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Psych Week 2 > ICL 8.5: Psychopharmacology of Anxiety Disorders > Flashcards

ICL 8.5: Psychopharmacology of Anxiety Disorders Flashcards

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1
Q

what are the overlapping symptoms seen in both major depressive disorder and anxiety disorders?

A

the core MDD symptoms are depressed mood and decreased interest/pleasure while the core anxiety symptoms are anxiety and worry

however, they have a lot of other similar symptoms like decreased concentration, sleep disturbances, fatigue –> this relates to the medications that are used for each and why there’s overlap between them

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2
Q

which NTs are implicated in anxiety?

A
  1. serotonin
  2. GABA
  3. NE

there is potential for interactions among noradrenergic, serotonergic, and dopaminergic neurons

glutamate, dopamine, CRF are also involved but those 3 are the main ones

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3
Q

what medications can be used to treat anxiety?

A
  1. SSRIs (fluoxetine)
  2. SSNRIs

SSNRIs: venlafaxine and duloxetine

TCA: imipramine, clomipramine –>

  1. tetracyclic and unicyclic antidepressants (mirtazapine)
  2. benzodiazepines
  3. azapirones (buspar;Buspirone)
  4. anticonvulsants (neurontin; gabapentin)
  5. antihistamine(vistaril or Atarax; hydroxyzine)
  6. beta Blockers
  7. antipsychotics (olanzapine)
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4
Q

which drug is the gold standard for OCD?

A

clomipramine

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5
Q

what are the various indications for the use of antidepressants?

A
  1. depression
  2. bipolar depression
  3. sleep disorders
  4. anxiety disorders
  5. eating disorders
  6. ADHD
  7. substance-related disorders
  8. pain syndromes
  9. IBS
  10. enuresis (bed-wetting)
  11. some dermatological disorders
  12. premature ejaculation
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6
Q

what is the general MOA of antidepressants?

A

we want to increase NT levels in the synapse via

  1. pre-synaptic reuptake inhibition
  2. blocking catabolism of NTs (break down)
  3. receptor agonist/antagonist effects = potentiate receptor action
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7
Q

how is serotonin normally transmitted across a synaptic cleft?

A

serotonin binds to the post-synaptic neuron causing a cascade of processes & resulting in a desired effect

if there’s high serotonin levels, serotonin molecules find to the same pre-synaptic neuron at the 5-HT1B auto receptor which stops the release of more serotonin = negative feedback loop!

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8
Q

what is the MOA of SSRI?**

A
  1. primary MOA is the selective inhibition of the serotonin transporter (SERT)
  2. the precise mechanism of SSRI therapeutic action is delayed disinhibition of serotonergic neurotransmission

this happens via desensitization of 5-HT1Aand 5-HT1Bauto receptors

what happens is when we give SSRIs to people, the clinical effect is only seen after 8 weeks with anxiety patients even though there’s an immediate increase in serotonin; why is that? it’s because of this desensitization of the 5-HT1Aand 5-HT1Bauto receptors

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9
Q

what are the 4 key pathways that occur that explain the MOA of SSRIs?

A
  1. blockade of serotonin reuptake pump which leads to an immediate increase in in the synapse AND the serotonin somatodendritic region
  2. chronic use of SSRIs causes ↑ somatodendritic serotonin concentration which desensitizes the somatodendritic 5-HT1Aautoreceptors, ↑serotonin at the presynpse
  3. desensitization of the terminal presynaptic 5-HT1Bautoreceptors and
  4. the desensitization postsynaptic serotonin receptors

this is why it takes 4 weeks for depression and 8 weeks for anxiety!

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10
Q

what are the effects of serotonin disinhibition? how does this help explain why SSRIs are used for various different disorders?

A

disinhibition of serotonergic neurotransmission pathway delivers serotonin to different places for different psychiatric disorders

  1. midbrain raphe to prefrontal cortex could hypothetically help mediate the antidepressant effects of SSRIs
  2. midbrain raphe to basal ganglia could hypothetically mediate therapeutic actions of SSRIs in OCD
  3. mesolimbic cortex and hippocampus could mediate therapeutic actions in panic disorders
  4. hypothalamus could mediate therapeutic actions in bulimia and binge-eating disorder
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11
Q

why is there a difference between the time course of the clinical effects vs. chemical effects of SSRIs?

