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B&B Part 2 > B&B Week 5 > Flashcards

B&B Week 5 Flashcards

1
Q

where is the hypothalamus located?

A

inferior to the thalamus and forms the walls and floor of the inferior portion of the third ventricle

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2
Q

how is the hypothalamus divided functionally?

A

can be divided into functional areas of nuclei along a lateral/medial axis and anterior/posterior axis

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3
Q

what is the function of the hypothalamus?

A

main regulator of homeostasis in the body

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4
Q

what is the function of the lateral region of the hypothalamus?

A

carries two way signals between forebrain and brainstem

eating, arousal

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5
Q

what is the function of the medial zone of the hypothalamus?

A

most functionally important nuclei are here

ADH secretion, satiety, GH secretion

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6
Q

what is the function of the anterior zone of the hypothalamus?

A

cooling of body temp, sleep, eating

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7
Q

what is the function of the posterior zone of the hypothalamus?

A

up regulation of body temp

arousal

wakefulness

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8
Q

what are the afferents that feed into the hypothalamus?

A

general somatic, visceral, gustatory information from SC and brainstem

limbic afferents–> from hippocampus (via fornix to mamillary bodies) and from amygdala

olfactory info

cortical info from forebrain

thalamus

retinal collaterals

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9
Q

what are the efferents that flow from the hypothalamus?

A

descending fibres to brainstem and spinal cord (visceral motor nuclei)

ascending fibres to forebrain

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10
Q

what is the function of the limbic system?

A

together with the hypothalamus, the limbic system provides an anatomical substrate for emotional, drive related and motivated aspects of behavior

comprises both cortical and subcortical structures

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11
Q

what are the cortical structures associated with the limbic system?

A

LIMBIC LOBE–> parahippocampal, cingulated and subcallosal gyri, which are interconnected by the cingulum

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12
Q

what are the subcortical structures associated with the limbic system?

A

hippocampus, amygdala, septal nuclei

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13
Q

what structure gives rise to the efferents that carry limbic information out into the forebrain, brainstem and spinal cord?

A

hypothalamus

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14
Q

where is the hippocampus?

A

cortex, in the medial temporal lobe

forms the floor of the lateral ventricle

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15
Q

what is the hippocampus responsible for?

A

learning and memory

it is informed of all sensations

regulates behavior, autonomic function, and endocrine function

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16
Q

where is the amygdala found?

A

deep within the uncus, rostral to the hippocampus

sits above and in front of the temporal horn of the lateral ventricle and is anterior to the tail of the caudate nucleus

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17
Q

what are the following portions of the amygdala responsible for?

  1. basolateral nuclei
  2. central nuclei
  3. corticomedial nuclei
A
  1. emotional significance to a stimulus–> integrates sensory information
  2. regulate visceral responses to emotional stimuli (fight/flight, physiological changes due to emotional state)
  3. smell of food and emotional response to food (appetite) and also release of cortisol
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18
Q

where are the septal nuclei located?

A

medial wall of the frontal lobe

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19
Q

what do the septal nuclei connect to?

A

olfactory bulb, hippocampus, amygdala

cholinergic neurons that have projections to hypothalamus, amygdala, hippocampus and frontal cortex

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20
Q

what does the papez circuit do?

A

experience of emotion involves reciprocal interactions between cortex and diencephalon

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21
Q

what structures are considered part of the limbic system?

A

hypothalamus (though it is structurally part of the diencephalon, the hypothalamus is functionally part of the limbic system), hippocampus, amygdala, septal nuclei, (papez circuit), parahippocampal, cingulated and subcallosal gyri

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22
Q

what structures make up the papez circuit?

A

mammillary bodies–> thalamus anterior nuclei–> cingulate cortex–> hippocampus–> back to mammillary bodies

each of these communicates with other structures

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23
Q

what are the key neurotransmitters of the limbic system and the hypothalamus?

A

NE, dopamine, serotonin

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24
Q

what physiological systems do the hypothalamus and the limbic system regulate in order to maintain homeostasis?

A
  1. endocrine secretion
  2. autonomic function
  3. homeostatic functions
    - thermoregulation
    - food intake
    - body water regulation
    - fluid balance
    - blood pressure
    - sleep wake cycles/circadian rhythms
  4. basic drives
    - motivation
    - goal oriented behaviors
    - emotional behaviours
  5. learning and memory (hippocampus only)
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25
Q

what is the role of the hypothalamus in the limbic system?

