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92 Cards in this Set
- Front
- Back
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Aminergic nerumomodulators have multiple receptors subtypes generated from?
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different genes or RNA splice variants. Different receptor subtypes can mediate different effects and can be targeted by diff drugs
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G-proteins have severe effects: what are they?
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modulate ion channels or trigger intracellular second messenger systms; thus, increasing or decreasing protein phosphorylation.
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How is dopamine synthesized?
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tyrosine-->DOPA (by tyrosine hydroxylase, the rate-limiting enzyme)-->dopamine (by dopa decarboxylase)
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What are the transporters of DA in the presynaptic terminal
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VMAT, DAT
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Which drugs block DA reuptake and promote release?
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methylphenidate and amphetamines
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Where are the DA neurons located?
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substantia nigra and ventral tegemental areas in the midbrain
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Whate are the terminal fields of DA?
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Caudate putamen, nucleus accumbens (ventral stiatum) important in reward, and VTA, frontal cortex, minbic cortex, amygdala, and hippocampus
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What roles do DA have?
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normal motor function, dysfunction, and phrarm trx
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Name the basal ganglia circuit loops
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Motor cortex, frontal cortex (cognitive), limbic cortex (emotion, reward, addiction)
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NE synthesis
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In side the VMAT, DA--> NE by DA-Beta-hydroxylase.
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What regulates the levels of NE or DA release and reuptake
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transporters
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Where is NE neurons located?
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Locus coerulus in the brainstem
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How is epinephrine synthesized?
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NE--> Epi by phenylethanolamine N-methyltransferase
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What is the target of NE?
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Same as DA: frontal, limbic, hippo, amygdala
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What is the target of Epi?
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restricted to subcortical regions.
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Serotonin synthesis?
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tryptophan--> 5-hydroxytrytophan--> serotonin.
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how are biogenic amines cleared?
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it is not degraded, it is re-uptaken
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Where are serotonin neurons located?
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raphe nuclei along the midline of the brainstem
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Serotonin target?
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Same as DA, and NE
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Histamine synthesis?
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Histidine --> histamine by histidine decarboxylase
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Histamine targets?
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Same as DA, NE, and Serotonin
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Which pathway mediates reward and addiction pathways?
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mesolimbic pathway, specifically the nucleus accumbens. Increases DA release
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Drugs that reduce positive reinforcements for: alcohol, opioid, cannabinoid
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etoh: disulfiram blocks acetagldehyde dehydrogenase, opiod/cannabinoid antagonists: naltrexone/rimonaban
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Overdose trx: opiates
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opioid antagonist- naloxone/narcan
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tolerance to opiates trx
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rotation of opiate
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withdrawal trx: alcohol, opiates
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alcohol: benzodiazeines, tapering to avoid seizures, opiates- clinidine, radid detox
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maintanence trx: opiate, nicotine
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opiate: methadone, buprenorphine, smoking- nicotine patch
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What area of the brain is involved in mood disorders?
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limbic system
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When a person is depressed, what are they lacking?
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they are lacking the capacity to adapt. Trx is to restore resilence
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What is the treatement of mood disorders: operational concept?
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Perturb, Assist, modify vulnerability
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Factors that perturb major depression?
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sleep deprivation (helps anti-depressants work faster, ECT (best therapy), Antidepressive Drugs
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What are factors that assist in adaptation?
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hopitalizaiton, supportive network, endorine supplements, regular exercise, social routine
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Factors that Modify adaptation and reduce vulnerability?
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lithium, psychotherapy, antidepressants,
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What drugs do you use for biopolar disorder?
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Mania: decrease dopa with Anti-psychotics (olanzapine, risperidol, clozapine) Induce remission: anticonvulsants (lamotrigine, topiramate), prevention/maintenance (lithium)
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menarchy and hypothyroidism is known to place people at higher risk for depression: T/F
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T
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What is the best therapy for recurrent depression?
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meds and cognitive-behavior psychotherapy.
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Which drugs are best for treating women with depression?
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anti-depressants and thyroxine
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How does Lithium work?
