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98 Cards in this Set

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name Parkinson's drugs
BROMOCRIPTINE, AMANTADINE, LEVODOPA (w/carbidopa), SELEGILINE (and COMT inhibitors), antimuscarinics (eg BENZOTROPINE)
what parkinson drugs act to increase DA levels?
L-dopa/carbidopa, amantidine
why is L-dopa paired with carbidopa?
tho L-dopa crosses BBB, a large % will be decarboxylated to DA in periph, so it is paired w/carbidopa, a DA decarboxylase inhib that does not cross the BBB
toxicity of L-dopa?
arrhythmias from periph conversion to DA; long term use can cause dyskinesia after admin, and akinesia b/t doses (="on-off phenomenon")
what parkinson drugs act to agonize DA receptors?
BROMOCRIPTINE, PRAMIPEXOLE, ROPINIROLE
MoA of BROMOCRIPTINE?
D2 agonist and D1 antagonist
Clinical uses of BROMOCRIPTINE?
parkinson's, **hyperprolactinemia**, suppression of lactation in non-nursing moms, acromegaly (mediated by D1 antag, b/c DA increases GH s/c)
what class is BROMOCRIPTINE in?
ergot alkaloid
what parkinson drugs act to prevent DA breakdown?
SELEGILINE (MAO-B inhib); ENTACAPONE, TOLCAPONE (COMT inhibitors)
what drug is SELEGILINE usu paired with?
is used as adjunctive agent w/ L-dopa, but may also enhance adverse effects of L-dopa
what parkinson drugs act to curb excess cholinergic activity?
antimuscarinics, eg BENZTROPINE
BENZTROPINE has the greatest effect on which parkinson's sx?
tremor, rigidity; but little effect on bradykinesia
MoA of SUMATRIPTAN?
5HT1D agonist, causes vasoconstriction
clinical uses of SUMATRIPTAN?
acute migraine, cluster headache attacks
toxicity of SUMATRIPTAN? contraindications?
coronary vasospasm, mild tingling; contraind in pts with CAD or prinzmetal's angina
toxicity of BENZODIAZEPINES?
sedation, tolerance, dependence, additive CNS depress w/etoh (less risk of cardioresp dep/coma than barbs)
toxicity of CARBAMAZEPINE?
diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver tox, teratogenesis, induction of P450
toxicity of ETHOSUXIMIDE?
GI distress, lethargy, headache, urticaria, Stevens-Johnson syndrome
toxicity of PHENOBARBITAL?
sedation, tolerance, dependence, induction of P450 (thus many drug interactions), cardioresp depress (->death), additive CNS depress w/etoh
toxicity of PHENYTOIN?
nystagmus, diplopia, ataxia, sedation, SLE-like syndrome, induction of P450; w/chronic use: gingival hyperplasia in kids, periph neuropathy, hirsutism, megaloblastic anemia (dec folate absor), malig hypertherm (rare); teratogenic (fetal hydantoin synd)
toxicity of VALPROIC ACID?
GI distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain
toxicity of LAMOTRIGINE?
Steven-Johnson synd
toxicity of GABAPENTIN?
sedation, ataxia
toxicity of TOPIRAMATE?
sedation, mental dulling, kidney stones, weight loss
MoA of PHENYTOIN?
use dependent blockade of Na channels (binds when in inactivated state and prolongs refrac period), inhib' glutamate release from excitatory presyn neurons
clinical uses of PHENYTOIN?
first line tonic clonic, first line status epilepticus prophylaxis, also used for partial seizures; also used as class IB antiarrhythmic
MoA of CARBAMAZEPINE?
use dependent blockade of Na channels (binds when in inactivated state and prolongs refrac period)
clinical uses of CARBAMAZEPINE?
