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228 Cards in this Set
- Front
- Back
glaucoma drugs
|
p. 307
|
|
which alpha agonists are used to treat glaucoma
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epinephrine, brimonidine
|
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which beta blockers are used to treat glaucoma
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timolol, betxolol, carteolol
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which cholinomimetics are used to treat glaucoma
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pilocarpine, carbachol, physostigmine, echothiophate
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which diuretics are used to treat glaucoma
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acetazolamide, dorzolamide, brinzolamide
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which prostaglandin is used to treat glaucoma
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latanoprost
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what classes of drugs are used to treat glaucoma
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alpha agonists, beta blockers, cholinomimetics, diuretics, prostaglandins (*mnemonic -- treating glaucoma is easy as ABCD)
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what is the effect of epinephrine in glaucoma
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increase outflow of aqueous humor
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what are the side effects of epinephrine treatment in glaucoma
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mydriasis, stinging
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what glaucoma should epinephrine NOT be used for
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closed-angle glaucoma
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what is the effect of brimonidine in glaucoma
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decreased aqueous humor synthesis
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what are the side effects of brimonidine treatment in glaucoma
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no pupillary or vision changes
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what is the effect of beta-blocker treatment in glaucoma
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decrease aqueous humor secretion
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what are the side effects of beta blocker treatment in glauzoma
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no pupillary or vision changes
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what is the effect of cholinomimetics in glaucoma
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ciliary muscle contraction, opening of trabecular meshwork, increase outflow of aqueous humor
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what are the side effects of cholinomimetics in glaucoma
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miosis, cyclospasm
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what is the effect of diuretic treatment in glaucoma
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inhibition of carbonic anhydrase --> decrease HCO3 secretion --> decrease aqueous humor secretion
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what are the side effects of diuretics in glaucoma
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no pupillary or vision changes
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what is the effect of prostaglandin (latanoprost) treatment in glaucoma
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increase outflow of aqueous humor
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what is the side effect of prostaglandin treatment in glaucoma
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darkens color of iris (browning)
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which drugs used to treat glaucoma increase outflow of aqueous humor
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cholinomimetics, prostaglandin, epinephrine
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can you use epinephrine in closed-angle glaucoma
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NO
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brimonidine is used to treat what eye disease
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glaucoma
|
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what kind of drug is latanoprost
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prostaglandin
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latanoprost is used to treat what eye disease
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glaucoma
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which glaucoma drugs decrease aqueous secretion
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beta blockers, diuretics
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L-dopa/carbidopa
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p. 307
|
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what does L-dopa stand for
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levodopa
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what is the mechanism of action of L-dopa/carbidopa
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increase dopamine level in brain
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what is L-dopa/carbidopa used to treat
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Parkinson's disease
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how is L-dopa different from dopamine
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L-dopa can cross the blood-brain barrier, dopamine cannot
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what happens to L-dopa after it crosses the BBB
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converted to dopamine by dopa decarboxylase
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what enzyme convertes L-dopa to dopamine
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dopa decarboxylase
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what is the function of carbidopa
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peripheral decarboxylase inhibitor
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why is carbidopa given with L-dopa
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increase L-dopa availability in CNS by inhibiting decarboxylase in periphery, also limits peripheral side effects
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what are the side effects of L-dopa.carbidopa treatment
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arrhythmias, dyskinesias
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why do patients taking L-dopa get arrhythmias
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peripheral effects of dopamine
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why do patients taking L-dopa get dyskinesias
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excess dopamine stimulation in CNS
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Parkinson's disease drugs
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p.308
|
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what drugs are used to treat Parkinson's disease
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dopamine agonists, MAO inhibitors, antimuscarinics
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specifically, which drugs are used to treat Parkinson's
