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NSG212 > mood disorder > Flashcards

mood disorder Flashcards

1
Q

depression is secondary only to…

A

hypertension

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2
Q

are men or women more likely to have depression

A

women

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3
Q

what is the youngest age depression has been diagnosed

A

3 years old

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4
Q

what neurotransmitters are associated with depression

A

serotonin, norepinephrine, dopamine

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5
Q

what is becks cognitive triad

A
  1. negative, self-deprecating view of self
  2. pessimistic view of the world
  3. belief that negative reinforcement will continue
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6
Q

what is the stress-diathesis model of depression factors

A

learned helplessness and cultural considerations
Environmental, interpersonal, life events combined with biologial predisposition, psychological stressors that trigger brain changes

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7
Q

what is diathesis biological model

A

genetic, biochemical, alterations in hormonal regulation from biological predisposition

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8
Q

what are the subtypes observed in major depressive disorder

A 
Psychotic features
Melancholic features
Atypical features 
Catatonic features
Postpartum onset
Seasonal affective disorder (SAD)
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9
Q

what are some things someone with grief will experience

A
  1. Sadness, despair, mourning
  2. Fatigue or low energy
  3. Tears
  4. Loss of appetite
  5. Poor sleep
  6. Poor concentration
  7. Happy and sad memories
  8. Mild feelings of guilt
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10
Q

what are some things someone will MDD will experience

A
  1. Worthlessness
  2. Exaggerated guilt
  3. Suicidal thoughts
  4. Low self-esteem
  5. Powerlessness
  6. Helplessness
  7. Agitation
  8. Loss of interest in pleasurable activities
  9. Exaggerated fatigue
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11
Q

what are the 5 types of loss and grief

A

uncomplicated, acute, anticipatory, disenfranchised, and complicated or maladaptive grief

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12
Q

What are the 5 kubler ross stages of grief

A
  1. denial
  2. anger
  3. bargaining
  4. depression
  5. acceptance
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13
Q

what are worden tasks of mourning

A
  • accept reality of loss
  • process the pain of grief while caring for self
  • adjust to the world without the deceased
  • find an enduring connection with the deceased while embarking on a new life
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14
Q

how long do symptoms need to be present to be diagnosed with PDD

A

2 years or more

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15
Q

is MDD or PDD worse

A

MDD is worse

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16
Q

what does PDD stand for

A

persistent depressive disorder

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17
Q

what are these tools: becks inventory, hamilton, and zung used for

A

depression

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18
Q

what are the key assessment findings for depression (feelings)

A

anergia, low self esteem, guilt, worthlessness, helpless/hopelessness

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19
Q

what is the assessment tool used for suicide potential

A

SAFE-t

ALWAYS used

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20
Q

What things will you look for when assessing someone for depression

A

impairment in thought process- concentration, decisions and judgement
avoiding contact with others

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21
Q

what areas do you need to assess for suicide potential

A

Mood
Anhedonia (inability to experience pleasure)
Anergia (lack of energy)
Anxiety
Feelings of:
Worthlessness, guilt, helplessness, and hopelessness
Anger and irritability

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22
Q

what are the communication considerations for a depressed patient

A
  • Person with depression may speak and comprehend very slowly.
  • extreme depression a person may be mute
  • sitting with a patient is a valuable intervention
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23
Q

what are some nursing interventions for depressed patients

A

Be present. Listen.
Assess for suicide risk
Form a trusting therapeutic relationship
Encourage patient to question negative assumptions and beliefs about self.
Encourage activities to raise self esteem
Encourage formation of supportive relationships

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24
Q

what physical symptoms may a depressed patient show

A

anorexia, insomnia, self care deficits and constipation

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25
Q

what are the targeted symptoms for pharmacologic therapy

A 
Sleep disturbance
Appetite disturbance (decreased or increased)
Fatigue
Decreased sex drive
Psychomotor retardation or agitation
Diurnal variations in mood (often worse in the morning)
Impaired concentration or forgetfulness
Anhedonia
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26
Q

what types of therapy may be used for a depressed person

A

cognitive-behavioral therapy [CBT], interpersonal therapy [IPT]) and antidepressant therapy

