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Psych 1 Flashcards

0
Q

What does the DSM contain?

A

Explicit diagnostic criteria in a checklist format.
Multiaxial system.
Neutral regarding etiology (except adjustment disorders and disorders induced by substances or general medical conditions)

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1
Q

What is the DSM?

A

Diagnostic and Statistical Manual of Mental Disorders

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2
Q

What are the criteria of Major Depressive Disorder?

A

Must have experienced 5 of the following in a single 2-week period (one of which must be either 1 or 2)

1) depressed mood most of the day, every day
2) loss of interest or pleasure in activities
3) unintentional weight loss/ gain, appetite loss/gain
4) insomnia/hypersomnia
5) psychomotor agitation / retardation
6) fatigue or loss of energy
7) feelings of worthlessness, excessive or inappropriate guilt
8) diminished ability to concentrate
9) recurrent thoughts of death, suicidal thoughts w/ or w/o plans or suicide attempt.

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3
Q

What information does the DSM not include?

A

etiology and treatment

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4
Q

What are the axises of the DSM’s multi-axial system?

A

I: maj. clinical syndromes and other conditions
II: personality disorders / mental retardation
III: physical disorders and other conditions relevant to understanding mental disorder
IV: psychosocial and environmental factors that could influence diagnosis / treatment / prognosis
V: Global assessment of function: 0-100 scale

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5
Q

What score on DSM axis V is associated w/ inpatient admission?

A

41-50

Serious symptoms or impairment (social, occupational, school)

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6
Q

What does DSM axis V score of 1-10 indicate?

A 
persistant threat to self or others
OR
inability to maintain minimum hygeine
OR
serious suicidal act with expectation of death
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7
Q

What are the biological factors that contribute to mental illness?

A

current physical disorders and history of physical illness
prenatal history
genetic factors
medications

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8
Q

What social factors contribute to mental illness?

A

family relationships and interractions
supports and stressors
racial, religious, socioeconomic, cultural background

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9
Q

What new diagnostic categories were added to DSM V?

A

Obsessive Compulsive and related
Trauma and Stressor relate
Disruptive, Conduct, and Impulse-control

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10
Q

What psychological factors are considered in mental illness?

A

Experiences in infancy, childhood, adolescence, adulthood

current psychological strengths and weaknesses

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11
Q

What is Akathisia?

A

Subjective feeling of muscular tension -> restlessness

Often caused by 1st gen antipsychotics

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12
Q

What is Catalepsy?

A

Waxy flexibility

ex. if patient limb is positioned, patient will unconsciously keep it in that position

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13
Q

What is Cataplexy?

A

Loss of muscular tone precipitated by emotion

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14
Q

What is akathisia and what is a common cause?

A

A feeling of muscular tension that leads to physical restlessness
Side effect of 1st gen antipsychotic drugs

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15
Q

Stereotypic movement

A

Repetitive, fixed pattern of movement (hand flapping, rocking, head banging)
-intellectual disability, autism

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16
Q

Describe Expressive vs. Receptive aphasia

A

Expressive (Broca’s): motor deficit - knows what is intended, but can’t find words
Receptive (Wernicke’s): word salad - fluid, nonsensical speech. Impairment of comprehension

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17
Q

What is circumstantial vs. tangential thinking?

A

Circumstantial: person eventually gets to the point, but indirectly
-overly abundant detail

Tangential: person never gets to point - derailed on a tangent

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18
Q

In what context are visual hallucinations most common?

A

Organic illness - medical or substance related

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19
Q

What is formication?

A

Tactile hallucination

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20
Q

What are Hypnogogic and Hypnopompic hallucinations?

A

“normal” types of hallucinations
Hypnogogic: occur upon falling asleep (falling)
Hypnopompic: occur upon waking (someone in the room)

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21
Q

What is the Moro reflex?

