⭐ LECTURE 5: ANTI-SPASTICITY DRUGS AND MUSCLE RELAXANTS Flashcards
Selective filtration of the CNS capillaries via tight junctions between capillary endothelial cells
BLOOD-BRAIN BARRIER (BBB)
nonpolar, lipid-soluble drugs
PASSIVE DIFFUSION
polar and lipophobic compounds
CARRIER-MEDIATED TRANSPORT
initiation of neurotransmitter release
PRESYNAPTIC ACTION POTENTIAL
no synthesis = no neurotransmitter
NEUROTRANSMITTER SYNTHESIS
storage of the neurotransmitter
STORAGE
block the transmitter catabolism in the presynaptic terminal
METABOLISM
site of drug action; increases synaptic activation
RELEASE
allows more neurotransmitters to stay in the synaptic cleft
RE-UPTAKE
serves as a negative feedback
IONIC CONDUCTANCE
Exerts a calming and relaxing effect
SEDATIVE-HYPNOTIC DRUG
Emotional state characterized by excessive feelings of worry, fear, and nervousness
Treated with anxiolytic drugs
ANXIETY
state of sleep
HYPNOSIS
inability to initiate, maintain, or achieve restful sleep
INSOMNIA
Reduces the activity level of a neuron making it less likely to fire
GABA
GABAA RECEPTOR for sedation
Alpha-1
Beta-2
Gamma-2
GABAA RECEPTOR for Anxiolytic
Alpha-2
Beta-3
Gamma-2
abundant in the limbic system including amygdala for panic and fear response
GABAA
Increase the affinitty of GABA that increases the influx of chloride ions at the postsynaptic cell and Results in decreased anxiety and greater feeling of calm
BENZODIAZEPINES
Increase affinity of GABA → chloride channel opening → membrane hyperpolarization
NON-BENZODIAZEPINES
Decrease the activity of excitatory neurotransmitters (ACh and Glutamate)
BARBITURATES
Exaggerated muscle stretch reflex that occurs following an INJURY TO THE CNS
SPASTICITY
Continuous, tonic contraction of specific muscles described as increased tension in skeletal muscle
SPASM
Binds to GABAA receptor increasing GABA induced inhibition at the synapse
DIAZEPAM (VALIUM)
Cause global decrease in CNS excitability → generalized sedation → skeletal muscle relaxation
CENTRALLY-ACTING ANTI SPASM DRUGS
Blocks mono and polysynaptic reflexes by activating GABAB receptors and blocking release of excitatory neurotransmitters
BACLOFEN (LIORESAL, TRILAXANT)
Stimulates alpha-2 adrenergic agonist receptors in the brainstem → decreased release of excitatory neurotransmitter (pre and postsynaptic inhibition)
CLONIDINE (CATAPRES) AND TIZANIDINE (ZANAFLEX)
Peripherally acting
DANTROLENE SODIUM (DANTRIUM, RYANODEX)
Blocks mono and poly synaptic reflexes by activating GABAA receptors that increases the influx of chloride ions at postsynaptic cell
DIAZEPAM (VALIUM, VALZEPAM, TRANKIL) AND CLONAZEPAM (RIVOTRIL, KLONOPIN)
Antiepileptic drug
Gabapentin
New analog of gabapentin that may also prove useful
Pregabalin
Centrally acting muscle relaxant
Centrally acting muscle relaxant
Inhibitory amino acid neurotransmitter
Glycine
Centrally mediated and carries no direct peripheral action on the affected muscles
CYCLOBENZAPRINE
Structurally related to diphenhydramine and carries relatively stronger anticholinergic weaker sedative properties
ORPHENADRINE
Prescribed for nocturnal leg muscle cramps
QUININE
Centrally acting muscle relaxant with an unknown mechanism
METAXALONE
Produces its muscle relaxant effect by depressing the interneuronal activity at the spinal cord level as well as in the descending tracts of the reticular formation
CARISOPRODOL
Prevents ACh release from presynaptic membrane, causing temporary calming of muscle contractions by blocking nerve impulse transmission at the neuromuscular junction
BOTULINUM TOXINS (BOTOX, DYSPORT, XEOMIN, MYOBLOC)
Gamma fibers are demyelinated for about 6 months resulting in a less irritable, weakened muscle
and is peripherally acting
PHENOL
