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178 Cards in this Set
- Front
- Back
- 3rd side (hint)
What do voltage-gated ion channels respond to?
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Changes in membrane potential.
(Metabotropic receptors can also modulate VG channels) |
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Give examples of VG channels.
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Na+ channels
K+ channels Ca2+ channels All located on neuronal axons |
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What are VG channels responsible for?
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Very fast action potentials from opening of the ion channel (due to changes in the membrane potential).
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How does a metabotropic receptor directly modulate a VG channel?
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On Ca2+ or K+ channels by G protein.
- Decreased Ca2+ = inhibition of NT release - Increased K+ channel opening (efflux) = slow inhibition - Direct action is LOCAL |
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How does a metabotropic receptor indirectly modulate a VG channel?
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By G protein and 2nd messengers.
Can occur over distances. |
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What do ionotropic (ligand-gated ion channel) receptors respond to?
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Respond to something (NT, neuromodulator) binding to it to open the ion channel.
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What are ligand-gated ion channels responsible for?
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Fast transmission from the opening of the ion channel (due to the NT activating the flow of specific ions through the channel).
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What is a ligand-gated ion channel typically like?
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They are typically made up of multiple subunits around a central pore. NT usually binds to one type of subunit.
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structure
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What do metabotropic (G protein-coupled) receptors respond to?
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The binding of a first messenger to set off the G protein cascade.
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What do metabotropic receptors generate?
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Second messengers, such as cAMP, IP3 and DAG (which then activate protein kinases).
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Compare metabotropic receptors to VG or LG ion channels?
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Metabotropic have longer lasting effects, but neurotransmission is slower.
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What is an excitatory post-synaptic potential (EPSP)?
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A small depolarization caused by the opening of Na+ or Ca2+ channels to allow influx.
(Not enough to cause AP unless summation to threshold) |
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What is an inhibitory post-synaptic potential (IPSP)?
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Hyperpolarization caused by 1) opening of K+ channel (efflux) or 2) opening of Cl- channel (influx).
Either one makes it harder for the cell to fire. |
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List general mechanisms of CNS drug action.
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1) Synthesis
2) Storage 3) Release 4) Reuptake 5) Metabolism ALSO: - Activation or blockage of pre- or post-synaptic receptors - Interference with 2nd messengers |
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What are hierarchical neuronal systems?
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- Clear anatomical distribution
- Large myelinated neurons (fast conduction) - Major sensory & motor functions |
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What are diffuse neuronal systems?
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- Broad distribution
- Neuronal systems that contain one of the monoamines (NE, EPI, DA, etc) - Single cells with many small synapses - Not myelinated (slow conduction) |
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What is GABA?
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The major inhibitory neurotransmitter in the brain. Causes IPSPs.
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What does GABA subtype A cause?
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GABA subtype A is a LG channel - it causes Cl- influx and hyperpolarization
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What goes GABA subtype B cause?
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GABA subtype B is a G protein-coupled receptor - it opens K+ channels or closes Ca2+ channels
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What do GABA-A antagonists do?
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Block fast IPSPs.
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What do GABA-B antagonists do?
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Block slow IPSPs.
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What are BDZs?
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BDZs are GABA-A agonists.
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What are antispasmotics?
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Antispasmotics, like Baclofen, are GABA-B agonists.
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What type of neurotransmitter is glycine? How does it work?
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Glycine is the major inhibitory neuron in the spinal cord.
MOA is increased Cl- conductance. |
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What type of neurotransmitter is glutamate?
What NT is similar to glutamate? |
Glutamate is the major excitatory NT in the brain.
- Aspartate is similar to glutamate. |
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What type of receptors does glutamate work on?
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LG-ion channels receptors:
- NMDA - AMPA - Kainate Metabotropic - mGluR 1-8 |
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Acetylcholine: CNS responses by G protein-coupled muscarinic receptors by causing?
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Slow excitation by decreasing K+ efflux
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ACh: how do nicotinic receptors work in the CNS?
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LG ion channel receptors -> cause excitation by increasing Na+ and K+ permeability
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Name the 4 monoamines.
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NE, EPI, DA, 5-HT
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What is the rate-limiting enzyme in catecholamine synthesis?
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The conversion of tyrosine to L-DOPA by tyrosine hydroxylase (TH)
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What is NET?
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NET is the NE transporter back into the pre-synaptic cell so that NE is conserved. It can be inhibited by cocaine & TCAs.
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What are autoreceptors?
