CNS drugs Flashcards
what do all GABAnergic drugs cause as a preliminary response
paradoxical disinhibition
what does GABAa activation cause
increased chloride entry into the cell. this results in membrane hyperpolarization
what do benzodiazepams do to GABA channels
they potentiate GABA. shifts the dose-response to the left. a smaller dose has the same effect. they just increase the frequency of opening the channel.
do benzos have GABAnergic activity
no they dont.
what does BZ1 mediate
sedation
what does BZ2 mediate
cognitive effect. mediates anxiety and impairment. anterograde amnesia.
what is alprazolam used for and why
anxiety, panic, phobias. long half-life
what is diazepam used for and why
anxiety, preop sedation, muscle relaxation, withdrawal. log half-life
what is lorazepam used for
anxiety, preop sedation, statis epilepticus. long half-life
what is midazolam used for
preop anesthesia. ultra short half-life
what is temazepam used for
sleep disorders. short half life
what is oxazepam
sleep disorders and anxiety
barbiturates mechanism
prolong the GABA activity. increase the duration of chloride opening. greater hyperpolarization.
are barbs GABAnergic
yes. they will open the channels by themselves. they have their own receptors.
what else do the barbs do?
inhibit complex I of the electron transport chain. through this mechanism they can cause irreversible toxicity
what are the barbs contraindicated in
porphyrias. this occurs because the barbs increase P450’s and all P450s have heme.
is there cross-dependence between the barbs, benzos, and ethanol
yes. people who have tolerance to alcohol will also show tolerance to the rest
withdrawal of benzo
rebound insomnia, anxiety, seizures when they were used at high doses or for antiepileptic
withdrawal from barbs and ethanol
anxiety, agitation, life-threatening seizures (delirium tremens)
what are the important interactions for the CNS depressants
their effects are additive with other CNS depressants, such as antihistamines, opiates, anesthetics, beta-blockers
what do barbs do to metabolic panel
induce lipid metabolism such as lipid soluble drugs, oral contraceptives, carbamazepine, phenytoin, warfarin
what are the non-BZ drugs
zolpidem and zoleplon
what are zolpidem and zoleplon
BZ1 agonists, they have less cognitive effects and are used in the treatment of insomnia.
what do we treat benzos with
flumazenil
what do all alcohols do to the CNS
cause depression. GABAmimetic activity. all alcohols cause metabolic acidosis.
what does ethylene glycol do
CNS depression, ATN due to crystals in the kidney,metabolic acidosis.
what does methanol do
causes respiratory failure, acidosis, ocular damage
what is the toxic metabolite of ethylene glycol
oxalic acid
what is the toxic metabolite for methanol
formaldehyde
what is the toxic metabolite of ethanol
acetyladehyde
what does ethanol do
CNS depression, acidosis
what does acute ethanol do to the body
N/V, HA, hypotension, combines with folate and thiamine
what is chronic alcoholism do to the body
hypoglycemia, fatty liver and lipemia, muscle wasting, gout
what are the drugs of choice for partial-simple or complex seizures
valproic acid, phenytoin, carbamazepine
DOC for general tonic clonic
valproic acid, phenytoin, carbamazepine
DOC for absence seizures
ethasuximide and valproic
DOC for statis epilepticus
lorazepam, diazepam, phenytoin, fosphenytoin
what is the mechanism of action for phenytoin
decreases axonal conduction by preventing Na+ influx through fast Na channels.
what other drug shares phenytoin’s mechanism
carbamezepine
what is the mechanism of action for benzos
increases inhibition by GABA mediated hyperpolarization
what other drugs share benzo’s general mechanism?
barbiturates, even though this isnt entirely accurate.
what is the general mechanism of action for lamotrigine, topiramate, felbrate
decreases the excitatory effects of glutamic acid.
what is the general mechanism for ethosuximide and valproic acid
decreases Ca influx through T type channels in thalamic neurons
phenytoin mechanism
blocks Na channels in the inactivated state.
does phenytoin prevent seizure propagation or initiation
does NOT prevent initiation, it does prevent propagation.
what are the uses of phenytoin
seizure states, except absence.
what are the kinetics for phenytoin
variable absorption, zero order elimination, nonlinear kinetics. it induces p450
SE of phenytoin
CNS depression. gingival hyperplasia, hirsutism, osteomalacia, megaloblastic anemia, anaplastic anemia. it is a teratogen responsible for cleft-lip and palate.
carbamazepine mechanism
identical to phenytoin. sodium channel blocker in the inactivated state.
uses of carbamazepine
DOC for trigeminal neuralgia. seizure states, and bipolar (manic phase). not for use in absence
SE of carbamazepine
induces its own metabolism. CNS depression, osteomalacia, megaloblastic anemia, aplastic anemia. exfoliative dermatitis (SJS), increases ADH release. teratogen: causes cleft lip and palate and spina bifida.
valproic acid mechanism
blocks sodium channels in the inactivated state but also blocks GABA transaminase and increases the GABA. blockade of T-type calcium channels. (similar to phenytoin and ethosuximide)
uses of valproic acid
seizure states including absence. the manic phase of bipolar. migraine prophylaxis.
SE of valproic acid
INHIBITS p450. hepatotoxic, thrombocytopenic, pancreatitis, alopecia. teratogen: spina bifida.
ethosuximide mechanism
blocks t-type calcium channels in the thalamus
uses of ethosuximide
absence seizures
felbrate and lamotrigine
blocks sodium and glutamate receptors
uses of felbrate and lamotrigine
adjuvant to seizure state medicines,
SE of felbrate and lamotrigine
hepatotoxic, aplastic anemia, SJS.
gabapentin mechanism
increases the effects of GABA
uses of gabapentin
seizure states and neuropathic pain esp. postherpetic neuralgia.
SE of gabapentin
sedation
