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opioid analgesics- Mechanism of action
open k+ channels, close ca+2 channels, decrease synaptic transmission.
Inhibit the release of Ach, NE, 5-HT, glutamate, substance P
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Dextromethorphan Clinical use
Pain and cough suppression
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Methadone
Acute pulmonary edema, maintenance for addicts
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Opiod analge toxicity
- Respiratory depression
- Constapation
- Pinpoint pupils
- CNS depression
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Overdose of Opiod Analgesic Treatment
- Naloxone
- Naltrexone (opiod receptor antagonist)
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Butorphanol Mechanism of action
Partial agonist at opioid mu receptors, agonist at kappa receptors
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Butorphanol Clinical Use
Pain, Causes less respiratory depression than Full agonists
Labor and Delivery
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Tramadol Mechanism of action
- Very Weak opiod agonist
- Inhibits 5-HT, NE reuptake
- (works on multiple transmitters Tam-it-all)
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Tramadol Clinical Use
- Chronic Pain
- Migraines
- (those with addictive personalities)
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Tramadol toxicity
Lowers seizure threshold
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Alpha agonist- Epinephrine MOA in glaucoma
Decrease aqueous humor production due to vasoconstriction
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Epinephrine Side effects
- Mydriasis
- stiniging
- not used in closed angle glaucoma
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Beta Blockers (Timolol, betaxolol, cartelolol) MOA in glaucoma
Decrease aquous humor secretion
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Diuretics (acetazolamide) MOA n Glaucoma
Decrease aqueous humor secretion due to decrease bicarb via inhibition of carbonic anhydrase
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Cholinomimetics (Direct: carbachol, pilocarpine)
Indirect( Physostigmine) MOA in Glaucoma
- increase outflow of aqueous humor
- contract ciliary muscle
- open trabecular meshwork
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Cholinomeimetics Side effects
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Prostaglandins (latanoprost) MOA in Glaucoma
Increase aqueous humor outflow
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Latanoprost Side effect
Darkens color of iris
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Can most Epilepsey Drugs be used to treat Simple Partial, ANd Complex Partial seizures
Yes all except, ethosuximide and Benzo's
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Phenytoin MOA & Use
Increase Na+ channel inactivation
- 1st Line Tonic Clonic
- Prophylaxis in Status Epilepticus
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Drugs Used to Treat 1st Line tonic Clonic Seizures
Phenytoin, Carbamazepine, Valproic Acid
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Carbamazepine MOA & Use
Increase Na+ channel inactivation
First Line for Trigeminal Neuralgia
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Lamotragine MOA and Use
Blocks Voltage Gated Na+ Channels
Tonic Clonic
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Gabapentin MOA & Use
Gaba Analog
inhibits HVA Calcium Channels
Tonic clonic, peripheral neuropathy, bipolar disorder
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Topiramate MOA
- Blocks Sodium Channels
- increase Gaba action
"TO mechanisms"
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2 drugs Increase Gaba Action alone
Phenobarbital and Benzo's
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Phenobarb MOA & Use
Increase Gaba
1st line Pregnant Woman
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Use for Absence Seizures
- Ethoosuximide ist line
- Valproic acid
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Ethosuximide MOA
Blocks thalamie T-type Ca+2 Channels
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Used for Status Epilepticus
Benzo's (diazepam, Lorazepam)
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Prevents Seizures of Eclampsia second to MgSO4
Benzo's Diazepam or Lorazepam
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Tiagabine MOA
Inhibits Gaba reuptake
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Vigabatrin
- Irreversibly inhibits Gaba Transaminase
- Increases Gaba
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General Epilepsy Drug Toxicities
- Diplopia
- Sedation
- Ataxia
- Dizziness
- Nystagmus
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Phenytoin Toxicities
- Gingival Hypeplasia
- Hirsutism
- Megaloblastic anemia (decrease Fol)
- Teratogenic (fetal hydantoin Syndrome)
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BarbiDURATEs (phenobarb, pentobarb, thiopental, secobarb) MOA
Facilitate Gaba Action by increaseing DURATion of Cl- channel opening-- > decrease neuron firing
(gaba is inhibitory)
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Barbiturates Use
Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
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Inducers of p450
- "BCGPQRS"
- Barbiturates Carbamazepine Griseofolvin Phenytoin Quinidine
- Rifampine St. Johns Wart Alchohol
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Benzo'a (FREnzo's) MOA
Facilitate Gaba action by increaseing FREquency of Cl- channel opening
decrease REM sleep
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Short Acting Benzo's
"TOM"
- Triazolam
- Oxazepam
- Midazolam
Highest Addictive potential
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Used Primarily for Alcohol withdrawl
Chlordiazepoxide, Diazepam
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Benzo Overdose Treatment
Flumazenil- competitive antagonist at GABA Benzo receptors
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Halothane (inhaled Anesthetic)
- Low MAC, More potent
- High blood solubility longer induction
- More Lipid Soluble-More Potent, longer
- induction & recovery time
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Nitric Oxide (inhaled Anesthetic)
- High Mac Low Potency
- Low Blood Solubility, Rapid Induction
- Low Lipid Solubility less potent
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Thiopental (Barbiturate/IV Anesthetics)
High Potency, High Lipid Slouble, RAPID entry to brain
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Midazolam (benzo/IV anesthetic)
MC Drug used for endoscopy
Can cause: Amnesia, with post-op Cardio/resp depression
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Ketamine (PCP analog)
Block NMDA receptor
(NMDA receptors For learning and Memory)
Less respiratory/cardio depression Good for kids!