A

typically acts as the effector of the limbic system

the fornix columns cut through the hypothalamus on their pathway to the mammillary bodies, dividing it into medial and lateral areas

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26
Q

what are the mammillary bodies?

A

distinct nuclei located in the posterior part of the hypothalamus

they receive information from the hippocampus and reciprocally relay to the anterior hypothalamic nuclei and the midbrain

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27
Q

what are the three regions of the medial nuclei of the hypothalamus and what nuclei are found in each region?

A
  1. anterior/preoptic–> preoptic, suprechiasmatic, supraoptic, paraventricular, anterior nuclei
  2. middle/tubercle–> dorsomedial, ventromedial, arcuate nuclei
  3. posterior–> mammillary bodies, posterior nuclei
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28
Q

describe the lateral nuclei of the hypothalamus

A

diffuse nuclei

long fibre tracts passing through and interconnecting the hypothalamus with rostral areas and brainstem

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29
Q

list the functions of the hypothalamus

A
  1. regulation of endocrine function
  2. regulation of autonomic function
  3. temperature regulation
  4. food intake regulation
  5. regulation of sleep/wake cycle and circadian rhythm
  6. reproduction and sexual function
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30
Q

how does the hypothalamus perform the following function?

regulation of endocrine functon

A

supraoptic and paraventricular nuclei produce hormones and they are stored in the posterior pituitary

releasing/inhibiting hormones are released that control anterior pituitary hormone production and release

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31
Q

how does the hypothalamus perform the following function?

regulation of autonomic function

A
  1. anterior hypothalamus activates parasympathetic response

2. posterior hypothalamus activates sympathetic response

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32
Q

how does the hypothalamus perform the following function?

temperature regulation

A

temperature sensitive neurons respond to skin and core body (blood) temp via:

  1. activating heat loss centre in anterior hypothalamus (resulting in cutaneous vasodilation and sweating) or
  2. by activating the heat gain center in the posterior hypothalamus (resulting in peripheral vasoconstriction, shivering)
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33
Q

how does the hypothalamus perform the following function?

food intake regulation

A

the feeding center is located in the lateral hypothalamus

satiety center is in the ventromedial nucleus

both areas integrate signals to affect feeding and drinking

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34
Q

how does the hypothalamus perform the following function?

regulation of sleep/wake and circadian rhythms

A

suprachiasmatic nucleus regulates the circadian rhythms (i.e with input from retina, +++serotonin innervation)

lesions result in abnormal sleep patterns

i.e anterior hypothalamus lesion leads to insomnia
posterior hypothalamus lesion leads to impaired wakefulness

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35
Q

how does the hypothalamus perform the following function?

reproduction and sexual function

A

neurons in the preoptic nucleus and the ventromedial nucleus are sensitive to estrogens and androgens–> involved in signalling hormone secretion and activating behavior

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36
Q

structurally, what is the limbic system?

A

a ring of cortex on the medial surface of the cerebral hemisphere and includes the:

  1. cingulate gyrus (just above the corpus collosum)
  2. parahippocampal gyrus (medial gyrus of the temporal lobe)
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37
Q

where is the entorhinal cortex found and what does it do?

A

the entorhinal cortex is found in the anterior part of the parahippocampal gyrus of the limbic system

it is responsible for receiving cognitive and sensory information from cortical association areas

this cortex transmits information to the hippocampal formation for consolidation and subsequently returns it to the association areas where it is encoded as memory traces

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38
Q

that structures are included in the hippocampal formation?

A
  1. hippocampus
  2. dentate gyrus

*these structures are characterized by their S shaped scroll/seahorse shape and are located on the floor of the lateral ventricle deep to the parahippocampal gyrus in the temporal lobe

the hippocampus is composed of several 3 layered areas of cortex that are rolled upon one another

nerve fibres originating from the hippocampus converge to form the FIMBRIA –> the fornix is a continuation of these fimbriae, receiving axons from the hippocampus

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39
Q

describe the course of the fornix

A

it is a continuation of the fimbriae that originate in the hippocampus

the fornix follows the course of the lateral ventricles with most fibres terminating anteriorly in the mammillary bodies of the hypothalamus

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40
Q

where does the dentate gyrus lie?

A

between the fibriae of the hippocampus and the parahippocampal gyrus

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41
Q

what shape are the amygdalae?

A

almond shaped

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42
Q

what does the hippocampus do?

