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Psychiatry > Psych > Flashcards

Psych Flashcards

1
Q

Depression Symptoms

A

AS
Anhedonia
Sadness

EASY
Energy
Appetite
Sleep
Yearning

ACID
Activity
Concentration
InDecisiveness

SUGR
Suicide
Unworthiness
Guilt
Rumination
SIGECAPS
Sleep (increased or decreased)
Interest (loss of)
Guilt (or other negative thoughts)
Energy (loss)
Concentration problems
Appetite (increased or decreased)
Psychomotor activity (retardation or agitation)
Suicidal thoughts
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2
Q

Depression DDx (14)

A 
Adjustment disorder w/ disturbance of mood
Persistent depressive disorder
Cyclothymic disorder
Bipolar disorder
Major depressive episode secondary to substance use or substance withdrawal
Major depressive episode secondary to medical condition
AD(H)D
Disruptive mood dysregulation disorder
Generalized anxiety disorder
PTSD
Premenstrual dysphoric disorder
Normal periods of sadness
Psychotic disorders
Borderline personality disorders
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3
Q

Psychoanalytic theory of depression:

Dysfunction

Precipitant

Key Features

A

Dysfunctional maturation

Real, threatened or perceived loss

Loss leads to anger and low self esteem; depression is “anger turned inward”

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4
Q

Behavioral theory of depression:

Dysfunction

Precipitant

Key Features

A

Dysfunctional social skills

Decrease in response contingent positive reinforcement (RCPR)

Not enough reward. dysphoria; clinical depression is a result of the secondary gain

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5
Q

Cognitive/behavioral theory of depression:

Dysfunction

Precipitant

Key Features

A

Dysfunctional attitudes and beliefs

Environmental stressor

Activation of depressogenic schema trigger negative interpretations of self/future which in turn cause other symptoms of depression

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6
Q

Learned helplessness theory of depression:

Dysfunction

Precipitant

Key Features

A

Dysfunctional attributional style

Negative events

Frequent “punishment” can cause an internalized, stable, and global interpretation of the world: specifically, a belief that your future actions will have no effect on outcome

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7
Q

Attachment theory of depression:

Dysfunction

Precipitant

Key Features

A

Dysfunctional object relations

Disrupted affectional bonds between mother and infant

Abnormal mother-infant bonding leads to disruptions in the development of object constancy, which may predispose to marked dependency needs and depression

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8
Q

MDD:

Male/Female

Age of Onset

Risks (3)

Genetic?

A

Female

30

Poverty
Life stress
Personality disorder

Yes

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9
Q

Approach to evaluating & treating mood disorders

A

DETRE

Diagnose
- consider other diagnoses

Educate
- side effects, response, treatment, prognosis

Treat
- SSRI, SNRI, DRI, 5-HT, Li, Lamotrigine, Psychotherapy

Re-Evaluate
- adherence, improvement, side effects, dose adjustment

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10
Q

Cumulative Risk Model

A

molecular and cellular factors interact with environmental and behavioral factors, with risks accumulating sufficiently in some individuals to produce clinical phenotypes

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11
Q

Serotonin (5-HT):

Origins

Involved Structures

Relevant Disorders

A

Dorsal raphe

Cortex (esp. frontal)
Thalamus
Midbrain
Basal ganglia
Cerebellum

Depression
Anxiety

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12
Q

Norepinephrine (NE):

Origins

Involved Structures

Relevant Disorders

A

Locus ceruleus

Limbic system (amygdala, hypothalamus)
Cortex
Thalamus

Depression
Anxiety

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13
Q

Dopamine (DA):

Origins

Involved Structures

Relevant Disorders

A

Ventral tegmental area (VTA)

Substantia nigra –> striatum
Tubulo-infidibular (pituitary)
Midbrain –> limbic/cortex
Nucleus accumbens

Schizophrenia
Addiction

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14
Q

HPA Axis

A

Hypothalamus –> [CRH] –> Anterior Pituitary –> [ACTH] –> Adrenal Cortex –> [Cortisol] –> Hypothalamus & Anterior Pituitary (negative feedback)

When we’re stressed & have to respond, HPA is stress response system
- in Depression, HPA turns on but doesn’t turn off

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15
Q

Yerkes-Dodson Law

A

Inverted U-shaped curve whereby low levels of anxiety yield low performance, some anxiety enhances performance, while high anxiety lowers performance again

