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92 Cards in this Set
- Front
- Back
- 3rd side (hint)
hypokinetic movements caused by what?
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reduced DA or increased ACh
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hyperkinetic movements caused by what
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increased DA relative to ACh
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PD defined by:
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50% loss of DA in substantia nigra which causes:
80% loss of DA in striatum |
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DA released from
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axonal varicosities
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end of dose wearing off effect
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when disease progresses and neuron availability and recycling mechanisms are no longer relavent
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What is responsible for the decrease in therapeutic window as PD progresses for Sinemet?
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end of dose wearing off effect occurs in brain only and there is a increased risk of toxicity in periphery
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cofactor of AAAD?
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pyridoxine (thus deficiency prevetns peripheral Ldopa conversion)
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on-off phenomenon
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sudden onset of PD during treatment due to sensitization of Glu in striatum associated with sawtoothing levodopa levels
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Early treatment of PD
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indirecting acting agonists and antimuscarinics to promote normal physiological actions; also use direct acting agonists because they are neuroprotective
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why is levodopa for late stage PD
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most effective when you need it most but most side effects
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HD neuronal unbalance
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loss of GABA and increased DA tone which leads to chorea
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Goal of Dystonia therapy
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anti-muscarinics, antispasmodics
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Tourette's neuronal imbalance?
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increased movement from DA (hyperdopaminergic)
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What are schizo positive symptoms? negative?
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positive: hallucinations and delusions
negative: poverty of speech, socially inapropes behaviors |
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What is the DA theory of schizophrenia?
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pharmacocentric: since DA antagonists work in schizo's, the disease must be caused by +DA
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but schizo brains have no increase or decrease in DA receptor number
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what is the hypofrontality hypothesis of psychosis?
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failure of parahippocampal gyrus to develop; this prefrontal cortex doesn't develop (- symptoms)and can't inhibit n. accumbens; disinhibition causes + symptoms
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Drugs that can control both negative and positive symptoms in schizos target whta?
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D4 receptors and 5HT receptors such as clozapine
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fallicy of DA theory of schizo?
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DA only induces + symptoms, no change in DA receptor #, PCP causes psychosis but not full range of symptoms
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EPSEs result from what?
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DA receptor blockade in regions of brain not intended for antipsychotic therapy, mainly the nigro-striatal pathway
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EPSEs
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extrapyramidal side effects: Dystonia, then akathisia, then parkinsonian
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Classes of antidepressants
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TCAs
Heterocyclics Antimanic Drugs MAOIs SSRIs (THAMS) |
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What are the new heterocyclics?
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NDRIs
SNRIs NaSSA |
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Theory of depression
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It is a consequence of brain biogenic amine deficiency
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NTs deficient in depression?
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NE (either increase or decrease) and 5HT (indoleamine)
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patients with reduced 5HT think of what?
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suicide ideation
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What is SAD?
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prolonged dark causes increased melatonin which inhibits 5HT-ergic neurons to cause depression
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What explans sleepiness in depressed patients?
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production of melatonin in depressed folk
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What explains efficacy delay?
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upregulation of NE receptors due to uprfulation of NE
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net effect of NE?
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it normally inhibits interneurons; massive influx inhibits noise
increased noise = depression |
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net effect of 5HT in brain?
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increases limbic input to cortex, without this, emotion pathways r fucked
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What is Quinidine?
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anti-arrythmic agent.
OD: slows dromotropy and causes arrhythmias |
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domotropic
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affecting AV conduction velocity of the heart
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What is serotonin syndrome?
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hyperthermia, rigidity, myoclonus, fluctuations in vital signs
(stiff, cold, twitching, unstable!) |
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Why is compliance higher in SSRIs?
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less side effects
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side effects of SSRIs?
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serotonin syndrome,
insomnia impotence increased risk of suicide |
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Why does MAOI have more effect on serotonin?
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because NE is also catabolized by COMT
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which MAO is responsible for 5HT and NE mostly?
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MAO-A; MAO-B does DA more
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What indicates use of SSRIs?
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reduced 5HIAA
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What indicates use of desipramine or nortriptyline?
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reduced VMA or MHPG
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What is the amphetamine procative test?
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patient improves with amphetamine which indicates use of a noradrenergic agent
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dexamethasone suppresion test?
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indicates use of a 5HT agent; if symptomes don't improve w dex, it means there is a problem with 5HT which regulates cortisol levels.
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manic phase
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bipolar phase where pts have grandiose thinking, insomnia, risk-taking, high self esteem
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rapid cyclers
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rapid shifts between manic and depressive
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switch phenomenon
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tricyclics with antimuscarinic activity can precipitate mania in a depressed patient
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Action of drugs used as anxiolytics
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CNS depressants, some without sedation (anxioselective)
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Conscienceness continuum
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CASH OSCD
Conciousness: Alertness Sedation Hypnosis Obtundation Stupor Coma Death |
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Binding sites on GABA
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1)GABA
2) Benzodiazepine 3) Barbituate 4) Beta Carbolines (inverse agonist) |
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Safest CNS depressant? Why?