A

learning and forming new memories

likely to be an initial storage site for memories

believed to be an encoding area that translates short term memories into long term memories

the overlying cortex is also involved in memory function

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43
Q

what happens if both medial parts of the temporal lobes are removed?

A

one cannot form new memories regarding facts or events and this condition is less severe if the overlying cortex is intact

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44
Q

what is the function of the amygdalae?

A

emotional learning and modulation of fear, anxiety, rage and aggression

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45
Q

what happens if there is bilateral amygdala damage?

A

Kluver-Bucy syndrome

characterized by changes in

  1. aggression (if complete, you get docility and fearlessness. if partial you get bursts of aggression)
  2. emotional depression
  3. visual agnosia
  4. hypersexuality
  5. inappropriate attention to sensory stimuli
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46
Q

what is the definition of normal personality?

A

personality refers to the combination of characteristics or qualities that form an individual’s distinct character

it is a complex pattern of deeply embedded psychological characteristics expressed in behaviors

internal characteristic

relatively constant over time

includes both biological (temperament) and learned (character) elements

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47
Q

list the 5 personality dimensions

A
  1. openness to experiences
  2. conscientiousness
  3. extraversion
  4. agreeableness
  5. neuroticism
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48
Q

what are the defining characteristics and antagonistic characteristics associated with the following personality dimension?

openness to experiences

A

defining: intellectual, creative, insightful
antagonistic: shallow, unimaginative, unreflective

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49
Q

what are the defining characteristics and antagonistic characteristics associated with the following personality dimension?

conscientiousness

A

defining: organized, efficient, dependable, perfectionist, persistent
antagonistic: careless, erratic, forgetful

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50
Q

what are the defining characteristics and antagonistic characteristics associated with the following personality dimension?

extraversion

A

defining: sociable, expressive, spontaneous, energetic, verbose
antagonistic: withdrawn, silent, shy, inhibited

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51
Q

what are the defining characteristics and antagonistic characteristics associated with the following personality dimension?

agreeableness

A

defining: cooperative, amiable, empathetic, respectful
antagonistic: antagonistic, harsh, impolite

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52
Q

what are the defining characteristics and antagonistic characteristics associated with the following personality dimension?

neuroticism

A

defining: insecure, self-critical, anxious, touchy, excitable, jealous
antagonistic: unemotional, autonomous

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53
Q

define personality disorder

A

an enduring patterns of inner experience and behaviour that deviates markedly from expectations of individuals culture in at least two areas: cognition, affectivity, interpersonal functioning, impulse control

this enduring pattern is:

  • inflexible and pervasive
  • causes subjective distress or functional impairment
  • is stable and of long duration
  • is not due to substance use or a general medical condition (i.e head trauma)

the personality disorders are grouped into three clusters based on descriptive similarities

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54
Q

what are the 3 clusters of personality disorders?

A
  1. Cluster A: paranoid, schizoid and schizotypal personality disorders
  2. Cluster B: antisocial, borderline, histrionic and narcissistic personality disorders
  3. Cluster C: avoidant, dependent, and obsessive compulsive disorders
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55
Q

how might someone appear that has a Cluster A personality disorder?

A

Cluster A: paranoid, schizoid and schizotypal personality disorders

individuals with these disorders may appear odd or eccentric

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56
Q

how might someone appear that has a Cluster B personality disorder?

A

Cluster B: antisocial, borderline, histrionic and narcissistic personality disorders

individuals with these disorders may often appear dramatic, emotional or erratic

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57
Q

how might someone appear that has a Cluster C personality disorder?

A

Cluster C: avoidant, dependent, and obsessive compulsive disorders

individuals with these disorders may appear anxious or fearful

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58
Q

why is the clustering system for personality disorders not always the best?

A

because it has not been consistently validated and individuals frequently present with co-occurring disorders from different clusters

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59
Q

what is the key personality pattern of a paranoid personality disorder? what would the medical presentation of the patient be?

A

cluster A

key personality pattern: distrust, suspicious, guarded, self righteousness such that others’ motives are interpreted as malevolent

presentation: “you have nothing to offer me”

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60
Q

what is the key personality pattern of a schizoid personality disorder? what would the medical presentation of the patient be?

A

cluster A

key personality pattern: detachment from social relationships and a restricted range of emotional expression

presentation: indifferent, remote, does not connect

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61
Q

what is the key personality pattern of a schizotypal personality disorder? what would the medical presentation of the patient be?