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16
Q

Syndrome

A

A set of signs & symptoms that occur together, representative of a morbid condition

Known phenomenology

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17
Q

Disorder

A

A morbid condition w/o a known basis or pathology

Known syndrome w/ time + characteristic associations

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18
Q

Disease

A

A morbid condition w/ characteristic signs & symptoms, w/ a known etiology, pathology, or physiology

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19
Q

DSM Diagnosis

A

(1) Identify presenting symptom(s)
(2) Determine if the symptom(s) is/are clinically significant (is it a mental disorder?)
(3) Rule out secondary causes
(4) Determine specific primary disorder
(5) Add subtypes & specifiers

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20
Q

Mini-Mental State Exam

A

Component of a full mental status exam that ssess only cognitive functions

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21
Q

Anorexia Nervosa:

Epidemiology

Course

Etiology

A

2nd decade (13-18), female, Caucasian, upper/middle social classes

most lethal, chronic, depression/anxiety comorbidity, improve w/ treatment

familial, serotonin abnormalities, HPA axis abnormalities, multifactorial (psychological, social, cultural, biological/genetic), 5HT abnormalities –> dysphoria

22
Q

Bulimia Nervosa:

Epidemiology

Course

Etiology

A

mid-adolescence to late 20s, diverse socioeconomic class, female

substance use problems, fluctuating symptoms w/ varying cycles of remissions & exacerbations, seasonal, psychiatric comorbidity

multifactorial (psychological, social, cultural, biological/genetic), 5HT abnormalities –> dysphoria

23
Q

Binge-Eating Disorder:

Epidemiology

Course

Etiology

A

similar to bulimia nervosa, but less severe

impulsive eating w/ no compensatory weight loss efforts

multifactorial (psychological, social, cultural, biological/genetic), 5HT abnormalities –> dysphoria

24
Q

Monoamine Hypothesis

A

Depression / anxiety results, in part, from inadequate monoamine neurotransmitter activity in the brain (serotonin, norepinephrine, dopamine)

All antidepressnats work, theoretically, by boosting the availability of one or more of these NTs in certain circuits of the brain

25
Q

Torsades de pointes

A

Fatal arrhythmiadue to TCA overdose (no risk in SSRIs)

26
Q

Hypertensive crisis: “cheese reaction”

A

Potential problem when prescribing MAOIs
Too much dietary tyramine –> abrupt increase in pulse & BP –> acute onset of hypertension
Treat by stopping MAOI & giving meds to reduce BP

27
Q

Serotonin Syndrome

A

Dangerously high serotonin levels when mix MAOIs w/ other antidepressants
–> elevated pulse & BP, confusion, muscle stiffness, & fever

28
Q

Dopamine Hypothesis

A

SCZ

  • Excess DA neurotransmission –> positive symptoms (hallucinations, delusions, disorganization of thought)
  • Deficit in DA transmission –> negative symptoms (apathy, alogia, anhedonia, amotivation, asociality)

All antipsychotics block DA receptors (esp D2)

29
Q

DA Pathways:
Mesolimbic

Associated with…

DA receptor activity in SCZ

DA receptor activity in SCZ w/ D2 blockade

Consequence

A

Positive symptoms

Elevated

Balanced

Reduction of hallucinations, delusions

30
Q

DA Pathways:
Mesocortical

Associated with…

DA receptor activity in SCZ

DA receptor activity in SCZ w/ D2 blockade

Consequence

A

Negative symptoms

Reduced

Further reduced

Worsens negative symptoms

31
Q

DA Pathways:
Nigrostriatal

Associated with…

DA receptor activity in SCZ

DA receptor activity in SCZ w/ D2 blockade

Consequence

A

Basal ganglia, movement disorders

Normal

Reduced

Induces Parkinsonism (extrapyramidal symptoms, EPS)

32
Q

DA Pathways:
Tuberoinfundibular

Regulates…

DA receptor activity in SCZ

DA receptor activity in SCZ w/ D2 blockade

Consequence

A

Prolactin

Normal

Reduced

Can cause hyperprolactinemia

33
Q

Atypical vs. Typical Antipsychotics

A

Decreased extrapyramidal symptoms (temporary, treat w/ anticholinergics)

Decreased tardive dyskinesia (s/t permanent writhing/chorea movement, switch to milder antipsychotic)

Decreased neuroleptic malignant syndrome (all-ver muscle rigidity due to high creatinine kinase, treat w/ benzos (muslce relaxants) & DA receptor agonist)

Decreased acute dystonic reaction (sudden single muscle group contraction, treat w/ intramuscular anticholinergic)

Elevated metabolic syndrome (elevated serum glucose, serum triglycerides, & body weight, risk of diabetes)

34
Q

Major Depressive Episode:

Minimum duration of symptoms

Minimum number of symptoms

Symptoms cause marked impairment?

