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PSYCHOPHARMA - MIDTERM > MODULE 16 > Flashcards

MODULE 16 Flashcards

1
Q

Serotonin is normally removed from the the synapse by reuptake sites on the presynaptic neuron. SSRIs block the serotonin reuptake sites, allowing serotonin to remain active in the synapse longer

A

The Role of Serotonin

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2
Q

implicated in mood regulation

A

Serotonin

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3
Q

To block the reuptake into presynaptic cell. The longer serotonin can remain in the synaptic cleft, the greater the possibility it can do its thing
at the receptors.

A

The Role of Antidepressants

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4
Q

T or F
How the Brain Reacts to this Artificial Manipulation?

  1. Brain does not take too kindly to such manipulation, and as such, it strikes back.
  2. Armed with feedback forces, presynaptic cells begin releasing more serotonin than usual, and in lockstep, the density level of the receptors diminishes.
  3. As antidepressants tries to continue accelerating serotonin activity, the brain responds by putting the hammer down.
A
  1. T
  2. F. presynaptic cells begin releasing less serotonin than usual
  3. T
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5
Q
  • also referred as tricyclics
  • many of these agents are dual-action in that they block the reuptake of both 5-HT and NorE
  • effective but are fraught with side effects that render them intolerable for patients
A

Cyclics

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6
Q
  • work by selectively blocking or inhibiting the reuptake of 5-HT.
  • side effects tend to be transient, with the exception of weight loss and sexual dysfunction.
A

SSRIs

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7
Q
  • dual-action; inhibit or block the reuptake of 5-HT and NorE.
  • side effects are similar to SSRI
A

SNRIs

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8
Q
  • mechanism is to selectively blocks the reuptake of NorE
  • provides energy boost, as well as for decreasing distractibility and improving attention span
  • not FDA approved for depression
A

NRIs

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9
Q
  • rarely used, due to their numerous and potentially serious and fatal drug-drug interactions and drug-food interaction.
  • Monoamine oxidase is an enzyme that circulates in the central nervous system to metabolize neurotransmitters at presynaptic nerve endings.
  • causes serious interaction to food containing Tyramine, an amino acid that plays a role in maintaining blood pressure and is metabolized by monoamine oxidase; it can result in hypertensive crisis.
  • it should NEVER be combined with SSRIs, it will cause
A

MAOIs

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10
Q

T or F (Cyclics)

A. As a class, they tend to be dangerous in overdose and can enhance the sedative effects of alcohol.
B. They are not sedating, in that they inhibit the effects of histamine, similar to the actions of Benadryl (diphenhydramine).
C. Can cause annoying side effects – dry mouth, blurred vision, constipation, urinary retention and
confusion – because they block the actions of acetylcholine.
D. They can cause orthostatic hypotension, a drop in standing blood pressure
E. There is no risk of tachycardia, or rapid heart rate
F. Weight loss is associated with a metabolic slowdown in carbohydrate and fat metabolism. In some individuals, it is contribute to by an increased craving for sweets and fats.
G. An increase in libido and ability to perform sexually is linked to the serotonergic effect

A

A. T
B. F. They are sedating
C. T
D. T
E. F. There is a risk of tachycardia
F. F. Weight gain
G. F. A decrease in libido and inability to perform sexually

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11
Q

Main side effects of SSRIs

A. Increased an__ty or an “activated” feeling
B. Se__ion
C. Insomnia
D. Sexual dy__nction
E. Weight gain, but less than the associated with cy__cs.

T or F - discontinuing is best done gradually to spare patients unnecessary upset

A

A. Increased anxiety or an “activated” feeling
B. Sedation
C. Insomnia
D. Sexual dysfunction
E. Weight gain, but less than the associated with cyclics.

Trueee

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12
Q

don’t necessarily fit into antidepressant family; DNR:linked to its action on dopamine and NorE

A

Atypical Antidepressants

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13
Q
  • usually combines mechanism of action of SSRIs with that of anxiety drugs – which targets 5-HT1A.
  • exerts dual-action effect by inhibiting serotonin reuptake, and by acting as a partial agonist at the 5-HT1A receptor.
  • has also been reported with associated minimal side effects: weight gain and fewer sexual side effects
  • Viibryd (vilazodone) and Brintellix (vortioxetine) are examples of
A

Hybrids

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14
Q

T or F
Initiating Antideppressant Selection: What is Important?
1. Know whether the antidepressant consistently underperform placebo.
2. Consider how well the antidepressant stands up to other competitors within the same genre.

