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78 Cards in this Set
- Front
- Back
Parkinsonism -
mechanism of dz -loss of _ neurons -excess _ activity |
loss of dopaminergic neurons
excess cholinergic activity |
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Parkinsonism -
name the drugs: "BALSA" |
Bromocriptine
Amantadine Levodopa (with carbidopa) Selegiline (and COMT inhib) Antimuscarinics |
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Which drugs...
Agonize dopamine receptors |
-Bromocriptine (ergot alkaloid and partial dopamine agonist)
-Pramipexole -Ropinirole |
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Which drugs...
increase dopamine |
-Amantadine (may increase DA release)
-L-dopa/carbidopa (converted to DA in CNS) |
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Which drugs...
prevent dopamine breakdown |
Selegiline (selective MAO type B inhibitor)
Entacapone (COMT inhibitor) Tolcapone (COMT inhibitor) |
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Which drugs...
curb excess cholinergic activity |
Benztropine (Antimuscarinic)
-improves tremor and rigidity -but little effect on bradykinesia |
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L-dopa's other daym
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levodopa
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l-dopa/carbidopa:
-mechanism |
-increases level of DA in brain.
-unlike DA, L-dopa can cross BBB and is converted by DOPA DECARBOXYLASE in the CNS to DA |
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L-dopa/carbidopa:
-toxicity -longterm toxicity |
-Arrhythmias (peripheral conversion to DA -> decreased by Carbidopa)
-Longterm -> dyskinesia following administration, akinesia between doses |
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Carbidopa
-mechanism |
A peripheral dopa decarboxylase inhibitor
-given with L-dop to increase bioavailability of L-dopa in brain, and to limit peripheral side effects (i.e. arrhythmias) |
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Selegiline
-mech -clin use -toxicity |
-Selective MAO-B inhibitor, thereby increased availability of dopamine
-adjunct to L-dopa in tx of Parkinson's dz -may enhance adverse effects of L-dopa |
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Sumatriptan
-mech, t 1/2 -clin use -tox & CONTRAINDICATOINS |
-5-HT(1D) Agonist -> Vasoconstriction (t 1/2 = 2hrs)
-for acute migraine, cluster HA attacks -Tox: coronary vasospasm, mild tingling CONTRAINDICATED in CAD or PRINZMETAL's ANGINA |
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1st Line Epilepsy drugs for
- tonic-clonic sz (3) - absence sz (1) - acute status sz (1) |
-phenytoin, carbamazepine, valproic acid
-ethosuximide -diazepam, lorazepam |
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1st line drug for trigeminal neuralgia
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carbamazepine
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epilepsy drug also a class Ib antiarrhythmic
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phenytoin
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epilepsy drug also used for peripheral neuropathy
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Gabapentin
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1st epilepsy drug in pregnant women, children
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phenobarbital
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Epilepsy drug also used for MYOCLONIC SZs
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valproic acid
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1st line for acute Status/generalized sz, also used for seizures of eclamspia
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benzodiazepines (diazepam, lorazepam)
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1st line to prevent seizures of eclampsia
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MgSO4
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1st line for PROPHYLAXIS of status/generalized szs
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phenytoin
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phenytoin
-mechansim -1st line for...(2) |
increases Na+ channel inactivation (use-dependent blockage)
-inhibition of glutamate release for excitatory presynamptic neuron -tonic-clinic sz, prophy for status/gen sz |
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carbamazepine
-mech -1st line for (1) -special use (1st line) |
increases Na+ channel inactivation
-tonic-clonic sz -trigeminal neuralgia |
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Lamotrigine
-mech -used for... (3) |
-blocks VOLTAGE-gated Na+ channels
-for partial (simple, complex) and tonic clonic szs |
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Gabapentin
-mech -used for... -special use |
increases GABA release
-for partial (simple, complex) and tonic clonic szs, and PERIPHERAL NEUROPATHY |
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Topiramate
-mech -used for... |
-blocks Na+ channels AND increases GABA action
-for partial (simple, complex) and tonic clonic szs |
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Phenobarbital
-mech -used for... (3) -special use |
-increases GABA-A action (by increases DURATION of Cl-channel opening)
-for partial (simple, complex) and tonic clonic szs -1st line in pregnant women and children |
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Valproic acid
-mech -1st line for -also used for -another use |
-increases Na_channel inactivation AND increases GABA concentration
