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Pharmacology II > Exam 3 - Behavioral Medicine > Flashcards

Exam 3 - Behavioral Medicine Flashcards

1
Q

MAJOR DEPRESSIVE DISORDER

A

…

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2
Q

Pharmacotherapy

A

Older agents are less specific and have a smaller therapeutic index. Ex: TCA.
2-3 fold OD = fatal.

Newer agents are more specific and have a wider therapeutic index. Ex: SSRIs.
Multiple fold OD = OK.

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3
Q

Placebo

A

Placebo effect takes place with anti-depressant medications, makes it difficult to determine if therapy is effective.

Trials confounded with placebo affect, some trials have poorly defined outcomes.

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4
Q

Depression, can be secondary to:

A
  • Hypothyroidism
  • Parkinson’s disease
  • Inflammatory conditions
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5
Q

What medications can cause depression?

A

Beta Blockers
Levetireacetam (Keppra)
Isotretinoin
Topiramate (Topamax)

Clonidine
Corticosteroids
OC
Methyldopa

Interferons (Ribovirin)
Tamoxifen

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6
Q

Anxiety

A
  • GAD, OCD, Panic disorder, PTSD, Phobias

- Can inhibit normal function; often associated with depression.

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7
Q

Why do people get depressed?

A
  • Due to depressed levels of monoamines (serotonin, NE).
  • Experience depression due to deficiency of catelcholamines.

-Meds address the issue to supplement the catelcholamines.

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8
Q

Reserpine

A

Antihypertensive; causes synapses to kick out catelcholamines, so they get metabolized.

Causes a deficiency of NE, epi. In addition to hypotension/bradycardia from drug, you’d see depression develop in patients.

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9
Q

If you give drugs to increase serotonin and fix deficiency, you should see “immediate” effect on depression.

Why don’t the drugs work immediately?

A

Therapeutic effect of drugs take weeks to become effective; can be 4-6 weeks.

A lot of pts D/C therapy early, so need to let them know therapeutic effect takes a while.

Mechanism of depression

  • Downstream effects:
  • Receptor expression
  • Gene transcription
  • No final theory how antidepressants work; just know they work
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10
Q

Three phases of treatment

A

Acute phase
Continuation phase
Maintenance phase

Often requires lifetime therapy.
Especially for recurrent symptoms.

Situational based - can get away with short-term therapy

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11
Q

Acute phase

A

First 6-12 weeks of treatment

  • Remission of symptoms
  • Important to educate patients on increased risk of SUICIDE during this time.
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12
Q

Continuation phase

A

4-9 months into treatment:

-Eliminate residual symptoms to prevent recurrence.

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13
Q

Maintenance phase

A

12-36 months into treatment:

-Prevent recurrence.

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14
Q

Non-pharmacologic therapy

A

Psychotherapy
-Affects are additive with antidepressants

ECT
Repetitive transcranial magnet stimulation (TMS)

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15
Q

PHARMACOLOGICAL THERAPY

A

..

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16
Q

How do you know what antidepressants to give?

A

Can’t predict which agent a patient will respond to.

Choice made empirically:

  • history of response
  • concurrent medical illness
  • presenting symptoms
  • cost
  • drug to drug interactions
  • ADR profile
  • Patient preference
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17
Q

Escitalopram (Lexapro)

A

Causes anorgasmia

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18
Q

Antidepressants

How long does it take to reach therapeutic effects?

A
  • 2 to 6 weeks for therapeutic effects
  • Adverse effects occur within hours to days
  • 20-30% failure rate with antidepressants
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19
Q

Failure Rate

A
  • Intrinsic resistance to therapy
  • Due to inadequate dosage or duration
  • Noncompliance
  • ADR or delay in therapy
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20
Q

Placebo effect efficacy/recurrence

A
  • 30-40% efficacy
  • Natural remission in 6-12 months
  • 50-70% experience recurrence
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21
Q

TCA vs. SSRI

A
  • Same efficacy
  • Differ in ADR profiles
  • Therapeutic doses and overdose
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22
Q

MAOI (monoamine oxidase inhibitors)

A
  • Oldest class
  • Non-specific MAOI A + B inhibitors
  • Prevent breakdown of catecholamines 5HT and NE
  • Prevent breakdown of NT; get more NT in synapse
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23
Q

TCA (tricyclic antidepressants)

A
  • Inhibit reuptake of 5HT and NE

- More NT in synapse

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24
Q

SSRI (Selective serotonin reuptake inhibitors)

A

Specifically inhibit reuptake of 5HT to leave in synapse

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25
Q

SNRI (Selective serotonin and NE reuptake inhibitors)

A
  • Inhibit reuptake of NE and 5HT

- Have a balance

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26
Q

What drug activates alpha-2 agonists and treats HTN?

A

Clonidine

  • acts as alpha-2 receptor agonist
  • decreases NE release
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27
Q

In general, MOA antidepressants:

A

-Enhance NE and 5HT effects, MOA not fully known

Long term therapy leads to adaptive and regulatory changes:

  • increased SE and NE receptor density
  • Increased 2nd messenger signaling via G proteins
  • Increased expressoin downstream of gene products
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28
Q

MAOIs - Name them, MOA, and main risk with taking them.

SPIIT

A
  • Iproniazid - first agent
  • Phenelzine (Nardil) - MC
  • Isocarboxazid
  • Tranylcypromine (Parnate) - MC
  • Selegiline transdermal (Emsam)

MOA: Irreversible inhibitor of MAO-A and MAO-B. Affects metabolism of 5HT, NE, and DA (dopamine).

Affect exogenous monoamines (tyramine).
-If you inhibit breakdown of NT, plus more NT being produced, and tyramine from diet = at risk for serotonin toxicity.

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29
Q

Iproniazid

A

Iproniazid

  • MAOI
  • Originally antituberculosis
  • Elevated mood in treated patients, so they started using it for depression.
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30
Q

ADR MAOIs

A
  • Postural hypotension (most common)
  • Weight gain
  • Decreased libido
  • Anorgasmia
  • HYPERTENSIVE CRISIS
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31
Q

How do MAOI cause postural hypotension?

A

-Postural hypotension
Older patients with less cardiovascular reserve - when they go from sitting to standing, their vessels don’t vasoconstrict, because there’s no release of NE/epi.
-If you have a higher set point of NE, bc its not degraded, you cant release extra amount to cause the vasoconstriction. Can’t adapt to the change in pressure.

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32
Q

What S/S are consistent with hypertensive crisis?

How do MAOI cause hypertensive crisis?

A
  • N/V and HA
  • Stiff neck
  • Diaphoresis
  • Looks likemeningitis, but BP: 200/110
  • Risk of CVA and hemorrhagic stroke

MAOI on top of something else increasing catelcholamine levels:

  • MAOI + SSRI/SNRI
  • MAOI + Tyramine intake

Increase catelcholamine levels and cause hypertensive crisis.