A

although the chemical effects of antidepressants are immediate (i.e. reuptake inhibition), clinical response is delayed for several weeks, because of downregulation (presynaptic auto-receptors, alpha & beta noradrenergic receptors, and 5HT receptors)

some may experience benefit as early as 1-2 weeks

2 weeks – most of the common side effects should subside

6 weeks – should be seeing some benefit; considered “adequate” trial before going to next step in treatment algorithm

8 weeks for anxiety disorders (and you need higher doses too)

12 weeks – full benefit at that dose; because it takes time to affect the manufacturing of proteins in our bodies

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12
Q

what are the common side effects of SSRIs?

A
  1. nausea
  2. headache
  3. bowel changes
  4. anxiety (short term BZD to help with this)
  5. sleep changes and vivid dreams

usually resolve within 2 weeks

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13
Q

what are some of the less common side effects of SSRIs?

A
  1. sexual dysfunction
  2. bruxism; grinding of teeth
  3. tinnitus
  4. weight changes
  5. decreased platelet binding = increased bleeding

most usually resolve with discontinuation

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14
Q

what are the serious side effects of SSRIs?

A
  1. photosensitivity
  2. Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH) = hyponitremia
  3. seizures
  4. impairment in kidney or liver functioning
  5. increased bleeding
  6. Serotonin Syndrome
  7. discontinuation syndrome (seen in SSRIs with short 1/2 life)
  8. suicidality
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15
Q

what are the symptoms of serotonin syndrome?

A
  1. myoclonus
  2. rigidity
  3. delirium
  4. hyperreflexia
  5. sweating
  6. diarrhea
  7. nausea
  8. tachycardia
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16
Q

what are the side effects of increased NE when using SSNRIs?

A
  1. tremors
  2. jitteriness
  3. increased heart rate
  4. increased blood pressure
  5. sweating
  6. sexual side effects
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17
Q

what are the side effects of using a medication that blocks histamine?

A
  1. sleepiness
  2. weight gain
  3. increased hunger
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18
Q

what are the side effects of using anticholinergic medications?

A

Red as a beet: Flushing, peripheral vasodilation

Mad as a hatter: delirium, confusion, poor memory, (visual) hallucinations

Hot as a hare: high temperature, high heart rate

Blind as a bat: Pupil dilation, blurred vision, increased intra-ocular pressure

Dry as a bone: decreased salivation, urinary retention, constipation, decreased sweating

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19
Q

which drug commonly causes serotonin syndrome?

A

tramadol

it causes direct release of 5HT from stored vesicles and decreased 5HT reuptake

serotonin syndrome is really hard to diagnose unless you have a good history

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20
Q

which drugs cause direct stimulation of 5HT receptors?

A
  1. buspar
  2. triptans
  3. tegretol
  4. LSD
  5. mescaline
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21
Q

which drugs cause direct release of 5HT from stored vesicles?

A
  1. amphetamines
  2. MDMA
  3. cocaine
  4. reserpine
  5. codiene,
  6. dextromethorphan
  7. pentazocine
  8. tramadol (Ultram)
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22
Q

which drugs cause increased abailability of 5HT precursors?

A

L-Tryptophan

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23
Q

which drugs cause decreased 5HT reuptake?

A
  1. SSRIs
  2. trazodone
  3. serzone
  4. effexor
  5. cymbalta
  6. dextromethorphan
  7. ultram (tramadol)
  8. demerol
  9. cocaine
  10. St. Johns Wort
  11. amphetamines
  12. tegretol
  13. methadone
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24
Q

which drugs cause decreased 5HT degradation?

A
  1. MAOIs

2. St. Johns Wort

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25
Q

what is the MOA of fluoxetine?

A

aka Prozac!

causes the inhibition of serotonin reuptake

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26
Q

what are the benefits of using fluoxetine?

A

it has the longest half-life of all antidepressants! this is important because other SSRIs with short 1/2 lifes have notorious withdrawal symptoms so fluoxetine is least likely to have discontinuation symptoms

also because of its long 1/2 life, you need 5 weeks washout recommended before MAO’s can be given

so it’s the only antidepressant with the option of a once weekly pill because of its long half life

tends to be more activating/ agitating/suppress appetite – if you’re using it for anxiety you have to let the patient know because you’re treating the anxiety but what you’re giving is also causing anxiety; so you need to start with small doses and add BZD short term until prozac kicks in

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27
Q

what are the pharmakokinetics of fluoxetine?