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Transporters that the released NT uses to go back into the pre-synaptic cell. The NT itself regulates this receptor.
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Monoamines are metabolized by _______ and _______
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COMT and MAO (monoamine oxidase)
COMT metabolism is extraneuronal; MOA metabolism happens in the cytoplasm of nerve terminals |
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What types of MOA enzymes are there and where do they act?
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MAO-A mostly works in the body. MAO-B mostly works in the brain.
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Describe dopamine and its actions.
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Causes slow inhibition of neurons. Works on specific systems that involve motor function, addition and pleasure/reward.
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Describe the DA receptors.
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D1-D5 are G protein-coupled.
D1 group (D1/D5): excitatory with Gs = increased cAMP D2 group (D2/D3/D4): inhibitory with Gi = decreased cAMP |
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Describe NE receptors, and what they are involved with in the brain?
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All NE receptors are metabotropic. Involved in attention and arousal (locus ceruleus).
Inhibitory in locus ceruleus (Alpha2 receptors -> hyperpolarization by increased K+ conductance) |
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How is NE excitatory in the brain?
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Indirect: inhibits inhibitory neurons (disinhibition)
Direct: inhibits K+ conductance through Alpha-1 and Beta receptors |
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Describe serotonin receptors.
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All except 5-HT-3 are metabotropic.
5-HT-3 is ionotropic with rapid excitation at a few specific sites |
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Is serotonin inhibitory or excitatory?
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In most areas 5-HT is inhibitory but depends on receptor subtype.
- Mostly by 5-HT-1A -> increased K+ conductance - 5-HT-1A & GABA-B share same K+ channels |
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Name the peptide transmitters.
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Opioid peptides, substance P, cholecystokinin, VIP, neuropeptide Y
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Name 2 prototypes of TCAs.
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Imipramine (Tofranil)
Amitripyline (Elavil) |
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What is the MOA of TCAs?
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Block reuptake of NE & 5-HT by pre-synaptic terminals, causing increased NE & 5-HT availability for post-synaptic receptors.
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Describe the pharmacokinetics of TCAs.
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- Relief of sx after 2-3 wks
- Well absorbed PO - Highly bound to plasma proteins - Long half lives (ex- protripyline, 80hrs) |
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TCA Metabolism?
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CYP450, and then glucuronidation; many active metabolites
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What are the CNA effects of TCAs?
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- In non-depressed individuals - dysphoria, anxiety, sedation, difficulty concentrating & thinking
- sleep problems corrected |
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What are the neurologic side effects of TCAs?
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Seizures
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What are the anticholinergic side effects of TCAs?
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- Dry mouth
- Blurred vision - Constipation - Urinary retention |
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What are the cardiovascular side effects of TCAs?
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- Orthostatic hypotension (peripheral alpha receptor blockade)
- Tachycardia (cardiac muscarinic blockade / inhibition of NE reuptake) - Arrhythmias * Avoid in pts with pre-existing cardiac disease * |
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Other side effects of TCAs?
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Excessive sweating, weight gain, manic excitement, precipitate glaucoma (elderly w/narrow angle)
- Rarely: Jaundice, agranulocytosis, teratogenic effects! |
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What happens when TCAs are used in overdose/suicide attempts?
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- SEVERE anticholinergic effects
- Convulsions - Coma - Respiratory depression - Shock - Death |
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How do you treat a TCA overdose?
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- Gastric lavage
- Activated charcoal - NaHCO3 - diazepam and/or physostigmine (AChEI) |
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What are other uses of TCAs besides depression?
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- Enuresis
- Agorophobia - OCD (clomipramine) - Neurogenic pain |
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What are the DDIs with TCAs?
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- Potentiate effects of: EtOH & other CNS depressants, anticholinergic drugs, biogenic amines (NE, EPI)
- Use of MAOI + TCA causes hyperpyrexia, convulsions, death, serotonin syndrome |
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What is serotonin syndrome?
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Rare & fatal drug interaction due to excessive 5-HT. Results in hypertension, tachycardia, hyperthermia, myoclonus, change in mental status
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How do you treat serotonin syndrome?
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No specific antidote, so supportive tx.
(Can give cyproheptadine, a 5-HT anatagonist, and BDZs to help control sx) |
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Heterocyclics: what is the MOA of Amoxapine (Asendin)?
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NE reuptake blocker
(not used much) |
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Heterocyclics: what is the MOA of Maprotiline (Ludiomil)?
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NE reuptake blocker
(not used much) |
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Heterocyclics: what is the MOA of Trazodone?
