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74 Cards in this Set
- Front
- Back
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what does Ach control? DA? ne? 5ht? glu? gaba?
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ach- memory, motor control
da- reward/reinforcement ne- mood/learning/memory/anxiety 5ht- mood/appetite/sleep pain glu- excitatory NT gaba- inhibitory NT |
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where does NE arise from and where does it project to
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arises from locus cereulus
projects to cortex cerebellum and spinal cord involved in learning, memory, psychosis, anxiety |
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where do serotonergic neurons arise from
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raphe nucleus and projects to cortex, cerebellum and spinal cord
involved in sensory gating, pain, mood, motivation, appetite, depression, compulsion |
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what is the monoamine hypothesis
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drugs that decrease NE / 5HT will cause depression
drugs that increase NE/5HT will decrease depression |
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if your anti depressant drugs don't work in 2 weeks, should you switch them?
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no it takes about 2-6 weeks for effects to kick in
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what beneficial effect does 5ht have specifically with neurons
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5ht promotes neurogenesis through BDNF
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what is the common effect of an antidepressant
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at first it'll block reuptake so there is a lot.
since there is a lot of NT in the cleft, over time, it'll cause downregulation of a1 and b1 adrenergic receptors and 5ht2 receptors |
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t or f antidepressant drugs promote neurogenesis
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true
serotonin stimulates BDNF to prevent neurodegeneration |
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how does stress have an effect on the body/neurons
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stress --> increase glutamate --> direct effect on neuron --> atrophy of dendrites --> decrease volume in hippocampus and amygdala and prefrontal cortex
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what is ketamines effect
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ketamine is an NMDA-R antagonist.
glutamate binds NMDA, if ketamine is blocking the receptor, glutamate can't bind. therefore, glutamate can't elicit its effect |
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what are the ways that NT does reuptake and degradation
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specific transporter uptakes NT and repackages it into secretory granules
other enzymes like MAO and COMT will alter chemical structure making it inactive |
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what is the first line antidepressant drug
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SSRI
last line is MAOI - reserved for people failing SSRI, TCA, and atypical antidepressants (buproprion/ nefazadone/mirtazapine) |
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generally, it is thought to best continue tx for how long after a relapse
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6 months
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what drugs do you NOT give with MAOi
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TCA
buproprion mirtazapine |
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what drug + lithium induces seizures
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SSRI + lithium = seizures
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what drugs can NOT be given with TCA
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tca should NOT be given with MAOi and SSRi (can cause serotonin syndrome)
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what drugs can NOT be combined w/ ssri
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tca
lithium |
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which drugs cause weight gain
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mirtazapone
tca lithium valproic acid maoi |
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what drugs do NOT cause weight gain
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ssri
buproprion |
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what are the main SE of TCAs
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anticholinergic- miosis, sweating, dry mouth, urinary retention, sweating
antihistamine - sedation anti adrenergic- orthostatic HYPOtension seizures weight gain, dizziness |
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list the TCAs in descending order of SE
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ami>imi>nor>des
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what is the MOA for TCA
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compete with NE/5ht at the transporter to prevent reuptake
has NO DIRECT EFFECT on nt synthesis, storage, or release chronically, it'll cause a2,b1 adrenergic and 5ht2 receptor and down regulation |
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what are the 2 big complications to watch out for when giving TCA
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resp depression
cardiac arrhythmias |
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what drug interactions do TCA have
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should NOT be taken w/
etoh --> CNS depression anticholinergic agents insulin/hypoglycemic agents --> increase hypoglycemia maoi |
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what are the pharmacokinetics of TCA
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rapidly absorbed, strongly bound to albumin
metbaolized in liver, excreted in kidney long t 1/2 10-70 hours |
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who do you have to be careful in giving TCA to
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BPH pts and cardiac arrhythmia pts
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which TCA has the most SE and why
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amitryptyline over imipramine/desipramine/nortryptyline because amitryptyline is a tertiary amine
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what are some other uses for TCA
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tx for anxiety, anuresis (imipramine), OCD, neuropathic pain (amytriptyline)
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what are the SE of venlafaxine and desvenlafaxine
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more activity at SERT than NET
SE: Dizziness, dry mouth, anorexia, SOMNOLENCE, increased sweating, NAUSEA, sexual dysfxn, possible serotonin syndrome low albumin binding |
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what is a major SE that we must watch out for w/ venlafaxine specifically
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HTN
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who should NOT be taking duloxetine
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BPH pts
hepatic insufficiency end stage renal dz |
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SNRi, like amitryptiline can be used to treat what
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neuropathic pain
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what is the MOA of MAOi
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MAO regulate degradation of catecholamines, 5ht and other endogenous amines
inhibitors prevent degradation |
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which MAO is more related to depression and which is more with parkinsons?
