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Pharm III > Lecture 7 (psych)- Exam 4 > Flashcards

Lecture 7 (psych)- Exam 4 Flashcards

1
Q

Medications for psychiatric disorders:
* What NTs are altered in the brain?

A
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2
Q

pathophysiology
* What receptor and behavior does serotonin, NE and DA deal with?

A
  • Serotonergic: 5HT receptor-> Mood and reproductive behavior
  • Noradenergic: NE receptor-> alertness and focus
  • DA: DA receptor->Cognitive function, motivation and awakeness
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3
Q

Selective serotonin reuptake inhibitors (Ssris)
* What is the MOA?
* Increases what? (effect)

A
  • Inhibits serotonin reuptake from synaptic cleft by blocking serotonin reuptake transporters (SERTs)
  • Effect: Increased serotonin activity related to improved mood
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4
Q

SSRIs
* What are the agents? (6)

A
  • Citalopram (Celexa)
  • Escitalopram (Lexapro)
  • Fluoxetine (Prozac)
  • Fluvoxamine (Luvox)
  • Paroxetine (Paxil)
  • Sertraline (Zoloft)
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5
Q

SSRIs
* What are the different components with agent selection ? (9)

A
  • History of response
  • Pharmacogenetics
  • Comorbidities
  • Medical history
  • Presenting symptoms
  • Potential for drug-drug interactions
  • Adverse effect profile
  • Patient preference
  • Cost
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6
Q
A
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7
Q
A
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8
Q

BBW-suicidal ideation
* Antidepressants increased the risk compared to placebo of what?
* Effect was no seen in who?
* What needs to be weighed?

A
  • Antidepressants increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in short-term studies in children, adolescents and young adults
  • Effect was not seen in adults older than 24 years
  • The risks should be weighed with benefits
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9
Q

BBW-suicidal ideation
* patients and families should be educated to watch for what?
* What needs to happen with prescribing practitioner?

A
  • Patients and families should be educated to watch for clinical worsening, suicidality, unusual behavior
  • Close observation and communication with prescribing practitioner recommended
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10
Q

Serotonin syndrome
* When does this occur?
* Usually the result of what? Give examples?
* What is CI?

A

Occurs when serotonin levels are too high
* Usually the result of drug interactions with antidepressants that cause increased levels of serotonin

Examples:
* Triptans
* Monoamine oxygenase inhibitors (MAOIs)
* St. John’s Wort
* Dextromethorphan
* Alcohol

CI: during or within 10 days of an MAOI

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11
Q

Serotonin syndrome
* What are the sxs?

A
  • Sweating (shivers)
  • Myoclonus
  • Autonomic nervous system instability
  • Rigidity - muscles
  • Temperature increase
  • Seizures

SMARTS

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12
Q

What is the txt of serotonin syndrome?(3)

A
  • Supportive care
  • Benzodiazepines
  • Cyproheptadine – serotonin antagonist (antitode)
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13
Q

What are the examples of SNRIs?

A

* venlafaxine (Effexor)
* duloxetine (Cymbalta)
* desvenlafaxine (Pristiq)
* milnacipran (Savella)-For FM
* levomilnacipran (Fetzima)**

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14
Q

What is the MOA of SNRIs? What is the effect?

A

MOA: inhibit serotonin and norepinephrine reuptake transporters in the synaptic cleft

Increased activity of serotonin and norepinephrine associated with increased mood

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15
Q
A

*baseline QTc recommended

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16
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A
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17
Q

*

SnRIs
* May increase what? Why? What need to need to monitor and when?
* What is more common with SSRIs?

A
  • May increase blood pressure and tachycardia (increased NE) – monitor BP before and after initiation
  • Nausea more common than with SSRIs – start low and titrate
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18
Q

Atypical antidepressants
* _ -line treatment in most cases
* What are examples of it being used?