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5-HT reuptake blocker
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Heterocyclics: what is the MOA of Bupropion (Wellbutrin)?
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MOA unknown.
(May block DA & NE reuptake) |
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Heterocyclics: what is the MOA of Venlafaxine (Effexor)?
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Blocks reuptake of NE & 5-HT (but 5-HT more)
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Heterocyclics: what is the MOA of Mirtazapine (Remerol)?
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5-HT reuptake blocker AND it increases amine release (Alpha-2 blocker)
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Heterocyclics: what is the MOA of Nefazodone (Serzone)?
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5-HT reuptake blocker
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Which heterocyclic has DA antagonist effects that cause restlessness, parkinsonism, tardive dyskinesia & amenorrhea-galactorrhea syndrome?
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Amoxapine (Asendin)
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Which heterocyclic causes less sedation and antimuscarinic effects than TCAs (but still some effects)?
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Maprotiline (Ludiomil)
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Which heterocyclic is a good hypnotic and causes priapism?
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Trazodone
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Which heterocyclic is used in depression and in smoking cessation?
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Bupropion
(Wellbutrin - depression) (Zyban - smoking cessation) |
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Which heterocyclic has a high risk of seizures, especially at high doses?
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Bupropion
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Which heterocyclic is a CYP450 inhibitor?
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Nefazodone (Serzone)
(But it's less sedating than Trazodone, and fewer sexual side effects than SSRIs) |
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Which heterocyclic has a sympathomimetic effect?
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At higher doses, Venlafaxine (Effexor) can increase pulse and BP.
At lower doses, it's like SSRIs. |
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Which heterocyclic has strong antihistamine effects, is more sedating and causes weight gain?
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Mirtazapine (Remerol)
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Which SSRI is a CYP450 inhibitor?
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Fluoxetine (Prozac)
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Which classes of drugs CAN'T MAOIs be co-administered with?
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TCAs and SSRIs
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What are the general adverse effects of SSRIs?
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Nausea, decreased libido, sexual dysfunction
(Serotonin syndrome when given with MAOIs) |
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What potency does nitrous oxide have and what is it's maximal safe concentration?
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It has low potency, & cannot produce Stage-III anesthesia on its own.
Maximal safe concentration = 70% |
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Name 4 volatile liquids mixed with gas to be used as inhaled anesthetics.
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1) Isoflurane
2) Halothane 3) Sevoflurane 4) Desflurane |
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What are IV general anesthetics used for?
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- To induce
- To maintain (in combination with other IV or inhaled drug) - For surgeries - In patients on mechanical ventilators |
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What is the general MOA of general anesthetics?
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Increasing action potential threshold (harder to fire) or interference with synaptic transmission.
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What part does GABA-A play in general anesthetics?
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General anesthetics bind to GABA-A receptor to potentiate GABA transmission by: increasing Cl- influx and hyperpolarization --> inhibition
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What does a low general anesthetic concentration do to GABA-A?
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It has an indirect effect at low concentrations - it enhances the efficacy of endogenous GABA (like BDZs)
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What does a high general anesthetic concentration do to GABA-A?
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It has a direct effect at high concentrations - it directly activates the GABA-A channel and opens it
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What else may be occurring for action with general anesthetics?
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- Increased K+ efflux -> hyperpolarization
- Decreased duration of action of nicotinic Na+ channels |
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Which general anesthetics DO NOT seem to function in the way of GABA-A, etc MOAs?
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Ketamine (dissociative), nitrous oxide, and xenon (inhibit NMDA excitatory receptors)
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Potency is _________ proportional to _________ solubility.
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directly
lipid |
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True or False?
Highly lipid soluble agents pass readily into brain and fat. |
True - more hydrophilic agents do NOT pass readily
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What is the minimum alveolar concentration of anesthetic (MAC)?
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The alveolar concentration of an anesthetic that is requires to prevent a response to a standardized painful stimulus in 50% of patients.
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A more potent anesthetic would have a ________ MAC value.
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Low
( ↓ MAC → ↑ Lipid Solubility → ↑ Potency ) |
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A more potent anesthetic would have a ________ oil-gas partition coefficient.
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High
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What is the effective MAC range?
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0.5 - 1.5 MAC is the goal range.
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MAC values are lowered in?
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- Elderly (need less, more sensitive)
- Hypothermia - When adjunct meds are used (opioids, sympatholytics, sedative hypnotics) |
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MAC values are ____________.
