psychotherapeutics ppt Flashcards

1
Q

what is the prevalence of depression annually in Canada in %

A

from 5 to 8.2 percent of the Canadian population afflicted annually.

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2
Q

what is the estimated lifetime prevalence of depression in the US for adults

A

16.2% lifetime prevalence

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3
Q

what is remission like in relation to depression

what is the risk of relapse after 1 time? after 2nd and third?

A

At least 50% of people following their first episode of major depression will go on to have at least one more episode and after the second and third episodes, the risk of further relapse rises to 70% and 90% respectively.

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4
Q

if taking antidepressants and you are no longer having symptoms when can you stop taking the
how long do you need to take them the second time?
third time?

A

after the first depression to stay on antidep for at least 9 months after symptoms subside,

the second time at least 5yrs after symptoms subside

the fthird time basically for life (she wasnt positive on those timelines)

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5
Q

what are 2 great screening questions for depressed pt

A

Screening for depression is 2Q: have they lost pleasure or interest in things in their life or are there still things they enjoy? Have felt sad down low depressed or hopeless?

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6
Q

which age and ethnicities are at disproportionate risk of suicide

A

Elderly Caucasian and Asian men over the age of 65 years and Asian women over 80 years are at disproportionate risk.

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7
Q

t or f a large amount of those who died by suicide had lost touch with their drs

A

f

75 % of elderly suicide completers were seen by their doctor within one month of death

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8
Q

when a pt has high levels of the following what risks for suicide does it mean that risk is very high and hospitalization may be immediately necessary

A
  • Internal emotional pain (e.g., feelings of shame, guilt, humiliation),
  • External stress (e.g., loss of spouse, job, legal troubles),
  • Agitation (e.g., from sleep loss, drug use, or excessive anger),
  • Hopelessness
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9
Q

what re the 2 major theories of et of depression

A

Monoamine neurotransmitter dysfunction

Neuroendocrine factors

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10
Q

which addition factors are thought to play a role in et of depression. examples of each

A

Additional factors thought to play a role in etiology of depression

  • Immune system-stress (going thru the hypothalamic pituitary renal system)
  • Genetic factors (family hx, genetic cofactors like alcoholism and depression)
  • Environmental factors (poverty, trauma in early childhood and beyond)
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11
Q

what is it called when a pt cant describe how they feel

A

alexithymia

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12
Q

which drugs may be associated with major depression

A

Reserpine, steroids, alpha-methyldopa, propranolol and hormonal therapy may be associated with major depression.
in class: Anticonvulsants, antimigraines, corticosteroids, hormonal drugs eg corticosteroids, GNRH, birth control, antiretrovirals, antimalarials

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13
Q

beyond the mentioned drugs what are other medical causes of depression

A

Active abuse or withdrawal from alcohol, cocaine, sedatives, opiates, cannabis, anxiolytics, hypnotics and amphetamines

Idiosyncratic reactions to other medications can occur

Medical conditions: hypothyroidism, cardio- vascular disease, etc.

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14
Q

depression has a **bidirectional relationship to which medical condition?

How does this work?

A

coronary artery disease can cause depression
and depression is an independent risk factor for coronary artery disease and its complications;
depression may contribute to sudden cardiac death and increase all causes of cardiac mortality;
and depression contributes to unhealthy lifestyle and poor adherence to treatment. “

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15
Q

in the graph she gave us how did depression following MI impact mortality

A

Depression was a significant predictor of mortality (hazard ratio, 5.74; 95% confidence interval, 4.61 to 6.87; P=.0006).

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16
Q

what are the two larger…(classes?) of older antidepressants

A
Tricyclic antidepressants (TCAs) 
Monoamine oxidase (MAO) inhibitors
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17
Q

TCAs what other medical condition are these used for?

egs of these?