A

Second-line treatment in most cases

May be considered first-line for specific situations
* Depression associated with insomnia
* Depression in elderly with anorexia and weight loss
* Minimal to no sexual side effects

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19
Q

Atypical antidepressants: Mirtazpine
* What is the MOA?

A

Inhibits alpha-2 receptors at presynaptic cleft
* Alpha-2 receptor activation normally decreases NE and 5HT3 in the synaptic cleft
* Alpha-2 inhibition will increase levels of NE and serotonin in the synaptic cleft

Selectively inhibits 5HT 2A and 3A so serotonin selectively binds to 5HT1A receptor (stronger link to depression)

Inhibits histamine-1 receptors - sedation

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20
Q

Atypical antidepressants: Mirtazapine
* What are the SE?(5)

A
  • Sedation
  • Increased appetite
  • Weight gain
  • Dry mouth
  • Sexual side effects = placebo (good for someone with sexual SE, insomina)
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21
Q

Atypical antidepressants: Trazodone and nefazodone
* What is the MOA?

A
  • Selectively binds to 5-HT2A receptors so more serotonin binds to 5-HT1A receptors
  • Weekly inhibits serotonin reuptake at the synaptic cleft – increasing serotonin
  • Strong histamine-1 receptor inhibitor – SEDATION
  • Alpha-1 receptor inhibitor – orthostatic hypotension, priapism
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22
Q

What is the BBW nefazodone?

A

Hepatic failure has been reported (1: 250,000 patients)

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23
Q

Trazodone is extensive metabolism via what?

A

CYP3A4

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24
Q

Atypical antidepressants: Trazodone and nefazodone
* What are the SE?(4)

A
  • Sedation (61% trazodone)
  • Dizziness (36%)
  • Dry mouth (27%)
  • Nausea (19%)
  • Orthostatic hypotension
  • Headache
  • Weight neutral
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25
Q

Atypical antidepressants: Vilazodone (Viibryd) and vortioxetine (Trintellix)
* What is the MOA
* Vilazodone is metabolism by what?

A

MOA:
* Strong inhibitors of serotonin reuptake at presynaptic cleft (like SSRIs)
* Bind selectively to 5-HT1 and stimulate receptors

Vilazodone extensive metabolism by CYP3A4

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26
Q

Atypical antidepressants: Vilazodone (Viibryd) and vortioxetine (Trintellix)
* What are the SE?(6)

A
  • Increased risk of serotonin syndrome
  • Anticholinergic
  • Nausea / diarrhea
  • Sexual dysfunction
  • Weight gain – vilazodone
  • Abnormal dreams – vortioxetine
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27
Q

Atypical antidepressants: Bupropion
* What is hte MOA?

A
  • Binds to NE and DA receptors at the presynaptic cleft inhibiting reuptake; no effect on serotonin
  • Blocks nicotinic receptors-benefits with smoking cessation
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28
Q

Atypical antidepressants: Bupropion
* What are the SE?

A
  • Least sexual side effects
  • Dry mouth
  • Nausea
  • Anxiety
  • Insomnia – take in the AM
  • Tachycardia
  • Decrease seizure threshold – especial in patients with history of seizures or eating disorders
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29
Q

Atypical antidepressants: Bupropion
* Cl in who?(4)

A

CI: bulimia or anorexia nervosa, use of MAOI inhibitor within last 14 days, seizure disorder

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30
Q

Tricyclic antidepressants
* What is tertiary and secondary medications? What is there is MOA?

A

Tertiary (imipramine, amitriptyline, clomipramine)
* Inhibit serotonin and NE reuptake transporters

Secondary (nortriptyline, desipramine)
* Inhibit only NE reuptake transporters

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31
Q

Tricyclic antidepressants
* Not recommened as what?
* Usually reserved as what?