A

Infant extends limbs when startled

Gone by 4 mos

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22
Q

Birth to 3 month milestones

A

Soc/ Lang: Smile to voice

Gross Motor: Improve head control, Follow past midline

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23
Q

4-5 month milestones

A

Social / language: Recognize parent, Coos

Gross motor: Roll over, sit propped up

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24
Q

6-7 month milestones

A

Social / language: Laugh and Babble

Gross motor: Sit unassisted, pass cube hand to hand

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25
Q

8-10 month milestones

A

Social / language: stranger anxiety, peek-a-boo, Moma / Dada (non-specific)
Gross Motor: Crawl, stand, Thumb finger grasp

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26
Q

12 month milestones

A

Social / language: Dada / Mama (specific) and first words

gross motor: walk and drink from a cup

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27
Q

Piaget’s theory of development and stages

A 
Piaget:  Cognitive
Birth - 24 month:  sensorimotor
3-6 years:  Pre-operational
8-10:  Concrete operational
11-18:  Formal operational
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28
Q

Erikson: theory of development and stages

A 
Erikson:  Psychosocial
Birth - 12mos:  Trust vs. Mistrust
1-2 yrs:  autonomy vs. shame vs. doubt
3-6 yrs:  initiative vs. guilt
6-10 yrs:  industry vs. inferiority
11-18 yrs:  identity vs. role confusion
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29
Q

Freud: theory of development and stages

A 
Freud:  psychosexual
Birth -12mos:  oral
1-2 yrs:  anal
3-6 yrs:  phallic
6-10 yrs:  latency
11-18 yrs:  adolescence
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30
Q

When in development is gender identity established?

A

Starts around 18 months, established by 24-30 mos.

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31
Q

When in development does object permanence develop and what is it?

A

Before 24 mos (part of Piaget’s Cognitive model - Sensorimotor stage)

When object disappears, child knows it still exists and will look for it.

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32
Q

What occurs in Freud’s phallic phase?

A

3-5 yrs
Genital focus
Preoccupation w/ illness and injury
Oedipal complex: focus on parent of opposite sex, competes w/ other parent for attention

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33
Q

At what point does a child understand death as final?

A

8 yrs. Prior to this, the concept of finality is not present. May understand that a person is “gone,” but expects return.

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34
Q

What is IQ? Mean IQ? Standard Deviation? Mental Retardation?

A

IQ is an objective intelligence test calculation
Mean is 100 w/ Standard deviation of 15
Mental Retardation is <70 (2 std. deviations below the mean)

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35
Q

At what stage of what theory of development do the concepts of conservation and reversibility emerge?

A

Concrete Operations (age 6-11) of Piaget’s Cognitive model

Conservation: volume remains the same in different size containers
Reversibility: water and ice are interchangeable

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36
Q

What is Freud’s Latency period?

A

age 6-11

Sexuality is repressed in favor of making same-sex friendships and participating in school and sport.

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37
Q

What is Industry vs. Inferiority?

A

Part of Erikson’s Psychosocial model. Age 5-13.
Understand’s family’s role in larger society.
Industry: strives for sense of accomplishment, sense of mastery over environment.
Inferiority: when can’t master a task

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38
Q

What is the leading cause of death in adolescents?

A

Accidents

- risky behavior, sense of indestructibility

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39
Q

The stages of early and middle adulthood include what age ranges?

A

Early: 20-40
Middle: 40-65

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40
Q

What is Erikson’s early adulthood stage?

A

Intimacy vs. Isolation (21-40)
Intimacy: must be able to make/honor commitments, sacrifice, and compromise
Without Intimacy -> Isolation -> withdrawal and depression

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41
Q

What is Erikson’s stage of middle adulthood and what ages does it include?

A

Generativity vs. Stagnation, 40-60
Generativity: provide guidance to next generation
Stagnation: no impulse to guide - unprepared for old age

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42
Q

What physical changes come with middle adulthood?

A

Decline in biological and physiological function
Medical illness (HTN, MI, Cancer)
Menopause
Change in physical appearance (wrinkles, obesity, balding)

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43
Q

What life period does phychiatric illness usually manifest?

