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41 Cards in this Set
- Front
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Glaucoma drugs
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1. alpha agonist:
EPI, brimonidine *decrease aq humor SYNTHESIS (vasoconstriction) *don't use EPI in closed angle glaucoma! 2. Beta-blocker: timolol, betaxolol, carteolol *decrease aq humor SECRETION 3.Diuretics: Acetazolamide *decrease aq humor secretion due to decreased bicarb 4. Cholinomimetics: Direct: pilocarpine, carbachol Indirect: physostigmine, echothiophate *increase outflow of aq humor; contract ciliary muscle and open trabecular meshwork **pilocarpine in emergencies 5. PGs: Latanoprost (PGF2alpha) *increase OUTFLOW of aq humor darkens color of iris (lengthens eye lashes) |
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Opioids
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Mu: morphine
delta: enkephalin kappa: dynorphin open K+ channels, close Ca2+ --> decrease synaptic transmission -inhibit release of ACh, NE, 5-HT, glutamate, substance P use: pain, cough suppression, diarrhea, pulm edema Tox: addiction, resp depression, pinpoint pupils, constipation, additive CNS depression with other drugs *do not develop tolerance to miosis and constipation |
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Butorphanol
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partial agonist at opioid mu receptors
agonist at kappa use: pain; less resp depression (can use in women in labor) Tox: causes withdrawal if on full opioid agonist |
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Tramadol
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weak opioid agonist
also inhibits 5HT and NE reuptake use: chronic pain, not addictive tox: similar to opioids **decreases seizure threshold |
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1st line tonic clonic
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Phenytoin
Carbamazepine Valproic acid |
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1st line px for status epilepticus
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Phenytoin
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1st line partial simple or complex
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Carbamazepine
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1st line absence
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ethosuximide
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1st line acute status epilepticus
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Benzo (diazepam or lorazepam)
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Tx tonic clonic AND absence
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valproic acid
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Phenytoin
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use-dependent blockade of Na channels; increase refractory period
-inhibit glutamate release from excitatory presynaptic tx: tonic clonic also a IB antiarrhythmic tox: nystagmus, diplopia, ataxia, sedation gingival hyperplasia hirsutism megaloblastic anemia (decrease folate absorption) peripheral neuropathy teratogen: fetal hydantoin syndrome SLE-like induces p450 Fosphenytoin for parenteral |
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Carbamazepine
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increases Na channel inactivation
TRI CARBs **first line trigeminal neuralgia, tonic clonic Tox: diplopia, ataxia agranulocytosis, aplastic anemia liver tox teratogen induces p450 SIADH Stevens-Johnson |
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Lamotrigine
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Blocks voltage-gated Na channels
tox: stevens johnson |
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Gabapentin
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GABA analog, but primarily inhibits HVA Ca2+ channels
tx: partial; tonic clonic; peripheral neuropathy, bipolar disorder Tox: sedation, ataxia |
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Topiramate
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blocks Na channels
increases GABA action Tox: sedation, mental dulling, kidney stones, weight loss |
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Phenobarbital
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partial seizures, tonic-clonic
increases GABAa action **1st line in pregnant; children tox: sedation tolerance, dependence induce p450 |
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Valproic acid
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1st line tonic clonic
also tx partial, absence, myoclonic seizures increase Na channel inactivation increase GABA concentration Tox: GI rare but fatal HEPATOTOX neural tube defects tremor weight gain CI in pregnancy |
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Seizures of preeclampsia
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MgSO4
Benzos |
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Seizures in pregnant women, children
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Phenobarbital
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Ethosuximide
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1st line absence
blocks thalamic T-type Ca2+ channels EFGH: Ethosuximide Fatigue GI HA urticaria Stevens-Johnson |
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Tiagabine
Vigabatrin Levetiracetam |
Tiagabine: inhibits GABA reuptake
used for partial seizures Vigabatrin: irreversibly inhibits GABA tarnsaminase to increase GABA -for partial seizures Levetiracetam: may modulate GABA and glutamate release -for partial and tonic-clonic |
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Barbiturates
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phenobarb, pentobarb, thiopental, secobarbital
facilitate GABAa action by increasing DURATION of Cl- channel opening, thus decrease neuron firing use: sedative, seizures, insomnia, induce anesthesia (thiopental) Phenobarb increases liver metab, used in Criglar-Najjar II to induce glucuronyltransferase Tox: resp or CV depression, induce p450 for OD: symptomatic |
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Benzos
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Facilitate GABAa action by increasing FREQUENCY of Cl- channel opening
decrease REM sleep use: anxiety, spasticity, status epilepticus: lorazepam, diazepam detox/DTs: chlordiazepoxide night terrors, sleepwalking, anesthetic, hypnotic OD: FLUMAZENIL (competitive antagonist at GABA benzo receptor) SHort acting: Triazolam Oxazepam Midazolam Alprazolam Med: (10-20h) Estazolam Lorazepam Temazepam Long: (days) Chlordiazepoxide Clorazepate Diazepam Flurazepam ***benzos, barbs, and alcohol all bind GABA(A)-R, a ligand-gated Cl channel |
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nonbenzo hypnotics