A

**(used for urinary retention as well due to this side effect)

imipramine and amitriptyline

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18
Q

TCAs: were they still used much after SSRIs

-how are these meds dangerous for pt

A

As soon as the new drugs came out these were mostly phased out. Theyre very cardiotoxic and can easily kill pt if takes OD. Gen only psychiatrists could provide

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19
Q

are there major restrictions with MAOI antidepressants? When are these used in r/t other antidepressants

A

**MAOI have many dietary and drug interactions. The only time they use these now is if someone doesnt have good result with other drugs. Theyd probably be tried after AAP and TCA

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20
Q

what were the two general classes of newer antidepressants

A

Selective serotonin reuptake inhibitors (SSRIs)

Serotonin/norepinephrine reuptake inhibitors (SNRIs)

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21
Q

how long must you take antidepressants before theyll begin working
why?

A

**Must be taken 2–4 weeks before depressive symptoms improve

-Why they take so long to work: some theories
Up-regulation of neurotransmitter
Hippocampus changes

Scientists believe the behavioral effects of antidepressants may be due to other changes that occur as a reaction to the changed serotonin levels. However, researchers don’t know what reactions include, and therefore cannot create medications that target them directly.

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22
Q

where are antidepressants in general absorbed and metabolized?
what route are they given through?

A

Given orally, absorbed from small bowel, metabolized extensively in the liver

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23
Q

do antidepressants interact with each other and other meds metb in the liver

A

yes

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24
Q

SSRIs are generally oxidatevely metabolized by CYP2D6 what are the different categories of this

A
ultrarapid metabolizer (UM); 
extensive, or normal, metabolizer (EM); 
intermediate metabolizer (IM); and 
poor metabolizer (PM). 
Between 5% and 10% of whites are classified as PM, ~5% are classified as UM, 20% to 30% are classified as IM, and the rest are EM
Some people d/t genotype may metabolize SSRIs differently
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25
Q

which neurotransmitter do traditional antidepressants mostly work on and how are they acting on it

A

Traditional antidepressants go after serotonin transporter proteins. These regulatory proteins take serotonin back into the nerve cell after it has been released in the process of signaling other neurons. Antidepressants keep the transporters from performing this function.

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26
Q

which area of the brain is sometimes found to be smaller in depressed people?
Is there a cnclusion on why this is?

A

Researchers have noticed that the hippocampus of a depressed person’s brain tends to be smaller than average. Some researchers hypothesize that a problem with neurogenesis causes both the small hippocampus as well as depression; others caution that the causal arrow may be reversed, with a small hippocampus leading to problems with neurogenesis and depression.

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27
Q

does chronic or long term use of antidep cause and inc or dec in neurogenesis

A

increases neurogenesis

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28
Q

what are the indications for use of antidepressants

A

Depressive symptoms persist at least 2 weeks
Impair social relationships or work performance
Occur independently of life events
-Treatment of anxiety disorders
-Enuresis management
-Neuropathic pain management

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29
Q

which kind of antidepressant is used for enuresis mgmt

A

TCAs

30
Q

what are contraindications for antidepressant use

A
Acute schizophrenia
Mixed mania and depression
Suicidal tendencies
Severe renal, hepatic, or cardiovascular disease
Narrow-angle glaucoma
Seizure disorders
31
Q

which antidepressant affects hemostasis and how?

therefore which drugs inc this risk

A

Because serotonin release from platelets is essential for hemostasis and psychotropic drugs interfere with serotonin reuptake, **these agents are associated with increased risk of GI bleeding.

Concomitant use of non-steroidal anti-inflammatory drugs (NSAIDS), acetylsalicylic acid (ASA), or warfarin increases this risk.

32
Q

what is the half life of SSRIs and are they quite protein bound or not

A

**Active metabolite with long half-life (24-72 hr). Highly protein bound.

33
Q

which age must you use caution with SSRIs and why

A

for some teens it may **inc risk of suicidal ideaton

34
Q

what is the primary mood stabilizing agent we looked at and what is it derived from

A

lithium carbonate is a naturally occuring metallic salt

35
Q

which mental health condition is lithium used for?

what aspect of this?