A
  • Not recommended as first line due to side effect profile
  • Usually reserved as last line therapy
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32
Q

TCAs
* What are the SE?(3)
* MC causes of death?(3)

*

A
  • Anticholinergic side effects
  • Serotonin syndrome
  • Cardiac toxicity – increase QTc / arrythmias
  • MC causes of death from TCAs: Convulsions, Coma, Cardiac toxicity
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33
Q

TCAs
* What is the warning?
* Inhibits what?

A
  • Warning: use with caution in patients with suicidality
  • Inhibit CYP450 enzymes
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34
Q

MAOIs
* What is the MOA?

A
  • Prevents the breaks down of serotonin, NE, or DA neurotransmitters pumped back into the presynaptic cleft
  • NT build up in presynaptic vesicles
  • More NT released
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35
Q

MAOIs
* What are the SE?

A

Serotonin syndrome
* Other medications that increase levels of serotonin should be held for 14 days after stopping MAOIs
* Time needed to regenerate MAOIs
* Hypertensive crisis

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36
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A
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37
Q
A
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38
Q

MAOIs
* What is the hypertensive crisis? (5)

A
  • Hyperthermia
  • Increased blood pressure
  • Increased heart rate
  • Arrythmias
  • Agitation
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39
Q

MOAIs
* MC with combining what? Ex? (3)
* What is the treatment?

A

MC with combining MAOIs with foods high in tyramine
* Cheese
* Wine
* Beer

Treatment:
* Phentolamine -> adrenergic antagonist
* Blocks NE receptors

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40
Q

Lithium
* What is the MOA?
* What is the therapeutic index?

A

MOA:
* Exact mechanism unknown
* Thought to inhibit conversion of inositol monophosphatase to inositol decreasing overall inositol levels
* OVERALL decrease in neurotransmitters (KNOW)

Narrow therapeutic index that requires close monitoring

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41
Q

Lithium
* What are the SE?

A
  • Nausea, vomiting, diarrhea
  • Tremor
  • Nephrogenic diabetes insipidus
  • Hypothyroidism
  • Leukocytosis
  • Weight gain
  • Sexual dysfunction
  • Cardiotoxicity
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42
Q

Lithium
* What is the cause of nephrogenic DI SE? What do you use?
* Why hypothyroidism SE?
* What are toxic levels?(6)

A

Nephrogenic diabetes insipidus – blocks ADH from binding to receptors; urine does not concentrate
* Loop diuretics, thiazide diuretics or triamterene may be used
* If hydrochlorothiazide used – decrease lithium dose by 50% and monitor potassium levels

Hypothyroidism – blocks TSH from releasing thyroid hormone

Toxic levels – renal failure, ataxia, confusion, dysarthria, coma, death

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43
Q

Lithium
* When are levels measured?

A

Levels should generally be measured
* 5-7 days after new or increased dose ( Goal levels: 0.8 to 1.2 meq/L)

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44
Q

Lithium
* Lithiumlevels are closely related to what? (3) Explain?

A

Lithiumlevels are closely related to renal function, salt balance, and water balance
* Dehydration causes higher lithium levels
* Increasing sodium intake causes lower lithium levels
* Decreased sodium intake causes an increase in lithium levels

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45
Q

Lithium
* What are the contrainations?(5)

A
  • Significant renal impairment
  • Sodium depletion
  • Dehydration
  • Significant cardiovascular disease
  • Pregnancy = cardiac anomalies
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46
Q

Lithium
* What are the baseline labs?(5)

A
  • Urinalysis
  • BMP (blood urea nitrogen (BUN), creatinine, calcium)
  • Thyroid function studies
  • Pregnancy test for women of childbearing potential
  • Electrocardiogram (ECG) for patients over age 40
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47
Q

Lithium
* What are the maintenance labs?

A
  • BUN and creatinine should be checked every two to three months during the first six months of therapy, and every 6 to 12 months thereafter
  • Thyroid function should be checked once or twice during the first six months, and every 6 to 12 months thereafter
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48
Q
A

Block voltage-gated Na+ channels; inhibit action potentials in excitatory neurons

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49
Q
*

CI? MONITOR?