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benzodiazepine because all others can cause death
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Brain stem activity/ bilateral thalamic and cortical activity is required for what?
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consciousness
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Parts of brain active and depressed during sleep?
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brainstem depressedl forebrain activated
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How is sleep atony accomplished?
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activation of gigantocellular region which activates glycinergic Renshaw interneuron which depresses LMN.
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How does ACh facilitate sensory traffic into cortex and thus arousal?
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increase thalamus to thalamo-cortical fiber firing rate to facilitate sensory traffic
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Why does sleepiness increase during the day?
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adenosine accumulates and binds to receptors on cholinergic neurons to decrease ACh release
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How does caffeine wake you up?
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antagonizes adenosine so it disinhibits ACh release and therefore facilitates sensory traffic.
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What pathologies can occur in stage IV of sleep?
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night enuresis and pavor nocturnus
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How do sedative hypnotics used to treat enuresis and pavor nocturnus?
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alter sleep cycle architecture
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pathology associated with early onset of REM
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depression
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what is differential rates of tolerance
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some mechanisms gain tolerance faster than the other so efficacy changes over time
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what is the safety factor built into barbituates?
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differential rates of tolerance:
tolerance to sedation increases faster than anti-resp and anti-epileptic tolerance TI antiseizure activity remains same while TI of sedation increases :) |
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mediates fear response
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amygdala nucleus
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NTs in amygdala
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GABA, Glu, 5HT, NE
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Why is fear learned?
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Glu in amygdala can undergo LTP through NMDA receptors
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main cause of seizure foci development
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trauma that reduces capacity to buffer extracellular K or cell packing
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what induces epilepsy?
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loss of inhibition
PDS - an elevated sustained resting potential |
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What does use-dependency mean in terms of Na channel antagonism?
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just like anesthetics, they work where more Na channels are open and therefore affects most active neurons the most
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Symptoms of non-migraine headache
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bilateral, nonthrobbing, usually stress related
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Treatment for nonmigraine headaches
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1) behavioral
2) NSAIDS 3) muscle relaxants |
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Excedrine
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ASA, acetominophen, caffeine combo (excedrine)
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how to avoid rebound headache
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taper nsaid dose
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vascular hypothesis of wolff?
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5HT maintains tone and vasoconstriction. During ischemia, vessels vasodilate and this loss of tone allows CT to be manipulated by pulsing pressure which causes pain
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sterile inflammatory hypothesis of migraines
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unknown inflammatory process that releases histamine and peptides
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biobehavioral hypothesis of migraines
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wave of depolarizatoin causes activation of opthalmic branch of trigem which is where headaches are thought to originate
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Why can't migraneuers absorb antimuscarinics?
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they have gastric stasis as a symptom
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What is MAC?
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minimum alveolar concentration - gas amnt in blood needed to produce no reflex response to a knife cut ED50 at RT at SL
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how does solubility affect speed of anesthesia?
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the more soluable, the longer the induction of anesthesia
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what is a closed system?
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the idea that gas (volatile) anesthetics can only go in lungs, blood, brain, and these 3 compartments will equilibrize
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only anesthetic to be biotransformed?
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liver
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how are most anesthetics terminated?
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exit lung just like they entered, except for halothane
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Overton-meyer hypothesis
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The Overton-Meyer hypothesis suggests that these drugs disrupt membrane fluidity changes transmembrane protein structures and thus activity of Na channels. Potency related to oil:gas partition.
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What does Enk do?
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reduces release of SubP from peripheral C fibers
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What do endorphins do?
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released by POMC and have paracrine effects
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Receptors in the enkephalin receptor system?
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Mu, kappa, delta, epsilon
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What do mu receptors mediate?
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Analgesia-mediating in suprasegmental and segmental systems
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What side effects are initiated by mu receptors?
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euphoria and respiratory depression
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kappa mediates what?
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spinal cord and CNS but not as potent as mu
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delta receptors mediate what?
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limbic and spinal cord; more emotional and behavioral
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How does mu cause euphoria
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increased DA,NE, forebrain
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how does Mu/delta/kappa cause respiratory depression?
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reduces sensitivity to CO2 in medulla
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how does morphine cause hypotension?
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direct histamine displacement from mast cells and delta medullary depression
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how is RUQ pain associated with morphine?
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morphine causes spincter of oddi spasms
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Why shouldn't you give oxygen to someone in a coma?
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O2 will stop hypoxic drive and cause breathing
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toxic triad of opiod toxicity
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Respiratory depression, Coma, Miosis
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