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27
Q

what does serotonin do and what is the precursor

A

Neurotransmitter. Precursor is tryptophan found in protein foods. Sleep, appetite, pain aggression libido, hormones

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28
Q

what does norepinephrine do and what is the precursor

A

Neurotransmitter. Precursor is dopamine. Arousal, Fight or Flight, Mood

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29
Q

what does dopamine do and what is the precursor

A

Neurotransmitter. Precursor is phenylalanine found in protein foods. Fine muscle movement, emotions-thinking, hypothalamus to release hormones, pleasure response

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30
Q

what does histmaine do

A

Neurotransmitter. Alertness, inflammation, gastric secretion

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31
Q

what does tyramine do

A

Not a neurotransmitter and cannot pass the BB barrier. Vasoconstrictor, found in food– especially fermented foods. MAO in the gut break it down—unless a drug inhibits MAO

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32
Q

what category does fluoxetine (prozac) fall into

A

SSRI

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33
Q

what is a syndrome caused by prosac

A

serotonin syndrome

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34
Q

what is serotonin syndrome

A

Rare and life-threatening event

Risk greatest when SSRI is administered in combination with monoamine oxidase inhibitor (MAOI), some cold medicines

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35
Q

how does SSRIs work

A

By blocking neuronal uptake there is more serotonin left at the synapse

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36
Q

why do SSRIs take up to 6 weeks to have full effect

A

The way SSRI block reuptake is by affecting the creation of transporter molecules which carry the serotonin back to the neuron. At first, there are plenty of old transporter molecules to do the job. It takes time to clear these out.

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37
Q

what happens if you suddenly stop SSRIs

A

Withdrawal sx: dizziness, tremors, GI

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38
Q

what are the rare life threatening symotomss of serotonin syndrome

A 
Abdominal pain, diarrhea, bloating
Restlessness, fever, high b/P
Mood swings, Delirium, seizures
Tonic rigidity
Apnea, death
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39
Q

how do you stop increased risks of taking SSRIs and MAOI

A

Need to wait 5 weeks after stopping SSRI before switching to MAOI, and 2 wks if going to SSRI from MAOI

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40
Q

what are the emergency measures to stop serotonin syndrome

A
  1. Discontinue SSRI

2. Symptomatic TX

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41
Q

what are the symptomatic treatment for emergency measures of SSRI (serotonin syndrome)

A 
A. Drugs to block serotonin receptors
B. Cooling blankets. 
C. Dantrolene or diazepam for  rigidity
D. anticonvulsants
E. artificial respiration
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42
Q

what are the neurotransmitter effects of Tricyclics (TCAs) ex. Amitriptyline

A

Inhibits reuptake of serotonin and norepinephrine

43
Q

what are the adverse effects of Tricyclics (TCAs) ex. Amitriptyline

A

Cardiac

44
Q

what are the condraindications of Tricyclics (TCAs) ex. Amitriptyline

A

MI, narrow angle glaucoma, pregnancy, hx of SZ

45
Q

what are risks associated with Tricyclics (TCAs) ex. Amitriptyline

A

OD of Tricyclics is very dangerous. Be aware of suicidal risk

46
Q

what is an example of MAOIs Used Tx resistant depression and Panic DO

A

Phenelzine (Nardil)

47
Q

what are the neurotransmitter effects of MAOIs

A

monoamines

Serotonin, norepinephrine, dopamine, histamine

48
Q

what are the adverse effects of MAOIs

A

Hypertensive Crisis

49
Q

what are some of the drug and food interactions of MAOIs

A

Drugs: Avoid over-the-counter (OTC) medications.
Food: Avoid foods containing tyramines

50
Q

what are the contraindications of MAOIs

A

Liver disease, HTN, CHF, cerebrovascular disease

51
Q

MAOIs prevent breakdown of norepinephrine, serotonin, dopamine resulting in what

A

Increased levels result in increased mood

52
Q

MAOIs inhibit breakdown of tyramine in liver which causes what

A

Increased levels (tyramine) lead to HTN, hypertensive crisis, CVA, and possible death

53
Q

what does transcutaneous delivery of an MAOI with a patch called the selegiline transdermal system (STS). help in

A

At doses up to 6mg over 24 h—no tyramine restriction in diet. Higher doses still require diet.