A
50
Q
*

__ INDUCER? CI? MONITOR?

A
51
Q
*

CI?

A
52
Q
A
For test always pick 2nd gen
53
Q
A
53
Q

Schizophrenia
* What is the MOA of the disease?

A
  • Exact pathophysiology unknown but thought to be secondary to a change in DA functioning in the brain
  • May also involve NE, serotonin, and GABA
54
Q

Antipsychotics
* How many DA receptors?
* What have the highest density in all pathways involved in psychotic disorders?
* What is the primary target of antipsychotic drugs?

*

A
  • There are five primary DA receptors in all pathways of the brain
    *** D1 and D2 have the highest density in all pathways involved in psychotic disorders
  • D2 is the primary target of antipsychotic drugs**
55
Q

Typical (1st generation) antipsychotics
* What is the MOA?
* What pathways are affected?
* Treats what?

A
  • Non-specifically block dopamine D2 receptors in all areas of the brain
  • Blockage impacts all four pathways
  • Treats only positive symptoms: Hallucinations, Delusions, Disorganized speech / behavior
56
Q

Typical antipsychotics

A
57
Q
A
58
Q

Typical antipsychotics
* Separated into what?

A

Separated into high potency and low potency based on affinity for D2 receptors

59
Q

Typical antipsychotics: high potency
* High affinity for what?
* Stronger what?
* More what?
* What are the examples? (4)

A

High affinity for D2 receptors
* Stronger antipsychotic effects
* More EPS and greater increase in prolactin levels
* Haloperidol
* Fluphenazine
* Prochlorperazine
* Tri-fluoperazine

60
Q

Typical antipsychotics: Low potency
* Less affinity to what?
* Blocks what? (3)
* What is the example?

A

Less affinity to D2 receptors

Blocks with other receptors
* Alpha adrenergic – hypotension
* Cholinergic
* Histamine – sedation, weight gain

Ex: Chlorpromazine

61
Q

Atypical (2nd Generation) Antipsychotics
* Blocks what? What does that cause?

A

Block dopamine D2 and serotonin 5HT2A receptors
* Serotonin normally inhibits DA release
* Serotonin blockage may increase DA at sites in the brain that need it

62
Q

Atypical (2nd Generation) Antipsychotics
* Transiently binds to what? What does that cause?
* What are the effects? (3)

A

Transiently bind DA receptors and disassociate quickly  more normal DA activity (compared to typical antipsychotics)
* Decreased EPS
* Decreased negative symptoms
* Increased cognition

63
Q

Atypical (2nd Generation) Antipsychotics
* What does it also block?(4)

A
  • Serotonin receptors
  • Alpha 1 receptors
  • Histamine 1 receptors
  • Muscarinic receptors
64
Q

Atypical (2nd Generation) Antipsychotics
* What are the examples?
* Each agent has what?
* What does it treat?

A

Examples
* risperidone (Risperdal)
* olanzapine (Zyprexa)
* quetiapine (Seroquel)
* ziprasidone (Geodon)
* aripiprazole (Abilify)
* lurasidone (Latuda)

Each agent has different affinity for other receptor blockage which results in specific side effect profiles

Treat positive and negative symptoms

65
Q

Atypical antipsychotic adverse effects

A
66
Q

Atypical antipsychotic adverse effects

A
67
Q
A
68
Q

antipsychotic adverse effects

A
69
Q

antipsychotic adverse effects

A
70
Q

EPS Symptoms

A
71
Q

EPS Symptoms

A
72
Q

EPS Symptoms

A
73
Q

Benztropine
* What is the MOA?
* What does it restore?
* What does it do to muscles?

A
  • Anticholinergic, antagonizes CNS Ach and histamine1 receptors
  • Restores the balance between Ach and DA
  • Muscle relaxation
74
Q

Benztropine
* What are the SE? (4)
* What are the precautions?(3)

A

Adverse effects:
* Anticholinergic
* Weakness
* Confusion
* Anhidrosis

Precautions: Not recommended for patients with tardive dyskinesia, narrow angle glaucoma, preexisting tachycardia

75
Q

Tardive dyskinesia
* What is the cause?