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additive
EX) N2O at 40% MAC + inhalant anesthetic at 70% MAC = 110% MAC |
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Rate of induction and recovery of inhaled general anesthetics are proportional to?
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1) Solubility of anesthetic in the blood
2) Concentration of anesthetic in the gas mixture 3) Respiratory rate 4) Pulmonary blood flow 5) Ateriovenous concentration gradient |
5 determinants
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Describe what the depth of inhaled anesthesia is related to.
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Depth of anesthesia results from the partial pressure (concentration) of anesthetic in the brain - the brain anesthetic concentration depends on its equilibrium with the blood anesthetic concentration.
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Describe the blood : gas partition coefficient in terms of induction.
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Blood is a large compartment that fills slowly before reaching brain. If the agent has ↑blood solubility there will be a slow induction time because it wants to spend time in the blood. If it has ↓blood solubility, then it has a rapid brain concentration & rapid induction.
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Achievement of a brain concentration of an inhaled anesthetic to provide adequate anesthesia requires?
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transfer of the anesthetic from the alveolar air to the blood AND from the blood to the brain
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Nitrous oxide and desflurane are relatively insoluble in blood - their blood:gas partition coefficient will be high or low?
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Low
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Halothane & isoflurane have moderate-to-high blood solubility - this means more molecules will...?
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More molecules will dissolve in the blood before the partial pressures change significantly - this means the concentration will increase less rapidly (slow induction)
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A higher concentration of anesthetic in the mix would do what to the rate of induction?
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It would make induction faster (gets faster into the blood).
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Anesthetic concentration in the blood is proportional to the ______ and ______ of ventilation.
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rate and depth
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An increase in pulmonary ventilation causes?
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A slight increase in low blood solubility agents but a bigger increase in higher blood solubility agents - so hyperventilation gives a rapid induction with slow induction agents.
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What is the effect of opioid induction in response to ventilation?
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Opioids cause a depression of respiration, so induction will be slow unless mechanically ventilated
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What effect does pulmonary blood flow have on inhaled anesthetics?
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More flow slows the rate of rise in arterial concentration - less flow will increase the rate of rise.
This is important for high solubility agents. |
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An increased arteriovenous gradient means?
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An increased time it will take to achieve equilibrium in the brain.
(venous blood has less anesthetic than arterial after tissue pickup -> gradient) |
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What are the highly perfused organs and what effect do they exert?
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Brain, heart, lungs, kidneys, liver, & spleen
These highly perfused organs exert the greatest effect during induction of anesthetics. |
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Describe elimination of inhaled anesthetics.
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Elimination is proportional to the rate of removal from the brain. Major route is through the lungs (some in the liver, ie, 40% halothane).
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Which is eliminated faster - blood insoluble or blood soluble inhaled agents?
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Blood-insoluble agents are limited faster (faster recovery).
(think blood:gas partition coefficient) |
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What do all inhaled anesthetics do to the mean arteriolar pressure (MAP)?
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All decrease MAP in proportion to their alveolar concentration.
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Halothane and Enflurane do what to blood pressure?
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Decrease BP by decreasing cardiac output (but little change in PVR)
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Isoflurane, desflurane, & sevoflurane do what to blood pressure?
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Decrease BP by decreasing PVR.
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What does halothane do to the pulse?
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Decreases SA node firing, causing bradycardia.
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What does desflurane, & isoflurane do to the pulse?
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Cause sympathetic activation, and tachycardia.
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All inhaled anesthetics, except N2O, does what to the respiratory system?
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- ↓ tidal volume & ↑ respiratory rate
- ↓ventilatory response to low O2 (ventilate mechanically) - Pooling of mucus (suctioning, atropine can ↓ bronchial secretions) |
3 things
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All inhaled anesthetics, except N2O, does what to the brain?
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- ↓ metabolic rate
- ↑cerebral blood flow due to ↓ vascular resistance (caution: ICP, head trauma) - ↓ "burst-firing" on EEG |
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All inhaled anesthetics, except N2O, does what to the kidneys?
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↓ GFR and ↓ renal blood flow
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All inhaled anesthetics, except N2O, does what to the liver?
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↓ hepatic blood flow
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Which volatile liquid causes hepatotoxicity?
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Halothane - liver damage at low O2 & with repeat exposures
- proteins made in its metabolism cause antibody formation & autoimmune hepatitis (transplant!) |
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Methoxyflurance and enflurane do what to the kidneys?
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Metabolism causes free fluoride ions that are nephrotoxic!
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What does sevoflurane do to the kidneys?
