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length of time AD take to work
3 or more weeks
factor associated with neural plasticity, resilience, and neurogenesis
brain derived neurotrophic factor
effective AD therapy do this
increase neurogenesis ans synaptic connectivity by increasing BDNF
AD drugs increase levels of
NE, 5HT, and dopamine which act to increase BDNF levels, promotes development of new connections in limbic, cortical, and hippocampal circuitry
Antidepressant Drugs increase
- the amount of NE and/or 5HT at cortical and
- limbic synapses.
Tricyclic Antidepressants (TCAs) block
the reuptake of NE and (to a lesser extent) 5HT into nerve terminals by blocking the transporter at presynaptic terminals (NET, SERT). They also block alpha 1 receptors.
MAO Inhibitors (MAOIs) block
the metabolic breakdown of NE and 5HT.
Selective Serotonin Reuptake Inhibitors (SSRIs)
block the reuptake of 5HT and (to a lesser extent) NE into nerve terminals by blocking the transporter at presynaptic terminals (NET, SERT).
Selective Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)
- block the reuptake of both NE and 5HT into nerve
- terminals by blocking the transporter at presynaptic terminals (NET, SERT).
anti-muscarinic, antihistaminic, and alpha 1 receptor -blocking actions
fluoxetine stuff and SE
- SSRI, geriatric and ped depression, bulemial PMDD, OCD
- metabolized into norfluoxetine- more active 3x
- AE- HA sweating, anxiety agitation, GI, weakness and fatique and sexual dysfn, weight and sleep changes. Numerous drug rxn CYP2d6 especially with TCA, neuroleptics, cardiac and BB drugs
- less rxn than fluoxetine. adult depression, OCD in 6yo, panic d/o, PTSD, social phobia, PMDD, schizo depression, brain injury beahvioral probs, premature ejac.
most delayed onset of effects of SSRIs
- Highly protein bound, 1 week to establish Css,
- weak inhibitor of CYP2D6 less likely to inhibit metabolism. NOT approved for children or depression. effective in reducing hot flashes in menopause
SSRI, s enatomer of citalopram- no evidence that SE profile is less than racemic. Used for GAD- generalized anxiety d/o. and adolescent depression
SSRI generalized AE
- mainly because of increased Serotonin levels, NVD, GI, usually emerge early and cease in first week.
- DISCONTINUATION syndrome- after abrupt WD,
agents at high risk for discontinuation syndrome
- short half lives and inactive metabolites like citalopram and escitalopram.
- fluoxetine has lowest DS risk
S/Sx of discontinuation syndrome
HA, malaise flu like sx, agitation, irritability, nervousness, and sleep changes
rare but dangerous elevation of 5HT- hyperthemia, muscle rigidity, myoclonus, rapid fluctuation in mental status and VS. liklihood increases with concurrent SSRI use
all SSRi can do this to depression
transform it into mania- should be stopped if develops, and mania therapy should be initiated
SNRI, dual inhibitors of both serotonin and norepi and is effective in treating pts with melancholia- severe form of depression. minimal protein binding conferring good bioavail, PTSD, PMDD, hot flashes in Ca
SE of venlafaxine/ desvenlafaxine
very similar to SSRIs, nausea constip, insomnia, HA, sedation and sex dysfn.
trmt for women who want to avoid estrogen therapy for menopause
- SNRI- well absorbed and good half life, tightly protein bound-- extensive oxidative metabolism
- GAD, mngt of fibromyalgia, chronic musculoskeletal pain- from OA or other
well tolerated w/ orthostatics w/ TCAs. greater seizure potential. does slightly inhibit dop reupake
nefazadone/trazadone and SE
- weak 5ht reuptake inhibitors, no anticholinergic or cardiotoxicity
- SE- Nef associated with hepatotoxicity
block the metabolism of NE, Dop, and 5ht that may leak out of symnaptic besicles when cell is at rest
- each inhibit MAO irreversably
- amphetamine like stimulant may produce agitation and insomnia
- certain forms of mild bipolar illness
MAOI AE and contra
- very toxic and unpredictable drug food interactions
- tyramine in certain foods such as cheese, meats, red wines. with MAOI get rapid release of catcholamines- occiptal HA, stiff neck. htn, tach, nausea, seizures, CVA. strict dietary restrictions.
- interact with SSRI- serotonin syndrome and buproprion-seizures
TCAs mech and SE
- NE reuptake block and some Sero. many AE
- alpha adrenergic, muscarinic, and H1 hist, narrow TI
- imipramine 5-6 dose is fatal, OR and QT prolong, muscarinic blockade - similar to atropine, ortho hypotndizziness, reflux tach, drowsiness.
- caution with use in old and young- may have poor compliance
bipolar dz trmt
AD meds can precipitate mania w/ MDD pts, could be related to epilepsy overrxtive brain. Anticonvulsants seem to have efficacy in trmt of mania- carbamazepine, valproate, lamotrigine, lithium has claming effect
lithium and valproate
most useful trmt for bipolar
lithium and lamotrigine
useful for aggresion in elderly dementia
useful for irritability and impulsivity
carbmazepine indi and SE
- elderly dementia
- skin rxn, hemat, vc, and liver
valproate indi rxn
- anticonvulsant for bipolar- agitation and aggresion in dementia- off label
- nv, thrombocytopenia abnormal coags, increased risk of suicide
lamotrigine indi and SE
long term maintenance of bipolar I, not for acute mania, risk of steven johnsons syndrome if not titrated- skin and mucous severe rxn- some suicidal ideation
lithium indi and SE
- manic-depressive- effective in 60-80% of mania, may involve phosphatidyl inositol PW
- AE- HA, dry mouth, polydipsia, polyuria, GI distress, tremor, fatigue, derm rxn, sedation, ataxia, slurred speech confusion convulsion, decrease thyorid fn. VERY LOW TI
- imipramine- prototypical