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15 Cards in this Set
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- Back
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monoamine hypothesis
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depression due to deficiency in one of three catecholamines:
serotonin norephinephrine dopamine |
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problems with monoamine hypothesis
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1) no antidepressant effect associated with drugs that increase neurotransmitters (cocaine, amphetamines) - won't treat antidepression
2) delay (2-3 weeks) b/w rise in neurotransmitters and clinical effects 3) decreased levels of serotonin only associated with few types of depression+ |
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serotonin
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most imp. NT for depression
synthesis: tryptophan + tryptophan hydroxylase 5-hydroxytryptphan + aromatic amino acid decarboxylase 5-hydroxytryptamine 5-HT receptors found in many tissues (CNS, blood vessels, smooth muscle, platelets, GI tract) therefore demostrate side effects in these tissues |
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phenylziine (nardil)
tranylcypromine (Parnate) |
monoamine oxidase inhibitors
non-selective, irreversible inhibitors severe interaction w/ food + drugs food: tryamin (cheese, beer, liver) - acts like amphetamine; displaces NE drugs: TCA, sympathomimetic (both dangerously increase BP - too much NE -> vasocon -> high BP), meperidine (fever) MAO destroys tyramine long lasting b/c irreversible |
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moclobemide
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reversible inhibitor MAO A (RIMA)
reversible + competitive inhibitor removes danger of tyramine effect (increase in NA leading to stroke) |
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MAO B inhibitors
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used in treatment of Parkinsons
involved in metabolism of DA and metabolism of protoxins -> toxins. |
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amytriptyline, imipramine, amoxapine
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tricyclic antidepressants
blocks reuptake of NA tricyclic antidepressants have many functional groups: a1 adrenergic antagonism h1 antagonism muscarinic antagonism 5HT and NA reuptake inhibiton |
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side effects for Tricyclic antidepressants
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H1 antagonism:
weight gain drosiness muscarinich antagonism: anti-SLUDGE (blocks parasymp. system - atropine effects) consipation, blurred vision, dry mouth, drowsiness block a receptors: decreased BP, dizziness |
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fluoxetine (prozac),
paroxetine (Paxil) sertraline (Zoloft) |
SSRI (serotonin selective reuptake inhibitor)
removed a1, muscarinic, histamine and NA reuptake blocker activites (unlike TCA) 5HT increases two ways: 1) increased levels of 5HT downregulate postsynaptic receptors (leading to improved mood) 2) increased levels of 5HT downregulate presynaptic (negative feedback) receptors = increased 5HT into synapse side effects: nausea, anorexia, insomnia, sexual dysfunction, increased suicide (?) much safer for overdose most prescribed antidepressants |
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buproprion (Wellbutin, Zyban)
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NDRI (noradrenaline/dopamine reuptake inhibitor)
help stop smoking - increased dopamine levels help reduce craving |
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Venlafaxine (Effexor)
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SNRI (serotonin-noradrenaline reuptake inhibitor)
-inhibit reuptake of 5HT, NA and some DA advantage: increase both 5HT and NA rapid effect (1 week) side effects: sexual dysfunction, impotence, anorgasmia |
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trazadone
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SARI (serotonin-2 antagonist / reuptake inhibitor)
extremely sedating (excellent non-dependence forming hypnotic) increase 5HT levels AND also block 5HT-2 receptors which are responsible for side effects associated with high 5HT levels (anxiety, agitation, sexual dysfunction) |
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mirtazapine
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noradrenergic/serotonin specific antagonists
block a2 negative feedback inhibition; increases release of NA and 5HT also possess 5HT-2 receptor blocking ability resulting in decreased side effects (reduced anxiety, agitation, nausea, insomina, sexual dysfunction) |
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electroconvulsive therapy (ECT)
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used in treatment of severe depression
patient lightly anaesthetized, ventilated and paralyzed with neuromuscular blockers side effects: confusion, memory loss |
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lithium
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mood stabilizer (treatment of manic phase)
monovalent ion mechanism: blocks conversion of IP to inositol - inhibition with IP3 formation, interference with cAMP formation mainly used prophylactically in bipolar, long half-life; narrow therapetuic window side effects: nausea, polyuria & thirst, tremor |
