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STEP Pharm I > Fibromyalgia and Sapasticity > Flashcards

Fibromyalgia and Sapasticity Flashcards

1
Q

What is the suspected cause of fibromyalgia?

A

Elevated levels of neurotransmitter function in theascending pathways of the spinal cord and diminished levels in the descending, modulatory pathways of people with fibromyalgia. Thiswould lead to amplification of all nociceptive signals arriving in the brainfrom peripheral tissues.

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2
Q

What are some of the symptoms of fibromyalgia?

A

-stiffness-unrefreshing sleep-tension headache-irritable bowel or bladder-difficulty concentrating

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3
Q

What are some of the currently most commonly used drugs for fibromyalgia (not just symptom relief)?

A

-acetaminophen-NSAIDs-TCAs-Cyclobenzaprine

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4
Q

What are the serotonin-Nor repute inhibitors used in fibromyalgia treatment?

A

-Duloxetine (Cymbalta)-Milnacipran (Savella)both labeled for use

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5
Q

Which does Doloxetine prevent uptake of more, serotonin or Nor?

A

Serotonin

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6
Q

Which does Milnacipran prevent uptake of more, serotonin or Nor?

A

NE 3x more

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7
Q

T or F. Neither Sero/NE Reuptake Inhibitor acts on a receptor

A

T. and neither affects Dopamine

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8
Q

How is Doloxetine metabolized?

A

CYP 2D6 and eliminated in urine

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9
Q

How is Milnacipran metabolized?

A

Does not involve CYP activity; eliminated in the urine as a mix of parental drug and metabolites.

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10
Q

Contraindications of Doloxetine or Milnacipran?

A

-liver dysfunction-chronic alcoholism -pre-existing CV conditions -closed-angle glaucoma-MAOIs

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11
Q

Why cant Doloxetine or Milnacipran be given to patients with underlying CV problems?

A

they increase heart rate and BP

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12
Q

BBW of Sero/NE reuptake inhibitors?

A

suicidal ideation

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13
Q

T or F. Both Sero/NE reuptake inhibitors can cause hyponatremia

A

T. Via SIADH potential

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14
Q

How does Pregabalin (Lyrica) work?

A

Fibromyalgia drug that is an analog of gabapentin (anti-seizure drug) that acts by inhibiting presynaptic alpha-2-delta subunits of L-type Ca2+ channels, thus, inhibiting the excitatory transmission of glutamate

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15
Q

What is the clinical of Lyrica?

A

Glutamate inhibition seems to alleviateneuropathic pain, anxiety and pain syndromes

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16
Q

How is Lyrica eliminated?

A

it is rapidly absorbed and eliminated in urine mostly unchanged with some tubular reabsorption (no known DD interactions)

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17
Q

Contraindications of Pregabalin (Lyrica)?

A

Rebound worsening of symptoms upon drug withdrawal. May cause dependence with continued use.Additive sedation may occur with other agents that affect the CNS in this manner. Patients should be monitored for worsening depression or suicidal thoughts /behavior.

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18
Q

AEs of Pregabalin?

A

Dizziness, sedation, blurred vision and xerostomia may occur; these are especially problematic in the elderly.

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19
Q

What should be monitored when giving Pregabalin (Lyrica)?

A

serum creatinine

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20
Q

What are the off-label drugs for Fibromyalgia?

A

-Amitriptyline (Elavil)-TCA-Fluoxetine (Prozac) -Cyclobenzaprine

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21
Q

What is Fluoxetine (Prozac)?

A

selective serotonin reuptake inhibitor (SSRI)

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22
Q

What are some skeletal muscle relaxers?

A

-Carisoprodol (Soma)-Cyclobenzaprine (Flexeril)-Methocarbamol (Relaxin)-Tizanidine (Zanaflex)

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23
Q

How does Methocarbamol (Relaxin) work?

A

No direct effect on muscle or excitation-contraction coupling. Effects thought to be due to generalized sedative action. Pain relief due to altered pain perception.

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24
Q

What are the FDA indications for Relaxin?

A

-tetanus-muscle spasm

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25
Q

How is Methocarbamol metabolized?

A

Hepatic dealkylation and hydroxylation with urinary elimination. NOTE: Significant hepatic and/or renaldysfunction has the potential to increase drug toxicity.

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26
Q

AEs of Relaxin?

A

Additive CNS depression with other depressant drugs, and alcohol.Common side effects include drowsiness, dizziness, lightheadedness, blurred vision, N/V, headache and irritability.

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27
Q

How does Tizanidine (Zanaflex) work?

A

PO agent that acts as an agonist on pre-synaptic α-2 receptors leading to decreased activation of polysynaptic spinal cord motor neurons with concomitant reduction in muscle tone but NOT muscle strength.

28
Q

Can Tizanidine (Zanaflex) be used as an anti-HTN?

A

No, weak in that area compared to other a2 agonists

29
Q

What is Zanaflex approved for?

A

-MS-spasticity-spinal cord trauma

30
Q

How is Zanaflex eliminated?

A

Extensive first-pass metabolism, short half-life with extensive renal excretion of long-lastingmetabolites.

31
Q

When is elimination of Tizanidine hindered?

A

with advancing age and in renal dysfunction (CrCl less than 25 ml/min)

32
Q

AEs of Zanaflex?

A

-hepatocellular toxicity-rebound hypertonicity, tachycardia, and HTN if not tapered off high doses-xerostomia, dizziness, sedation, hypotension (via a2 action)

33
Q

DD interactions of Tizanidine?

A

-additive CNS depression with CNS depressants-Additive hypotensive effects with a2 agonists

34
Q

What are some 2 agonists that would be contraindicated with Zanaflex?