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by competing with Na
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Substance Abuse vs Substance Dependence: which one has the all the symptoms of addiction including withdrawal, tolerance
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Substance Dependence.
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What are they symptoms of addiction caused by?
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scarring of the brain, decreased brain metabolism
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What are the changes of Neurotransmitters in alcohol use?
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Increase dopamine, gaba, optiates, decrease in serotonin and glutamate.
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What are the effects of opiates, gaba, glutamate, dopamine, serotonin?
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Dopamine: pleasuare reward, craving; serotoninmood, pain, impulsivity; opiates:pain, pleasure; gaba: alertness, sedation, glutamate: learning, memory
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differences of meth and coccaine
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Meth: longer half life, targets DA release, no medical use; Coccaine: targets DA reuptake, used medically
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opiods vs opiates: what are they?
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opiods: anything that binds to opiod receptor, opiates: are synthetic
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Whats a type of semi-synthetic opiate?
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heroin, methacodone.
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what's the number one abused illicit drug among seniors>
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opiates
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Are there pathological consequences to gambling?
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yes
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True/false: addiction and its consequences is the same, except the target (gambling, sex, drugs, etc) is different
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yes
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Drugs of abuse and affect on brain functioning: Which part of the brain does it affect for the following: positive reinforcement, negative reinforcement, urges/cravings, inmpairedinhibior control
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nucleus accumbens (liking), amygdala and hippocampus (anxiety-provoking), anterior cingulate and insula (wanting), frontal lobes (disinhibition)
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What is the brain's pleasure center?
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dopamine pathway in the limbic system
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Areas of the brain affected during intoxication
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VTA (specifically, the nucleus accumbens)
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Areas of the brain affected from addiction
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Anterior cingulate (from the orbitofrontal cortex)= decrease activity causing andedonia.
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Name some TCA's
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imipramine, desipramine, amitriptyline,nortriptyline, clomipramine
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What is the pharmacologic activity of TCA's?
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inhibit the reuptake of biogenic amines (NE, 5HT),CNS depressant (sedation, loss of energy), anti-muscarinic (causes dry mouth, blurred vision, constipation, increased sweating), alpha-adrenergic blockers (orthostatic hypotension)
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Clinical uses of TCA's
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depression, enuresis (imipramine), chronic pain (amitriptyline)
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Adverse rxns of TCA's
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Besides one associated with its pharmacologcal effects, it cause withdrawal syptoms (nausea, headache), overdoss can be treated with physostigmine (can cross BBB), weight gain!
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Mechanism of mirtazaine, trasondone, bupropion
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Second-genteration antidepressants: mirtazapine: blocks 5HT and alpha-adrenergic receptors, trazodone: blocks 5HT receptors. Bupropion (well-butrin): blocks NE, serotonin, and dopa re-uptake.
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SSRI:Name some
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Fluosectine, paroxetine, fluvoxamine, sertraline, citalopram, escitalopran
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SSRI: why don’t they produce cardiovascular or antimuscarinic effects?
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they have little effect at the alpha reeptors and muscarinic receptors
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SSRI: side effects
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nausea, GI upset, headache, insomnia, nrvousness, sexual dysfunction.
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Serotonin and NE reuptake inhibitors (SNRI's): name two drugs
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duloxetine, venlafaxine
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MAOI: Name some
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isocarboxazid, phenelzine, tranylcypromine
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MAOI: how does the drug effect become terminated?
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Inhibition of MAO is irreversible so enzyme regeneration terminates the drug effect.
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MAOI: Pharm activity
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inhibits oxidative deaminatioj of catecholamines and serotonin so NE and 5HT stay around longer due to the inhibition of fo monoamine oxidase.
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MAOI: Pham effects
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CNS: mood elevation, amphetamine like activity, Cardio: orthostatic hypotension (from NE)
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MAOI: Adverse effects
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irreversible nature (must wait 10-14 before giving another drug), hypertensive crisis (MAOI causes the build up of some chemical in the gut that causes it), CNS stimulation (dizziness, headache, inability to sleep), orthostatic hypotension, inhibiton ejactualtion, hypertensisve crisis
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Serotonin syndrome: what is it?