A

fluoxetine has a ton of drug-drug interactions so it’s really only given by itself because it interacts with CYP450 –> so generally want to avoid in elderly b/c med interaction issues, 2D6, 3A4)

non-linear pharmacokinetics: dose increases lead to disproportionately greater increases in plasma drug levels

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28
Q

what is the MOA of sertraline?

A

aka zoloft

inhibition of serotonin reuptake

possibly some more dopaminergic activity than other SSRIs, but generally well tolerated and no specific unique areas

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29
Q

what are the pharmacokinetics of sertraline?

A

zoloft has a 1/2 life of 26-32 hours

it also has linear pharmacokinetics so the dose increases relative to expected increase in plasma drug level

this is why it’s generally recommended in medically ill patients because it doesn’t have any drug-drug interactions

30
Q

what is the MOA of citalopram?

A

aka Celexa

it inhibits serotonin reuptake

31
Q

what are the side effects of citalopram?

A

celexa has a recommended max dose of 40mg due to cardiac rhythm abnormalities

this limits the efficacy of celexa

32
Q

what are the pharmacokinetics of citalopram?

A

it has multiple CYP 450/medication interactions, including grapefruit juice

  1. linear pharmacokinetics (dose increases lead to expected increase in plasma drug level)
  2. large age-related change in plasma drug level, so geriatric patients should start at half recommended dose –> also most geriatric patients are on a lot of other medications so you don’t want to combine it with other meds that could increase QT interval
33
Q

what is the MOA of escitalopram?

A

aka lexapro

it’s structurally similar to citalopram; it’s an active enantiomer

it’s the SSRI that is the most “selective” for serotonin!!!

it’s also often used in medically ill due to low drug-drug interactions and good tolerability

34
Q

what is the MOA of paroxetine?

A

paxil is an SSRI

it also has anti-histaminic and anticholinergic effects

it’s a good SSRI for anxiety! but just warm them about the discontinuation symptoms

35
Q

what are the side effects of paroxetine?

A

paxil tends to be sedating and can cause weight gain due to anti-histaminic effects

avoid in pregnancy (used to be category D; has teratogenic effects)

36
Q

what are the pharmacokinetics of paroxetine?

A
  1. short half life so has the MOST discontinuation symptoms
  2. many CYP 450/medication interactions
  3. non-linear pharmacokinetics (dose increases lead to disproportionately greater increases in plasma drug levels)

large age-related change in plasma drug level, so geriatric patients should start at half recommended dose

37
Q

what is discontinuation syndrome?

A

discontinuation from a medication can cause flu like symptoms like:

  1. NVD
  2. jittery/agitation
  3. electric shock sensations
  4. emotional lability
  5. temperature fluctuations

symptoms usually resolve within 1-2 weeks are stopping the medication, but can have residual symptoms that last for 1-6 months

38
Q

which medications are most likely to cause discontinuation syndrome?

A
  1. paroxetine
  2. venlafaxine

both have really short 1/2 life

39
Q

what is the MOA of vilazodone?

A

viibryd has more affinity as a 5HT1A partial receptor agonist (like buspirone) and less affinity as SSRI –>so it blocks the transporter and also by itself has some serotonin-like effect

it was actually nicknamed “SPARI”: Serotonin Partial Agonist/Reuptake Inhibitor

very highly protein bound and tends to be activating

40
Q

what is the MOA of vortioxetine?

A

trintellix has SSRI activity but it also works at 5 serotonin receptors on the post-synaptic neuron

  1. 5HT 1A – agonist (like buspirone and vilazodone)
  2. 5HT 1B – partial agonist
  3. 5HT 1D – antagonist
  4. 5HT3 – antagonist (like ondansetron)
  5. 5HT7 – antagonist
41
Q

what are SNRIs?

A

similar concept in mechanism of action to that of SSRIs, but they block the reuptake of both serotonin and norepinephrine into the presynaptic neuron

side effects are similar to SSRIs, plus symptoms of adrenaline/epinephrine –> ALL have risk of hypertension!!!

42
Q

which drugs are SNRIs?

A
  1. Effexor / Venlafaxine
  2. Cymbalta / Duloxetine
  3. Pristiq / Desvenlafaxine
  4. Fetzima / Levomilnacipran
43
Q

what is venlafaxine?