1st line tonic clonic
1st line trigeminal neuralgia
good for partial seiz
2nd line bipolar d/o
MoA of LAMOTRIGINE?
blocks voltage-gated Na channels
clinical uses of LAMOTRIGINE?
partial, tonic clonic
MoA of GABAPENTIN?
increases GABA release
clinical uses of GABAPENTIN?
partial, tonic clonic, peripheral neuropathies (neuropathic pain syndromes)
MoA of TOPIRAMATE?
inactivates Na channels (same as phenytoin, carbamazapine); potentiates GABA-ergic transmiss; blocks glutamate at AMPA/kainate receptors
clinical uses of TOPIRAMATE?
partial, tonic clonic
MoA of PHENOBARBITAL?
inc GABA-A action by inc DURATION of Cl channel opening, thus dec neuronal firing
can barbituates alone be lethal?
yes; b/c at high doses, barbs can directly activate GABA channel
clinical uses of PHENOBARBITAL?
partial, tonic clonic
1st line in pregnant women, kids
contraindic of BARBITUATES?
**porphyria**
tx of BARBITUATE o.d.?
sx management (assist respirations, inc BP, etc)
MoA of VALPROIC ACID?
inc GABA accumulation, inc Na channel inactivation
clinical uses of VALPROIC ACID?
1st line myoclonic, tonic clonic
partial
absence (2nd line unless pt has other seizures too)
mood stabilizer in mania
MoA of ETHOSUXIMIDE?
blocks low-threshold T-type Ca channels (provide pacemaker current in thalamic neurons)
clinical uses of ETHOSUXIMIDE?
1st line absence seizures
MoA of BENZODIAZEPINES?
enhance GABA-A by inc FREQUENCY of Cl channel opening
Clinical uses of BENZOS?
anxiety, spasticity, detox (esp etoh), night terrors, sleepwalking, 1st line status epilepticus (lorazepam and diazepam)--also used to prevent seizures of eclampsia
Tx for BENZO O.D.?
FLUMAZENIL (competitive agonist at GABA receptor)
name BENZOS
DIAZEPAM, LORAZEPAM, TRIAZOLAM, TEMAZEPAM, OXAZEPAM, MIDAZOLAM, CHLORDIAZEPOXIDE, ALPRAZOLAM
short acting BENZOS?
TRIAZOLAM, OXAZEPAM, MIDAZOLAM
(TOM thumb)
name inhaled anesthetics
HALOTHANE, ENFLURANE, ISOFLURANE, SEVOFLURANE, METHOXYFLURANE, NITROUS OXIDE
how does potency of inhaled anesthetics relate to lipid solubility?
potency is directly proportional to lipid solubility
clinical effects of inhaled anesthetics?
myocard dep, resp dep, naus/emesis, inc cerebral blood flow (dec cerebral metabolic demand)
SE/toxicity of inhaled anesthetics?
malig hyperthermia (w/gen predisp, causes massive release of Ca stores, tonic musc contrac); hepatotox (HALOTHANE); nephrotox (METHOXYFLURANE); proconvulsant (ENFLURANE)
what is the solubility and potency of NITROUS OXIDE? how does this impact is usage?
used in conjunction w/others b/c can't produce complete anesth alone; low blood and lipid solubility, thus fast induction and low potency, which permits close regulation of the level of anesth; is also least likely to dec BP or inc pCO2
classes of IV anesthetics?
barbituates, benzos, ketamine (arylcylcohexamines), opiates, propofol
name BARBITUATES
PHENOBARBITAL, PENTOBARBITAL, THIOPENTAL, SECOBARBITAL
time of onset on THIOPENTAL?
unconsciousness 15-30sec after admin
what characteristics are responsible for fast onset/short duration of THIOPENTAL?
high pot, high lipid solubility (crosses BBB fast, but also has fast redistribution to other organs)
clinical uses of THIOPENTAL?
induction of anesth in combo w/inhaled anesth', often in short surgical procedures
effect of THIOPENTAL on cerebral blood flow?
it decreases cerebral blood flow and O2 consumption by brain
what drug is most commonly used for endoscopy?
MIDAZOLAM
clinical indications for BENZOS
pre-op sedation, intra-op sedation (if analgesia not required), in combo w/other agents
why is MIDAZOLAM a good pre-op agent?
it produces antegrade amnesia (loss of mem after admin of drug), which calms pt
what type of anesthesia does KETAMINE produce?
dissociative anesthesia (=catatonia, amnesia, analgesia w/o loss of consc)
clinical indications of KETAMINE
trauma cases where CV support needed; in kids during painful procedures, to facilitate pt coop
CV effects of KETAMINE?
stim' sympathetic NS -> CV stim (inc HR, art BP, CO)
effects of KETAMINE on cerebral blood flow?