A

Young adulthood - most are chronic
Bipolar 30
Major Depression 40
Schizo men 10-25, women 25-35 (women have 2nd peak in middle age)

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44
Q

What are the most common reasons for mortality in young adulthood?

A 
MVC
Homicide
Suicide
Other injury
Mental illness is a major risk factor for all!!
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45
Q

Cohorts in The Study of Adult Development

A

Privelaged males - Harvard grads born ~1920
Inner City males - socially disadvantaged born ~1930
Middle class, intellectually gifted women born ~1910

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46
Q

In the Study of Adult Development, what distinguishes Happy-Well from Sad-Sick?

A 
No objective physical disability at 75
Subjective physical health at 75
Longer length of undisabled life
Mental health
Social support
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47
Q

How does sleep change in old age?

A

Decreased: Total sleep time, REM %, Stages 3 and 4 sleep
Increased: Sleep latency and nightly awakenings

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48
Q

What aspects of pharmacy does aging affect?

A

Volume of Distribution
Elimination half-life

NO EFFECT ON ABSORPTION

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49
Q

3 Unipolar disorders

A

Major Depressive Disorder
Dysthymic disorder
Depressive Disorder NOS

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50
Q

What is a Dexamethasone test?

A

Given to a patient with depression or suspected depression - Dexamethasone is synthetic cortisone
In non-depressed patients, glucocorticoid synthesis is suppressed.
In depressed patients it is not (50% of pts w/ MDD)

Indicates increased liklihood of melancholia, psychotic features, and suicide.

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51
Q

What is the monoamine theory of depression?

A

Depression is result of dysregulation of monoamines:
Serotonin: people who committed suicide have low levels in CSF and low numbers of platelet uptake sites on platelets.
–Indirect evidence: SSRIs are effective
Norepinepherine: correlation between downregulation of B-adrenergic receptors and reponse to SNRIs
Dopamine: Drugs that decrease DA may induce depression. Drugs that increase DA help treat

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52
Q

At what point in development do gender differences in depression manifest?

A

Puberty

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53
Q

What gene polymorphism is linked to depression and SSRI response?

A

5-HTT : serotonin transporter

Ask what meds have worked for family members - likely to work for patient.

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54
Q

What does acute phase treatment for MDD consist of?

A

Usually 6-8 weeks w/ 2x monthly visits to monitor symptoms, medication adherence, side effects, dose adj, etc.

Antidepressants should be switched if no clear effect in 4-6 weeks

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55
Q

What is the continuation phase of MDD treatment?

A

After acute phase / pharmacotherapy : 6mos - 1 year of treatment to prevent relapse and ensure remission.

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56
Q

What is Dysthymia?

A

Less severe than MDD
Patients are depressed + 2 of:
CHASES: Concentration, Hopeless, Appetite, Sleep, Energy, Self Esteem
Symptoms most days for 2+ years (children and adolescents 1yr)

57
Q

What symptoms are missing in Dysthymia compared to MDD?

A

Anhedonia, Guilt / Worthessness, Psychomotor abnormality, suicidal ideation.

58
Q

What is premenstrual dysphoric disorder?

A

Similar to MDD symptoms associated with menstrual cycle. Symptoms present with almost every cycle with last week of luteal phase, remitting shortly after menstrution begins.

59
Q

How is PMDD treated?

A

SSRI first line pharmacotherapy (luteal vs. full cycle: no diff)
also: lifestyle: exercise, diet (decrease sodium and caffeine)
vitamin B6, E, Ca, Mg

60
Q

Define a manic episode

A

Persistently elevated, expansive, or elavated mood lasting 1 week or more plus 3 of the following (4 if only irritable)
DIG FAST
Distractability, Indiscretion, Grandiosity, Flight of Ideas, Activity Increase, Sleep deficit, Talkativeness

Impaired functioning may -> psychosis

61
Q

What is hypomanic disorder?

A

Same as manic, but shorter lived. 4 days vs. one week.