A

effexor is an SNRI that has variable serotonergic versus noradrenergic effects based on dosing –> at lower doses increases 5HT but at higher doses increases NE too

it’s the least protein bound of all antidepressants so it’s not affected by coumadin

shortest half life so has the most discontinuation symptoms

44
Q

what is duloxetine??

A

cymbalta is an SNRI that has equal serotonergic/noradrenergic input

it’s also FDA approved for diabetic neuropathy and fibromyalgia too

pain accompanied by depression or anxiety is when you’d use duloxetine

45
Q

what are the side effects of duloxetine?

A

cymbalta has potential for liver toxicity, so do not use in someone who is already hepatically compromised

most common side effect is nausea

46
Q

what is desvenlafaxine?

A

Pristiq is the SNRI form of venlafaxine after its undergone metabolization by CYP2D6 in the liver

however, it does not have the changing serotonergic / noradrenergic effect based on dose, like venlafaxine does

it’s excreted relatively unchanged (not affected by P450)

47
Q

what is levomilnacipran?

A

Fetzima is an SNRI that is the active entantiomor of Milnacipran (Savella) for fibromyalgia

more selective for NRI initially, but as dose gets higher it becomes more equal for SRI (kind of the opposite of Venlafaxine)

48
Q

which SNRI is excreted renally?

A

levomilnacipran (fetzima)

most other SNRIs are hepatic

49
Q

what is the MOA of buspirone?

A

buspar is an agonist at the serotonin 5-HT1A receptor

can be as effective as BZDs for GAD, but takes 1-2 weeks of daily use for onset of anxiolytic activity –> so when you can’t use BZDs, use buspirone!

50
Q

what are the drug-drug interactions involved with buspirone?

A

the levels of Buspar are increased by:
1. blood pressure pills (verapamil, diltiazem),

  1. antibiotic (erythromycin),
  2. anti-fungal (itraconazole),
  3. grapefruit juice

so be careful if someone is taking buspirone and also one of these things

51
Q

what is gabapentin?

A

neurontin is is an analogue of GABA and is used to treat seizures and neuropathic pain

however, it’s used off-label often in psychiatry for the treatment of generalized anxiety if there’s alcohol use

side effects: dizziness, drowsiness, peripheral edema/swelling

52
Q

what is hydroxyzine?

A

vistaril/atarax is is an antihistamine, similar to diphenhydramine

watch out for anticholinergic effects; also has side effects of drowsiness and dizziness

can be prescribed PRN for anxiety!

53
Q

what is the MOA of B blockers?

A

it competitively antagonizes norepinephrine & epinephrine at the beta adrenergic receptors

it’s useful for reducing peripheral physical symptoms of performance anxiety such as tremor, sweating, tachycardia, blushing which is good for public speaking, musical concert, etc. –> this is good for anxiety too though because if you limit the physical symptoms they’ll calm down

used to treat tremor

contraindicated in people with severe breathing problems (asthma, COPD, etc) and recent myocardial infarction

54
Q

what’s the difference between the use of SSRIs for anxiety vs. depression?

A

many SSRIs are off-label for a lot of the anxiety disorders, but are still considered first line treatments

most benzos are FDA approved for most anxiety disorders, yet are considered to have more of an augmentation role rather than primary, unless there is basically no other choice (usually because of intolerability to SSRIs)

for anxiety, the SSRI doses should start at lower doses than you would normally start for depression (because of likelihood of initial activation)

however the target doses end up being in a higher range than you would use for depression

55
Q

what are sedative hypnotics?

A

a heterogeneous class of drugs that includes benzodiazepines, barbiturates, and various hypnotics

sedative = lowers excite & calms the awake patient

hypnotic = produces drowsiness & promotes sleep

56
Q

what are the various conditions that benzodiazepines are used to treat?

A
  1. anxiety disorders
  2. agitation
  3. insomnia and other sleep disorders
  4. akathisia (restlessness)
  5. tremor
  6. TMJ (jaw pain)
  7. catatonia
  8. seizures
  9. skeletal muscle relaxation
57
Q

what is the MOA of benzodiazepines?

A

GABA(A) receptor agonist

GABA(A) receptors are sensitive to BZD/barbiturates but GABA(B) receptors are not

BZDs interact at the α2 subunit, then provide a boost (indirect agonist) to endogenous GABA by allowing an influx of Cl into the post-synaptic neuron

there is a high density of BZD receptors within the amygdala, suggesting it is an important site for the actions of anxiolytic drugs

58
Q

what is the structure of the GABA(A) receptor? where do BZDs bind?