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Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics (BALSA)
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which dopamine agosts are used to treat Parkinson's
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L-dopa/carbidopa, bromocriptine, pramipexole, ropinirole, amantadine
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what is the action of bromocriptine in Parkinson's
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ergot alkaloid, partial dopamine agonist
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what is the action of amantadine in Parkinson's
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enhances dopamine release
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what MAOI is used to treat Parkinson's
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selegiline
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what is the mechanism of selegiline
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selective MAO type B inhibitor
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what antimuscarinic is used to treat Parkinson's
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benztropine
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what is the effect of benztropine in Parkinson's
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improves tremor, rigidity, little effect on bradykinesia
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Sumatriptan
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p. 308
|
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what is sumatriptan used for
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acute migraine, cluster headache attacks
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what is the mechanism of sumatriptan
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5-HT1D agonist
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what is the half life of sumatriptan
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less than 2 hours
|
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what are the side effects of sumatriptan
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chest discomfort, mild tingling
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what are the contraindications for sumatriptan
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patients with CAD or Prinzmetal's angina
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Epilepsy drugs
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p. 308
|
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which drugs are used for simple and complex partial seizures
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phenytoin, carbamazapine, lamotrigine, gabapentin, topiramate, phenobarbital
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what types of seizures is phenytoin indicated for
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simple and complex partial, tonic-clonic, status epilepticus
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what types of seizures is carbamazepine indicated for
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simple and complex partial, tonic-clonic
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what types of seizures is lamotrigine indicated for
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simple and complex partial, tonic-clonic
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what types of seizures is gabapentin indicated for
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simple and complex partial, tonic-clonic
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what types of seizures is topiramate indicated for
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simple and complex partial
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what types of seizures is phenobarbital indicated for
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simple and complex partial, tonic-clonic
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what drugs can be used for tonic-clonic seizures
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phenytoin, carbamazapine, lamotrigine, gabapentin, phenobarbital, valproate
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what drugs can be used for absence seizures
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valproate, ethosuximide
|
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what drugs can be used for status epilepticus
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phenytoin, benzodiazapines (diazepam, lorazepam)
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what types of seizure is valproate indicated for
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tonic-clonic, absence
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what types of seizure is ethosuximide inidcated for
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absence
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what type of seizure are benzodiazepines indicated for
|
status epilepticus
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other than anti-seizure, what else is phenytoin used for
|
class 1B anti-arrhythmic
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how should a patient taking carbamazepine be followed
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monitor LFT's weekly
|
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which seizure drugs have adjunct use
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gabapentin, topiramate
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which seizure drug is safest in pregnant women
|
phenobarbital
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which seizure drug is used in Crigler-Najjar II
|
phenobarbital
|
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what are the advantages of phenobarbital
|
can be used in pregnant women, Crigler Najjar II
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Epilepsy drug toxicities
|
p. 309
|
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what are the side effects of benzodiazepines
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sedation, tolerance, dependence
|
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what are the side effects of carbamazepine
|
diplopia, ataxia, CYP induction, blood dyscrasias, liver toxicity
|
|
what are the side effects of ethosuximide
|
GI distress, lethargy, headache, urticaria, Stevens-Johnson syndrome
|
|
what are the side effects of phenobarbital
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sedation, CYP induction, tolerance, dependence
|
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what are the side effects of phenytoin
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nystagmus, diplopia, ataxia, sedation, ginigival hyperplasia, hirsutism, anemias, teratogenic
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what are the side effects of valproate
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GI distress, rare by fatal hepatotoxicity, neural tube defects (spina bifida)
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what are the side effects of lamotrigine
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life-threatening rash, Stevens-Johnson syndrome
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what are the side effects of gabapentin
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sedation, movement disorders
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what are the side effects of topiramate
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sedation, mental dulling, kidney stones, weight loss