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Morphine/Fentanyl Use As IV anesthetic
Concious Sedation/general anesthesia
- (morphine histamine release itchy nose
- fenttanyl no histamine release)
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Propofol
Potentiates Gaba (inhibitory)
Rapid Anesthesia induction and short procedures
"milk of amnesia"/ high TG content/< N/V post op than thiopental
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Local Anesthetics
Esters: Procaine, Cocaine, Tetracaine
AmIdes: LIdocaIne, MepIvacaIne, BupIvacaIne
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Local Anesthetic MOA
Block Na+ channels, most effective in rapidly firing neurons
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Order of Nerve Blockade (local anesthetics)
Small myelinated> small Umylenated>large myelinated> large unmyelinated
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Order of Loss (local Anesthetics)
Pain>temp>touch>pressure
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Local Anesthetics excep cocaine should be given with?
Vasoconstrictors (Epinephrine) to enhance local action
decrease bleeding, increase anesthesia
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Neuromuscular Blocking Drugs Use
(Depolarizing and Nondepolarinzing)
Muscle Paralysis in surgery or mechanical ventilation
Selective for motor nicotinic receptor
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Succinylcholine (Depolarizing) MOA
imitates Ach at Nicotinic M receptors acting non-competitively, but then blocks the receptor
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Succinylcholine Reversal blockade
Phase I: Prolonged depolarization (block made worse/potentiated by cholinesterase inhibitors)
Phase 2: Repolarized but blocked- antidote is chonesterase inhibitors ie Neostigmine
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Nondepolarizing Neuromuscular Blockers
(Tubocurarine, atracurine,
mivacurium)
Competitive Ach receptor blocker
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Reversal Of Non-depolarizing blockers
Neostigmine, edrophonium, other cholinesterase inhibitors
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Dantroline MOA & Use
Preents the realeas of Ca+2 from SR of skeletal muscle
Malignant Hyperthermia-caused by use of inhaled anesthetics and succinylcholine together
Neuroleptic Malignant Syndrome- caused by toxicity of antipsychotic drugs
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Neuroleptic Malignant Syndrome
Muscle rigidity Fever, delirium, autonomic instability
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Malignant hyperthermia:
Myoglobinuria, excessmuscle contraction, hyperthermia, body decreases O2 supply, can't remove CO2 & regulate body temp
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Parkinsons Drugs
- "BALSA"
- Bromocriptine
- AMantadine
- Levodopa + Carbidopa
- Slegiline (COMT inhibitors)
- Antimuscarinics (Benztropine)
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Selegiline
- Inhibits MAO-B
- Prevents Breakdown of Dopamine in brain
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Entacapan, Tolcapan
inhibit COMT which usually converts levodopa to 3-O methyldopa.
SO it Increase [ Levodopa] in CNS which is then converted to dopamine by DDC (Dopamine DeCarboxylase)
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Alzheimers Drugs
Memantine- NMDA receptor antagonist prevents excitotoxicity mediated by Ca+ 2
Donepezil/Rivastigmine/Galantamine- Ach cholinesterase inhibitor therfore increase Ach
- Remember Alzheimers decrease Ach
- NMDA involved in learning and memory
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Huntigtons Disease & Treatment
Increase Dopamine, decrease GABA + Ach
Haloperidol Dopamine Receptor Antagaonist (decrease dopamine
Respirine + Tetrabenazine
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Sumatriptan
5-HT 1B/1D Agonist causes vasoconstriction
Migraines, Cluster headaches
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