A
  • DA blockade by antipsychotics causes the body to create more DA receptors
  • These receptors are more sensitive to DA causing increased signaling to motor areas of the brain
  • Result = TD
76
Q
A
77
Q

TD TREATMENT
* What are VMAT2s?
* What happens when you block VMAT2s?

A

Vesicular monoamine transporter 2 (VMAT2) packages DA into presynaptic vesicles

VMAT2 inhibition
* Decreases the amount of DA in presynaptic vesicles
* Less DA released
* Down regulates postsynaptic DA receptors
* Improves symptoms of TD

78
Q

VMAT2 Inhibitors: Valbenazine
* What are the SE?

LY

A

Adverse effects:
* Dizziness
* Nausea
* Imbalance / falls
* QT prolongation

79
Q

VMAT2 Inhibitors: Deutetrabenazine
* What are the SE?

LY

A
  • Somnolence
  • Anticholinergic effects
  • Imbalance / falls
  • QT prolongation
80
Q

Adjustment Disorder
* What is it?
* Sxs could cause what?

A
  • Maladaptive behavioral or emotional symptoms develop w/in 3 mos. of a stressor and resolve w/in 6 mos.
  • Symptoms could cause significant or insignificant impairment in function.
81
Q

Adjustment Disorder
* What is the treatment?

A
  • First-line: Individual psychotherapy and group therapy
  • +/- short-term pharmacotherapy for insomnia, anxiety or depression
  • Watch out for self-medication with ETOH, drugs, stimulants
82
Q

Depressive Disorder: Major Depressive Episode
* Duration?
* What must be present?
* No signs of what?
* Episode is not the result of what?

A
  • Depressive signs and symptoms present for most days during a 2-week period
  • Depressed mood or anhedonia must be present
  • No signs of mania
  • Episode is not a result of bereavement
83
Q

Major Depressive Episode DSM-5 Criteria: “SIG E CAPS”
* Must have at least five of the following symptoms for at least a 2-week period:, must include either number 1 or number 2:

* KNOW

A
84
Q

What is the phq-9? What are the levels?

LY

A

Used for depression scale
* 0 to 4 = normal
* 5 to 9 = mild depression
* 10-14 = moderate depression
* 15-19 = moderately severe depression
* ≥ 20 = severe depression

85
Q

MDD – treatment general Principals
* What are the treatment? (general)

A
86
Q

MDD – treatment general Principals
* What is partial and full remission?

A

Remission induction
* Partial remission: Period <2 mos w/o symptoms or persistent symptoms for 2 or more months
* Full remission: 2 months or more without any significant symptoms

Prevention of relapse

87
Q

MDD – treatment
* What type of therapy?
* What medications?

A

Psychotherapy – cognitive behavioral therapy ,etc

Second generation anti-depressants:
* SSRI
* SNRI
* Atypical antidepressant
* Serotonin modulators

First generation
* Tricyclic antidepressants
* Monoamine oxygenase inhibitors

88
Q

Depression treatment review
* All antidepressants considered what?
* Agent selection based on what?

A
  • All antidepressants considered equally efficacious
  • Agent selection based on patient / antidepressant properties and adverse effects
89
Q

Depression treatment review
* What medication is considered first line?
* Failure to respond to one agent does not predict what?
* What is the Most common dose dependent ADRs ?(3)

A

SSRIs considered first line secondary to safety in OVERDOSE and tolerability profile
* Failure to respond to one agent does not predict response to another
* Most common dose dependent ADRs GI (N,V,D), anxiety, headache

90
Q

Depression treatment review
* What is the goal?
* Start how?

A
  • Goal=return to previous level of functioning
  • Start at lowest recommended dose
91
Q

MDD Pharmacotherapy
* Start dose how? Then what?