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33
Q

Important education point on MAOI risk:

A

MAOI = irreversible inhibitors

  • Because they’re irreversible inhibitors, the drug sticks around for 2 weeks.
  • Wait the “2 week washout period” before starting a new drug!!!
  • Still at risk for CVA and death after drug is discontinued
  • Takes 2 weeks to regenerate enzymes
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34
Q

How do you treat hypertensive crisis?

A

Antihypertensives

  • IV ACE inhibitors
  • IV beta blockers

Drop BP until they get through wash out period and start metabolizing the catelcholamines again.

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35
Q

What are dietary restrictions on patients taking MAOI? Why?

A

NO TYRAMINE or it will increase production of catelcholamines.

Aged cheese
Sour cream
Yogurt
Cottage cheese
Wine / Beer
Aged and processed meats
MSG
Fava beans
Soy sauce
Coffee
Sauerkraut
Licorice

Do not consume with MAOIs!
So many food interactions, run into issues with compliance that lead to toxicity.

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36
Q

What drugs have similar affects (to increasing tyramine intake) when taken with MAOIs?

A

Medications that will increase catelcholamines in the synapse:

  • Amphetamines in ADHD
  • Appetite suppressants
  • Asthma meds
  • Cocaine
  • Decongestants (pseudoephedrine)
  • Robitussin
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37
Q

Tricyclic antidepressants (TCAs)

AACDDIN

A 
Amoxapine (Asendin)
Amitriptyline (Elavil)*
Clomipramine (Anafranil)
Desipramine (Norpramin)*
Doxepin (Sinequan)*
Imipramine (Tofranil)
Nortriptyline (Pamelor)*
  • Derived from phenothiazines (antipsychotics)
  • Not as specific as SSRI
  • MOA: Inhibit the reuptake for 5HT and NE.
  • Used to be first-line therapy for depression, now replaced with SSRIs (due to toxicity profile).
  • Also used to treat insomnia and neuropathic pain.
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38
Q

What phenothiazine is used as an anti-emetic?

A

-Promethazine (Phenergan)

  • Used as anti-emetics, like Reglan, because they’re dopamine antagonists.
  • Blocking dopamine helps with N/V on chemoreceptor trigger zone.
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39
Q

When prescribing was limited, what could be prescribed for sleep that wasn’t a controlled substance?

A
  • TCAs

- Trazadone

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40
Q

What TCA treats neuropathic pain of fibromyalgia?

A

Amitriptylene

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41
Q

What TCA treats nocturnal aneuresis?

A

Imipramine (Tofranil)

  • Treats nocturnal aneuresis (bed wetting)
  • Anticholinergic side effects - “dry as a bone”
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42
Q

ADR of TCAs -

A
  • Sedating drugs at normal doses. Used for sleep. BUT HIGH doses, cause agitation and seizures.
  • Midriasis (dilation)
  • Hyperthermia in high doses
  • Urinary retention
  • Dry mouth/skin
  • Decreased bowel motility
  • Red is cutaneous vasodilation
  • HR increases.

-Cardiac conduction delays - Na channel blocker, causes conduction delays that lead to arrythmias!!!

  • Block alpha receptors, leads to orthostatic hypotension.
  • Sexual dysfunction due to affected penile blood flow
  • Weight gain
  • Sedation

Used for neuropathic pain and sleep, mostly.
Safer antidepressants can be used.

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43
Q

Why is there an increase in suicide during the acute phase?

A
  • Avolition: normally can’t act on SI thoughts, but now they have more energy to act on thoughts of self-harm.
  • Higher burst of energy
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44
Q

SSRIs

CEFFPS

A 
Citalopram (Celexa)
Escitalopram (Lexapro)
Fluoxetine (Prozac, Sarafem)
Fluvoxamine (Luvox)
Paroxetine (Paxil)
Sertraline (Zoloft)
  • Safer alternative to TCAs, because they ONLY work on serotonin receptors.
  • TCAs work against Na channels, alpha receptors, muscarinic receptors.
  • MOA: prevent reuptake of 5HT increasing the synaptic concentration. Selective for 5HT transporter.
  • First-line for major depressive disorder.
  • Patients can take 10 to 30-fold overdose without being fatal.
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45
Q

What is the relationship between Citalopram (Celexa) and Escitalopram (Lexapro)?

TEST QUESTION

A

They’re enantiomers.

Conversion of dose:
-Escitalopram => Citalopram
-10mg E = 20mg C
If on 20mg of Citalopram, switch them to 10mg Escitalopram.

  • Every dose of Citalopram is double the dose of Escitalopram.
  • Citalopram 40mg = 20mg Escitalopram
  • Racemic mixture: Citalopram (50% of it is escitalopram).
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46
Q

Fluoxetine (Prozac, Sarafem)

-Fem?

A

Sarafem

  • Treats premenstrual disorder
  • fem = female
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47
Q

ADR SSRI

A

-Less ADR than TCAs, because they have a low affinity for alpha, histamine, and muscarinic receptors = fewer SE, better tolerated :)

  • Less weight gain
  • GI upset
  • Sexual dysfunction
  • HA
  • Insomnia
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48
Q

What can result from abrupt SSRI discontinuation?

A

Abrupt D/C leads to withdrawal:

  • Sleep disturbance
  • Rebound anxiety and depression
  • Taper them off dose slowly!!
  • Does NOT occur as frequent in agents with longer half-lives or metabolites (fluoxetine).
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49
Q

If you’re tapering a patient off of an SSRI, but they start experiencing sleep disturbance, anxiety, or depression; what do you do?

A

If they have SE when coming off of the drug, you need to increase the dose and restart the titration.

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50
Q

If you’re worried about patient compliance when using an SSRI and tapering off, which drug is preferred?

A

Fluoxetine

  • Longer half-life
  • Active metabolite so you have a better taper in affect rather than an abrupt discontinuation.
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51
Q

What SSRI causes QT interval prolongation?

A
  • Citalopram

- Escitalopram

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52
Q

What is the black box warning associated with SSRIs?

A

Increased risk of suicidality in children, adolescents, and young adults.

  • Acute phase of treatment
  • Applies to SSRIs, SNRIs, misc.
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53
Q

What are the possible mechanisms of suicide increase in SSRIs?

A
  • Increased energy (akathisia) acutely leads to depressed patients acting on their suicidal thoughts.
  • May lead to manic episode in bipolar patients.
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54
Q

SNRIs

A 
Venlafaxine (Effexor)
Desvenlafaxine (Pristiq)
Duloxetine (Cymbalta)
Milnacipran (Savella)
Levomilnacipran (Fetzima)
  • MOA: Non-tricyclic antidepressants, which target SERT and NET transporters. Prevent uptake of serotonin/NE.
  • Fewer SE than TCAs.
  • Other indications: fibromyalgia, peripheral neuropathies.
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55
Q

What SNRIs are used for neuropathic pain?

A

Duloxetine (Cymbalta)

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56
Q

What is the relationship between Venlafaxine (Effexor) and Desvenlafaxine (Pristiq)?