A

cluster A

key personality pattern: acute discomfort in close relationships, cognitive or perceptual distortions, and eccentricities of behavior

presentation: odd, may blur reality and fantasy, difficult to report symptoms

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62
Q

what is the key personality pattern of a antisocial personality disorder? what would the medical presentation of the patient be?

A

cluster B

key personality pattern: disregard for, and violation of, the rights of others

presentation: superficially charming, hostile when confronted

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63
Q

what is the key personality pattern of a borderline personality disorder? what would the medical presentation of the patient be?

A

cluster B

key personality pattern: instability in interpersonal relationships, self-image, and affects; marked impulsivity

presentation: unpredictable, impulsive, suicide risk

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64
Q

what is the key personality pattern of a histrionic personality disorder? what would the medical presentation of the patient be?

A

cluster B

key personality pattern: excessive emotionality and attention seeking behavior

presentation: “everything hurts all over”

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65
Q

what is the key personality pattern of a narcissistic personality disorder? what would the medical presentation of the patient be?

A

cluster B

key personality pattern: grandiosity, need for admiration, lack of empathy

presentation: “i am special; my problem is unique”

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66
Q

what is the key personality pattern of a avoidant personality disorder? what would the medical presentation of the patient be?

A

cluster C

key personality pattern: social inhibition, feelings of inadequacy, hypersensitivity

presentation: hesitant, embarrassed, self conscious

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67
Q

what is the key personality pattern of a dependent personality disorder? what would the medical presentation of the patient be?

A

cluster C

key personality pattern: submissive and clinging behaviour related to an excessive need to be taken care of

presentation: seeks constant reassurance and feedback

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68
Q

what is the key personality pattern of a obsessive-compulsive personality disorder? what would the medical presentation of the patient be?

A

cluster C

key personality pattern: preoccupation with orderliness, perfectionism, control

presentation: “i have researched by symptoms extensively”

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69
Q

how are psychiatric disorders diagnosed?

A
  1. take a full hx of HPI, PMI, meds, social hx, family hx etc…
  2. general and detailed physical exam with focus on presenting symptoms
  3. include a neuro exam to get a sense of brain, nerves, muscles
  4. psychiatric exam–> determine person’s mental condition; MSE is an important part of the clinical assessment process
  5. diagnosis of psych disorders involves use of the DSM V
    * DSM IV and earlier used an axial diagnosis system–> DSM V has no axes
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70
Q

why is the mental status exam (MSE) an important part of the psychiatric clinical assessment process?

A

because it provides a structured way of observing and describing a patient’s current state of mind, under the domains of appearance, attitude, behaviour, mood and affect, speech, thought process, thought content, perception, cognition, insight and judgement

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71
Q

what is the purpose of performing the MSE as part of the psych assessment?

A

obtain a comprehensive cross-sectional description of the patient’s mental state which, when combined with the biographical and historical information of the psych hx, allows the clinician to make an accurate diagnosis and formulation, which are required for coherent treatment planning

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72
Q

briefly state what each axis stood for in DSM IV

A
  1. axis I–clinical syndromes (i.e depression, schizophrenia)
  2. axis II–developmental disorders and personality disorders (i.e autism, mental retardation//paranoid, borderline)
  3. axis III–physical conditions which play a role in the development, continuance or exacerbation of axis I and II disorders (i.e brain injury or HIV/AIDS)
  4. axis IV–severity of psychosocial stressors
  5. axis V–global assessment of functioning
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73
Q

what are the fundamental features of an anxiety disorder?

A

unwanted emotions (panic attacks), thoughts (obsessions) and actions (avoidance)

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74
Q

list the different types of anxiety disorders

A
  1. panic/agorophobia
  2. phobic disorders
  3. trauma-related disorders
  4. OCD
  5. generalized anxiety disorder
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75
Q

what is panic/agorophobia disorder?

A

recurrent, discrete periods of intense fear or discomfort with 4 or more of the following:

  1. palpitations
  2. tachycarida
  3. sweating
  4. trembling
  5. dyspnea
  6. choking
  7. chest pain
  8. nausea
  9. chills/hot flashes
  10. dizziness
  11. derealization
  12. fear of losing control
  13. fear of death
  14. paresthesias
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76
Q

what are the types of panic/agorophobia disorders?

A
  1. unexpected
  2. situationally bound (always occur)
  3. situationally predisposed (sometimes)
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77
Q

define agorophobia

A

fear of being in a place that may be difficult to escape from in case of a panic attack

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78
Q

what are the types of phobic disorders?