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which anti-epileptic drug is teratogenic
|
phenytoin
|
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which anti-epileptic drug can cause dependence
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benzodiazepines, phenobarbital
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which anti-epileptic drug can cause neural tube defects
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valproate
|
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which anti-epileptic drugs can cause GI distress
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valproate, ethosuximide
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it is necessary to check LFT's with which anti-epileptic drugs
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carbamazepine, valproate
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which anti-epileptic drugs cause CYP induction
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phenobarbital, carbamazepine
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which anti-epileptic drugs can cause blood problems
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carbamazepine, phenytoin
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which anti-epileptic drugs can cause Stevens-Johnson syndrome
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lamotrigine, ethosuximide
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which anti-epileptic drugs can cause diplopia
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carbamazepine, phenytoin
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Phenytoin
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p. 309
|
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what is the mechanism of phenytoin action
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use-dependent blockade of Na+ channels
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what is the clinical application of phenytoin
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grand mal seizures
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what are the toxicities of phenytoin
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nystagmus, ataxia, diplopia, lethargy
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what are the chronic toxicities of phenytoin
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gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia, malignant hyperthermia (rare)
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should pregnant women take phenytoin
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NO -- teratogenic
|
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why does phenytoin cause megaloblastic anemia
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causes decreased vitamin B-12
|
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Barbiturates
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p. 309
|
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name 4 barbiturates
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phenobarbital, pentobarbital, thiopental, secobarbital
|
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what is the mechanism of barbiturate action
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increase duration of Cl channel opening --> decreased neuron firing --> facilitate GABA-A action
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how do barbiturates facilitate GABA-A action
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increase duration of Cl channel opening which decreases neuron firing (Barbidurate increases duration
|
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is barbiturate action on the CNS stimulatory or inhibitory
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inhibitory
|
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what is the clinical application of barbiturates
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sedative for anxiety, seizures, insomnia, anesthesia induction (thiopental)
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which barbiturate is used for anesthesia induction
|
thiopental
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what are the side effects of barbiturates
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dependence, additive CNS depression effects with alcohol, respiratory or CV depression (death), drug interactions due to CYP induction
|
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what should you find out before giving a patient barbiturates
|
what other medications they take, because of CYP induction and many drug interactions
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what happens if you give barbiturates to a patient in alcohol-induced coma or DT's
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they might DIE!! Because of additive effect of barbiturates and alcohol --> respiratory depression
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when are barbiturates contra-indicated
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porphyria
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can barbiturates cause dependence
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YES
|
|
My friend Barb was very anxious so her doctor gave her barbiturates to increase the duration of the time she could speak in public without freaking out and having a seizure. She became so dependent on it that she recommended it to her friend Portia who couldn't take it because of porphyria. One day Barb drank too much alcohol and took her barbiturates and never woke up! THE END
|
clinical pharmacology made ridiculous. Period
|
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Benzodiazepines
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p. 309
|
|
name a bunch of benzodiazepines
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diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide (all have ZZZ in them)
|
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what is the mechanism of benzodiazepines
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increase frequency of Cl channel opening --> facilitate GABA-A action (Frenzodiazepines increase frequency)
|
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which GABA receptors are facilitated by barbiturates and bezodiazepines
|
GABA-A
|
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what are the clinical applications of benzodiazepines
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anxiety, spasticity, status epilepticus (diazepam), detoxification (alcohol withdrawal, DT's)
|
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which benzodiazepine can be used for status epilepticus
|
diazepam
|
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what drugs can be used to treat alcohol withdrawal
|
benzodiazepines
|
|
which benzodiazepines are short-acting
|
TOM thumb: Triazolam, Oxazepam, Midazolam
|
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what are the toxic effects of benzos
|
dependence, additive CNS depression effects with alcohol
|
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how are benzos better than barbiturates
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less respiratory depression and coma risk
|
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how do you treat benzo overdose
|
flumazenil
|
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what is flumzenil used for
|
benzo overdose
|
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how does flumazenil work
|