-1st line for tonic-clonic -for partial (simple, complex) and tonic clonic szs -also for ABSENCE szz -also for myoclonic szs |
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ethosuximide
-mech -1st line for |
-blocks thalamic T-type Ca2+ channels
-absence szs |
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benzodiazepines (diazepam, lorazepam)
-mech -1st line for ... (1) -also used for... (1) |
-increases GABA-A action
-ACUTE status/generalized szs -for seizures of eclampsia (MgSO4 is 1st line to prevent) |
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Benzo toxicities
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-Sedation
-Tolerance -Dependence |
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Carbamazepine toxicity
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-Diplopia
-Ataxia -AGRANULOCYTOSIS, APLASTIC ANEMIA -LIVER toxicity -teratogenesis -induction for cytochrome P-450 |
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Ethosuximide toxicity
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-GI distress
-Lethargy -HA -Urticaria -Stevens-Johnson syndrome |
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Phenobarbital toxicity
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Sedation
Tolerance/dependence Induction of cytochrome P-450 |
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Phenytoin toxicity
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-Nystagmus
-Diplopia -Ataxia -Sedation -GINGIVAL HYPERPLASIA (kids) -HIRSUTISM -megaloblastic anemia (decrease folate absorption) -teratogenic (fetal hydantoin syndrome) -SLE-like syndrome -induction of cyt P-450 -malignant hyperthermia (rare) |
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Valproic acid toxicity
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-GI distress
- HEPATOXICITY (rare but fatal -must MEASURE LFTs) -NTD (spina bifida) -tremor -weight gain |
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Lamotrigine toxicity
(1) |
Stevens Johnson syndrome
-(hypersensitivity complex affecting the skin and the mucous membranes ~ toxic epidermal necrolysis) |
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Gabapentin
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Sedation
Ataxia |
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Topiramate
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Sedation
Mental dulling KIDNEY STONES Weight loss |
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Barbiturates
- name 4 |
Phenobarbital
Pentobarbital Thiopental SECObarbital |
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Barbiturates
-mechanism |
factilitate GABA-A action by increasing DURATION of Cl- channel opening (thus decreasing neuron firing)
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Barbiturates
-clin use -contraindicated in... (1) |
-sedative for anxiety
-sezures -insomnia -induction of anesthesia (thiopental) *Contraindicated in porphyria |
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Barbiturate toxicity
-important: -additive effect with (1) -_ or _ depression (can lead to death) -drug interactsion d/t ) |
-Dependence
-ADDITIVE CNS depression with Alcohol -resp or CV depression can lead to death -drug interaction d/t induction of liver microsomal enzymes (cyt P-450) |
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Treatment for Barbiturate overdose
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Symptom mgmt (assist respiration, increase BP)
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Benzodiazepines
name them (8) |
diazepam, loarzepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam
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Benzos
-mechanism: facilitate GABA-A action by... hint: "FREnzodiazepines" |
increasing FREQUENCY of Cl-channel opening
-most have long half-lives and active metabolites |
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Short-acting benzos
"TOM thumb" |
Triazolam
Oxazepam Midazolam |
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Benzos - clinical use
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-anxiety, spasticity
-acute STATUS EPILEPTICUS (lorazepam and idazepam) -detoxification (esp alcohol withdrawal - DTs) -night terrors -sleep walking |
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Benzo toxicity
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dependence
ADDItive effect with EtOH *less risk of resp depression ad coma with barbiturates |
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Benzo overdose treatment
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FLUMAZENIL
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Flumazenil
-mech |
competitive antagonist at GABA receptor
-treat benzo overdose |
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Anesthetics Principles
-to reach CNS, drugs must be ___-soluble (cros BBB) or be actively transported |
lipid-soluble
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Anesthetic drugs with decreased solubility in BLOOD have ___ induction and recovery times (slow or rapid?)
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rapid
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Anesthetic drugs with increased solubility in LIPIDS have ___ potency = 1/MAC
MAC = ? |
increased potency
MAC = minimal anesthetic concentration |
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N2O has low blood and lipid solubility.
Is induction fast or slow? Is potency high or low? |
Induction fast
Potency low |
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Halothane has high blood and lipid solubility.