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Degradation by CO2 absorbents releases vinyl ether, causing proximal tubular necrosis!
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What is malignant hyperthermia syndrome?
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Genetic disorder of skeletal muscle from mutations on ryanodine receptors of SR => ↑free Ca2+
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Who does malignant hyperthermia syndrome occur in?
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Susceptible pts that got combo of muscle relaxants and inhaled anesthetics (esp. halogenated)
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What are the symptoms of malignant hyperthermia syndrome?
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Hyperthermia, tachycardia, hypertension, muscle rigidity & contractions, metabolic acidosis (lactic acid)
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How do you treat malignant hyperthermia syndrome?
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Dantrolene (blocks ryanodine receptor); cooling; restore pH back to 7.4
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What specific cardio effects does halothane have?
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sensitizes heart to catecholamines by increasing automaticity -> arrhythmias
(so use EPI, etc with caution) |
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What specific CNS effects does enflurane have?
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Seizures (high doses)
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What is the chronic toxicity of inhaled anesthetics?
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Increased risk of spontaneous abortion and decreased fertility
N2O causes megaloblastic anemia |
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Short-acting barbiturates, like thiopental, for induction & short surgeries can cause what side effects?
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Large doses -> myocardial depression
Hypotension, ↓ SV, ↓ CO Resiratory & circulatory depression ↓ brain metabolism & O2-use Less ↑ cerebral blood flow (good for head trauma) |
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Which BDZs are used pre-op for sedation and amnesia?
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Diazepam (Valium)
Lorazepam (Ativan) Midazolam (Versed) - used most |
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What is Flumazenil?
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A BDZ antagonist; can use for reversal
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What is Naloxone (Narcan)?
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An opioid antagonist - reverses respiratory depression
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Increased doses of opioids can cause?
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Chest wall rigidity during surgery (impaired breathing) - also post-op respiratory depression
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Opioids are useful in what type of patients?
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Cardiac patients
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Name 4 opioids.
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Morphine
Fentanyl Alfentanil - fast onset Remifentanil - fast onset/recovery (esterases) |
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What is neuroleptanesthesia?
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General anesthesia induced by the intravenous administration of neuroleptic drugs in combination with inhalation of a weak anesthetic.
EX) fentanyl + droperidol (like Haldol) + N2O |
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Describe characteristics of Propofol.
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Fast onset/recovery - less N/V - for general anesthesia or conscious sedation - hypotension and decreased CO during induction - acidosis in kids
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Describe characteristics of Etomidate.
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- For cardiac patients
- Minimal cardio & respiratory depression - NOT analgesic, so use with opioids |
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Describe characteristics of Ketamine.
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- Dissociative: catatonia, amnesia, analgesia
- NMDA receptor blocker - Lipophilic = fast distribution |
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Is ketamine a cardiac stimulant?
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Yes, it causes increased pulse, CO, BP, cerebral blood flow & O2 use, and ICP
But ok in high-risk elderly b/c they're pulse & BP won't drop |
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Name 3 characteristics of MAOIs.
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- Long duration of action
- Irreversible inhibitors of MAO - Sympathomimetic effects |
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Name 3 MAOIs.
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- Tranylcypromine (Parnate)
- Phenelzine (Nardil) - Isocarboxazid (Marplan) |
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How do MAOIs work?
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Inhibitors block deamination of catecholamines and 5-HT by MAO (both subtypes) - this prevents degradation of NTs, so more molecules in synapse
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Antidepressant effects of MAOIs are mostly due to inhibition of MAO-A - why?
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MAO-A metabolizes NE, 5-HT, and tyramine
MAO-B acts on dopamine |
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Which opioid cannot be given with MAOIs due to a deadly reaction?
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Meperidine (Demerol)
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What is a tyramine hypertensive crisis?
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Tyramine (like amphetamine) is taken up by catecholamine nerve terminals & causes release of NT into synapse
- Pts should avoid tyramine-containing foods while on MAOIs |
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BDZs are mainly used for?
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- Sedative-hypnotics
- Anxiolytics - Anticonvulsants |
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MOA of BDZs and Barbiturates?
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Potentiate action of GABA at GABA-A receptor (they have their own binding sites)
- BDZ: ↑frequency of channel opening - Barb.: prolong opening of Cl- channel |
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Describe the relationship between BDZs and GABA and Barbiturates and GABA.
