief in spinal cord comes from inhib. of substance P action - sedation at high doses
29
what are the FDA indications for baclofen?
multiple sclerosis muscle spasm spasticity spinal cord trauma
30
how is baclofen eliminated?
extensive renal elimination
31
what could happen if you give baclofen in pts with renal failure?
``` drug accumulation can lead to: encephalopathy abdominal pain seizures respiratory depression ```
32
what could happen if a pt suddenly stops taking baclofen?
BBW of rebound neural activity: - seizures - confusion - hallucinations - psychiatric disturbances (esp. in pts w/ previous CNS conditions) - increased spastcity (maybe-->rhabdomylolysis, MODS, death)
33
dose adjustment of antidiabetic agents may be necessary for which drug that treats spasticity?
baclofen (can cause increased BG)
34
what do you have to remember about taking pts off of baclofen?
tapered dosing over 2 wks
35
Dantrolene MOA
decreases muscle contraction by directly interfering (ryanodine receptor) w/ Ca2+ release from the SR w/i skeletal muscle cells -effectively uncouples the excitation-contraction process
36
what are the FDA indications for dantrolene?
malignant hyperthermia multiple sclerosis neuroleptic malignant syndrome spasticity
37
why does dantroline have a delay in immediate administration?
it has to be reconstituted
38
how is dantrolene metabolized & eliminated?
hepatically metab. renally eliminated
39
what are the monitoring parameters for dantrolene?
LFTs
40
IV dantrolene combined w/ CCB in treatment of malignant hyperthermia may produce what?
Vfib & CV Collapse
41
what are some common adverse effects of dantrolene?
muscle weakness-->drooling, dysarthria, enuresis, myalgias & backache