Antidepressants drug names and facts Flashcards
6 anti-depressant categories
- Cyclic Antidepressants
- MOAI’s
- SSRI’s
- Serotonin and Norepinephrine Reuptake Inhibitors
- Norepinephrine Reuptake Inhibitors
- Atypical antidepressants
MAOI’s Action
- inhibits monamine oxidase (MAO)- an enzyme used to break down catecholamines (norepinephrine, dopamine, serotonin) in neurons
- bond cannot be broken, function only returns when new enzymes are made
Tricyclic Antidepressants
- metabolized in the liver
- highly bound to plasma protein
- can easily become toxic if another drug is admin. that is also highly protein bound, very difficult to remove drug from body
First Generation
Tricyclic and MAOI’s
Second Generation
SSRI’s
Heterocyclics
Tofranil
imipramine
- Tricyclic
- powerful sedation and anticholinergic effects
Elavil
amitriptyline
- Tricyclic
- powerful sedation and anticholinergic effects
Anafranil
clomipramine
- Tricyclic
- powerful sedation and anticholinergic effects
- originally for depression, has anti-obsessional effects
- now primarily used for OCD (also depression, anxiety, panic, ADHD)
- can also be administered through injection
Sinequan
doxepin
- Tricyclic
- powerful sedation and anticholinergic effects
Palemor
nortriptyline
Tricyclic antidepressant and nerve pain medication
- lower sedation and aniticholinergic effects
- metabolite of Elavil
- NE and Seretonin reuptake inhibitor
- metabolized in liver
- excreted in urine and feces
- highly protein bound
- long half life (28-31 hrs)
- SE: nausea, drowsiness, sedation, worsening of symptoms, dry mouth, blurred vision
- slow onset, leads to elevated mood, better sleep
Tricyclic Uses
- depressive symptoms (especially for resistant or long term depression)
- chronic pain
- anxiolytic effects
- analgesic effects
Nopramin
desipramine
- metabolite of Tofranil
Tricyclic Mechanism of Action
- block presynaptic reuptake transporter for NE and/pr seretonin (aka NET nd SERT)
- block postsynaptic receptors for histamine, acetylcholine, and norepinephrine (why you get mroe side effects- not specific)
Tricyclic Pharmocokinetics
- given orally, easily absorbed
- long half life, in body longer
- taking at bedtime relieves sedation SE - metabolized in liver
- clinical effects are longer in elderly
- crosses placenta
Tricylcic Therapeutic Effects
- no dependence potential
- slow onset of action
- wide array of effects on CNS
- elevate mood
- increase physical activity
- improve appetite and sleep
Tri. Side Effects
- Dirty- reacts with many receptor side
- dry mouth ,blurred vision, dilated pupils
- confusion, disorientation, agitation
- sedation
- most side effects subside over time
Tri. Drug interactions
- Reacts with a lot of drugs!
- antipsychotics, benzo’s, sedatives, antiepileptics
- OTC weight loss
- MAOI’s
Heterocyclics
- blocks NE reuptake (blocks NET)
- mild anticholinergic effects
- sedating
Ludiomil
maprotoline
- hetercyclic
- long half life
- can cause seizures
Ascendin
amoxapine
- heterocyclic
- better at relieving anxiety and agitation (in addition to depressive symptoms)
- can lead to parkinson like SE
- active metabolite
- OD is fatal
Desyrel
trazodone
- almost no anticholinergic effects
- heterocyclic
- commonly prescribed for sleep due to sedation effect
- absorption increased when taken with a mean
- Olelptro- new formulation- extended release
MAO’s facts
- limited use due to serious SE
- Strict dietary restrictions
- any food with tyramines (wont be broken down bc MAOI enzyme is blocked, builds up in body)
(alcohol, specific meats, fruits and veggies, specific cheese, caffeinated food and drinks)
- any food with tyramines (wont be broken down bc MAOI enzyme is blocked, builds up in body)
- long time for therapeutic effect
MAOI’s uses
- atypical, long term depression
- anorexia and bulimia
- bipolar depression
- panic disorder and phobias
MAOI SE
- low HR
- hypotension
- anticholinergic effects
- agitation
- lethal dose if 6-10 times usual dose is taken
Eldapril (Emsam)
selegiline
- MAOI
- transdermal patch- slow continuous absorption
- food and drug interactions not a concern bc absorbed through skin
- SE- skin irritation
SSRI action and effects
- block presynaptic transporter for seretonin reuptake (SERT)
- depression, anxiety do, bipolar
- safe with elderly
- highly tolerated
SSRI SE
- neutral for weight gain (except with paroxetine, Paxil)
- GI upset, headache, dizziness, insomnia, agitation
- sexual dysfunction (up to 80%)
- RARE- neuroleptic malignant syndrome- increased body temp
- serotonin syndrome- too much serotonin causing cognitive disturbance, agitation, and restlessness
- ANS dysfunction- fever, chills, sweating, high bp, diarrhea, increased HR