competitive antagonist at GABA receptor
|
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can a patient become benzodiazepine dependent
|
YES
|
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are barbiturates or benzodiazepines used for alcohol withdrawal
|
benzodiazepines
|
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Antipsychotics (neuroleptics)
|
p. 310
|
|
what is another name for antipsychotics
|
neuroleptics
|
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name 4 antipsychotic drugs
|
thioridazine, haloperidol, fluphenazine, chlorpromazine
|
|
how do you keep benzos straight from antipsychotics
|
Benzos help 3rd year Jon Kazam be less anxious around patients: Shazam Kazam! Without antipsychotics patients talk like a crazy 'zine (well, not perfect, but I'm working on it)
|
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what is the mechanism of most antipsychotics
|
block dopamine D2 receptors
|
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what is the clinical application of antipsychotics
|
schizophrenia, psychosis
|
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what are the side effects of antipsychotics
|
extrapyramidal side effects (EPS), sedation, endocrine, muscarinic blockade, alpha blockade, histamine blockade
|
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what is a long-term effect of antipsychotic use
|
tardive dyskinesia
|
|
what is neuroleptic malignant syndrome
|
a side effect of antipsychotics; rigidity, autonomic instability, hyperpyrexia
|
|
how do you treat neuroleptic malignant syndrome
|
dantrolene, dopamine agonists
|
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what is tardive dyskinesia
|
side effect of neuroleptics; stereotypic oral-facial movements, may be due to dopamine receptor sensitization
|
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what is the "rule of 4" with EPS side effects from antipsychotic drugs
|
evolution of EPS side effects: 4 hours -- acite dystonia, 4 days -- akinesia, 4 weeks -- akasthesia, 4 months -- tardvie dyskinesia
|
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is tardvie dyskinesia reversible
|
often irreversible
|
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what is fluphenazine used for
|
schizophrenia, psychosis
|
|
Atypical antipsychotics
|
p. 310
|
|
name 3 atypical antipsychotics
|
clozapine, olanzapine, risperidone
|
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what type of antipsychotic is clozapine
|
atypical
|
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what type of antipsychotic is olanzapine
|
atypical
|
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what type of antipsychotic is risperidone
|
atypical
|
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what is the mechanism of atypical antipsychotics
|
block 5-HT2 and dopamine receptors
|
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what is the mechanism of clozapine
|
block 5-HT2 and dopamine receptors
|
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what is the mechanism of olanzapine
|
block 5-HT2 and dopamine receptors
|
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what is the mechanism of risperidone
|
block 5-HT2 and dopamine receptors
|
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what is the clinical application of clozapine
|
schizophrenia positive and negative symptoms
|
|
what is the clinical application of olanzapine
|
schizophrenia positive and negative symptoms, OCD, anxiety disorder, depression
|
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what is the clinical application of risperidone
|
schizophrenia positive and negative symptoms
|
|
how are atypical antipsychotics different from classic ones
|
atypicals treat positive and negative symptoms of schizophrenia, fewer extrapyramidal and anticholinergic side effects than classic antipsychotics
|
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which antipsychotics should be used to treat positive and negative symptoms of schizophrenia
|
atypical ones -- clozapine, olanzapine, risperidone
|
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which antipsychotics should be used for fewer side effects
|
atypical ones -- clozapine, olanzapine, risperidone
|
|
what is a potential toxicity of clozapine
|
agranulocytosis
|
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which antipsychotic drug can cause agranulocytosis
|
clozapine
|
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what test must be done weekly on patients taking clozapine
|
WBC count because of potential agranulocytosis
|
|
Lithium
|
p. 310
|
|
what is the mechanism of action of lithium
|
unknown; may be related to inhibition of phosphoinositol cascade
|
|
what is the clinical application of lithium
|
mood stabilizer for bipolar disorder
|
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how does lithium help people with bipolar disorder
|
prevents relapse and acute manic episodes
|
|
what are the side effects of lithium
|
tremor, hypothyroidism, polyuria, teratogenic
|
|
is it OK for women taking lithium to get pregnant
|
NO -- teratogenic
|
|
what does lithium cause polyuria
|
ADH antagonist --> nephrogenic diabetes insipidus
|
|
Antidepressants
|
pg 311
|
|
What do the following drugs inhibit: 1. MAO inhibitors, 2. Desipramine/maprotilline, 3. Mirtazapine and 4. Fluoxetine/trazodone?
|
1. MAO 2. NE reuptake 3. Alpha 2-R 4. 5HT reuptake
|
|
All of the above actions are ------synaptic
|
PRE
|
|
List the Tricyclic Antidepressants
|
pg 311 Imipramine, amitriptyline, desipramine, nortriptyline, clomipramine, doxepin
|
|
What are the three C's of their toxicity?
|
Convulsions, Coma, Cardiotoxicity (arrythmias). Also respiratory depression, hypyrexia.
|
|
How about toxicity in the eldery?
|
confusion and hallucinations due to anticholinergic SE
|
|
What is the mechanism of TCA?
|
block reuptake of NE and 5HT
|
|
What is the clinical uses of TCAs?
|
Endogenous depresion. Bed wetting - imipramine. OCD- clomipramine.
|
|
How are tertiary TCA's different than secondary in terms of side effects?
|
Amitriptyline (tertiary) has more anti-cholinergic effects than do secondary (nortriptyline). Desipramine is the least sedating.
|
|
what are the SE of TCAs?
|
sedation, alpha blocking effects, atropine-like anti cholinergic side effects (tachycardia, urinary retention)
|
|
Fluoxetine, sertraline, paroxetine, citalopram are what class of drugs?
|
pg 311 SSRI's for endogenous depression
|
|
How long does it take an anti-depressant to have an effect?
|
2-3weeks
|
|
How does the toxicity differ fromTCA's and what are they?
|
Fewer than TCA's. CNS stimulation - anxiety, insomnia, tremor, anorexia, nausea, and vomiting.
|
|
What toxicity happens with SSRI's and MAO inhibitors given together?
|
Seratonin Syndrome! Hyperthermia, muscle rigidity, cardiovascular collapse
|
|
What are heterocyclics?
|
pg 312 2nd and 3rd generation antidepressants with varied and mixed mechanisms of action. Used major depression.
|
|
Examples of heterocyclics?
|
trazodone, buproprion, venlafaxine, mirtazapine, maprotiline
|
|
Which one is used for smoking cessation?
|
Buproprion. Mechanism not known. Toxicity - stimulant effects, dry mouth, aggrevation of pyschosis
|
|
Which one used in GAD?
|
Venlafaxine - inhibits 5HT and DA reuptake. Toxicity - stimulant effects
|
|
which one blocks NE reuptake
|
maprotiline
|
|
Which one increases release of NE and 5HT via alpha 2 antagonism?
|
mirtazapine. Also potent 5HT Rantagonist. Toxicity - sedation, increase serum cholesterol, increase appetite
|
|
What is trazodone and it' SE?