A

-Clonidine-Methyldopa-Guanfacine-Guanabenz

35
Q

What should be monitored if giving Zanaflex?

A

LFTs

36
Q

What is Carisoprodol (Soma)?

A

PO drug that has CNS action in reticular activating system and spinal cord leading to sedation and altered perception of pain. It is believed (but not proven) that generalized sedation is the basis for the muscle relaxation. NO DIRECT EFFECT on neuronal conduction, neuromusculartransmission or muscle excitability.

37
Q

How is Soma metabolized?

A

Extensive hepatic metabolism (CYP2C19) to several (less) active compounds with ultimate elimination in the urine. Renal or hepatic dysfunction increases the potential for retention of drugand/or metabolites, thereby increasing toxicity.

38
Q

AEs of Carisoprodol (Soma)?

A

Drowziness and dizziness are most common, together with other CNS manifestations likeagitation, insomnia, vertigo, ataxia; systemic effects of sedation include asthenia, temporary vision loss, mydriasis, orthostatic hypotension.

39
Q

What should be monitored if giving Soma?

A

serum creatinine/BUN

40
Q

What is Soma indicated for?

A

musculoskeletal pain

41
Q

How does Cyclobenzaprine (Flexeril) work?

A

central action possible at the level of the brain stem to induce muscle relaxation

42
Q

What is Flexeril indicated for?

A

muscle spasm or fibromyalgia (off-label), NOT for relief of cerebral or spinal cord disease

43
Q

How is Cyclobenzamine eliminated?

A

Undergoes enterohepatic recirculation and extensive hepatic metabolism (CYP3A4, 1A2, 2D6) with reduced clearance in elderly and with hepatic impairment.

44
Q

AEs of Flexeril?

A

significant antimuscarinic activity can produce drowsiness, xerostomia, and dizziness, constipation, etc. -QT prolongation Falls are common in elderly

45
Q

Contraindications of Flexeril?

A

-other anticholinergics, TCA, and 1st gen antihistamines -drugs also prolonging QT

46
Q

What are the drugs for spasticity?

A

-Baclofen (Lioresal)-Botulinum toxin-Dantrolene (Dantrium)-Tizanidine (Zanaflex)

47
Q

Note about drugs for spasticity

A

Although these drugscan indeed produce muscle relaxation, they do so at drug doses that produce significantsedation and so are not commonly employedfor this purpose.

48
Q

How does Baclofen (Lioresal) act?

A

complex; acts as GABAb agonist at multiple levels in spinal cord, producingeither inhibitory signals or hyperpolarizing andthereby reducing the excitatory (aspartate and glutamate) polysynaptic pathways.

49
Q

How does Baclofen cause pain relief in the spinal cord?

A

inhibition of substance P action.NOTE: In high doses, baclofen producessedation, although not as effectively as diazepam [Valium], therefore some drug activity is doubtless derived from supraspinal actions.

50
Q

FDA Indications of Lioresal:

A

multiple sclerosis, muscle spasm, spasticity, spinal cord trauma

51
Q

How is Lioresal eliminated?

A

renal (caution with renal failure)

52
Q

What can happen with high doses of Baclofen in patients with renal dysfunction?

A

drug accumulation can lead to encephalopathy, abdominal pain,seizures and respiratory depression.

53
Q

AEs of Baclofen?

A

Abrupt discontinuance of therapy should be avoided (Black Box warning) as “rebound” neural activity can result in seizures, confusion, hallucinations, psychiatric disturbances (especially in those with preexisting CNS conditions!) and increased spasticity (perhaps advancing torhabdomyolysis, multisystem failure and death). Tapered dosing should occur over 2 or more weeks

54
Q

Other AEs of Baclofen?

A

-can increase blood glucose -drowsiness-renal failure with abrupt withdrawal

55
Q

Contraindications of Baclofen?

A

-diabetics-other anti-HTN and MAOIs-other CNS depressants

56
Q

How does Dantrolene (Dantrium) work?

A

dantrolene decreases muscle contraction by directly interfering (ryanodine receptor) with calcium ion release from the SR within skeletal muscle cells.Effectively it “uncouples” the excitation-contraction processDantrolene does not work like a calcium channel blocker, e.g.,verapamil, nor does it block Ach release from the endplate.

57
Q

FDA uses of Dantrium?

A

-malignant hyperthermia-MS-spasticity-neuroleptic malignant syndrome

58
Q

T or F. Dantrolene has little or no effect oncardiac or smooth muscle at doses used for skeletal muscle relaxation.

A

T. The extent of its CNSeffect is not known.

59
Q

How is Dantrolene given?

A

oral or IV (solubilized with surfactant + water - very alkaline, producesthrombophlebitis; administered into fast running infusion or large vein). Need for reconstitutiondelays immediate administration!

60
Q

How is Dantrolene eliminated?

A

Hepatic metabolism with inactive metabolites renally eliminated. May cause hepatic toxicity when employed chronically.

61
Q

What patient population is especially at risk for hepatic toxicity with Dantrolene?

A

Females >35 yrs, MS patients, and those with concurrent multiple drug therapy (especiallyestrogens). Regular liver function tests are recommended

62
Q

What can Dantrolene do if given during caesarean section?

A

can cross placenta and cause ‘floppy’ child syndrome

63
Q

AEs of Dantrolene?

A

-muscle weakness leading to drooling, enuresis, myalgia, dysarthria and backache

64
Q

Contraindications of Dantrolene?

A

-other depressants, - IV with CCBs in the Tx of malignant hyperthermia

65
Q

Giving Dantrolene IV with CCBs in the Tx of malignant hyperthermia can cause what?

A

Vfib and CV collapse

STEP Pharm I (36 decks)

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