INC' cerebral blood flow (thus is NOT used in head trauma cases)
SEs of KETAMINE?
halluc, bad dreams, disorientation
name opioids used as IV anesthetics
MORPHINE, FENTANYL
MoA of MORPHINE
binds mu-opioid recep -> dec NT release from presyn nocioceptive neurons, and hyperpol' and inhib' postsyn neurons
clinical uses of MORPHINE?
severe pain, acute pulm edema (venodil->dec preload->dec perception of SOB)
SEs of MORPHINE?
dependence, w/drawl, O.D., constipation (dec motility), biliary colic (inc sphincter of Oddi tone), naus/vom
sx of OPIOID withdrawal?
lacrimation, rhinorrhea, sweating, gooseflesh, nausea, tachypnea
sx of OPIOID O.D.?
coma, pinpoint pupils, resp dep
tx for OPIOID O.D.?
NALOXONE (=pure antag at opioid mu recep)
uses of PROPOFOL?
rapid anesth induction and short procedures (similar pharm-dynam as thiopental, but w/less postop nausea)
what are the 2 types of local anesthetics?
ester and amide anesthetics
name ester anesthetics
PROCAINE, COCAINE, TETRACAINE
name amide anesthetics
LIDOCAINE, MEPIVACAINE, BUPIVACAINE
MoA of local anesthetics?
block Na channels by binding on inside of membrane, thus block nerve conduc
how does charge affect mech/binding of local anesthetics?
tert amine local anesth' penetrate memb in uncharged form, bind as charged form
what dosing adjustments must be made for local anesthetics when used on infected (acidic) tissue?
must use more, b/c in acidic envir anesth' are charged and can't penetrate membrane effectively
what is the order of nerve blockade by local anesthetics?
rapidly firing>slowly; smaller>larger; myelinated>unmyel (less impt)

ex. very small unmyel pain fiber>small myel ANS fiber>large myel ANS fiber
order of sensation loss with local anesthesia?
pain>temp>touch>pressure
what type of drug are local anesthetics commonly paired with? why?
vasoconstrictors (alpha-1 agonist, eg. epi)-> enhance local action, inc duration of action (limits removal/metab of drug), dec bleeding
clinical uses of local anesthetics?
minor surg procedures, spinal anesthesia
toxicity of local anesthetics?
CNS excitation (restlessness, paresthesias, tinnitus, convulsions); myocard dep and hypotens, except cocaine, which causes vasocons and hypertens
clinical uses of neuromuscular blocking drugs
musc paralysis in surg or mechanical ventilation
name depolarizing neuromusc blockers
SUCCINYLCHOLINE
MoA of SUCCINYLCHOLINE?
PHASE 1 (prolonged depol): binds motor nicotinic recep, opens Na chan, memb depol, transient fasic'->flaccid paralysis

PHASE 2 (repolarized but blocked): memb partially repol', but is desens'd to ACh, preventing further APs
Is there an antidote to SUCCINYLCHOLINE during PHASE 1 blockade?
no
what happens if give cholinesterase inhibitor during PHASE 1 SUCCINYLCHOLINE blockade?
the block is potentiated by AChE inhib
is there an antidote to PHASE 2 SUCCINYLCHOLINE blockade?
yes: AChE inhib (eg neostigmine)
name nondepolarizing neuromuscular blocking drugs
TUBOCURARINE, ATRACURIUM, MIVACURIUM, PANCURONIUM, VECURONIUM, RAPACURONIUM
MoA of nondepol neuromusc blockers?
competitively block chol transmiss at nic recep by preventing ACh from binding to receptor
can nondepol neuromusc block be reversed?
yes: AChE inhibitors (eg neostigmine, edrophonium, etc)
concomittant admin of what two drugs causes malignant hyperthermia?
inhalation anesthetics (except N2O) and succinylcholine
clinical uses of DANTROLENE?
tx of malignant hyperthermia, and neuroleptic malignant syndrome
MoA of DANTROLENE?
prevents release of Ca from sarco retic of skel musc