Is induction fast or slow? Is potency high or low? |
Induction is slow
Potencty is high |
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Inhaled Anesthetics
-name them -mechanism? unknown! |
Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide
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Inhaled anesthetics
effects what happens to cerebral blood flow? |
myocardial depression
respiratory depression nausea/emesis INCREASED CEREBRAL BLOOD FLOW (decreased cerebral metabolic demand) |
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Inhaled anesthetics: Toxicity
-Halothane -Methoxyflurane -Enflurane |
Halothane - Hepatotoxicity
Methoxyflurane - Nephrotoxicity Enflurane - Proconvulsant *malignant hyperthermia (rare) |
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Intravenous anesthetics:
name the types (5) Hint: B.B. King on OPIATES PROPOses FOOLishly |
Barbiturates (thiopental)
Benzodiazepine (Midazolam) arylcyclohexamines (Ketamine) Opiates (morphine/fentanyl) Propofol |
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Barbiturates (IV anesthetic)
-Thiopental features -Anesthesia use -Termination of effect -effect on cerebral blood flow? |
high potency, high lipid solubility, rapid entry into brain
-for induction of anesthesia and SHORT surgical procedures -DECREASES cerebral blood flow |
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Benzos (IV anesthetic)
-Midazolam -Anesthesia use -toxicity/antidote |
-most common drug for ENDOSCOPY
-adjunctive to inhaled anesthetics and narcotics -tox - resp depression, decreased bp (tx: flumazenil), AMNESIA |
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Ketamine (IV anesthetic)
-mech -tox -effect on blood flow? |
-PCP analog - act as DISSOCIATIVE ANESTHETICS
-CV stimulants tox - disorientation, hallucination, bad dreams *INCREASES cerebral blood flow |
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Opiates (IV anesthetic)
-morphine, fentanyl |
used with other CNS depressants during general anesthesia
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Propofol (IV anesthetic)
-use -less __than thiopental |
-for rapid anesthesia induction and SHORT procedures
-less post-op nausea than thiopental |
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LOCAL anesthetics
-type of compounds (2) -name them |
ESTERS: procaine, cocaine, tetracaine
AMIDES: lidocaine, mepivicaine, bupivacaine (2 i's in name) |
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LOCAL anesthics
-mechanism *how do tertiary amines bind? |
block Na+ channels by binding to specific receptors on inner portion of channel
*tertiary amine local anesthetics penetrate mb in uncarged form, then bind to ion channels as charged form |
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LOCAL Anesthetic principles
1 of 3: how much anesthetic needed in infected tissue? |
Infected tissue is acidic -> anesthetics are charged and cannot penetrate membrane effectively.
*More anesthetics needed in this case |
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LOCAL Anesthetic principles
2 of 3: order or nerve blockade; order of sensation loss |
Nn blockade:
Diameter: small > large Myelin: myelinated > unmyelinated *Size factor predominates over myelination: v.small unmyelinated pain fibers > small myelinated autonomic fibers > large myelinated autonomic fibers Order of sensation loss: Pain (first) > temp > touch > pressure (last) |
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LOCAL Anesthetic principles
3 of 3: why given with vasoconstrictors (epi)? |
to enhance local action
-decreases bleeding -increases anesthesia by decreases systemic concentration |
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LOCAL Anesthetic
-clinical use -if allergic to esters? give what? |
minor surgical procedures
spinal anesthesia -if allergic to esters, give amide |
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LOCAL anesthetic toxicities
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CNS excitation
severe CV toxicity (BUPIVICAINE) HTN hypotension Arrhythmias (COCAINE) |
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Neuromuscular blocking agents
-use |
for mm. paralysis in surgery or mechanical ventilation
*selective for motor (vs. autonomic) NICOTINE receptor |
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Name the
-Depolarizing neuromusc blocker (1) -Nondepolarizing (6) |
-Succinylcholine
-Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rapacuronium |
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Depolarizing nueromuscular blocker = Succinylcholine
*Reversal of blockade with ?: PHASE 1 PHASE 2 |
PHASE 1 (prolonged depolarization) - NO ANTIDOTE (block potentiated by cholinesterase inhibitors)
PHASE 2 (repolarized but blocked) - ANTIDOTE = CHOLINesteraSE INHIBITOR (eg, NEOSTIGMINE) |
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Nondepolarizing neuromuscular blocking agents - mechanism
-reversal of blockade with... (3) |
-competitive with ACh for nicotinic receptors
*reversal of blockade with NEOSTIGMINE, EDROPHONIUM, and other cholinesterase inhibitors |
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Dantrolene
-clinical use (2) |
-for MALIGNANT HYPERTHERMIA (caused by concomitatn use of inhalation anesthetics except N2O and succinylcholine)
-also to treat NEUROLEPTIC MALIGNANT SYNDROME (toxicity of antipsychotic drugs) |
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Dantrolene
-mechanism |
prevents release of Ca2+ from sarcoplasmic reticulum of skeletal muscle
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