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Zolpidem, Zaleplon, Eszopliclone
act at BZ1 receptor subtype; reversed by FLUMAZENIL use: insomnia tox: ataxia, HA, confusion *rapid metab by liver, so short duration |
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Anesthetics
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CNS drugs must be lipid soluble to cross BBB or be actively transported
Decreased solubility in blood: rapid induction and recovery time Increased solubility in lipid = increased potency = 1/MAC MAC: min alveolar concentration at which 50% pop is anesthetized, varies with age N2O: low blood and lipid solubility, fast induction and low potency Halothane: high lipid and blood solubility, high potency, slow induction Mechanism: lungs: increase rate and depth of ventilation --> increased gas tension Blood: increased blood solubility = increase blood/gas partition coeff = increase solubility = increase gas required to saturate blood = SLOWER onset of action Tissue: increase AV concentration gradient = increase solubility = increase gas required to saturate tissue = slower onset |
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Inhaled anesthetics
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-ane
+ nitrous oxide effect: myocardial depression, resp depression, nausea/emesis, increase cerebral blood flow (decrease cerebral metabolic demand) tox: Halothane: hepatotox methoxyflurane: nephrotox Enflurane: seizures N2O: expansion of trapped gas malignant hyperthermia |
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Thiopental
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high potency, high lipid solubility, rapid entry into brain
-induction of anesthesia and short surgical procedures -effect terminated by rapid redistribution into tissue and fat -decrease cerebral blood flow |
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Midazolam
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MC drug for endoscopy
-used with gas anesthetics and narcotics may cause severe postop resp depression decrease BP amnesia |
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Arylcyclohexylamines
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Ketamine
PCP analog; dissociative anesthetic BLocks NMDA receptors CV stimulant disorientation, hallucination, bad dreams increase cerebral blood flow (ACTIVE DREAMS!) |
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Opiates
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Morphine, fentanyl
used with other CNS depressants during general anesthesia fentanyl: no histamine release |
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Propofol
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Rapid anesthesia induction and short procedures
less postop nausea than thiopental **potentiates GABAa -not for long term use bc high in TGs |
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Local anesthetics
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Esters: procaine, cocaine, tetracaine (1 I)
Amides: lidocaine, mepivacaine, bupivacaine (2 I's) BLock Na channels by binding to specific receptors on inner portion of channel -preferentially bind activated Na channels, so most effective in rapidly firing neurons tertiary amines penetrate membrane in uncharged form, then bind ion channels as charged form 1. infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively (more needed) 2. Orer of nerve blockade: small myelinated > small unmyelinated > large myelinated > large unmyelinated order of loss: pain > temp > touch > pressure 3. Except cocaine, given with vasoconstrictors (EPI) to enhance local action; decrease bleeding, increase anesthesia by decrease systemic concentration use: minor surgical procedures, spinal anesthesia Tox: CNS excitation, severe CV tox (bupivacaine), HTN, hypotension, arrhythmias (cocaine) |
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Succinylcholine
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depolarizing, non-competitive neuromuscular blocker
for muscle paralysis in surgery or mechanical ventilation *selective for motor (vs autonomic) nicotinic receptor) Phase I: prolonged depolarization; no antidote; block potentiated by cholinesterase inhibitor Phase II: repolarized but blocked; cholinesterase inhibitor reverses (neostigmine) tox: hyperCa, hyperK |
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Nondepolarizing neuromuscular blockers
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-curar
vecuronium, rocuronium are rapid onset competitive: compete with ACh for receptors reverse blockade with cholinesterase inhibitor |
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Dantrolene
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tx: malignant hyperthermia (caused by -anes and succ) neuroleptic malignant syndrome (antipsychotics)
Mech: prevent release of Ca from sarcoplasmic reticulum of skeletal muscle |
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Parkinson's drugs
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BALSA:
Bromocriptine: DA agonist; ergot derivative pramipexole, ropinirole (non-ergot) Amantadine: increase DA release; tox = ataxia Levodopa/carbidopa: increase DA in CNS Selegiline: MAO-B inhibitor, prevents DA breakdown entacapone, tolcapone (COMT inhibitors, prevent L-dopa degradation) Benztropine: antimuscarinic, improves tremor and rigidity, but little effect on bradykinesia) Surgery: lesion STN Deep brain stimulation |
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L-dopa/carbidopa
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Increase DA in brain
L-dopa crosses BBB, converted to DA by dopa decarboxylase Carbidopa: peripheral decarboxylase inhibitor Tox: arrhythmias dyskinesia after dose; akinesia between doses |
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Selegiline
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Selectively inhibits MAO-B (in Brain), which normally metabolizes DA over NE and 5HT
use with L-dopa -may enhance adverse effects of L-dopa |
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Alzheimer's drugs
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Memantine:
NMDA receptor antag; helps prevent excitotox mediated by Ca Tox: dizziness, confusion, hallucinations (like ketamine) Donepezil, galantamine, rivastigmine AChE inhibitors Tox: nausea, dizziness, insomnia |
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Huntington's drugs
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Disease: increase DA, decrease GABA and ACh
reserpine + tetrabenazine: amine depleting Haldol: DA receptor antag |
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Sumatriptan
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5-HT 1b/1d agonist
vasoconstriction inhibition of trigeminal activation and vasoactive peptide release Use; migraine, cluster HA Tox: coronary vasospasm, mild tingling CI: CAD or Prinzmetal's, pregnant |
