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Pharm Spring 2023 > Muscuolsketal Medications > Flashcards

Muscuolsketal Medications Flashcards

1
Q

What conditions May require modification of musculoskeletal activity (Antispastics / antispasmodics)

A
  1. Severe spasticity
  2. Acute spasms due to muscle injury
  3. Amyotrophic lateral sclerosis (ALS)
  4. Malignant hyperthermia
  5. Dystonia
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2
Q

What conditions May require modification of musculoskeletal activity (neuromuscular blockers)

A
  1. Surgical relaxation
  2. Endotracheal intubation
  3. Ventilation control
  4. Convulsions
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3
Q

What is the primary inhibitory neurotransmitter (muscular neurotransmission)

A

GABA
*stimulating GABA perpetuates a state of non-excitement

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4
Q

What is the primary excitatory neurotransmitter (Muscular nuerotransmission)

A

Glutamate
*blocking glutamate reduces excitatory impulses

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5
Q

What is the goal of musculoskeletal acting medications

A

To reduce the hyperactive stretch reflex by
1. Reducing the activity of fiber exciting the primary motor neuron
OR
2. Enhance the activity of inhibitory internuncial neurons

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6
Q

What will the musculoskeletal acting drugs do (MOA)

A
  1. Reduce activity of fiber that excite the primary motor neuron
    *resulting in less reflex
  2. Enhance inhibitory neuron activity (resulting in less / reduced hyperactive stretch reflex)
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7
Q

What are the antispasmodics with analgesic effects (muscle relaxants)

A
  1. Baclofen
  2. Cyclobenzaprine
  3. Tizanidine
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8
Q

What are the antispasmodics with sedative effects (muscle relaxants)

A
  1. Carisoprodol (soma)
  2. Methocarbamol (robaxin)
  3. Metaxlone (skelaxin)
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9
Q

What are the antispasmodics (muscle relaxants( useful in

A
  1. Acute spasms due to muscle injury
  2. Severe / chronic spasm
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10
Q

What are the adverse reactions of muscle relaxants

A
  1. Excessive sedations
  2. Dizziness
  3. Confusion
  4. Headache
  5. Dependency
  6. Blurry vision
  7. Asthenia
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11
Q

What are the anticholinergic toxicities of muscle relaxants

A
  1. CNS depression
  2. Peripheral anticholinergic SE
    *Dry mouth
    *constipation
    *urinary retention
  3. Highest risk with the elderly
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12
Q

What are the anticholinergeric SEs of muscle relaxants

A
  1. Hot as a hare
  2. Dry as a bone
  3. Blind as a bat
  4. Red as a beet
  5. Mad as a hatter
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13
Q

What is the MOA of botulinum Toxin A, B

A
  1. Inhibits synaptic release of Ach by clipping vesicle fusion proteins in the presynaptic nerve terminal
  2. Direct acting muscle relaxation
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14
Q

What are some things to keep in mind about Botulinum Toxin A, B

A
  1. Injections are made directly into muscle
  2. Duration last 2 to 3 months
  3. Toxicities
    *muscle weakness, falls
  4. BBW
    *potential spread of toxin leading to excessive weakness
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15
Q

Are neuromuscular blocking drugs polar or non polar

A
  1. Highly polar
    *administer parenteral
    *do not readily cross cell membranes, not strongly bound to peripheral tissue
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16
Q

What is the normal elimination of neuromuscular blocking drugs

A
  1. The metabolites are not enough ton cause significant blockade during / after anesthesia
  2. After several days in the ICU the metabolites may accumulate causing prolongs of paralysis
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17
Q

What are the non depolarizing muscle relaxants

A
  1. Atracurium
  2. Cisatracurium
  3. Pancuronium
  4. Rocuronium
  5. Vecuronium
18
Q

What are the depolarizing muscle relaxants

A
  1. Succinylcholine
    *causes transient contraction then prolonged flaccid paralysis
    *duration of action lasts 5 to 10 minutes
19
Q

What is the MOA of non depolarizing muscle relaxants

A
  1. Competitive antagonist at nACh rejectors, especially at neuromuscular junctions which will prevent the depolarization caused by Ach
    *duration last 20to 60 minutes
20
Q

