Neuromuscular Blockade and Muscle Spasms Quiz

Neuromuscular Blockade and Muscle Spasms

• Neuromuscular blockade learning points include terminology, neuromuscular transmission, spasticity-causing medical conditions, neuromuscular blocking drugs, and skeletal muscle relaxation mechanism.

• Muscle spasms treatment also includes drug uses, reversal mechanisms, safe pharmacy management, look-alike/sound-alike issues, and warnings.

Key Terms

• Acetylcholinesterase
• Anaphylactic shock
• Botulinum toxin
• Central-acting muscle relaxants
• Clonus
• Depolarizing neuromuscular blockers
• Endotracheal intubation
• End plate
• Neuromuscular junction
• Nondepolarizing competitive blockers
• Peripheral-acting muscle relaxants
• Sarcomere
• Sole plate
• Spasticity
• Amyotrophic lateral sclerosis (ALS)
• Cerebral palsy
• Multiple sclerosis
• Tetanus

Overview of Neuromuscular Function

• Skeletal muscle contraction results from communication between peripheral nerves and muscles.
• Acetylcholine (ACh) carries messages between nerve cells and muscle cells.
• Acetylcholine-filled vesicles are found in the motor neuron's endplate.
• Calcium is released to cause ACh release, and drugs that affect ACh release/depletion cause muscle relaxation.

Overview of Neuromuscular Blockade

• ACh binds to nicotinic receptor sites on the muscle soleplate.
• ACh binding triggers sodium, calcium, and potassium ion influx, increasing endplate potential.
• Endplate potential exceeding 15 mV produces an action potential, leading to muscle contraction.

Overview of Botulinum Toxin

• Found naturally (e.g., botulinum toxin, black widow spider venom)
• Decreases acetylcholine release.
• Used to temporarily remove wrinkles, treat excessive sweating, uncontrollable blinking, or migraines.

Skeletal Muscle Relaxants

• Categorized by site of action and mechanism of action.
• Two primary mechanisms involve central nervous system depression or blockade of nerve transmission between the motor endplate and skeletal muscle receptors.

Peripheral-Acting Skeletal Muscle Relaxants

• Includes non-depolarizing (e.g., atracurium, cisatracurium, pancuronium, rocuronium) and depolarizing (e.g., succinylcholine) agents.
• Used in surgery, general anesthesia, and intubation.
• Improper use can be dangerous, potentially fatal.

Botulinum Toxin Type A Uses

• Temporary wrinkle removal
• Excessive sweating control
• Treating uncontrollable blinking
• Treating migraines (not FDA approved for cerebral palsy related spasticity)

Neuromuscular Blocking Agent Adverse Reactions

• Allergic reactions (rash, redness, bronchospasm, laryngospasm, anaphylaxis)
• Muscle pain
• Respiratory depression
• Cardiac arrest
• Injection site reactions (itching, burning)
• Hypotension
• Vasodilation
• Tachycardia or bradycardia
• Pulmonary edema
• Hyperkalemia (depolarizing agents)
• Additional botulinum toxin-type A adverse reactions include droopy eyelids, headaches, nausea, flu-like symptoms, and redness.

Reversal of Neuromuscular Blockade

• Anticholinesterase drugs (neostigmine, pyridostigmine) inhibit ACh esterase, increasing acetylcholine.
• Adverse reactions include salivation, muscle twitching, weakness, abdominal cramping, nausea, increased bronchial secretions, and difficulty breathing.

Strategies for Safe Use of Neuromuscular Blocking Agents

• High-alert classification due to potential for harm from improper use.
• Risks include permanent injury, respiratory arrest, and death.

Recommendations for Pharmacy Practice with NMBAS

• Product selection, storage, and access limitations are crucial.
• Warning labels are necessary.
• Proper ordering and dispensing practices are essential.

Overview of Spasticity

• It is a debilitating motor disorder affecting 12 million worldwide.
• Interferes with daily living, inhibits walking, causes fatigue/stiffness, and disrupts sleep.
• Positive symptoms include increased muscle tone, exaggerated tendon reflexes, and hyperexcitable stretch reflexes.
• Negative symptoms include muscle weakness and reduced endurance.

Pathophysiology of Spasticity

• Four phases: decreased muscle contractility, increased muscle tone, decreased reflex excitability and stiff/contracted muscles are involved

Conditions That Produce Spasticity

• Spinal cord injury, stroke, cerebral palsy, amyotrophic lateral sclerosis (ALS), multiple sclerosis, and muscle strain lead to spasticity.

Spinal Cord Injury

• Initial paralysis.
• Loss of tendon reflexes below the injury level.
• Increased muscle tone, exaggerated tendon jerks, and involuntary muscle spasms.
• Stronger reflex connections develop.

Amyotrophic Lateral Sclerosis (ALS)

• Damage to upper motor neurons causes decreased acetylcholine release.
• Acetylcholine desensitization of motor nerves leads to muscle weakness and cell death.

Neurotransmitters Involved in Spasticity

• Acetylcholine, y-aminobutyric acid (GABA), glycine, and glutamate play roles in spasticity.

Drugs Used to Treat Spasticity

• Peripheral-acting drugs (e.g., botulinum toxins, dantrolene) and central-acting drugs (e.g., baclofen, diazepam, tizanidine) treat spasticity.

Drugs Used to Treat Muscle Strain

• Drugs like cyclobenzaprine, methocarbamol, orphenadrine, and chlorzoxazone+acetaminophen+codeine are used.
• Central acting drugs are often used.

Adverse Reactions and Warnings for Muscle Strain Treatments

• Dizziness, drowsiness, blurred vision, and urine discoloration are possible adverse reactions.
• Warnings include impairments to driving, alcohol avoidance, possible habit formation, and the need to take with food.

Additional Look-Alike Drug Warnings

• Be aware of look-alike/sound-alike drug names (e.g., baclofen and Bactroban, Lioresal and Lotensin, diazepam and Ditropan, tizanidine and nizatidine, and cyproheptadine and cyclobenzaprine) to avoid errors.