A

Enantiomers

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57
Q

SNRI ADR

A
  • Nausea, GI disturbances (higher than SSRI).

- Sexual dysfunction.

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58
Q

What SNRI causes increases in systolic BP?

A

Venlafaxine

  • Dose related increases in systolic BP.
  • Happens because you block the reuptake of NE.
  • Not good for HTN pts; do SSRI instead.
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59
Q

What SNRI causes nausea, dry mouth, constipation, insomnia, diaphoresis?

A

Duloxetine (Cymbalta)

Nausea, dry mouth, constipation, insomnia, diaphoresis.

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60
Q

Mixed Serotonergic Agents

A
  • Trazodone
  • Nefazodone
  • Vilazodone (Viibryd) (new)
  • MOA: 5-HT2 antagonists and 5-HT reuptake inhibitors (block serotonin reuptake and receptor).
  • ADR: hypotension, dizziness, SEDATION.

Often prescribed for sleep if avoiding narcotics.

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61
Q

Trazodone (Desyrel) ADR

A

Trazodone (Desyrel)

  • Blocks alpha 1 receptors, causes dizziness and hypotension (w/ reflex tach).
  • Causes priapism!!
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62
Q

Why is Nefazodone (Serzone) used less frequently?

A

Nefazodone (Serzone)

-less use; cases of liver failure

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63
Q

Bupropion (Wellbutrin) MOA

A

Bupropion (Wellbutrin)

  • MOA: Inhibits reuptake of NE and DA, so more is in the synapse.
  • May enhance release of NE and DA as well to increase levels.
  • Used for opioid addiction, overeating, use for weight loss.
  • Also used for smoking cessation (Zyban).
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64
Q

How often do you take SR formulation and XL formulation of Bupropion (Wellbutrin)?

A

SR formulation = 2x daily
XL formulation = 1x daily

  • Don’t mess up dosing - can halve it or double it.
  • Leads to toxicity or increase in depressive symptoms.
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65
Q

If you have a patient on antidepressants who is having sexual dysfunction, what medication should you switch them to?

A

Buproprion

-Less sexual dysfunction than SSRIs.

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66
Q

Bupropion (Wellbutrin) ADR

A
  • ADR: Nausea, vomiting, tremor, insomnia, dry mouth
  • Agitation in some patients

-SEIZURES and ARRYTHMIAS – dose related; avoid in those who have a history of it!!!!

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67
Q

MISC ANTIDEPRESSANTS

A

…

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68
Q

Mirtazapine (Remeron)

A
  • MOA: Antagonist at presynaptic alpha-2 receptors.
  • Increases NE and serotonin release.
  • Antagonizes 5-HT2 and 5-HT3 receptors.
  • Antagonizes histamine receptors (see ADR).
  • ADR: Somnolence, weight gain, dry mouth, constipation
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69
Q

Vortioxetine (Trintellix)

A
  • Newer agent
  • MOA: Acts as SSRI; 5HT agonist, partial agonist, and antagonist at various receptor subtypes.
  • Affects 5HT3, 1A, 7, 1D, and 1B (don’t memorize this).

-CYP2D6 poor metabolizers may accumulate drug

  • Switch over to if they have failed other therapies for depression.
  • ADR: diarrhea, ejaculation dysfunction, nausea, orgasm dysfunction
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70
Q

If a patient is on Vortioxetine (Trintellix) and has an increase in side effects, what occurs?

A

-If they have poor CYP2D6 metabolism, the drug accumulates and causes more side effects.

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71
Q

What is Serotonin Syndrome?

A

Major effects:

  • Altered mental status (seizures/agitation/comatose)
  • Hyperthermia
  • Autonomic instability (hypotensive/tachycardia).
  • Increased muscle tone (clonus)
  • R/O infection, amphetamine toxicity, etc.

S/S - sweating, hyperthermia, brady/tachycardia, hyper/hypotension, altered mental status/seizures, clonus, rhabdomyolysis.

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72
Q

When is a pt likely to experience Serotonin Syndrome?

A

-Can occur when taking multiple serotonergic medications at once (drugs that inhibit serotonin uptake)

  • Mixing drugs from classes (TCA + SSRI).
  • Including tyramine interactions (eating foods with tyramine).
  • Seen most with MAOIs! Like Selegiline and Rasagiline.
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73
Q

If you have a patient diagnosed with major depressive disorder and a MRSA pneumonia, how do you treat?

A

Put them on Linezolid and make sure they’re NOT on any SSRIs.

-SSRI + Linezolid = increases risk of Serotonin Syndrome.

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74
Q

How do you treat serotonin syndrome?

A

Management

  • Aggressive supportive care
  • Hydration w/ IV fluids
  • Evaporative cooling (when hyperthermic).
  • Dantrolene - used to treat malignant hyperthermia.
  • Cyproheptadine - has some serotonin-blocking effects to help.
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75
Q

Dantrolene

A
  • Used to treat episodes of malignant hyperthermia.
  • Peripheral muscle relaxer, so they’re less acidotic.

**Also used in NMS

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76
Q

Cyproheptadine

A
  • 1st generation antihistamine
  • Blocks effects of serotonin.
  • Also used to stimulate appetite in muscle wasting syndrome.
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77
Q

Methylene Blue

A

Used for staining met hemoglobinemia.

When a patient is blue, but well-oxygenated, it can turn a blue patient pink.

Used as a dye for PTH glands to see where you need to resect, but acts as an MAOI. Pt getting PTH resection was on SSRI and not screened for interaction, pt started to get hyperthermic, muscles locked up, and had serotonin toxicity with it!!!

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78
Q

When would you want to use an agent with a long half-life or active metabolites?

A

Ex: Fluoxetine

  • Good for patients with compliance issues
  • May not need as long of a taper to prevent withdrawal, levels go down naturally.
  • Be careful when adding on new medications.
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79
Q

If you had a pt on Fluoxetine for a while, but you wanted to discontinue it and start a new drug - What would you do?

A

Do not want to do it at the same time, because there will still be levels of fluoxetine (plus new drug).

Adding the new drug right away puts you at risk for serotonin toxicity.

Need to titrate down Fluoxetine. 1 week in, can start adding the new drug.

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80
Q

Chronic therapy leads to _____________.

A

Tissue accumulation; may lead effects to stay around longer.

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81
Q

What happens when you give antidepressants to a patient with cirrhosis?

A

Because these drugs are metabolized in the liver, the half-life may be extended in cirrhotic patients.

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82
Q

How do you therapeutically monitor these drugs?

A
  • Drug levels don’t assess therapeutic efficacy.
  • Drug dosage titration should be based on symptomatic response.
  • Full effects may take up to 6 weeks
  • Important patient education point!
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83
Q

After 6 weeks, if they had partial improvement:

A

May need to increase their dose.

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84
Q

After 6 weeks, if they had no improvement:

A

Switch to another agent.