A

Start with lowest dose
* Dose titration increment and timing depend on specific agents
* Generally every 2 to 4 weeks

92
Q

MDD Pharmacotherapy: Onset of effects
* Some improvement should be seen in what?
* Patients with little improvement by 2 to 4 weeks, what is reasonable?
* Patients with improvements, what should you do?
* Consider a medication change if what?

A
  • Some improvement should be seen in 2 weeks
  • Patients with little improvement by 2 to 4 weeks – reasonable to increase antidepressant dose
  • Patients with improvements – hold same dose for 8 to 12 weeks prior to increasing dose
  • Consider a medication change if not in remission after 6 to 12 weeks on maximum dose
    * Could be a SWITCH or an ADD (non-SSRI antidepressant
93
Q

MDD Pharmacotherapy
* When do you get peak effects?
* Do not discontinue how? Why?

A

Peak effects
* Up to 12 weeks

Do not discontinue abruptly to avoid discontinuation syndrom
* GI distress, insomnia, dizziness, ataxia, paresthesia

94
Q
A
95
Q

Depression treatment review
* Response=
* Some patients respond when?
* Average time to response with citalopram is what?
* Patient generally improve after what?

A
  • Response = variable
  • Some patients respond in 1-2 weeks
  • Average time to response with citalopram 6 weeks
    * 56% of responders – response occurred at or after 8 weeks
  • Patients generally improve after 6 to 8 weeks
96
Q

Mdd –other therapies
* What are some of the therapies?

A

Vagal nerve stimulation

Transcranial magnetic stimulation

Electroconvulsive therapy (ECT)
* Effective in all types of MDD – generally treatment resistant, but….
* Few contraindications
* Greatest concern is transient memory loss

97
Q

Special populations: pregnancy
* Risk of what during pregnancy?
* What is considered safe?
* What medication is not okay?

A
  • Risk of depression reoccurrence during pregnancy if antidepressants stopped is high
  • Most SSRIs and SNRIs considered safe in pregnancy
  • Paroxetine associated with congenital cardiac abnormalities
98
Q

Special populations: Elderly
* What is first line?
* Avoid agents with what?
* What improved appetite and sleep?

A
  • SSRIs generally first-line
  • Avoid agents with anticholinergic adverse effects
  • Mirtazapine – improves appetite and sleep
99
Q

Special populations: Peds
* What is first line?
* Watch for what?

A
  • SSRIs / SNRIs generally first-line
  • Watch for suicidal ideation
100
Q

In Summary on Depression
* What is the non-pharm?
* What is the pharm?

A

Non-pharmacology
* Psychotherapy
* Exercise, regular meals, socialization (activities to treat anhedonia)

Pharmacology – initiate SSRI anti-depressant

101
Q

In Summary on Depression
* What is the patient education?

A
  • Adverse drug effects
  • Do not stop medications abruptly
  • Signs/symptoms of worsening, call the office or 911-ER
102
Q

Dysthymic Disorder (Persistent Depressive Disorder)
* What is it?
* MDD develops in how many patients?
* More common in who?
* Onset?

A
  • Chronic, persistent mild depression
  • MDD develops in 10-20% of patients
  • Women > men
  • Onset typically young adulthood
103
Q

Persistent Depressive Disorder
* What is most effective?
* First line meds?
* What are two other options?

A
  • Psychotherapy plus pharmacotherapy most effective
  • First-line antidepressants (SSRIs, SNRIs, bupropion)
  • Psychotherapy
  • Insight-Oriented (Psychoanalytic) Therapy
104
Q

Persistent Depressive Disorder
* What is the most common psychotherapy? WHat is it?

A
  • Insight-oriented therapy
  • Treatment of choice
  • How life events, desires, past and current relationships, and unconscious conflicts affect your feelings and contribute to feelings of depression
105
Q

Cyclothymic Disorder
* What is the pharmacotherapy?