A

bipolar

To treat/prevent manic episodes

36
Q

is lithium poorly absorbed

A

no. easily absorbed

37
Q

what is a concern in relation to lithium dose

A

-very toxic if overdosed

Monitor serum concentrations frequently
Narrow range between therapeutic and toxic levels

38
Q

what is unique about the pharmacokinetics of lithium

what is a prerequisite for this therapy (in r/t pharmacokinetics)

what studies must be done beforehand

A

Not metabolized by the body

  • **Entirely secreted by the kidneys
  • *Adequate renal function is prerequisite

Before therapy begun, baseline studies necessary
Renal, cardiac, thyroid

39
Q

when considering antidepressant therapy what are some of the factors considered when selecting a drug

A
Client’s age
Client’s medical conditions
Previous history of drug response-can include family hx of what they take
Specific medication’s adverse effects
Cost of medication
40
Q

t or f
antidepressants have established dosing thats been proven to work for almost everyone.

Peoples doses will inc according to their weight and renal function

A

Antidepressant dosage should be individualized according to clinical response

Initiated with small, divided doses
Gradually increased until therapeutic or adverse effects occur

41
Q

why is the duration of drug therapy after symptoms subside after the second and third depressions so long

A

the chance of relapse severely increases and the neural pathways for depression get reinforced each episode

42
Q

with lithium is it usually taken for only a short time

why is it most often stopped

A

Long-term therapy is usual practice due to high recurrence rate if medication discontinued
Most often discontinued because of adverse effects or client’s noncompliance

43
Q

which antidepressants lethality d/t it being highly toxic was most emphasized

A

**TCAs

44
Q

what is serotoning syndrome and can it be fatal

A

Overstimulation of serotonin receptors
Triad of mental, autonomic, and neurological disorders:

YES!**Can be fatal; hold medication

45
Q

what are the symptoms of serotonin syndrome

A

Symptoms include confusion, agitation, tachycardia, dyspnea, high or low blood pressure, myoclonus, tremors, chills, rigidity, and hyper-reflexia.

46
Q

when in relation to a dose does serotonin syndrome usually occur

is it only with an overdose that this can occur

A

It usually presents within 24 hours following the administration of therapeutic doses, intentional overdose, or inadvertent drug interactions.

47
Q

what can happen if you d/c your antidepressants suddenly?
does this apply to most or just some meds?
under what circumstances can this occur very rapidly?

A

antidepressant discontinuation syndrome which is reported with d/c of most antidepressant medications

wfor those on long term therapy or meds w short half life this can occur rapidly (even in days) and may be more intense

48
Q

how slowly should doses be tapered of antidepressants

A

gradually over 6-8wks to avoid antidep d/c syndrome

in my notes she mentioned even slower to stop rebound depression

49
Q

whatre antidepressant d/c syndrome symptoms from SSRI d/c

how long does this last

A
Dizziness, dysphoria, GI upset
Sleep problems, lethargy, headache
Anxiety/hyperarousal
More serious symptoms
Aggression, hypomania, mood disturbances, suicidal tendencies

(lasting from several days to several weeks)

50
Q

anitdepressant d/c syndrome from TCAs symptoms

A
TCA symptoms
Hypersalivation
Diarrhea
Urinary urgency
Abdominal cramping
Sweating
51
Q
which medication (specific name) would pts not be given over \_\_g d/t risk of fatal overdose.
what is therapeutic dose?
 what class is this med?
A

Venlafaxine (Effexor): an SSNRI, **** can have fatal overdose with as little as 1g, therapeutic dose around 75mg

52
Q

not sure if worth memorizing but what are other antidepressants listed

A
  • bupropion (wellburin, zyban)
  • maprotiline
  • mirtazapine (remeron)
  • trazodone (desyrel)
  • venlafaxine
53
Q

which of the antidepressants has a risk of seizures for doses over 450mg/day, & with hx of seizures

A

bupropion

54
Q

which of the folowing increases sleep and is often given w stimulant antidepressant like buprpion

A

trazodone

55
Q

what effects does mirtazapine have

A

decreases anxiety, agitation, insomnia, and migraine headaches as well as depression.