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85
Q

If a patient fails one SSRI, like Citalopram:

A

It doesn’t mean they won’t respond to another agent.

Citalopram (Celexa)
Escitalopram (Lexapro)
Fluoxetine (Prozac, Sarafem)
Fluvoxamine (Luvox)
Paroxetine (Paxil)
Sertraline (Zoloft)
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86
Q

Venlafaxine, Duloxetine, Buproprion (newer agents): drug interactions

A

Have fewer PK interactions.

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87
Q

SSRI: drug interactions

A

Have variable effects with CYP inhibition.

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88
Q

TCA: drug interactions

A

TCAs can be extensively metabolized by CYP enzymes.

  • Usually metabolized by CYP2D6 and CYP3A4.
  • Start low and titrate up.

CYP inhibitors will increase TCA levels ~ increased risk of toxicity.

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89
Q

What’s an important TCA reaction?

A

TCAs are highly protein bound.
-If a competitor drug comes and knocks TCA off of protein, it can increase free fraction of drug, therefore increasing TCA toxicity.

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90
Q

Any drug that affects serotonin can contribute to serotonin toxicity:

A
  • Linezolid
  • Methylene blue
  • Triptans (Suma, Riza, Almo)
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91
Q

If your patient on an SSRI has a migraine, why is it bad to prescribe them -triptans?

A

Triptans

  • Sumatriptan
  • Rizatriptan
  • Almotriptan

Triptans directly activate the serotonin receptors to vasoconstrict blood vessels. With further serotonin activation ~ would lead to further constriction, possible ischemia.

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92
Q

If you have an ICU patient with a history of MDD on an SSRI, but now they have a MRSA pneumonia, what can you do?

A

Do not have time to wait the “washout period” of 2-5 weeks like you normally would.

Stop SSRI and start Linezolid; need to treat them through the side effects.

If you kept them on SSRI during Linezolid treatment, they’re at a higher risk for serotonin toxicity.

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93
Q

What drugs cause QT interval prolongation?

A

For tx resistant depression, pts may be put on atypical antipsychotics with citalopram.

Putting them on both: increases risk for Torsades.

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94
Q

Sedative effect:

A
  • Trazadone
  • TCA

Synergistic effects with alcohol and benzodiazepines.

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95
Q

St. John’s Wort:

A

-Herbal supplement; used to treat mild to moderate depression.

  • MOA: Hypericin in it works as MAOI, increases catelcholamine effects.
  • At risk for serotonin toxicity when you use it with other antidepressants. Don’t want pts to take both.
  • ADR: dry mouth, dizziness, confusion, allergic reactions
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96
Q

What are important drug interactions of St. John’s Wort?

A
  • CYP3A4 and PGP inducer

- Inducing CYP3A4 metabolism will lower drug levels more quickly for those metabolized by CYP3A4.

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97
Q

Does FDA regulate supplements, like St. John’s Wort?

A

No; they have less oversight.

  • Use a reputable brand
  • Use same brand, to make sure you have the same amount of drug.

Oxycut is off the market for hepatotoxicity.

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98
Q

Elderly

A
  • Frequently overlooked, less management for depression.
  • Increased suicidality > 65yrs.
  • High risk for adverse effects, because they have less physical reserve.
99
Q

Pediatrics

A
  • More depression than once thought
  • Medications not as well studied; harder to perform studies on them.
  • Only fluoxetine has indication for patients < 18 years
  • Black box warning for increased suicide risk in acute treatment
100
Q

Pregnant and lactating patients

A
  • 14% incidence of serious depression during pregnancy
  • Often need to treat with SSRI during pregnancy to make sure mom is taken care of.
  • Mother on SSRIs prior to pregnancy more likely to relapse (stop taking care of themselves, commit suicide, etc.).
  • Babies with SSRI exposure more likely to be underweight and have pulmonary issues (may delay surfactant production).
  • TCA not recommended when pregnant!
101
Q

If a mother was taking SSRI during pregnancy, when the child is born, will they potentially have withdrawal effects?

A

If exposed during pregnancy and SSRI is not continued after birth, baby can be agitated.

  • Will have issues regulating BP, HR, etc.
  • Will go away with time.
102
Q

When treating a new patient, what should you start with?

A

Generally, start with SSRI or newer agent.

103
Q

What drugs are avoided?

What drugs are a “last resort”?

A

TCAs not preferred, due to adverse effects.
-May be used in neuropathic pain.

MAOIs are last resort; has failed all other therapies.

104
Q

If you have treatment failure:

A

-Assess compliance and adequate duration/dosing

  • May switch between agents in same or different class
  • Patient may fail sertraline, but fluoxetine may work

-Assure adequate “washout period” has occurred prior to starting new agent (1-2 weeks).

-May need to add additional therapy for tx resistant patients:
Lithium, atypical antipsychotics (aripiprazole - most common).

105
Q

BIPOLAR DISORDER

106
Q

Bipolar Type 1

A

Manic episode +/- depressive episode

107
Q

Bipolar Type 2

A

Major depressive disorder +/- hypomanic episode

108
Q

Cyclothymic disorder

A

Chronic fluctuations between subsyndromal and hypomanic episodes

109
Q

What causes mania?

A 
CNS disorders
Infections
Electrolyte abnormalities
Endocrine disorders
Alcohol intoxication or withdrawal
Hallucinogens
Steroids
110
Q

Goals of therapy for Bipolar:

A
  • Pt should remain on a mood stabilizer for their lifetime (lithium, valproic acid, etc.).
  • Meds are added for acute symptoms.
111
Q

Non-pharm therapy

A
  • Adequate nutrition, sleep, exercise, stress reduction
  • Mood charting
  • Supportive counseling
112
Q

Lithium (Lithobid) MOA/Kinetics

A
  • No unified theory for its MOA.
  • Modulate gene expression, has neuroprotective effects
  • Well absorbed in GI tract (salt)
  • Distributed throughout the body, no protein binding
  • Not metabolized, excreted unchanged in the urine
  • Resembles sodium in the body
113
Q

What’s a risk with lithium?

A

It presents as a salt in the body, so when your body wants to hold onto salt, it will hold onto lithium. If it wants to get rid of sodium, it will get rid of lithium too.

NARROW THERAPEUTIC INDEX

114
Q

If you put a patient on a diuretic, what happens?

A

Lose fluid, BP decrease

Body response is to increase the ADH to hold onto salt and water (will hold onto more lithium too).

115
Q

Lithium

A
  • Still considered first line therapy for mood stabilization.
  • Efficacy may be delayed several weeks!
  • NOT good for acute manic episodes.
  • Can prevent manic episodes and reduce suicide risk

NARROW THERAPEUTIC INDEX

  • Serum monitoring NEEDED.
  • Critical for treatment success, make sure patient is at a therapeutic level.
  • Therapeutic level: 0.5-1.2 mEq/L (measured like salt).
116
Q

What happens with abrupt D/C of Lithium?

A
  • May lead to remission of symptoms.
  • Can see it combined with other mood stabilizers.

