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Psychopharm > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

6 anti-depressant categories

A
  1. Cyclic Antidepressants2. MOAI’s 3. SSRI’s4. Serotonin and Norepinephrine Reuptake Inhibitors5. Norepinephrine Reuptake Inhibitors6. Atypical antidepressants
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2
Q

MAOI’s Action

A
  • 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
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3
Q

Tricyclic Antidepressants

A
  • 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
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4
Q

First Generation

A

Tricyclic and MAOI’s

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5
Q

Second Generation

A

SSRI’sHeterocyclics

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6
Q

Tofranil

A

imipramine- Tricyclic- powerful sedation and anticholinergic effects

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7
Q

Elavil

A

amitriptyline- Tricyclic- powerful sedation and anticholinergic effects

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8
Q

Anafranil

A

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

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9
Q

Sinequan

A

doxepin- Tricyclic- powerful sedation and anticholinergic effects

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10
Q

Palemor

A

nortriptylineTricyclic 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

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11
Q

Tricyclic Uses

A
  • depressive symptoms (especially for resistant or long term depression)- chronic pain- anxiolytic effects- analgesic effects
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12
Q

Nopramin

A

desipramine- metabolite of Tofranil

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13
Q

Tricyclic Mechanism of Action

A
  • 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)
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14
Q

Tricyclic Pharmocokinetics

A
  • 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
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15
Q

Tricylcic Therapeutic Effects

A
  • no dependence potential- slow onset of action- wide array of effects on CNS- elevate mood- increase physical activity- improve appetite and sleep
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16
Q

Tri. Side Effects

A

-Dirty- reacts with many receptor side- dry mouth ,blurred vision, dilated pupils- confusion, disorientation, agitation- sedation- most side effects subside over time

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17
Q

Tri. Drug interactions

A
  • Reacts with a lot of drugs!- antipsychotics, benzo’s, sedatives, antiepileptics- OTC weight loss- MAOI’s
18
Q

Heterocyclics

A
  • blocks NE reuptake (blocks NET)- mild anticholinergic effects- sedating
19
Q

Ludiomil

A

maprotoline- hetercyclic- long half life- can cause seizures

20
Q

Ascendin

A

amoxapine- heterocyclic- better at relieving anxiety and agitation (in addition to depressive symptoms)- can lead to parkinson like SE- active metabolite- OD is fatal

21
Q

Desyrel

A

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

22
Q

MAO’s facts

A
  • 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)- long time for therapeutic effect
23
Q

MAOI’s uses

A
  • atypical, long term depression- anorexia and bulimia- bipolar depression- panic disorder and phobias
24
Q

MAOI SE

A
  • low HR- hypotension- anticholinergic effects- agitation- lethal dose if 6-10 times usual dose is taken
25
Q

Eldapril (Emsam)

A

selegiline- MAOI- transdermal patch- slow continuous absorption- food and drug interactions not a concern bc absorbed through skin- SE- skin irritation

26
Q

SSRI action and effects

A
  • block presynaptic transporter for seretonin reuptake (SERT)- depression, anxiety do, bipolar- safe with elderly- highly tolerated
27
Q

SSRI SE

A
  • 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
28
Q

Paxil

A

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

29
Q

Celexa

A

citalopram- SSRIlow interaction effect with other drugsmore rapid onset- absorbed orally- half life 33 hours (once daily dose)- helps reduce alcohol consuption

30
Q

Lexapro

A

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 MAOISE- nausea, ejaculation DO, drowsiness, sweating

31
Q

Luvox

A

fluvoxamine (derivative of fluoxetine)SSRI for anxiety and depressionfewer SEgood complianceLuvox XR- tx for socal anxiety and OCD

32
Q

Prozac

A

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: energizingSE: 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

33
Q

Zoloft

A

sertraline- SSRI- fewer SE (few anticholinergic, antihistamine and adverse cardio effects)- more potent and effective- greater risk for serotonin effect

34
Q

Effexor

A

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

35
Q

Cymbalta

A

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

36
Q

Remeron

A

mirtazepine- dual action (increases release of NE and SE- different mechanism)- drowsiness, appetite, weight gain- absorbed orally, half life 20-40 hrs

37
Q

Wellbutrin

A

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

38
Q

Strattera

A

atomoxetine- Selective Norepinephrine reuptake inhibitor (SNRI)- nonstimulant used for ADHD

39
Q

Monoamine hypothesis

A

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

40
Q

Neurogenic theory

A
  • 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
41
Q

STAR Study (Rush et al)

A
  • looking at effectiveness of anti-dep. in normal setting- 4 levels with different methods or med. combosLEVEL 1:citalopram- only 30% achieved remission- 10-15% decreased sx by half- average 6 wk responseLEVEL 2: Zoloft, Wellbutrin or Effexor Or CBT- 25% became sx free- CBT results were comparable- med was mroe rapidly effective than CBTLEVEL 3: mirtazepine or nortriptyline- 10-20% achieved remissionLEVEL 4: MAOI or Parnate- 7-10% became sx freeOVerall, - 60% achieved remission- many withdrew- with each additional tx strateggy, odds for remission fall
42
Q

TAKE home for CLients on anti-dep.

A
  • 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

Psychopharm (4 decks)

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