Change in function, no impairment, no psychosis

62
Q

What is a mixed episode?

A

Criteria for both MDD and Manic episode are both met (except duration) EVERY DAY for 1 week

63
Q

What is BPAD and how are types I and II defined?

A

Bipolar Affective Disorder
Type I: requires one manic episode (MDE common (80-90%), not a requirement)
Type II: must have both hypomanic and MDE w/ no history of mania or mixed episodes. Significant imparement due to MDE

64
Q

At what age does BPAD usually manifest?

A

BPAD-I: 18
BPAD-II: 20
if first manic episode at 40+ start medical work-up

65
Q

Enlarged 3rd ventricle is the most common imaging finding of what disorder?

A

BPAD

66
Q

What is the prognosis for BPAD I?

A

Worse than MDD
50-60% achieve control w/ mood stabilizers
20-30% do not remit to baseline
30% have significant social decline

67
Q

What is the prognosis for BPAD II?

A

Not well studied
Chronicity
5-15% -> BPAD I

68
Q

What is appropriate pharmacotherapy for BPAD I?

A

Lithium, Valproic Acid, Atypical and Typical antipsychotics

May need sedative for manic disorders - benzidiazapine or antypsychotic

69
Q

What is cyclothymia?

A

For 2 yrs: presence of multiple periods of hypomania and non-MDE depressive symptoms

Cannot be w/o symptoms for >2 mos.

Clinically significant distress / impairment.

70
Q

What is adjustment disorder w/ depressed mood?

A

Depressive symptoms w/in 3 months of identifiable stressor
Impairment in function. Does not meet other criteria, does not meet criteria fore bereavement.
Symptoms resolve w/in 6 mos post-stressor.

71
Q

Depression commonly precedes the diagnosis of what major illness?

A

Pancreatic cancer.

72
Q

Criteria for substance induced mood disorder

A

Symptoms during or w/in one month of intoxication or withdrawal.
If pre-existing history of recurrent mood disorder or if symptoms persist for > 1 month post - likely primary mood disorder.

73
Q

What are catatonic features?

A

Immobility, purposeless activity, negativism, mutism, posturing, stereotypies, echolalia, echopraxia

74
Q

What substances are associated with mania?

A

Cocaine/Amphetamines
Stimulants
L-Dopa
Antidepressants

75
Q

Specifiers for mood disorder with Peripartum Onset

A

Symptoms w/in 4 weeks of delivery

Major Depressive, Mania, Mixed

76
Q

What is rapid cycling in mood disorder?

A

at least 4 episodes of depressive, manic,hypomanic, or mixed within a 12 month period.

5-15% w/ BPAD
> in women

77
Q

What must be demonstrated before prescribing antidepressants?

A

Clinically significant distress or impairment of social, occupational or other important areas of functioning.

78
Q

In patients w/ significan comorbid anxiety what drug should be avoided?

A

Bupropion

79
Q

What drug treatment is recommended for depression patients w/ significant anxiety?

A

Antidepressant w/ benzodiazepine (endpoint in mind - use for 1st month while acclimating to antidepressant)

80
Q

How long does it take for full response to antidepressant therapy? Why?

A

may be improvement in 1-2 weeks

Need to wait 4-8 weeks to fully asses response. Treatment results in downregulation of receptors - takes time.

81
Q

What is the #1 risk factor for recurrence of depressive symptoms after treatment?

A

Patient being initially treated to RESPONSE rather than REMISSION.

82
Q

How should antidepressants be discontinued?

A

Taper over weeks.
May have to switch to longer half-life drug.
Plan for event of relapse
Monitor

83
Q

Does an increased blood level of SSRI increase liklihood of response?

A

No.

Increased drug level does not improve probability of response

84
Q

What SSRI has the longest half-life? How long?

A

Fluoxetine

T1/2 = 7-10 days (active metabolite)

85
Q

What are side effects of SSRIs?