Valproic acid
Carbamazepine

117
Q

What’s the first sign your patient’s lithium levels are too high?

A

Fine tremor in the hands at rest

118
Q

Acute Adverse Effects of Lithium?

A

SE peak when drug levels peak, 1 to 2 hours after dose

  • GI distress, osmotic diarrhea
  • Muscle weakness, lethargy
  • Polydypsia, nocturia
119
Q

Osmotic diarrhea

A

Occurs with lithium, because there’s more “salt” in the GI tract.

120
Q

Lithium - Chronic Adverse Effects?

IMPORTANT AF

A
  • Fine hand tremor
  • Nephrogenic DI
  • Nephrotoxicity (glomerular sclerosis, interstitial nephritis)
  • Hypothyroidism - interferes with hormone synthesis. Hypothyroidism can be confused with depressive episodes.

-Reversible cardiac effects
T-wave flattening/inversion, AV block, bradycardia

-Acne, pruritic dermatitis, psoriasis exacerbation
-Weight gain
-Slurred speech, ataxia
-Overdose
>Acute or chronic
>Seizures, coma, dysrhythmias

121
Q

How do you ameliorate fine hand tremor?

A

Use long-acting formulations or beta blockers.

122
Q

How do you ameliorate nephrogenic DI?

A
  • Treat with loop or thiazide diuretics.
  • Helps regulate sodium you’re eliminating in the kidneys!
  • When you re-regulate, helps fix DI. :)

-Must watch lithium and potassium levels.

123
Q

If you have drug-induced DI, what do you do to tx?

A

Can D/C drug, use a diuretic, or can give artificial ADH - vasopressin.

124
Q

What interactions lead to accumulation of Lithium?

A

Dehydration, sodium restriction, vomiting, diarrhea, heart failure, cirrhosis

Gastroenteritis

125
Q

What drugs lead to lithium accumulation?

A

Thiazide diuretics, NSAIDs, ACE inhibitors, salt restriction

NSAID induced AKI
ACEI induced AKI

126
Q

Lithium and CYP!!

A

Lithium is not metabolized by CYP, so there’s no CYP enzyme interactions. YAY.

127
Q

ANTICONVULSANTS FOR BIPOLAR DISORDER

A

Lithium is the mainstay mood stabilizer for bipolar disorder

Other drugs are antiepileptics.

128
Q

Valproic Acid (Depakote, Depacon)

A
  • Go to mood stabilizer for BPD in US.
  • Adults usually on valproic acid for BPD, kids usually on it for seizures.
  • MOA: may mimic GABA at post-synaptic receptor sites.
  • Synergy with other agents, like lithium/carbamazepine, but increases risk for adverse effects.
  • Need therapeutic drug monitoring 50-125mcg/ml.
  • Baseline and follow up hepatic function tests NEEDED.
129
Q

ADR Valproic Acid

A

Better tolerated than Lithium!! Wider therapeutic index.

Commonly causes GI distress, find hand tremor, and sedation.

  • Hepatotoxicity
  • Hyperammonemia
  • Ataxia/Lethargy
  • PLT aggregation inhibition
130
Q

When working up BPD pt for altered mental status, what can the cause be?

A

Substance abuse

Ammonia levels - common cause for altered mental status in valproic acid patients.

131
Q

Carbamazepine (Tegretol)

A
  • MOA: Anticonvulsant properties: inhibiting neuronal sodium channels
  • Not a first line agent
  • Useful in lithium refractory patients

Therapeutic monitoring 4-12mcg/ml

132
Q

ADR Carbamazepine (Tegretol)

A
  • CNS depression: ataxia, lethargy, nystagmus, seizures
  • Cardiac conduction changes
  • SIADH!!!! Can cause hyponatremia.
133
Q

If pt is on therapy for bipolar disorder, Na is 119, and seizing - What drug caused this?

A

SIADH

Caused by carbamazepine

134
Q

What drug induces CYP3A4?

A

Carbamazepine (Tegretol)

-Affects anticonvulsants and oral contraception

135
Q

What drug dispalces carbamazepine from serum proteins?

A

Valproic acid

When combining, need to adjust dose to see how pt tolerates it.

136
Q

Oxcarbazepine (Trileptal)

A
  • Inhibits CYP2C19 and induces CYP3A4
  • No monitoring available.
  • ADR: dizziness, sedation, HA, ataxia, GI disturbance
  • SIADH (more than carbamazepine)
137
Q

If pt on carbamazepine had SIADH, what do you AVOID switching to?

A

Don’t switch to Oxcarbazepine (Trileptal)

Higher risk of SIADH

138
Q

Lamotrigene (Lamictal)

A
  • MOA: blocks sodium channels, inhibits glutamate release
  • Has antidepressant and mood stabilizing effects
  • ADR: SJS!!!
139
Q

When prescribing Lamotrigene (Lamictal) to a patient on valproic acid, how do you prescribe it?

A
  • Lamotrigene (Lamictal) dose must be CUT in half.

- Valproic acid will decrease clearance of drug and it can reach higher levels of toxicity/risk for SJS.

140
Q

Why would a patient stop taking Lamotrigene (Lamictal)?

A

If they have a new rash or pruritus.

Occurs most often with valproic acid and lamotrigene combination.

141
Q

ANTIPSYCHOTICS

142
Q

1st generation

A
  • Phenothiazines

- Block DA2 receptors (dopamine)

143
Q

2nd generation

A
  • Atypical antipsychotics

- Block DA2 and 5HT-2a receptors

144
Q

Both generations

A
  • Treat acute mania, put pt in a sedative state
  • Especially effective for those with agitation, aggression, and psychosis.
  • Chronic and acute therapy
145
Q

What are chronic adverse effects of antipsychotics?

A

Worsening type 2 DM
Weight gain
Hyperlipidemia

146
Q

ALTERNATIVE AGENTS FOR BIPOLAR DISORDER

147
Q

Benzodiazepines

A
  • Good for acute mania, agitation, panic, insomnia

- Good for pts who can’t tolerate mood stabilizers

148
Q

Calcium channel antagonists

A

-Inhibit NT release and synthesis

  • Verapimil may stabilize moods
  • Nimodipine penetrates BBB and has anticonvulsant properties.
  • Tx resistant patients
149
Q

How do you treat bipolar disorder?

A
  1. Start with mood stabilizing agents
    - Lithium, carbamazepine, valproic acid, or 2nd. gen. antipsychotic.
  2. If they have acute anxiety, insomnia, agitation
    - Add benzodiazepine
    - Oxcarbazepine is an alternative option
    - May need to start with 2 agents for severe manic episodes!
  3. Inadequate response
    - Lithium plus anticonvulsant/SGA
    - Anticonvulsant plus anticonvulsant or SGA (valproic acid plus carbamazepine or SGA).

SGA = second generation antipsychotic

150
Q

Manic episodes cause extra energy, but patients with severe manic episodes may present with agitation in ER with restraints.