What is the MOA for TCSs (tricyclic Antidepressants)

A
  1. Inhibits presynaptic reuptake of norepinephrine and serotonin
    *tertiary amines have greater affinity for serotonin transporter
    *secondary amines have greater affinity for norepinephrine transporter
21
Q

What are the tertiary amines

A
  1. Amitriptyline
  2. Doxepin
  3. Elavil
  4. Sinequan, silenor
22
Q

What are the secondary Amiens

A
  1. Nortriptyline
  2. Desipramine
  3. Pamelor
  4. Norpramin
23
Q

What is the difference between secondary and tertiary amines

A

Tertiary
1. Amitriptyline most SE
2. Doxepin = extremely sedating
Secondary
1. Better tolerated
*TCAs have a narrow therapeutic index can be anal in overdose due to cardio toxicity and seizures
*Avoid in suicidal patterns

24
Q

How are TCAs used for analgesia

A
  1. Reduce pain signaling / messages in the spinal cord by enhancing the concentration of serotonin and or norepinephrine
25
Q

What is the starting dose of TCAs

A

10 to 25 mg at bedtime and tirade to pain relief every 7 to 14 days
*usually stop at 50 mg

26
Q

What are the side effects of TCAs

A
  1. Tachycardia (Cardiovascular, orthostatsis)
  2. CNS
  3. Anticholinergic (weight gain*)
  4. Sedation* / sexual SE

** are the most limiting

27
Q

What are the CI off TCAs

A
  1. MAOI within 14 days, recent MI
  2. History of CV disease, lowering seizures threshold (more seizures)
  3. EKG monitoring
28
Q

What are the key drug interactions of TCAs

A
  1. CNS depressants
  2. Lithium (lowering of seizure threshold)
  3. Clonidine
  4. Additive risk serotonin syndrome
29
Q

What are the therapeutic monitoring of TCAs

A
  1. Used to verify adherence or toxicity bc efficacy
  2. Nortriptyline
    *most evidence for using concentration to attain efficacy
30
Q

What are clinical pearls of selective norepinephrine repuptake inhibitors (SNRIs) (Co-analgesics for pain)

A

Duloxetine (cymbalta)
1. Nausea
2. Stop if liver function tests are declining
3. No analgesic advantage with doses >60mg once or twice daily
Venlafaxine (Effexor)
1. Dose adjust in renal and hepatic dysfunction

31
Q

What is the MOA of anti seizure drugs (Carbamazepine / oxcarbazepine)

A
  1. Decreased repetitive action potential firing which inactivates sodium channels and will reduce pain signals
32
Q

What are the CI of carbamazepine / oxcarbazepine

A
  1. CI is hypersensitive to TCAs
    *Steady state is in 21 to 28 days
33
Q

What are the warnings of carbamazepine / oxcarbazepine

A
  1. Hyponatremia
  2. Fetal harm
  3. Suicidality
  4. Ghost capsule in feces
34
Q

What are the neurological ADRs of carbamazepine

A
  1. Drowsiness
  2. Ataxia
  3. Vertigo
  4. Diplopia
  5. Blurred vision
35
Q

What are the hematologic ADRs of carbamazepine

A
  1. Agranulocytosis
  2. Severe blood dyscrasias
36
Q

What are the dermatological ADRs of carbamazepine

A
  1. Pruritis
  2. SJS / TEN
37
Q

What are the GI/Hemostasis ADRs of carbamazepine

A
  1. Weight gain
  2. Osteoporosis
38
Q

How is oxcarbazepine (trileptal) compared to carbamazepine

A
  1. Less adverse effects
  2. Increased incidence of Hyponatremia
  3. More expensive
39
Q

What drug has the MOA of inhibition of presynaptic reuptake of norepinephrine and serotonin

A

Doxepin

40
Q

What drug has the MOA of reduced excitiation and enhance inhibition of motor neurons

A

Tizanidine

41
Q

What drug has the MOA of decreased repetitive action potential firing which downstream reduces pain signals

A

Carbamazepine

Pharm Spring 2023 (27 decks)

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