56
Q

what is lithium dosage based on

A

Serum lithium levels
Control of symptoms
Occurrence of adverse effects

Lower doses recommended for older adults, clients with conditions that impair secretion

57
Q

which population is at high risk of lithium toxicity

A

*** older adults

58
Q

what is the general dosing of lithium mg/day and when can toxicity stat (at what dose) mEq/L of blood?

A

900 – 1500 mg/d

  1. 8-1.4 mEq/L therapeutic range during acute mania
  2. 4 – 1.0 mEq/L maintenance range (toxicity can start at **1.5 mEq/L)
59
Q

what s/s should you teach pt to watch for when taking lithium

A

signs of toxicity: diarrhea, polyuria, nausea, vomiting, tremors, slurred speech, mental confusion, coma

60
Q

the effects of lithium can be seen after ___ days

because of a short half life lithium must be taken ____x day

A

Effects begin in 7-14 days

Short half life so needs to be taken 2-3x/day

61
Q

what nutritional counseling to give patients regarding lithium

A

ask them abt their daily diet, salt intake etc to determine what their dose will be
***** importance of adequate fluid and sodium intake (When decreased sodium intake, kidneys retain lithium -> toxicity)

62
Q

which of the three other meds (not lithium) emphasized for bipolar has many serious side effects and is used for rapidly cycling BPD

A

carbamazepine (tegretol)

63
Q

which other meds are used for bipolar

A
  • carbamazepine
  • valproate sodium
  • lomotrigine
64
Q

info about carbamazeipine
used for?
SE?

A

400 – 1000 mg/d
Most effective for mixed states, rapid cycling
SE’s – sedation, ataxia, aplastic anemia, agranulocytosis
Monitor for blood dyscrasias (fever, lethargy, etc)
Need to wear sunscreen – risk of dermatitis, Stevens-Johnson Syndrome (life-threatening hypersensitivity skin condition, starts with flu-like symptoms)

65
Q

which two bipolar meds can cause blood dyscrasias

A

carbamazepine and valproate

66
Q

valproate for BPD

SE to watch for

A

500 – 2000 mg/d; Highest blood level for effect. Highest dose is 60 mg/kg/d
SE’s – GI upset, weight gain, alopecia, teratogenicity, liver problems
Monitor for hepatotoxicity, thrombocytopenia
Best for mixed states, rapid cycling, secondary mania. Ineffective for depression
Selenium for hair loss
Polycystic ovary disease!

67
Q

lomotrigine for BPD
what is it
what is it used for
SE

A

Anticonvulsant, best for Bipolar depression
Improved cognition, excellent tolerance, serious autoimmune rash
Adverse Effects: blurred vision, watch for Stevens-Johnson Syndrome
Valproate interaction
12.5 to 25 mg/wk increments. Dose range of 75 to 300mg/d.

68
Q

The most serious adverse effect of tricyclic antidepressant (TCA) overdose is:

A. Seizures
B. Hyperpyrexia
C. Metabolic acidosis.
D. Cardiac arrhythmias.

A

D. Cardiac arrhythmias.

69
Q
A 17 year old client is prescribed Cipralex (escitalopram). What should the nurse monitor for?
A. Hormonal irregularities
B. Liver function
C. Effect to take place within a week
D. Suicidal ideation
A

D. Suicidal ideation

70
Q

In administration of Depakote or valproic acid what is a common concern?

A. Requirement for frequent level testing
B. Can cause potassium depletion
C. Should not be used with other heart medications
D. Should be taken in the morning

A

A
clients taking Depakote needs to have their drug levels tested as well as liver function and possibly other areas.

Depakote is another BPD med.
She says this wont be on quiz