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- BDZs ↑ GABA binding to Cl- channel
- BDZs ↑ frequency of channel opening - Barbs ↑ duration of openness |
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Pharmacological Effects of Sedative-Hypnotics - Sedation:
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- Decrease response to constant level of stimulation
- Anti-anxiety - Disinhibition - Anterograde amnesia - No psychomotor depression |
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Pharmacological Effects of Sedative-Hypnotics - Hypnosis:
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- Fall asleep fast
- Decrease REM sleep - Tolerance |
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Pharmacological Effects of Sedative-Hypnotics - Anesthesia:
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1) Barbiturates (thiopental, methohexital) - highly lipophilic, short acting, no antidote
2) BDZs (diazepam, midazolam) = adjuncts, longer lasting, reverse with flumazenil |
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Pharmacological Effects of Sedative-Hypnotics - Anticonvulsant:
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- Most can ↓ spread of seizure
(Clonazepam, lorazepam; PB, methabarbital (prodrug of PB)) |
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Pharmacological Effects of Sedative-Hypnotics - Other Effects:
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1) Muscle relaxation (carbamates, BDZs)
2) Respiratory (death from resp arrest), problem in COPD pts 3) Cardio (↓ contractility), problem in hypovolemia, CHF |
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What is Buspirone (Buspar) and its MOA?
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Anxiolytic only - partial agonist at 5-HT-1A receptors (no effect on GABA or BDZ binding sites)
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What is Zolpidem (Ambien) and its MOA?
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Hypnotic for insomnia tx - facilitates GABA inhibition by binding to BDZ binding site (but not structurally related to BDZs)
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Describe 3 characteristics of Zolpidem (Ambien).
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- ↓ REM
- Respiratory depression w/high dose - less likely for tolerance - ↓ dose in elderly, liver disease, and pts taking CIMETIDINE |
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What is Zaleplon (Sonata)?
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Hypnotic for insomnia - good for ↓ sleep latency but not for maintaining sleep (metabolized rapidly)
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What is Eszopiclone (Lunesta) and its MOA?
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Hypnotic for insomnia - binds at GABA-BDZ receptor
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Name 2 alcohols used as sedative-hypnotics.
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- Ethchlorvynol (Placidyl)
- Chloral Hydrate (Noctec) |
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Choral hydrate is metabolized to what?
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to trichloracetic acid - a toxic metabolite that accumulates
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What is Glutethimide (Doriden)?
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An older sedative hypnotic that is part of the piperidinedione group - schedule II drug for abuse potential
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Name the carbamate used as a sedative-hypnotic before BDZs.
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Meprobamate (Miltown, Equanil)
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Which type of drugs are most used for anxiety states?
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BDZs
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Which BDZ is best for panic / phobic attacks?
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Alprazolam (Xanax)
(Buspirone takes a week for effects) |
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Which drugs are best for sleep disorders?
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- BDZs w/short half-life - estazolam (Pro-Som), triazolam (Halcion)
- Zolpidem (Ambien), Zaleplon (Sonata) |
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What is chlordiasepoxide (Librium) used for?
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Alcohol withdrawal / detox
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How do local anesthetics work?
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they bind to voltage-gated Na+ channels, decreasing Na+ influx into neuron and inhibiting depolarization and AP generation
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Which form must a local anesthetic be in to gain entrance into the neuron?
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Unionized form
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Which form must a local anesthetic be in to bind to its site of action?
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Ionized form
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How are ester local anesthetics metabolized?
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By plasma & tissue esterases - creates PABA (caution hypersensitivity, or pt taking sulfonamide antibiotics)
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How are amide local anesthetics metabolized?
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Dealkylation & hydrolysis by liver microsomal enzymes
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Procaine has a _______ onset of action and a _______ duration of action.
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short onset
short duration |
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Chloroprocaine is used in obstetrics because..?
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It has a short duration of action and a margin of safety
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Tetracaine is more or less potent than procaine?
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More potent, so also more toxic.
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Compared to procaine, lidocaine is...?
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More potent, has faster onset, and a longer duration of action
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Mepivacaine is similar to lidocaine but...?
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it has a quicker onset and a prolonger duration
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Name 3 Dibucaine characteristics.
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- High potency
- High toxicity - Long duration |
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What toxicity does Bupivacaine have and where is it commonly used?
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Cardiotoxicity is possible, but rare.
Used during labor b/c it doesn't affect motor of abdominal muscles |
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Compare Ropivacaine to Bupivacaine.
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Ropivacaine is less potent, but has less cardiotoxicity
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What does the metabolism of Prilocaine yield?
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Orthotoluidine, which can accumulate and cause methemoglobinemia
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