|
primarily inhibits seratonin reuptake. Toxicity - sedation, nausea, priapism, postural hypotension
|
|
Give 2 examples of MAO
|
pg 312 phenelzine. Tranylcypromine
|
|
Mechanism and Clinical Uses?
|
non selevtive MAO inhibition. Atypical antidepressant, anxiety, hypochondriasis
|
|
What is the toxicity with tyramine ingestion (in foods) and meperidine?
|
Hypertensive crisis
|
|
Other toxicities?
|
CNS stimulation, contraindicated with SSRI's or B-agonists
|
|
What is the mechanims of selgiline (deprenyl)?
|
pg 312 Selectively inhibits MAO-B, increasing DA
|
|
what is the clinical use and toxicity?
|
adjunctive agent to L-dopa for Parkinsons. May enhance adverse effects of L-dopa
|
|
Analgesics/ Anesthetics
|
pg 312
|
|
General principles
|
pg 312
|
|
What is the significance of drugs with decreased solubility in blood?
|
rapid induction and recovery times . Ie. N20
|
|
What is the significance of drugs with increased solubility in blood?
|
increased potency = I/ MAC. Ie. Halothane
|
|
Inhaled Anesthetics
|
pg 312
|
|
list them
|
halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide
|
|
What is good about lower solubility?
|
the quicker the anesthetic response, and the quicker the recovery
|
|
What are these drug's effects?
|
myocardial depression, respiratory depression, nausea/emesis, increase cerebral blood flow
|
|
What toxicity mactches the following drugs 1. Halothane 2. Methoxyflurane 3. Enflurane 4. Rare
|
1. Hepatotoxcity 2. Nephrotoxicty 3. Proconvulsant 4. Malignant hyperthermia
|
|
IV anesthetics
|
pg313
|
|
What do barbituates, benzodiazepines, arylcyclohexylamines and narcotic analgesics have in common?
|
they are IV anesthetics
|
|
What the pharmacokinetics and uses of thiopental?
|
high lipid solubility, rapid entry into brain. Used for induction of anesthesia for short surgical procedures. Terminated by redistribution from brain. Decreased cerebral blood flow
|
|
Give an example of a benzo and what is this class's shortcoming?
|
midazolam used for endoscopy. Used with gaseous anesthetics and narcotics. May cause severe post-op respiratory depressio and amnesia
|
|
What does Ketamine (PCP analog and an arylcyclohexylamine) do?
|
dissociative anesthetic. Cardiovascular stimulant. Causes disorientation, hallucination, bad dreams. Increases cerebral blood flow.
|
|
How are narcotic analgesics used? Examples?
|
Morphone and fentanyl are used with CNS depressant during general anesthesia.
|
|
What is the advantage of propofol
|
used for rapid anesthesia induction and short procedures. Less post-op nausea than thiopental
|
|
Local anesthetics
|
pg 313
|
|
Name some esters?
|
procaine, cocaine, tetracaine,
|
|
Name some amides?
|
lidocaine, bupivacaine, (amides have two I's in name!)
|
|
What is the mechanism and clinical use?
|
bind receptor and block Na channels. Tertiary amine local anesthetics penetrate membrane in uncharge form, then bind charged form. Use for minor surgical procedures, spinal anesthesia.
|
|
How do you decide to use ester or amides?
|
if allergic to esters, give amides
|
|
what is the toxicity
|
CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, arrhythmias (cocaine)
|
|
In infected ________ tissue, anesthetics are charged and cannot penetrate membrane. Therefore, ______ anesthetics are needed.
|
acidic; more
|
|
What is the order of nerve blockade for size and myelination? Which factor predominates?
|
small diameter> large diameter. Myelinated fibers> unmyelinated fibers. Size factor predominates
|
|
what is the order of loss of sensation?
|
pain first, then temp, then touch, then pressure
|
|
Why would you give these drugs with vasoconstrictors?
|
to enhance local action
|
|
Opiod analgesics
|
pg 313
|
|
List as many as you can.
|
morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan
|
|
Mechanism: They act as _____ for opiod receptors to modulate synaptic transmission
|
agonists
|
|
which drugs act at the mu, delta, kappa receptors?
|
morphine enkephalin, dynorphin
|
|
Clinical use?
|
pain, cough supression (dex), diarrhea (loperamide), acute pulmonary edema, methadone maintenance programs
|
|
What are the major toxicities?
|
addiction, respiratory depression, constipation, miosis, additive CNS depression wth other drugs
|
|
Tolerance does not develop to __________and ______
|
miosis and constipation
|
|
How would you treat toxicity?
|
naloxone, naltrexone (opiod R antagonist)
|