A
  • Mood stabilizers and antimanic drugs are first-line treatment: Carbamazepine, valproate
  • Caution with antidepressants - can cause increased hypomanic or manic episodes
106
Q

Cyclothymic Disorder
* What is the psychosocial therapy?

A
  • Assist patients in learning to recognize their condition and learning to cope with their mood swings
  • Lifelong treatment usually needed
107
Q

What is the difference between bipolar one and two?

A
108
Q

Manic Episodes
* What is it? How long?
* What needs to be present?
* Results in what?
* Rule out what?

A
  • Abnormally and persistently elevated or irritable mood lasting at least one week
  • 3 or 4 manic symptoms present
  • Results in social or occupational dysfunction
  • Rule out medical vs. substance abuse being the cause
109
Q

Hypomanic episode
* Duration?
* What needs to be present?
* What is not there?

A
  • At least 4 continuous days (present most of the day) of abnormally and persistently elevated or irritable mood
  • 3 or 4 manic symptoms present
  • No significant social or occupational dysfunction
110
Q

Bipolar Disorder Treatment
* Treatment for bipolar disorder is divided into what?
* Different strategies for those experiencing what?
* Often necessary to do what?

A
  • Treatment for bipolar disorder is divided into acute and maintenance phases
  • Different strategies for those experiencing mania, hypomania, or depression
  • Often necessary to try different medications to find optimal treatment
111
Q

Bipolar Disorder Treatment
* What are the four categories of medication?

A
  • Anticonvulsants & mood stabilizers
  • Antidepressants (can often worsen mood symptoms)
  • Antipsychotics
  • Benzodiazepines
112
Q

Bipolar – acute treatment with SEVERE mania
* What is first line?
* What happens if no response in 1-3 weeks? Again no response?

A

First-line therapy:
* Lithium plus antipsychotic OR
* Valproic acid plus antipsychotic

If no response in 1 to 3 weeks
* Switch to alternative mood stabilizer (lithium or valproic acid)
* Continue antipsychotic

If still not response in 1 to 3 weeks after switch
* Alternative regimens recommended

113
Q

Bipolar – acute treatment: SEVERE mania
* Regimens considered equal; specific choice depends on patient-specific factors:

A
  • Renal insufficiency – avoid lithium
  • Hepatic insufficiency – avoid valproic acid
  • Pregnancy – avoid valproic acid and lithium
114
Q

Bipolar – acute treatment: HYPOMANIA or mild mania
* What is first line?
* What are other appropriate therapies?

*

A
*
115
Q

Bipolar – acute treatment: HYPOMANIA or mild mania
* When do you an alternative agent?
* What are the examples?

A
  • Alternative agents – do not respond or are intolerant to antipsychotics, lithium, or anticonvulsants
  • Benzodiazepines – clonazepam, lorazepam
116
Q

Bipolar major depression
* What is not indicated?
* What is first line?

A
  • No antimania therapy indicated
  • First-line: Quetiapine or lurasidone
117
Q

Bipolar major depression
* What is second line?

LY

A

Second-line (first-line monotherapy ineffective or intolerable):
* Olanzapine plus fluoxetine
* Valproate monotherapy
* Quetiapine or lurasidone plus lithium or valproic acid
* Lithium plus valproic acid or lamotrigine

118
Q

Bipolar disorder - maintenance therapy
* What is first line?

A
  • Same regimen that treated acute bipolar mood episode
  • Attempt to transition to monotherapy to decrease adverse effects and increase compliance
119
Q

Bipolar disorder - maintenance therapy
* What is the second line therapy?

A
  • Lithium
  • Valproic acid
  • Quetiapine
  • Lamotrigine
120
Q

Bipolar disorder - maintenance therapy
* What are the four goals?

A

Goals:
* Delay / prevent relapse
* Decrease suicide risk
* Promote psychosocial functioning
* Minimize adverse drug events

Pharm III (14 decks)

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