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MAOa = depression
MAOb= parkinsons |
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which MAOi , phenelzine, tranylcypromine, selegiline is an MAOb inhibitor specifically
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selegiline
also transdermal patch used to treat parkinsons if given in high doses, it can inhibit MAO-a as well and treat depression |
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what are the SE of MAOi
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sexual dysfxn
insomnia orthostatic hypotension dizziness anticholinergic effects |
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phenelzyine has what associated SE
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hepatotoxicity and damage
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which other drug besides maOi has sexual dysfxn
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snRi
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if you had a depressed patient that keeps falling asleep, what drug would you give? if they had trouble sleeping, what drug would you give
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if they can't stay awake, give MAOi because its se is insomnia.
if they can't fall asleep, give snRi because it causes somnolence |
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what foods should you NOT eat while on MAOis
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aged cheese
pods of fava beans yeast extract herring (smoked fish) these induce the tyramine induced hypertensive crisis. tyramine acts on nerve terminals causing NT to leak from storage vesicles into the cytoplasm. this is then deactivated by MAO-b --> increase in BP |
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what are teh drug interactions with MAOis
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CNS stimulants -appetite suprpesants, decongestants, ephedrine
anything that increases 5HT levels (TCA, burpropion, mirtazapine) |
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if a patient needs an antidepressant but is wary about gaining weight, which drug should you prescribe her?
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ssri
no weight gain SE |
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what is the MOA for citalopram, fluoxetine, paroxetine, sertraline, escitalopram
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these are SSRis and they prevent reuptake of serotonin specifically
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what drugs can NOT be used with SSRI
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lithium --> seizures
TCA |
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what SE has been a/w fluoxetine specifically
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akathesia
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why should you watch kids that are taking ssri
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they have a higher chance of suicide in the first few weeks
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what can happen to a bipolar pt when taking ssri
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sudden swtich to mania
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if you withdraw ssri what sx can appear
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myoclonus, malaise, chill, muscle aches, sleep disturbances, GI sx
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what are the drug interactions with ssri
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should NOT be used with tca, lithium,
ssri may cause increased [ ] of clozapine and may precipitate seizures has a synergistic effect with CNS depressants |
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if you give SSRi with MAOi what can it cause
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serotonin syndrome
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which ssri is the most sedating, which is the most stimulating
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sedating = paroxetine
stimulating = fluoxetine |
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what eating disorder can you give ssri as a treatment for
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bulimia
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name the atypical antidepressants
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bupropion
nefazodone mirtazapine |
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what is teh MOA of bupropion
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inhibits reuptake of NE and DA
antidepressant effects likely dt increased NE |
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the effects of the DA levels are used for what other treatment
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cessation of smoking
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what are the SE of bupropion
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dry mouth
tremor nausea ha does NOT cause weight gain, daytime drowsiness (snri and tca), sexual dysfxn (snri, maoi) |
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what is the MAO for nefazadone
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5ht2 antagonist
inhibits presynaptice 5ht1 autoreceptors and increases 5ht levels |
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what are the SE of nefazadone
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dry mouth
dizziness orthostatic hypotension nausea asthenia hepatotoxicity |
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what are the drug interactions with nefazadone
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strong interactions w/ triazolam (facilitates sleep), alprazolam (benzodiazepine tx for acute anxiety)
strong inhibitor of CYP3A4 |
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what is the MOA of mirtazapine
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acts as an antagonist at presynaptic a2AR autoreceptor and heteroreceptors to increase levels of NE and 5HT
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what are teh SE of mirtazapine
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weight gain
somnolence dry mouth constipation |
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what is a rare SE of mirtazapine
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agrnulocytosis
elevated liver fxn tests |
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what is teh path behind bipolar disorder
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deficiency of catecholamiens --> depression and excess of catecholamines --> mania
bipolar disorders is a deficiency in 5HT dysregulation of tehse neurotransmitters produce a cyclic rhythm disturbance in the CNS --> hyperactive G proteins |
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what is the MOA for lithium carbonate and lithium citrate
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prevents the hydrolysis fo iniositol phosphate to inositol
inhibits GSK so you don't get apoptosis and amyloid formation |
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why do you have to be careful with giving lithium if your patient is on a low na+ diet or thiazides
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it is renally absorbed in the proximal tubules
increased reabsorption by na+ depleting diuretics na+ depletion promotes li retention |
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what can lithium be used as a treatment for
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SIADH because the se are polyuria or polydipsia
lithium may induce nephrogenic diabetes insipidus |
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what are some mild SE of lithium
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hypothyroidism
alopecia weight gain abd pain sedation |
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what are some adverse effects in pregnancy
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ebsteins malformation
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what are the severe SE of lithium
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mental confusion
hyperreflexia gross tremor seizures coma death |
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what are the drug interactions with lithium
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diuretics- depletetion of na+ causes retention of li
nsaids- facilitate proximal tubular reabsorption of li+ |
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what are the other uses of lithium
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acute mania (but valproic acid or cabamazepine is better)
prevention of RECURRENCE of bipolar depression adjunct to antidepressant tx in MAJOR DEPRESSION |
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what is valproic acids SE
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GI sx
nv anoreixa sedation or ataxia is rare |
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can you substitute valproic acid for lithium?
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no, in the beginning it is equally effective, but after a few weeks, it is not as efficacious for maintenance
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carbamazepine's long term side effects are what
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drowsiness, vertigo ataxia, blurred vision, n/v, blood dyscrasia
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