A
  • side-effects generally not expected @ normal dosing*
  • GI distress: N/V/D (if persistent diarrhea - change drugs)
  • Migraine / Tension headache exacerbation (transient)
  • Sexual dysfunction, decreased libido (ejac. dysfunction, anorgasmia) - can lower dose and add bupropion
  • Weight change - esp. Paroxetine (gain)
  • Insomnia - Fluoxetine
  • Sedation - Paroxetine
86
Q

How are SSRIs metabolized?

A

All in liver, P450 (inhibition of CYP2D6)
Citalopram, Escitalopram, and Sertraline have fewest P450 interactions.
Fluvoxamine has most interactions.
Fluoxetine and Paroxetine interfere w/ opiates (prevent conversion to active form)

87
Q

What side effects are seen with SNRIs?

A

Same as SSRI (GI, Sexual, activation)
with addition of NE related
-dose dep. HTN, increased HR, sweat, dry mouth, constipation, dilated pupils

88
Q

What are some reasons for using Bupropion? When should it not be used and what are major risks?

A

Smoking cessation
No serotonergic activity: no sexual dysfunction (may improve sexual function)
Minimal weight changes

Not useful as anxiolytic
Seizure risk in high doses (above FDA dose of 450 mg)
Do not use in bulemic patients - electrolyte imbalance

89
Q

What are side effects of Mirtazapine?

A 
Sedation at LOW doses
Weight gain (anti-histamine)
Less impact on sexual function than SSRI and SNRI
90
Q

What is Vilazadone’s MOA?

A

SSRI + 5-HT1A agonism

Has more GI side effects than other SSRIs
supposedly fewer sexual side effects, but flawed study - looked at patients w/ depression related SD

91
Q

What is Trazadone used for? Side effects?

A

Infrequently used as antidepressant. Used for insomnia.
SSRI + 5-HT2 agonist
Higher doses - orthostatic hypotension and priapism

92
Q

What is the TCA MOA?

A

Block NET and SERT - SNRI like activity
Antagonize a1, histamine, muscarinic Ach receptors

-potentially fatal in OD

93
Q

What are TCAs used for?

A

Depression

Migraine, neuropathies, enuresis, trigeminal neuralgia

94
Q

What are TCA side effects?

A

Antihistamine: weight gain, sedation
Antiadrenergic: orthostatic hypotension, dizziness
Anticholinergic: dry mouth, constipation, urinary hesitancy, blurred vision, agg. narrow angle glaucoma, sedation

Cardiac (Na+ channels): tachycardia, flat T wave, QT prolong, depress ST

    • baseline EKG if over 40 or cardiac hx
    • no subsequent monitoring unless new symptoms
95
Q

What is the physiological distribution of MAOs?

A

MAO-A and -B in brain

MAO-A major MAO outside of the brain

96
Q

How can MAOi use result in hypertensive crisis? How is it treated?

A

MAO-A inhibition can -> tyramine induced NE released in gut -> HTN
treated with alpha-antagonist: phentolamine

97
Q

What is the 2 week rule of antidepressants?

A

Must wait 2 weeks before administering a restricted drug (interactions) or eating a restricted food.

Exception: fluoxetine - long half-life - must wait 5 weeks to start MAOi after stopping fluoxetine

98
Q

What is electroconvulsive therapy recommended for?

A

Drug resistant MDD, bipolar, or acute onset schizophrenia

  • -2+ medication failures
  • -acute suicidality

70% response in treatment-resistant patients.

99
Q

How should Lithium levels be monitored in patient? What is the range of therapeutic concentrations?

A

0.6-1.2 mEq/L
Draw 12 hrs. after last dose.
Check at start of treatment, then every 3-4 months until stable, then every 6 months.

100
Q

What is Ebstein’s Anomoly and what is it associated with?

A

Tricuspid valve is licated toward apex of RV. May be ASD present.
Associated with Lithium used in first trimester of preg.

101
Q

What are the 3 levels of consciousness in the topographic theory of the mind?

A

Conscious: what you are aware of
Preconscious: can become aware w/ effort
Unconscious: can not become aware of - still influential

102
Q

How is the topographic model inadequate?

