What is the MOA of the first-line Alzheimer disease treatment
Donepezil - cholinesterase inhibitor - Boost the amount of ACh in the brain -> higher ACh in synapse, more likely to have a signal -> improve symptoms of dement
What is the first-line treatment for anxiety disorders
g
Justify the use of tPA in ischemic stroke
Alteplase
Identify two subclasses of sedative-hypnotics to treat insomnia. Include MOA
f
Explain the rationale for the use of fosphenytoin for seizure prophylaxis following TBI
Anticonvulsant - stabilize neuronal membranes & decrease seizure activity by increase efflux/decrease influx Na+ across cell membrane during generation nerve im
Outline how cannabinoids would alter action potentials to improve MS-related spasticity.
Cannabinoids decrease the release of pre-synaptic glutamate-> decrease the amplitude of EPSPs-> decrease excitability of motor pathway in CNS ->
Distinguish abortive and preventative pharmacotherapies for migraine headache.
h
Justify the use of diuretics in the treatment of Meniere's disease
Theoretically improves symptoms by reducing the endolymph volume but high-quality studies on the effect of diuretics are lacking
Identify the MOA of the six different drug therapies used to manage PD symptoms
COMT inhibitor (Tolcapone)) and MAO-B inhibitor (Selegiline) ->
Identify a physiologic rationale for the declining efficacy of carbidopa-levodopa treatment over time in PD.
d
What is the MOA of the second-line Alzheimer disease treatment
Memantine - NMDA receptor blocker - decreases effects of glutamate (known to cause neuronal toxicity)
Rationalize the use of mannitol in acute TBI
reduce ICP by reducing blood viscosity -> increases cerebral blood flow and oxygen transport and constricts pial arterioles -> reduce cerebral blood volume, ICP
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