A
  1. F. consistently outperforms placebo.
  2. T.
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15
Q

Initiating Antideppressant Selection
Other Important Things to Consider:
1. How the depression p___ents.
2. Personal and family hist__y
3. Drug cha___teristics.
4. Reasonable ex___tations
5. I___ial response
6. Let the client c__ose

A
  1. How the depression presents.
  2. Personal and family history
  3. Drug characteristics.
  4. Reasonable expectations
  5. Initial response
  6. Let the client choose
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16
Q

Managing Antidepressant-Induced Sexual Dysfunction
1. Consider medical po___lities first.
2. Don’t a___tly discontinue.
3. Dosage r___tion.
4. Tale the antidepressant a__er sexual activity.
5. Medications that treat se__al dys__nction
6. Drug h___days.
7. Sw__ch to an antidepressant that typically causes fewer sexual side effects.
8. Augm___tion

A
  1. Consider medical possibilities first.
  2. Don’t abruptly discontinue.
  3. Dosage reduction.
  4. Tale the antidepressant after sexual activity.
  5. Medications that treat sexual dysfunction
  6. Drug holidays.
  7. Switch to an antidepressant that typically causes fewer sexual side effects.
  8. Augmentation
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17
Q

Antidepressant Effects on Sleep

  • most of these agents are sedating and suppress REM sleep.
  • sedating ___ typically block the actions of serotonin and histamine (amitriptyline and doxepin)
  • some ___ do not suppress REM (trazodone and nefazodone) but liver toxicity can be a side effect
A

Cyclic Antidepressants

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18
Q

Antidepressant Effects on Sleep

-appear to slow the onset of sleep and increase the number of awakenings – leading to an overall poor sleep cycle

A

SSRIs

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19
Q

Antidepressant Effects on Sleep

-effects on sleep is similar to the SSRIs; sleep continuity and REM are compromised by these antidepressants and
their NorE effects are unfriendly to sleep initiation and continuation.

A

SNRIs

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20
Q

Antidepressant Effects on Sleep

  • commonly have three-fold action (especially mirtazapine) of NorE, 5-HT and histamine inhibition.
  • helps users get to sleep quickly and stay asleep longer.
  • weight gain
A

Atypicals

21
Q

T or F

  • antidepressants have PHYSIOLGICAL effects on depressive symptoms and are effective but the mildest cases of
    depression.
A

TRUE

22
Q

T or F

Antidepressants has been successful when:
1. the user begins feeling more energetic, brighter and motivated after several days of use
2. the energy and motivation boost discourages the user to act in his/her best interest
3. the user concluded from day 1 that use should be time-limited and that the drug had magical powers to solve problems
4. the user thought through the process of antidepressant use, understanding their benefits and limitations and did not subscribe to false hope.

A
  1. T
  2. F. propel the user
  3. F. drug had no magical powers
  4. T.
23
Q

CHOOSING THE BEST TREATMENT FOR DEPRESSION
It is important to distinguish between:

-the emotional reaction stems from a relatively minor event; it is transient

A

Reactive Sadness

24
Q

CHOOSING THE BEST TREATMENT FOR DEPRESSION
It is important to distinguish between:

  • a normal response to a major interpersonal loss; experience can be tremendously painful and is more
    prolonged than reactive sadness; patient clearly relates sadness to the loss
A

Grief

25
Q

CHOOSING THE BEST TREATMENT FOR DEPRESSION
Medical Illness and Medications That Can Cause Depression

  • a pathological process characterized by: depressed mood or irritability. loss of interest in normal life activities, increasing impairment of normal functioning, irrational or exaggerated erosion of self-esteem, dramatic and specific change in vegetative patterns and the appearance of nonspecific physical complaints, and depression
    can occur in response to psychological stressors or may emerge without clear-cut precipitating events.
A

Clinical Depression

26
Q

CHOOSING THE BEST TREATMENT FOR DEPRESSION
Medical Illness and Medications That Can Cause Depression

  • low grade, chronic depression; less severe than clinical depression and typically does not interfere
    with daily functioning.
A

Dysthymia

27
Q

When Do We Prescribe Antidepressants?
Vegetative/Physiological Symptoms Reflecting a Biochemical Dysfunction:

  1. Sleep d___bance
  2. Ap___ite disturbance
  3. Fa___ue
  4. Chronic systemic in___mation
  5. Decreased sex d___e
  6. Rest___ess, agi___ion, or psychomotor ret___ation
  7. D___nal variations in mood
  8. Impaired concentration and for___ulness
  9. Pronounced an___onia
A
  1. Sleep disturbance
  2. Appetite disturbance
  3. Fatigue
  4. Chronic systemic inflammation
  5. Decreased sex drive
  6. Restlessness, agitation, or psychomotor retardation
  7. Diurnal variations in mood
  8. Impaired concentration and forgetfulness
  9. Pronounced anhedonia
28
Q

Phases of Treatment (for clinical depression with sustained vegetative symptoms; marked vegetative symptoms)