54
Q

what is an NDRI

A

bupropion (Wellbutrin) acts on norepinephrine and dopamine

55
Q

what is an SSRIA

A

vilazodone (Vibryd) serotonin reuptake inhibitor and agonist

56
Q

what is an NASSA

A

mirtazapine (Remeron)acts on norepinephrine and serotonin

57
Q

what is an SARI

A

Nefazodone (Serzone) or Buspirone (Buspar)

58
Q

what is an SSNRI

A

Venlafaxine (Effexor) and others inhibit reuptake of serotonin and norepinephrine

59
Q

what does an Electroconvulsive therapy (ECT) do

A

Procedure (like surgery) consents, anesthesia, muscle paralytics.

60
Q

what are the potential adverse reactions of Electroconvulsive Therapy (ECT)

A

Confusion, Memory lapses

61
Q

when would Electroconvulsive Therapy (ECT) be indicated

A

Patient is suicidal or homicidal.
Agitation or stupor is extreme.
Life-threatening illness is a result of the refusal of foods or fluids.
History includes a poor drug response or a good ECT response.
Standard medical treatment has no effect.

62
Q

Bipolar spectrum disorders arecharacterized by two opposite poles:

A

mania and depression

63
Q

what are the Psychological Co-morbidity of bi polar

A

Anxiety disorders
Panic attacks
Behavioral disorders
Substance and anxiety disorders worsen the prognosis and greatly increase the risk of suicide

64
Q

what are the medical co-morbidity of bi polar

A

Cardiovascular
Cerebrovascular
Metabolic disorders
Conditions associated with manic symptoms (e.g., central nervous system [CNS] tumors or trauma, hypothyroidism, seizure disorders, human immunodeficiency virus [HIV])

65
Q

what are the biological theories of bi polar

A

Genetics
Neurobiological
Neuroendocrine
Neuroanatomical

66
Q

what are the psychological influences and cultural considerations of bi polar

A
  • Stressful life events can trigger bipolar spectrum disorders(BSDs).
  • Child abuse a factor in severity
  • Cultural differences and beliefs can
  • vastly complicate the issue.
  • Hearing voices may be seen as divine
67
Q

what are some hypomania symptoms

A
  • Talks, jokes, may be crude or sexual
  • Pressured speech
  • Mood persistently elevated, euphoric inappropriate
  • Grandiose, judgement is poor
  • Deceased attention span
  • Overactive
  • Hypersexual, voracious appetite, decreased need for sleep, financially extravagant
68
Q

what are some symptoms of acute mania

A
  • Labile Mood, good humor to rage
  • Intrusive, demanding of attention
  • Profane, sexually crude remarks
  • Flight of Ideas and clang -association (Manic Mechanic)
  • Grandiosity that is out of contact with reality, extremely poor judgement
  • Intensified distractibility and lack of attention
  • No time for sex, eating or sleep—too busy!
69
Q

what are the symptoms of delirious mania

A
  • totally out of touch with reality
  • clanging speech
  • destructive, aggressive, out of control
  • may have hallucinations, delirum
  • aimless hyperactivity- unless restrained, exhaustion, death may result
  • too disorganized to do anything
70
Q

what are the physical/safety/ personal/ legal risks for mania

A

dehydration, cardiac status, exhaustion, unable to care for self, inappropriate sexual/ financial activity, hospitalization required, may need commitment

71
Q

what is the planning for acute phase

A

medical stabilization, maintaining safety, self-care needs

72
Q

what is the planning for continuation phase of mania

A

maintaining med adherence, psychoeducational teaching, referrals

73
Q

what is the maintenance phase of mania

A

preventing relapse

74
Q

what are some of the interventions of acute mania

A 
Structure in a safe milieu
Nutrition
Sleep
Hygiene
Elimination
75
Q

Teamwork Especially Important When….

A

Patient is out of control.
Patient is using power plays with the staff.
Patient uses splitting as a way to distract staff and to loosen staff limits.