How do you treat the severely manic episode?

A
  • Big dose IM Haldol

- IM Ativan

151
Q

ANTIPSYCHOTICS

152
Q

A1 receptors on vasculature

A

Control BP, constrict vessels

Agonized by NE, epi, DA

153
Q

A2 receptors

A
  • Clonidine agonizes A2 receptors

- Activating prevents NE release

154
Q

Schizophrenia presentation

A
  • Patient loses touch with reality, brain creates false reality
  • Hallucinations – especially hearing voices
  • Delusions – fixed false beliefs
  • Ideas of influence – actions influence by external forces

Patient’s affect

  • Flat, inappropriate, or labile
  • Personal hygiene suffers
  • Decreased medication compliance
  • Relapse, hospitalization
  • High rate of substance abuse Ethanol, nicotine, etc.
155
Q

Positive symptoms of schizophrenia

A

Too much dopamine in nucleus mesocaudate.

  • Suspiciousness
  • Unusual thought content
  • Hallucinations
  • Conceptual disorganization
156
Q

Negative symptoms of schizophrenia

A

Hypoactivity of dopamine in frontal cortex.

  • Flat affect
  • Alogia - not able to come up with words for things.
  • Anhedonia
  • Avolition - not able to act on thoughts they’d like to.
157
Q

Cognitive symptoms of schizophrenia

A

Hypoactivity of dopamine in frontal cortex.

  • Impaired attention
  • Impaired memory
  • Impaired executive function
158
Q

Goals of therapy for schizo:

A
  • Therapy should be assertive during first 5 years.
  • Patient most likely to have most psychosocial deterioration during this time.

-Treat for 3 months to see response.

159
Q

1st g. Antipsychotics MOA

A

Chlorpromazine (Thorazine)
Prochlorperazine (Compazine)
Fluphenazine (Prolixin)
Haloperidol (Haldol)

  • MOA: D2 receptor antagonist; block effects of dopamine and decrease the positive symptoms.
  • Less hallucinations, delusions
  • Good for acute psychotic episodes.
  • May worsen negative symptoms due to decrease pre-frontal cortex signaling.
  • Can have more flat affect or avolition.
160
Q

1st g. Antipsychotics ADR

When dopamine is blocked, prolactin is raised and causes:

A

-Prolactin is increased when dopamine is blocked: gynecomastia, menstrual irregularities.

161
Q

1st g. Antipsychotics ADR

When dopamine is blocked, Ach is raised and causes:

A

-Ach is increased when dopamine is blocked:
»Dystonia – involuntary muscle contractions
»Face, neck, tongue.

162
Q

1st g. Antipsychotics ADR

What is one of the major limiting factors from 1G antipsychotics?

A

Extrapyramidal side effects (EPS) – major limiting factor.

Results from dopamine blockade in caudate putamen.

Parkinson-like symptoms
»Catatonia
»Motor rigidity
»Tremor

163
Q

1st g. Antipsychotics ADR

Chronic dopamine antagonism, leads to upregulation of dopamine receptors. What does this cause?

A

-Akathisia - restless agitation; will see pacing, shuffling feet.

Tardive dyskinesia !!
»Chewing, licking movements
»Tongue protrusions
»Limb movements

164
Q

1st g. Antipsychotics ADR

Alpha 1 antagonism causes:

A

Dizziness, postural hypotension, and reflex tachycardia.

165
Q

1st g. Antipsychotics ADR

Antimuscarinic causes:

A

Mad as a hatter, blind as a bet, red as a beat

-Good for parkinsonism
-Bad for tardive dyskinesia
Less ach = more da.

166
Q

1st g. Antipsychotics ADR

Histamine 1 receptor antagonist causes:

A

Sedation, weight gain, hyperlipidemia, diabetes

167
Q

1st g. Antipsychotics ADR

Effects on the heart?

A

QT prolongation
Tachycardia
Sodium channel blockade

168
Q

Neuroleptic Malignant Syndrome (NMS)

A

S/S
-Hyperthermia, altered mental status, HTN
-Lead pipe rigidity
»Can lead to rhabdo
»Heat and acid build up, myoglobin in kidneys leads to renal insufficiency.

  • Caused by high potency D2 blockers
  • Seen most often with Haloperidol and Fluphenazine
169
Q

1st g. Antipsychotics LISTTTTTT

A
  • Chlorpromazine (Thorazine)
  • Prochlorperazine (Compazine)
  • Fluphenazine (Prolixin)
  • Haloperidol (Haldol)
170
Q

Prochlorperazine (Compazine)

A

-Used for HA/N/V

171
Q

Chlorpromazine (Thorazine)

A

-Most common

172
Q

What 1st g. antipsychotics cause acute dystonia and Neuroleptic Malignant Syndrome?

A

Haloperidol
Fluphenazine
-More D2 blocking ability
-More dystonia and NMS

Less likely to see with thorazine, because not as potent of a blocking D2 receptor.

173
Q

If you have a patient with an acute dystonic reaction from Haloperidol, how do you treat them?

A

Chlorpromazine

  • Better drug for them.
  • Not as potent in treating positive symptoms of schizophrenia.

Know if pt needs high potency or low potency.

174
Q

What drugs have more antimuscarinic / antihistaminic effects and cause sedation?

A
  • Chlorpromazine
  • Thioridazine

HIGH sedation.
Also cause orthostatic hypotension.
Less likely to see EPS.

175
Q

What are the high potency D2 blockers and cause extrapyramidal side effects (EPS)?

A
  • Haloperidol
  • Fluphenazine

Cause EPS, i.e. Parkinson-like symptoms:
»Catatonia
»Motor rigidity
»Tremor

176
Q

Which drug is highest risk of seizures?

177
Q

What drug causes highest elevation of prolactin?

A

-Thioridazine
Gynecomastia
Menstrual irregularity

178
Q

Which one causes most weight gain?

179
Q

Why are first generation antipsychotics important?

A

-Very effective to treat positive symptoms, but SE lead to discontinuation.

180
Q

If someone is acute, agitated, and having a lot of hallucinations/delusions, how do you treat?

A

Knock them out with IM Haloperidol.

181
Q

How do you treat extrapyramidal symptoms (EPS)?

A

EPS

  • Parkinsons symptoms
  • Includes dystonic reactions, akathisia
  • Treated with anticholinergics (usually antihistamines)
  • Diphenhydramine (Benadryl)
  • Benztropine (Cogentin)
  • Trihexyphenidyl (Artane)

Can also use benzodiazepines if above fails.. Help GABA work better (cause CNS depression, relax muscles).

182
Q

How do you treat tardive dyskinesia?

A

Can’t do much about it :(
AVOID by using second generation drugs.

Tx:

  • Avoid anticholinergics, they will worsen by increasing dopamine release!
  • Discontinue treatment
  • “Drug holidays”
  • Switch to second generation agent
183
Q

How do you treat Neuroleptic Malignant Syndrome (NMS)?