A

Does not address reasons behind symptoms and treatment

103
Q

What are the elements of the structural model?

A

Ego: conscious and unconscious aspects. Moderates Id and Superego. Descision making.
Id: completely unconscious. Sex and Aggression.
Superego: mostly unconscious. conscience and values.

104
Q

What is transferrance? Countertransferrance?

A

Unconscious redirection of feelings/ desires from the past toward the therapist.

Countertransferrence: reverse - therapist projects feelings toward patient

105
Q

What is psychodyanamic therapy?

A

based on Freud’s theory of uncovering unconscious aspects of patient’s life leading to greater self-understanding

Focus on: unconscious conflicts, repressed feelings, family issues from early life, difficulty w/ current relationships

106
Q

What is psychoanalysis?

A

Most intensive and rigorous form of psychotherapy.
3-6 sessions / week
Treated by psychoanalyst
pt. on couch, therapist behind

107
Q

What is behavioral therapy?

A

Use of classical and operant conditioning to directly change maladaptive behavior.

Improve symptoms w/o focusing on underlying history

108
Q

What are the 3 main parts of systematic desensitization?

A

Relaxation: learn techniques
Heiarchy: establish heiarchy of anxiety provoking stim.
Desensitization: apply relaxation to imagined scenes in therapy sessions

109
Q

Graded exposure vs. systematic desensitization

A

Systematic desensitization: walk through imagined scenes in therapy

Graded exposure: same system, but practiced in real life. Patient has “homework”

110
Q

Flooding vs. Implosion therapy

A

Flooding: patient is exposed to real-life stimulus w/o ability to escape - belief that escape contributes to anxiety. W/o escape, patient sees that situation is survivable and fear decreases.

Implosion: same idea, but imagined in setting of therapy.

111
Q

Describe Cognitive Behavioral Therapy

A

Combines Cognitive and Behavioral therapy
Psychopathology is the product of distorted thinking which negatively impacts behavior and mood.
Collaborative, goal oriented.
Cognitive: recognize, discuss, challenge automatic thoughts
Behavioral: apply relaxation techniques, graded exposure, etc.

112
Q

What is dialectical behavioral therapy?

A

Specific to treatment of Borderline Personality Disorder
Individual + group therapy.
Patients seen weekly for about a year
goals:
Reduce self-destructive / injurious behavior
Improve interpersonal skills

113
Q

What does “psychotic” mean?

A

Hallucinaton
Delusion
Disorganized speech and behavior

114
Q

What is the cause of positive psychotic symptoms?

A

Malfunction in mesolimbic system

115
Q

What is the cause of negative symptoms?

A

Defect in Mesocortical or prefrontal cortical.

Problem with nucleus acumbens reward pathway likely

116
Q

What does schizophrenia consist of?

A

2 or more of the following for 1 month:
Hallucination
Delusion
Disorganized speech
Grossly disorganized or catatonic behavior
Negative symptoms

Or only 1 if bizarre delusions, continuous commentary hallucinations, 2 or more voiceds conversing

117
Q

How does NMDA hypofunction explain schizophrenic symptoms?

A

In mesolimbic path: Glutamate -> NMDA -> GABA -> inhibit DA release
in schizo: NMDA does not inhibit DA: elevated DA -> (+) symptoms

Mesocortical path: No GABA interneurons! Glutamate -> NMDA -> DA release
schizo: Glutamate -> NMDA -> decreased DA release -> (-) symptoms

118
Q

What is schizophreniform?

A

Same criteria as Schizophrenia, but only 1-6 mos.
Most go on to Schizophrenia.
Does not require decline in functioning, though it may be present.

119
Q

Describe schizoaffective disorder

A 
Schizo symptoms (2+ for 1 month) + mood disorder
preceeded or followed by 2 weeks of delusions or hallucinations w/o mood disorder
120
Q

what constitutes deusional disorder?