76
Q

what kind of communication do you want to use when someone is manic

A
  • Display a firm, calm approach.
  • Express short, concise explanations or statements.
  • Remain neutral.
  • Maintain consistency.
  • Conduct frequent staff meetings to agree on approach and limit setting.
  • Hear and act upon legitimate complaints.
  • Firmly redirect energy.
77
Q

Control during the acute phase of hyperactive behavior almost always includes immediate treatment with

A

antipsychotic medication. However, when a patient is dangerously out of control, seclusion or restraints may also be indicated

78
Q

what is the positive of using seclusion for manic episodes

A

Reduces overwhelming environmental stimuli.
Protects a patient from harm to self or others.
Prevents the destruction of property.

79
Q

Seclusion is warranted when documented data (collected by the nursing and medical staff) reflect the following:

A
  • Risk of harm to others or self is substantial.
  • Patient is unable to control actions.
  • Problematic behavior has been sustained.
  • Other measures (e.g., setting limits beginning with verbal de-escalation or using chemical restraints) have failed.
80
Q

what is the first line therapy for mania

A

Lithium Carbonate & Valproic Acid (Depakote)

81
Q

how does Lithium Carbonate work in the body

A

Alters sodium transport in nerve and muscle cells and inhibits the release of norepinephrine and dopamine.
but
Does not inhibit the release of serotonin.

82
Q

what are some of the expected side effects of Lithium

A 
Fine hand tremors
Polyuria
Mild thirst
Mild nausea
General discomfort
Weight gain
83
Q

what is something to be aware of when looking at side effects of lithium

A
  • Some of the expected SE are similar to s-sx toxicity!

- Ex.) fine hand tremor is expected—Coarse tremors are sign of toxicity

84
Q

what labs should you monitor if someone is taking lithium

A

serum levels

85
Q

what is therapeutic blood level of lithium

A

0.8-1.4

86
Q

what is the maintenance blood level of lithium

A

0.4-1.3

87
Q

what is the toxic blood level of lithium

A

1.5-2.0

88
Q

what are the early ss of toxicity of lithium

A

n/v/d, thirst, polyuria, slurred speech

89
Q

what are the advanced ss of toxicity of lithium

A

course hand tremor, confusion, persistent GI upset, incoordination, EEG changes

90
Q

what are the severe ss of toxicity of lithium

A

ataxia, tinnitus blurred vision, stupor, seizures… death

91
Q

what is the early level of lithium toxicity

A

<1.5

92
Q

what are the interventions of early lithium toxicity

A

withhold dose, get Li level changing dose

93
Q

what is the advanced level of lithium toxicity

A

1.5-2.0

94
Q

what are the interventions of advanced lithium toxicity

A

depend on severity

95
Q

what is the level for severe lithium toxicity

A

2.0-2.5

96
Q

what are the interventions for severe lithium toxicity

A

no antidote, emetic, gastric lavage, treatment to hasten excretion

97
Q

what are the long term effects of lithium

A

Hypothyroidism
Kidney disease
Nephrogenic diabetes insipidus

98
Q

what is the teaching for lithium

A
  • Monitor Lithium levels
  • Normal Diet, normal sodium intake
  • 6 glasses of water a day
  • Do not take diuretics
  • Stop Lithium if sweating excessively, diarrhea, vomiting—and call MD
  • Kidney function tests yearly
  • TSH level yearly
99
Q

what are some meds that are anticonvulsants

A
  • divalproex sodium, valproic acid
  • (Depakote)
  • carbamazepine (Tegretol)
  • lamotrigine (Lamictal)
100
Q

what are some anxiolytics for mania

A
  • clonazepam (Klonopin)

- lorazepam (Ativan)

101
Q

how are anxiolytics used ofr mania

A

fast acting
treatment-resistent mania
psychomotor agitation

102
Q

what are some atypical antipsychotics

A 
olanzapine (Zyprexa)
risperidone (Risperdal)
aripiprazole (Abilify)
ziprasidone (Geodon)
quetiapine (Seroquel)
103
Q

how are atypical antipsychotics used in mania

A

sedative properties

NSG212 (7 decks)

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