A
  • Discontinue offending agent
  • Cool patient
  • Hydrate patient to limit muscle damage

Dantrolene (Dantrium)
»Peripheral skeletal muscle relaxant to loosen lead pipe rigidity.
»Also used for malignant hyperthermia in surgery (and Serotonin Syndrome).

Bromocriptine – dopamine receptor agonist
»Can also use for NMS. :)

184
Q

If you give a high potency D2 blocker, what SE occur?

A

Dystonia
EPS

Treated with: anticholinergics

185
Q

Acute Dystonia

A
  • Spasm of muscles of tongue, face, neck, back

- Tx: Benztropine or diphenhydramine

186
Q

Akathisia

A
  • Subjective experience of motor restlessness; may experience anxiety or agitation
  • Tx: Reduce dose or use low dose propranolol
187
Q

Neuroleptic Malignant Syndrome

A
  • Catatonia, stupor, fever, unstable pulse and blood pressure, myoglobinemia; can be fatal
  • Tx: STOP neuroleptic, use bromocritpine, dantrolene, and supportive measures.
188
Q

SECOND GENERATION ANTIPSYCHOTICS

189
Q

Benefits of 2nd gen. or “atypical antipsychotics”:

A
  • Fewer extrapyramidal and prolactin effects; avoid chronic probs.
  • More efficacy for NEGATIVE and COGNITIVE symptoms.
  • Less tardive dyskinesia with prolonged use. Already knew that….

Should be first line unless contraindicated!!!!!

190
Q

2nd g. Antipsychotics MOA

A

-MOA: Less affinity for D2 receptors in striatal tract, has D3 and D4 receptor blockade
(Lessens EPS symptoms).
-5HT-2 receptor antagonist.

  • Stops serotonin activity on frontal cortex, leads to inhibition of mesocortical dopamine.
  • Increases dopamine in frontal cortex, decrease in nucleus ac.
191
Q

What 2nd g. Antipsychotics cause highest risk of weight gain???

A

EWWWW

  • Olanzapine
  • Clozapine

Recommended to switch agents with > 5% weight gain

192
Q

What 2nd g. Antipsychotics have lowest risk of weight gain?

A
  • Ziprasidone
  • Aripiprazole

Recommended to switch agents with > 5% weight gain

193
Q

Aripiprazole - other use?

A

Used for treatment resistant depression as well, better SE profile.

194
Q

What 2nd g. Antipsychotic causes glucose intolerance and new onset diabetes?

A

Clozapine

Hyperlipidemia is common with the 2nd gen drugs too -
Metabolism tanks with these drugs!!

195
Q

What is clozapine reserved for?

A

Treatment resistant schizophrenia.

  • Black boxed warning for agranulocytosis!!!
  • Need to sign with pt/provider registry.
  • Must do serial CBC to prevent development of agranulocytosis.
196
Q

ADR: 2nd g. Antipsychotics

A

-QT prolongation
-Orthostatic hypotension, esp. with IV/IM doses.
Elderly are high risk, but can develop tolerance over 2-3 months.

Pts with acute agitation are being treated with IM 2nd gen. antipsychotics like Ziprasidone and Olanzapine.

197
Q

Why don’t you use 2nd g. Antipsychotics to treat elderly patients with dementia?

A

Black box warning

-Increased mortality in elderly patients with dementia related psychosis

198
Q

What 2nd. g. Antipsychotics cause sedation?

A
  • Clozapine
  • Olanzapine
  • Quetiapine

Sedation

QHS dosing
-Dose at night, will help them sleep better.

199
Q

What 2nd. g. Antipsychotics cause dry mouth and constipation (anticholinergic effects)?

A
  • Clozapine
  • Olanzapine

Dry mouth
Constipation

200
Q

What 2nd. g. Antipsychotics cause seizures?

A
  • Clozapine
  • Olanzapine

Overdoses of drugs will cause seizures and cardiac conduction delays.

201
Q

If you have a patient with benzodiazepines on 2nd. g. Antipsychotics will see ?

A

Synergy from both drugs:

  • Sedation
  • Orthostatic hypotension
  • Anticholinergic effects
202
Q

If you put someone on 2nd. g. Antipsychotics on a dopamine blocking drug, like Metoclopramide (Reglan) or Promethazine (Phenergan), what will you see?

A

Increased EPS,

Metoclopramide (Reglan) or promethazine (phenergan).

  • Used for N/V, gastroporesis.
  • Dopamine blockers, increase EPS with the 2nd gen drugs.
203
Q

Clozapine

A

Agranulocytosis

204
Q

2nd gen. antipsychotics LISTTTT

A 
Aripriprazole 
Clozapine 
Iloperidone 
Paliperidone
Olanzapine 
Quetiapine (Seroquel) *MC
Risperidone (Risperdal) *MC
Asenapine
Lurasidone

don’t cause EPS as much.

205
Q

Other 2nd. gen. agents:

A

Brexipiprazole (Rexulti)
Iloperidone (Fanapt)
Cariprazine (Vraylar)
Pimavanserin (Nuplaszid)

New agents

206
Q

What do you monitor for pts on antipsychotics?

A 
Weight
Blood pressure
Fasting plasma glucose
Fasting Lipids
Other antipsychotic side effects
>>EPS, etc.
207
Q

Pt w/ acute, agitated, psychotic episode.

How do you manage acute treatment and initiate medication therapy?

A

Manage by decreasing positive symptoms - they’re having a paranoid episode.

-Benzodiazepines can help calm/sedate the patient.
-Use high potency dopamine blocker to knock down - halperidol and olanzapine.
»Usually IM.
-Titrate up dose as tolerated.
-Change agents if there’s no improvement in 3-4 weeks.

208
Q

How do you manage patients with compliance issues?

A

Consider giving a long acting injectable form, IM

  • Olazapine
  • Risperidone
  • Ziprasidone
  • Aripiprazole
  • Haloperidol
209
Q

For a patient whose treatment naive with first break of schizo:

A

Start with aripripizole, risperidone, or ziprasidone.

-More benign drugs.

210
Q

If they’ve been previously treated with an antipsychotic for schizo:

A
  • Any antipsychotic except clozapine (need weekly CBCs).

- Avoid any that had poor efficacy before.

211
Q

Patient that had an inadequate response with antipsychotics in previous stages:

A

-Use any antipsychotic monotherapy except clozapine…

212
Q

Patient that had inadequate clinical response with two antipsychotics? Multiple failures.

A

Clozapine monotherapy recommended; esp if they’re extremely suicidal.

Can use multiple drugs at a time, but can cause SE. Start with benign drugs and increase… Refer to specialty.

213
Q

How do you discontinue antipsychotics?

A
  • Taper over 2+ weeks

- Restart at lowest dose if withdrawal occurs and do a slower taper

214
Q

How do you switch doses?