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Interaction of SSRI with MAOI's and L-tryptophan producing changes in mental status, twitches, yoclonus, hyper-reflexia, swating, penile erection , shivering tremor, headache. Seizures, coma. Trx. All serotonerigic drus should be stopped.
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Lithium: How does it stabilize mood?
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cuts down on high's and lows in biploar disorder by replacing Na.
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Lithium: adverse reaction
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low-therapeutic index. Plasma levels of lithium are directly propotional to toxic dose. Causes cardiac arrythmia, polyuria, polydipsia, inhbits action and ADH, weight gain, edema (from na retention). Trx with propanolol
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Barbituates: 3 fxns
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CNS Depression: increase duration of Cl channel opening (hyperpolarization)by increasing effects of GABA, increase [barbituates] can activate gaba receptors.. At very high concentrations they can affect other ion channels and they can decrease the release of other NT's
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Barbituates: Effects of CNS, Cardiovascular system, Tolerance, Dependence
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CNS: depression (dose-dependent ranging from coma to death). Cardiovascular: hypotension and cardiovascular collapse. Tolerance: due to adapotation at the celluar level and induction of their own metabolism. Dependence: drug-seeking behavior as well as physical dependence. Withrawal or abstinence synrome can occur
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Barbituates: Clinical Uses
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trx of anxiety and insomnia, anticonvulsant, anestehsia, induction of coma
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Barbituates: adverse effects
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acute intermittent porphyria
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Barbituates: drug interactions
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cross tolerance with other CNS depressants, induction of CYP450:results in acceleration of metabolism and decrease plasma concentrations of other drugs (birth control or warfarin)
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Alcohol: withdrawal syndrome and trx
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delirieum tremens. Trx with barbituates
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Methanol intoxication: what causes it and what are it's symptoms
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metabolite (formaldehyde and formic acid) causes nerve damage and blindness.
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Methylxanthines: name some
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caffeine, theophylline, theobromine.
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Methylxanthines: mechanism of action
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CNS stimulant, antagonist at adenosine receptors. Adenosine is an inthibitory NT, thrus it decreases the inhibitor effects of adenosine which increases CNS stimulation
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Methylxanthines:Pharm effects of CNS, peripheral, tolerance, withdrawal, dependence
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CNS. Increase alertness, Perpheral: vasoconstriction, diuresis,
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Methylxanthines: Clinical uses
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trx of headaches. Not good for trx of CNS depressant overdose (produces wide-awake drunk).
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Name some sympathomimetics:
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amphetamine, methylphenidate, pemoline
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amphetamine: mechanism of action
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releases DA and NE and inhibits reuptake.
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amphetamine: pharm effects
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CNS: improve performance on dull repetitive tasks, increase wakefulness, produce acute mood elevation. Peripheral effects cardiac stimulation, appetite suppressant. Tolerance, dependece. Withdrawal includes prolonged sleep, fatigue, depression, and intense hunger
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amphetamine: clinical uses
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adhd, narcolepsy, weight reduction.
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amphetamine: adverse effects
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dizziness, tremor hyperirritability, insomnia, depression hyperthermia, convulsions, coma. Paranoid psychosis, tachycardia, hypertension, headache, stroke
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methyphenidate: mechanism of action
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releases dopamine
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methylphenidate: clinical uses
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adhd, narcolepsy
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methylphenidate: adverse actions
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insominia, restlessness, talkativeness, behavioral disturbances, visual hallucinations, slurred speech, struttering, ataxia, vertigo, uncontrollable facial and tongue movements. Few cardiovascular effects (vs. amphetamines)
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pemoline: mechanismof action
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releases dopamine
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Coccaine: distribution
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highly-perfused tissue first (brain) then the rest of the body. Absorbed faster via smoking vs. i>V.
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Coccaine: mechanism of action
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blocks the reuptake of DA and NE and serotonin
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Coccaine: clinical uses
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anesthetic.
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