-begins with the first dose and extends until the patient is asymptomatic (6-8 weeks)

A

Acute Treatment

29
Q

Phases of Treatment (for clinical depression with sustained vegetative symptoms; marked vegetative symptoms)

  • to avoid acute relapse, it is strongly suggested that patients continue treatment for a minimum of 6 months beyond the acute phase.
A

Continuation Treatment

30
Q

Phases of Treatment (for clinical depression with sustained vegetative symptoms; marked vegetative symptoms)

  • relapse prevention is an important aspect of treatment, especially in those patients
    judged to have recurrent episodes (or at risk for
A

Maintenance Treatment

31
Q

Chronic treatment follows these guidelines:

-at the end of the continuation phase, gradually reduce the dose (over a period of 4-6 weeks to avoid acute discontinuation withdrawal symptoms) and, assuming no return of depressive symptoms, discontinue. Educate the
patient to be alert to any signs of recurrence (poor sleep, fatigue, etc.) and should this occur, contact the treating doctor ASAP.

A

First Episode

32
Q

Chronic treatment follows these guidelines:

a) With Risk Factors which include family history of mood disorders, first episode occurring prior to the age of 18, and/or most recent episode has severe symptoms. Recommend life-long medication treatment to prevent
recurrence.

b) Without Risk Factors: gradually discontinue medications.

A

Second Episode

33
Q

Chronic treatment follows these guidelines:

-recommend life-long treatment

A

Third or Later Episodes

34
Q

Chronic treatment follows these guidelines:

-recommend life-long treatment

A

Third or Later Episodes

35
Q
  • a depression that is mostly or partially resistant to treatment
  • the genesis is linked to how neurotransmitters are born: not all human beings are able to manufacture the same
    amount of neurotransmitters
  • neurotransmitter production is controlled by genotype
  • only 30% of depressed subjects achieve remission on first trial
  • monotherapy is not adequate for most depressed subjects particularly long term
A

Treatment-Resistant Depression (TRD)

36
Q
  • refers to the addition of medication from different chemical classes or the combination of antidepressants.
A

Augmentation

37
Q

a “kick starter” when combined with SSRI

A

Lithium

38
Q
  • (T4: Synthroid and Levothroid; T3: Cytomel);
  • some researchers suggested that thyroid hormone augmentation might correct a hypothyroid state.
A

Thyroid Supplements

39
Q
  • activate both the NorE and dopamine
A

Stimulants

40
Q
  • few of the second-generation antipsychotic have also shown effectiveness as augmenters to the traditional antidepressants.
A

Atypical Antipsychotics

41
Q
  • folic acid type derivative that helps normalize amounts of neurotransmitters by aiding in their synthesis and subsequent generation; depressed patients consistently have lower folate concentrations.
A

Deplin (l-methylfolate)

42
Q
  • now considered by many to be one of the best natural alternatives in the treatment of mild to moderate depression; aids in methionine synthesis and acts as a precursor to neurotransmitter development.
A

SAMe (S-adenosylmethionine)

43
Q
  • eicosapentaenoic acid (EPA): critical in heart function; and docosahexaenoic acid (DHA):
    critical in brain function; they both affect calcium, sodium, and potassium ion channels that regulate cellular electrical
    activity in the heart and brain.
A

Omega-3 Fatty Acids

44
Q
  • combination of antipsychotic and antidepressants
A

Olanzapine/fluoxetine combination

45
Q

T or F
What Influences a Less Than Adequate Response?

  1. Many depressed individuals are dosed adequately
  2. Not switching to other antidepressant classes if symptoms persist longer
  3. Patients skip or forget doses
  4. Substance abuse
  5. Diagnosed medical conditions
  6. Underlying bipolar disorder
  7. Resolved clinical syndromes
A
  1. F. are not dosed adequately
  2. T
  3. T
  4. T
  5. F. Undiagnosed medical conditions
  6. T
  7. Unresolved clinical syndromes
46
Q

Other Mechanical Strategies in Treating TRD:

-mimics seizures

A

Electroconvulsive Therapy (ECT)

47
Q

Other Mechanical Strategies in Treating TRD:

  • stimulates underactive neuron
A

Repetitive Transcranial Magnetic Stimulation (rTMS)

48
Q

Other Mechanical Strategies in Treating TRD:

-invasive procedure; implantation of device called an NCP System in the upper chest;

A

Vagal Nerve Stimulation (VNS)

49
Q

Other Mechanical Strategies in Treating TRD:

-dissociative anaesthetic with hallucinogenic properties (IV); to ameliorate severe depressive symptoms in
people who have responded poorly to antidepressants (those who are acutely suicidal)

A

Ketamine

PSYCHOPHARMA - MIDTERM (5 decks)

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