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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
What is the starting dose of TCAs
10 to 25 mg at bedtime and tirade to pain relief every 7 to 14 days *usually stop at 50 mg
26
What are the side effects of TCAs
1. Tachycardia (Cardiovascular, orthostatsis) 2. CNS 3. Anticholinergic (weight gain*) 4. Sedation* / sexual SE ** are the most limiting
27
What are the CI off TCAs
1. MAOI within 14 days, recent MI 2. History of CV disease, lowering seizures threshold (more seizures) 3. EKG monitoring
28
What are the key drug interactions of TCAs
1. CNS depressants 2. Lithium (lowering of seizure threshold) 3. Clonidine 4. Additive risk serotonin syndrome
29
What are the therapeutic monitoring of TCAs
1. Used to verify adherence or toxicity bc efficacy 2. Nortriptyline *most evidence for using concentration to attain efficacy
30
What are clinical pearls of selective norepinephrine repuptake inhibitors (SNRIs) (Co-analgesics for pain)
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
What is the MOA of anti seizure drugs (Carbamazepine / oxcarbazepine)
1. Decreased repetitive action potential firing which inactivates sodium channels and will reduce pain signals
32
What are the CI of carbamazepine / oxcarbazepine
1. CI is hypersensitive to TCAs *Steady state is in 21 to 28 days
33
What are the warnings of carbamazepine / oxcarbazepine
1. Hyponatremia 2. Fetal harm 3. Suicidality 4. Ghost capsule in feces
34
What are the neurological ADRs of carbamazepine
1. Drowsiness 2. Ataxia 3. Vertigo 4. Diplopia 5. Blurred vision
35
What are the hematologic ADRs of carbamazepine
1. Agranulocytosis 2. Severe blood dyscrasias
36
What are the dermatological ADRs of carbamazepine
1. Pruritis 2. SJS / TEN
37
What are the GI/Hemostasis ADRs of carbamazepine
1. Weight gain 2. Osteoporosis
38
How is oxcarbazepine (trileptal) compared to carbamazepine
1. Less adverse effects 2. Increased incidence of Hyponatremia 3. More expensive
39
What drug has the MOA of inhibition of presynaptic reuptake of norepinephrine and serotonin
Doxepin
40
What drug has the MOA of reduced excitiation and enhance inhibition of motor neurons
Tizanidine
41
What drug has the MOA of decreased repetitive action potential firing which downstream reduces pain signals
Carbamazepine

Pharm Spring 2023 (27 decks)

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