Muscle Relaxants Flashcards
1
Q
Anti-spastic Drugs
A
- Refers to agents specific for skeletal muscle
-
Reduce spasticity that interferes with daily living
- Such as that caused by cerebral palsy, multiple sclerosis, and spinal cord injuries
2
Q
Anti-spasmodic Drugs
A
- Refers to an agent that relieves spasms
- Adjuncts to rest, PT, and other measures for relief of discomfort ass. with MSK disorders
- Widely used but not superior to NSAIDS
- May be used when NSAIDS are not effective for a particular patient
3
Q
Classification of Drugs
A
4
Q
Spasticity
A
Characterized by:
- ↑ activity in 1a afferents ⇒ ↑ tonic stretch reflexes
- ↑ flexor muscle spasms
- Muscle weakness
- Also input from higher centers in the CNS
5
Q
Role of GABA
A
- GABA released from inhibitory interneuron in spinal cord
- Major role in modulating 1a afferents and alpha motor neurons
- Transmitter of the Ia “axon” is probably glutamate
- Two GABA receptors named A and B
6
Q
GABA-A Receptors
A
-
Chloride ion channel
- Binding of GABA to the receptor ⇒ channel opens
- Chloride to flow down its electrochemical gradient
- Binding of GABA to the receptor ⇒ channel opens
-
Present on:
-
Dendrites of alpha motor neurons
- Reversal potential for chloride close to or more ⊖ than resting membrane potential
- Activation ⇒ influx of chloride ⇒ hyperpolarization or stabilization of the neuron
-
Terminals of 1a afferents
- Reversal potential for chloride above resting potential
- Activation ⇒ chloride efflux ⇒ depolarization
- GABA mediated depolarization alone is not robust enough to cause neurotransmitter release
- ⊗ neurotransmitter release by disrupting the activation of Na+ channels and Ca2+ influx
-
Dendrites of alpha motor neurons
7
Q
GABA-A Receptor
Activation
A
Benzodiazepines ⊕ effect of GABA at GABA-A receptors
8
Q
GABA-B Receptors
A
-
Metabotropic receptors
- ↑ K+ conductance ⇒ hyperpolarization of cellular membranes
- ↓ Ca2+ influx
-
Present on:
-
Terminals of the 1a afferents
- Mediates presynaptic ⊗ of the release of excitatory neurotransmitters
-
Dendrites of alpha motor neurons
- Causes hyperpolarization
-
Terminals of the 1a afferents
9
Q
GABA-B Receptor
Activation
A
Baclofen mimics the action of GABA at GABA-B receptors
10
Q
α2 Adrenergic Receptors
A
Activation ⇒ ↓ cAMP
- On 1a afferent terminal ⇒ ↓ release of glutamate
-
On alpha motor neurons ⇒ ⊗ activity of the neuron
- Mechanism is not clear
11
Q
Benzodiazepines
MOA
A
Diazepam and other benzodiazepines:
Act by ⊕ allosteric modulation of GABA-A receptor activity in the CNS including the spinal cord
Interact with their own receptor on GABA-A complex ⇒ ↑ binding of GABA to its receptor site ⇒ more frequent opening of the chloride channel
12
Q
Benzodiazepines
Effects
A
-
Antispastic effect in pts w/ spinal cord transection
- Action involves effects directly in the cord
- ↓ spasticity associated with many etiologies
- ↓ of muscle tone in pts w/ central lesions usu. requires large, sedating doses
13
Q
Baclofen (Lioresal)
MOA
A
GABA-B agonist
14
Q
Baclofen (Lioresal)
Pharmacokinetics
A
-
Rapidly and completely absorbed after PO administration
- Oral administration not always effective
- Long-term intrathecal infusion used
- T½ about 3-4 hr
- Excreted primarily unchanged through renal excretion
- Give cautiously (with reduced dosage) in pts w/ impaired renal function
15
Q
Baclofen (Lioresal)
Uses
A
-
As effective as diazepam in reducing spasticity
- Alleviating sx of spasticity from MS
- Esp. flexor spasms and concomitant pain, clonus and muscular rigidity
- Value in pts w/ spinal cord injury and other spinal cord diseases
- Alleviating sx of spasticity from MS
- Less sedating than the benzodiazepine
-
May reduce muscle strength
- Less than benzodiazepines
- Not for skeletal muscle spasm from rheumatic disorders
- Baclofen has not helped patients with stroke
- Have not tolerated this drug well