A

-Taper 1st agent over 2 weeks after 2nd antipsychotic has been started low and titrate it up

215
Q

Withdrawal symptoms of antipsychotics:

A 
Insomnia
Nightmares
Headache
GI symptoms
Restlessness
Increased salivation/sweating
216
Q

ANXIOLYTICS

217
Q

Drugs that cause anxiety:

A
  • Antipsychotics – akathisia
  • Digoxin toxicity
  • Stimulants, sympathomimetics
  • Hallucinogens
  • Stimulants
  • Anticholinergics
  • Drug withdrawal (EtOH, opioids, benzodiazepines)
218
Q

Digoxin

A

Used in HF and Afib to help heart pump better.

Too much = anxiety

219
Q

Acute Anxiety

A

Acute panic attack

-Tx: benzodiazepine

220
Q

Chronic Anxiety

A

-Tx: antidepressants

221
Q

Alternative agents

A

Buspirone

Sec. Gen. Antipsych.

222
Q

Antidepressants

A 
FDA approved:
-Venalfaxine ER, duloxetine
SNRIS ^
-Paroxetine, escitalopram
SSRI ^
-Imipramine = 2nd line; higher ADRs. (TCA)
  • Effective for long term GAD, not acute panic attack.
  • Prevent acute panic attack from occurring tho.
  • 3 to 6 weeks until full efficacy seen.
223
Q

Benzodiazepines

A
  • MOA; potentiate effects of GABA
  • Good for acute panic attacks
Alprazolam (Xanax)
Chlordiazepoxide (Librium)
Clobazam (Onfi)
Clonazepam (Klonopin)
Clorazepate (Tranxene)
Diazepam (Valium)
Lorazepam (Ativan)**
Midazolam (Versed)
Oxazepam (Serax)**
Temazepam (Restoril)**
Triazolam (Halcion)**
224
Q

Chlordiazepoxide (Librium)

A

Used for prevention of alcohol withdrawal

225
Q

Clobazam (Onfi)

Clonazepam (Klonopin)

A

Prevention of seizure

226
Q

Diazepam (Valium)

A

Used for acute seizures and anxiety

227
Q

Lorazepam (Ativan)**
Oxazepam (Serax)**
Temazepam (Restoril)**
Triazolam (Halcion)**

A

“Lot benzodiazepines”

-Better for older patients, because they don’t have active metabolites or they’re water-soluble, so more easily eliminated by the kidneys.

228
Q

Other uses for benzos:

A

seizures, acute agitation muscle relaxant, sedation

229
Q

Onset of action related to drug lipophilicity

HIGH LIPOPHILICITY:

A

Diazepam and clorazepate –

  • high lipid solubility; cross BBB.
  • Onset within 30-60 minutes

Compared to lower lipophilicity: oxazepam (better for elderly; more water-soluble).

230
Q

What metabolizes benzos?

What are the exceptions? LCO

A

CYP3A4 metabolize most benzodiazepines

Except lorazepam, clonazepam, oxazepam

LCO better for old people to avoid med interactions.

231
Q

Benzodiazepines ADR

A

Drowsiness, sedation, psychomotor impairment, ataxia
Seen initially, tolerance develops

Paradoxical excitation - can occur in kids; just need more dose to calm them down.

Memory impairment
Synergistic with other depressants (EtOH)

232
Q

Withdrawal of chronic use of benzos:

A
  • Agitation, tremor, sweating, tachycardia, seizure
  • Rebound anxiety
  • Must be titrated off slowly!!
233
Q

Buspirone (Buspar)

A
  • Non-benzodiazepine anxiolytic
  • No anticonvulsant, hypnotic, dependence, impairment properties
  • Second line for GAD due to lack of consistent efficacy…
  • Takes 2+ weeks for efficacy
  • MOA: Serotonin 5HT-1A agonist
  • ADR: N/D/HA
  • Metabolized by CYP3A4
234
Q

Beta blockers

A
  • MOA: Blunt physiologic effects of anxiety. Reduce effects of endogenous catecholamines.
  • Useful for sweating, tachycardia, tremor, blushing

-Used in performance based situations

Agents used: propranolol (Inderal), atenolol (Tenormin)

235
Q

When do you take beta blockers for performance?

A
  • Take 1 hour prior to performance
  • Take a test dose at home to determine tolerance, adverse effects

BP may bottom out, cause dizziness.. Test dose critical.

236
Q

Urgent symptoms of anxiety?

A
  • Begin with short term benzodiazepine

- Begin SSRI or SNRI therapy for chronic use; benzo can cover until these kick in. :)

237
Q

Non-urgent symptoms

A

SSRI, SNRI

  • If no adequate response to therapy, switch to another agent.
  • If still no adequate response consider imipramine or other TCA.
238
Q

ADD/ADHD

239
Q

Stimulants

A
  • First line therapy
  • MOA: Block MA Oxidase. Inhibit reuptake of DA and NE.
  • Amphetamines increase the release of catecholamines into synapse.
  • Often available in extended release formulations, dosed 1x daily.
  • IR products dosed 2-3 times daily
  • Controlled 2 substance (highest control w/ med use).

CONTROL 2
CONTROL 2
CONTROL 2

240
Q

Stimulant LIST

A

Methylphenidate (Ritalin, Metadate, Concerta, Quillivant)

Daytrana patch - slap it on in the am.

Dexmethylphenidate (Focalin)

Mixed amphetamine salts (Adderall)
»Amphetamine&raquo_space;Dextroamphetamine

Lisdexamphetamine (Vyvanse)
»Prodrug converted to dextroamphetamine; prodrugs prevent abuse. Need liver to activate drug, so drug isn’t in the active form when its snorted by stupid druggies. :)

241
Q

ADR of stimulants:

Black box warning:

Withdrawal effects:

Other concerns?

A

Reduced appetite, weight loss, GI upset, Insomnia, Headache, Irritability, Tachycardia, hypertension

Black box warning for psychotic episodes, hallucinations, abuse and dependence :(

High abuse potential!
-Avoid in patients with history of drug dependence

Withdrawal effects
- Depressed mood

Concern for growth stunting

  • Minimal in most children
  • Perform “drug-free” trials yearly
242
Q

Non-stimulants alternatives: Atomoxetine (Strattera)

A
  • Selective norepinephrine reuptake inhibitor
  • Approved for use in adults
  • Slower onset of action (2-4 weeks vs. 1-2 hours)
  • No abuse potential
  • ADR: GI disturbance, Hypertension/tachycardia, Liver injury

Black box warning for suicidal ideation!!!!!!!!!!!!

243
Q

Non-stimulants: Alpha 2 agonists

Guanfacine
Clonidine

Patients on stimulants in morning time and these “nonstimulants” or depressants at night time QHS.

Help them sleep better.

A

Alpha 2 agonists
Guanfacine and Clonidine
-Pills or patch
-Guanfacine XR (Intuiv)

  • MOA: Prevent catecholamine release. Increase blood flow to prefrontal cortex (improves memory). Not as effective as stimulants.
  • ADR: Sedation (subsides in 2-3 weeks), hypotension, constipation

Pharmacology II (10 decks)

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