- Neuromuscular impairment- ataxia, increased reflexes, myoclonus,
- hallucinations
- withdrawal syndrome
- finish effects: flulike symptoms, insomnia, nausea
- suicidality, sleep disturbance, apathy, physiological sx
Paxil
paroxetine
- most specific SSRI for depression and GAD
- long half life
- most implicated in serotonin syndrome and psychosis
- high risk to fetus
- significant weight gain
Celexa
citalopram - SSRI low interaction effect with other drugs more rapid onset - absorbed orally - half life 33 hours (once daily dose) - helps reduce alcohol consuption
Lexapro
escitalopram - SSRI for major depression and GAD - more selective and less SE - admin orally, not highly protein bound - half life ~32 hours - metabolized and excreted through urine - do not take with MAOI SE- nausea, ejaculation DO, drowsiness, sweating
Luvox
fluvoxamine (derivative of fluoxetine) SSRI for anxiety and depression fewer SE good compliance Luvox XR- tx for socal anxiety and OCD
Prozac
fluoxetine
- SSRI usecd for depression, oCD, anxiety and panic, etc
- administered orally
- absorbed in GI tract
- highly protein bound
- metabolized in liver
- excreted through urine
- long half life (7-10 days)
- effects: energizing
SE: insomnia, changes in weight, sex dysfunction, sedation, anxiety, nausea
- significant drug interactions- do not use with MAOIs
- can trigger mania, may increase risk of suicidal thinking
Zoloft
sertraline
- SSRI
- fewer SE (few anticholinergic, antihistamine and adverse cardio effects)
- more potent and effective- greater risk for serotonin effect
Effexor
venlafaxine
- mixed SE and NE reuptake inhibitor (dual action)
- SE blocks at lower does
- at high doses also blocks dopamine (DAT)
- lacks anticholinergic or antihistaminic effects
- more sexual Se
- increased BP, extreme sleepiness!
- extended release approved for GAD and panic
- can trigger bipolar
- few drug interactions
- active metabolite (desvenlafaxine; Pristiq) used for depression
Cymbalta
duloxetine
- dual action (blocks more fully than Effexor) for depression and anxiety and pain
- 12 hr half life
- may induce mania
- Nausa is most common SE
Remeron
mirtazepine
- dual action (increases release of NE and SE- different mechanism)
- drowsiness, appetite, weight gain
- absorbed orally, half life 20-40 hrs
Wellbutrin
bubroprion
- dual action (NE and DOPA reuptake inhibitor:NDRI)
- orally admin
- absorbed din GI
- first-pass effects
- significant affinity for plasma
- metabolized in liver
- active metabolites
- excreted in uring
- used for depression, pain, adhd, addiction
- nervousness and nausea SE
- less likely to lead to weight gain sedation or sexual dysfunction
- abuse potential bc of dopamine increase
Strattera
atomoxetine
- Selective Norepinephrine reuptake inhibitor (SNRI)
- nonstimulant used for ADHD
Monoamine hypothesis
Depression is caused by NT deficiency. less NT are available in the cleft… THerefore, an increase in POST synaptic monoamine receptors occurs in an effort to capture all available NT. Now, there are no more NT available and people are depressed.
- problem with this theory bc drugs cause NT change quickly but effect is weeks later
Neurogenic theory
- existing neurons are able to repair themselves and brain is capable of making new neurons
- New neurons are produced in hippocampus and frontal cortex
- stress (depression) reduces neurogenisis in these areas and damages neurons
- delay occurs bc of time needed for new neurons to develop
- CREB (intracellularly response-element binding protein) activates genes that control production of BDNF (brain derived neurotropic factor)
- BDNF prtects neurons and prevents death of neurons
- hyp. that stress decreases BDNF
- antidepressants increease levels of BDNF in hippocampus
**When there is chronic stress, it impacts the BDNF gene, which prevents the BDNF from keeping neurons healthy
STAR Study (Rush et al)
- looking at effectiveness of anti-dep. in normal setting
- 4 levels with different methods or med. combos
LEVEL 1:citalopram - only 30% achieved remission
- 10-15% decreased sx by half
- average 6 wk response
LEVEL 2: Zoloft, Wellbutrin or Effexor Or CBT - 25% became sx free
- CBT results were comparable
- med was mroe rapidly effective than CBT
LEVEL 3: mirtazepine or nortriptyline - 10-20% achieved remission
LEVEL 4: MAOI or Parnate - 7-10% became sx free
OVerall,
- 60% achieved remission
- many withdrew
- with each additional tx strateggy, odds for remission fall
TAKE home for CLients on anti-dep.
- may take 6-8 weeks to see treatment effect
- side effects may subside
- physiological not psychological sx will see relief
- dont drink
- dont stop taking cold turkey