A

1 month of non-bizarre delusions
No marked impairment of judgement or function
Normal behavior.

121
Q

What are the treatments for EPS in patients on antipsychotic therapy? (Parkinsonism, Acute dystonia, Akathisia)

A

Parkinsonism: PO anticholinergic - Benztropine
Acute dystonia: IM or IV anticholinergic - Benadryl
-once stable, PO Benztropine
Akathisia: Beta blocker, Benzodiazapine, Anticholinergic

122
Q

In patients taking antipsychotics, what causes tardive dyskinesia?

A

Chronic DA blockade -> upregulation of receptors

Takes >6 mos. to develop, irreversible

123
Q

What symptoms accompany increased prolactin in patients on antipsychotics?

A

Galactorrhea, amenorrhea, poor fertility, sexual dysfunction, demineralization of bone.

124
Q

What is Neuroleptic Malignant Syndrome?

A

Potentially fatal side effect of antipsychotics
Muscle rigidity, hyperthermia, diaphoresis, dysphagia, tremor, incontinence, altered consciousness, mutism, tachycardia, elevated or labile BP

125
Q

How is NMS treated?

A

Neuroleptic Malignant Syndrome

  • Dantrolene
  • DA agonist
126
Q

What is the effective treatment for drug-resistant schizophrenia?

A

Clozapine - atypical antipsychotic
Used when failure of 2+ other drugs.
Risk: agranulocytosis
Also - weight gain, diabetes, myocarditis

127
Q

How is clozapine use monitored?

A

CBC every week for 6mos, then every 2 weeks.

128
Q

What did the CATIE study reveal about antipsychotics?

A

Olanzapine most effective despite side effects

Perphenazine (mid-potency typical) as effective as atypicals except olanzapine

129
Q

What part of brain is particularly associated w/ anxiety disorder?

A

Amygdala
Basal nucleus -> coping
Central nucleus -> passive fear (anxiety)

130
Q

What is the basis of the neurochemical model of anxiety?

A

NE, 5-HT and GABA antagonist administration can induce panic attacks
NE and 5-HT neurons promect to limbic cortex - implicated in anxiety
Benzodiazepine efficacy (via GABA potentiation) - supports idea.

131
Q

What medical disorders need to be ruled out before diagnosing anxiety?

A

cardiomyopathy
endocrinopathy
respiratory disease

132
Q

What medications are associated with casuing anxiety?

A

Beta blocker withdrawal

corticosteroids

133
Q

What drug is most effective for panic disorder?

A

Paroxetine

SSRI

134
Q

What drugs are useful for treating social phobia disorder?

A

Paroxetine
Beta blockers - for specific performance anxiety situations
Benzodiazepines - not useful for comorbid depression. Care in pts. w/ drug/alcohol use

135
Q

PTSD criteria and symptoms

A

Traumatic event must involve death, serious injury, or threat.
Reaction must include intense fear, helplessness or horror.
Re-experiencing
Avoidance of stimuli assoc. with trauma and numbing of general responsiveness
Persistent increased arousal.

136
Q

What is treatment for PTSD?

A

Anxiety mgt
Antidepressant
Psychotherapy
Lifetstyle mgt.

137
Q

What is first line treatment for anxiety disorders?

A

SSRI, but not bupropion

138
Q

What benzodiazepines avoid liver metabolism?

A

Oxazepam
Temazepam
Lorazepam

Metabolized by glucoronidation only - not microsomal oxidation
Good for liver disease and elderly patients

139
Q

What is treatment for insomnia?

A

Meds are not first line therapy
First: Review underlying causes - mental illness, medication
Consider sleep hygeine

140
Q

What medications may be used to treat insomnia?

A

Benzodiazepines - short term use.
decreases time to sleep onset, increases duration of sleep.
may experience rebound insomnia upon withdrawal - taper meds.

Non-benzo receptor agonists (Zolpidem, Zaleplon, Eszopliclone)
-lack other benzo properties, retain sedative-hypnotic effect.

M2 (19 decks)

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