A

GABAA receptor has several subunits: 2α, 2β and 1γ

BZDs interact at the junction of subunit α and γ

in the middle of the subunits is a Cl- ion channel that gets opened and hyper polarizes the cell when GABA or BZD bind to the GABA(A) receptor

*flumazenil is a BZD antagonist that you should know!! used to treat BZD overdoses!

59
Q

what’s the difference between BZD and barbiturate interactions at the GABA(A) receptor?

A

BZDs interact at the α2 subunit, then provide a boost (indirect agonist) to endogenous GABA by allowing an influx of Cl into the post-synaptic neuron

Barbiturates instead directly stimulate the Chloride channel, keeping them open 4-5x longer.

60
Q

which benzodiazepines are short acting vs. long acting?

A

SHORT ACTING
1. alprazolam/xanax (high potency)

  1. temazepam/restoril

LONG ACTING
1. clonazepam/klonopin (high potency)

DON’T NEED LIVER METABOLISM
1. lorazepam/ativan

  1. temazepam/restoril
61
Q

how are benzodiazepines metabolized in the body?

A

phase 1 and phase 2 metabolism in the liver

62
Q

interaction with which substances increase BZD levels?

A
  1. cimetidine
  2. antabuse
  3. estrogen & oral contraceptives
  4. erythromycin
  5. macrolide antibiotics
  6. itraconazole & ketoconazole
  7. SSRIs
63
Q

interaction with which substances decrease BZD levels?

A
  1. carbamazepine (Tegretol)
  2. antacids, food
  3. cigarette smoking
64
Q

BZD increase the levels of which medications?

A
  1. digoxin

2. phenytoin (Dilantin)

65
Q

what are the adverse effects of BZDs?

A

this is why we don’t use BZD as much as we could considering their efficacy!

  1. dose dependent CNS depression; excessive daytime drowsiness,
  2. cognitive impairment and confusion (tasks involving visuospatial ability & sustained attention)
  3. psychomotor impairment & risk of falls
  4. paradoxical reactions
  5. depression
  6. intoxication, abuse and dependence; breakthrough withdrawal reactions
  7. amnestic syndromes
  8. respiratory depression with alcohol, barbiturates, tricyclic & tetracyclic drugs, dopamine receptor antagonists, opioids, antihistamines
66
Q

what is the clinical presentation of physiological BZD withdrawal?

A

risk increases after 2 weeks daily use, and further increases significantly after 3-4 months of continuous use

most common effects (mild & 1-3 days) = GI, sweating, tremor, lethargy dizziness, headaches, increased acuity for smell & sound, restlessness, insomnia, irritability, anxiety, tinnitus, unsteadiness, palpitations, depersonalization

rare but severe side effects = severe & prolonged depression, hallucinations, protracted tinnitus, opisthotonos, choreoathetosis, myoclonus, bizarre involuntary muscular movements, delirium with catatonic features, panic & agoraphobia

seizures are a higher risk if high dose, >4 months of therapy, using other drugs associated with seizure induction, and a prior history of seizures; more seizures reported with Alprazolam than all other BZDs combined

usually lasts for 4-12 weeks; rarely (10-15% of chronic BZD users) can have a protracted withdrawal syndrome lasting 6-12 months

67
Q

which drugs are used to treat panic disorder?

A

First line: SSRI’s, BDZ’s

Others: TCA, MAO’s, SNRI’s

68
Q

which drugs are used to treat social anxiety disorder?

A

First line: SSRI, BDZ’s

Others: anticonvulsants, MAO’s, antipsychotics

69
Q

which drugs are used to treat specific phobia?

A

First line: SSRI, BDZ’s

70
Q

which drugs are used to treat generalized anxiety disorder?

A

First line: BDZ’s

Others: Buspirone, TCA, SSRI’s, SNRI’s, Mirtazapine, Bupropion, Hydroxyzine, antipsychotics

71
Q

which drugs are used to treat OCD?

A

First line: SSRI’s

Others: TCA

72
Q

which drugs are used to treat PTSD?

A

First line: SSRI’s SNRI’s

Others: TCA, MAO’s, Alpha blockers, antipsychotics

Psych Week 2 (18 decks)

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