Psychosis may occur?

Hospitalization may occur?

May be caused by drugs or other medical conditions?

A

2 weeks

5

Yes

Yes

Yes

No

35
Q

Manic Episode:

Minimum duration of symptoms

Minimum number of symptoms

Symptoms cause marked impairment?

Psychosis may occur?

Hospitalization may occur?

May be caused by drugs or other medical conditions?

A

1 week (unless hospitalized)

3 (4 if the mood is only irritable)

Yes

Yes

Yes

No

36
Q

Hypomanic Episode:

Minimum duration of symptoms

Minimum number of symptoms

Symptoms cause marked impairment?

Psychosis may occur?

Hospitalization may occur?

May be caused by drugs or other medical conditions?

A

4 consecutive days

3 (4 if the mood is only irritable)

No

No

No

No

37
Q

Striatum D2/3 receptors

A

Decreased in number in patients w/ addiction
- less DA synthesis & transmission –> fewer DA receptors –> experience less reward, no reinforcement from natural reinforces (food, etc.)

Low receptor availability: risk factor for addiction

38
Q

Main problems with stimulants (cocaine, amphetamines)

A

Cardiovascular (hypertension, vasospasm, arrhythmias, sudden cardiac death)

Cocaethylene production if cocaine is used w/ alcohol (neurotoxic & increased risk of cardiac death, alcohol increased blood levels of cocaine by 30%)

39
Q

Main problem with opiates

A

Overdose risk

40
Q

Substance Use Disorder Recovery

A

a process of change through which an individual achieves abstinence and improved health, wellness and quality of life

41
Q

Efferent Copy Proposal

A

Hallucinations result from a breakdown in the monitoring of internal speech

We’re usually able to readily distinguish b/n external verbal material & our own internally-generated “inner speech” by making an “efference copy” that serves as a monitor

Pts w/ SCZ may not be making efferent copies & thus can’t tell the difference b/n internal/external speech, perceiving the inner speech as “alien”

42
Q

Misplaced Salience Hypothesis

A

Salience (the sense that something is important) may be driven by amygdala & other limbic inputs

In delusions, there may be a misrepresentation of salience that corresponds biologically to NMDA receptor dysfunction & the role of DA in controlling signal to noise

Pts w/ SCZ attach greater salience on events or situations which contributes to increased arousal & scanning, further reinforcing the delusional beliefs

43
Q

Cognitive dysfunction –> thought disorganization in SCZ

A

Dysfunctional excitatory-inhibitory circuits in the prefrontal cortex give rise to impairments in working memory

Pts w/ SCZ lose track of the general idea that prompted their speech and hence jump from one thought to another, without a connecting, overarching theme or goal

speech appears like “loose associations”

44
Q

Suicide Risks

A 
Male
White
Old > teen
Unmarried
Protestant
MDs > dentists
Rural
West
45
Q

Somatic Symptom:

Mechanism (conscious / unconscious)

Motivation (conscious / unconscious)

A

Unconscious

Unconscious

46
Q

Factitious

Mechanism (conscious / unconscious)

Motivation (conscious / unconscious)

A

Conscious

Unconscious

47
Q

Malingering

Mechanism (conscious / unconscious)

Motivation (conscious / unconscious)

A

Conscious

Conscious

48
Q

NE abnormalities in specific personality traits

A

Emotional reactivity
Arousal
Extraversion

49
Q

5HT abnormalities in specific personality traits

A

Inhibition of impulse / affect

50
Q

ACh abnormalities in specific personality traits

A

Lethargy
Depression
Decreased exploration

51
Q

DA abnormalities in specific personality traits

A

Novelty-seeking

Histrionic (theatrical) traits

Psychiatry (6 decks)

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