A

either specific phobia or social phobia

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79
Q

what are examples of specific phobic disorders?

A

severe, excessive, persistent fear; typically avoided, recognized as irrational

can be due to animals, nature, situational, blood-injection injury and others

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80
Q

what are social phobia disorders?

A

severe, persistent fear of social interactions and performance in social situations

can be generalized (most social situations) or specific (i.e only if a meal is served)

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81
Q

name two trauma-related anxiety disorders

A

PTSD and acute stress disorder

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82
Q

what is PTSD?

A

anxiety disorder

must have been exposed to trauma, and have been having the following sx for the past year:
re-experiencing
avoidance and numbing
hyperarousal

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83
Q

what is acute stress disorder?

A

anxiety disorder

must have been exposed to trauma, other PTSD syx but less than one month

emotional numbing, reduced awareness, derealization, depersonalization, dissociative amnesia

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84
Q

what is obsessive compulsive disorder?

A

anxiety disorder

obsessions–> unwanted, recurrent thoughts, actions or images, “ego-dystonic”

compulsions–> repetitive behaviours intended to reduce stress or prevent harm

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85
Q

what is generalized anxiety disorder?

A 
excessive anxiety lasting more than 6 months, associated with:
restlessness
tension
difficulty concentrating
irritability
insomnia
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86
Q

what is the etiology of anxiety disorders?

A

typically chronic and arise in stressful life situations

more common in WOMEN (except for OCD which is equal)

often associated with other anxiety disorders, mood disorders, substance abuse and EDs

genes and environment interact with each other and independently predispose to anxiety disorders

both conditions fear reactions and maladaptive beliefs play a role (i.e some is learned)

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87
Q

what is the pathophysiology of anxiety disorders? i.e what neural structures and neurotransmitters are involved?

A

limbic system is important, especially the AMYGDALA

neurotransmitters: GABA, serotonin (raphe nucleus) and NE (locus ceruleus)

complex interaction between several brain areas (cortex, amygdala, hippocampus, HPA axis)

OCD–> orbitofrontal cortex has interactions with amygdala and basal ganglia

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88
Q

what are the cognitive pathways associated with anxiety disorders?

A

anxiety sensitivity–> fear of fear, due to beliefs about consequence of being afraid (i.e ridicule)

stimulus–> perceived threat–> apprehension–> body sensation–> interpretation of sensations

tendency in panic disorder to overanalyze body sensations which creates more panic–> vicious cycle

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89
Q

what is the treatment for anxiety disorders?

A

take into account patient preference, addiction potential and relapse rates etc…

meds: SSRIs, benzodiazepines

CBT: especially through exposure therapy and cognitive restructuring

combination

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90
Q

what are the risk factors for mood disorders?

A
  1. family member with mood disorder
  2. women more than men
  3. care taking position
  4. history of abuse
  5. stress
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91
Q

what role does genetics play in mood disorder risk?

A

highly heritable, especially in bipolar disorders

common genes exist for schizophrenia and bipolar

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92
Q

what is the pathophysiology of mood disorders?

A

most convincing evidence involved 5-HT1A receptors

HPA axis could play a role (as it controls cortisol and circadian rhythms)–> depressed patients are shown to be hypercortisolemic and have bigger pituitary glands, bigger adrenal glands and increased CRH

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93
Q

what are the subtypes of mood disorders?

A
  1. depressive disorders (unipolar depression)
  2. bipolar disorders
  3. other mood disorders
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94
Q

list the types of depressive disorders

A
  1. major depressive disorder
  2. dysthymic disorder
  3. minor depression
  4. DDNOS
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95
Q

what are the characteristics of major depressive disorder?

A

2 or more weeks of depressed mood plus anhedonia (inability to feel pleasure) plus 4 other depressed symptoms

physical symptoms–> appetite change, sleep disturbance, psychomotor agitation, low energy

psychological symptoms–> guilt, suicidal ideation, poor concentration

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96
Q

what is dysthymic disorder?

A

2 or more years of depressed mood on most days with other depression symptoms

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97
Q

what is minor depression?

A

fewer symptoms than major depression and shorter time span; meds are not effective

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98
Q

what is DDNOS?

A

doesnt meet criteria for major or minor depression or dysthymic

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99
Q

what is the treatment for depressive disorders?

A

psychotherapy for all types

antidepressants for major depression and dysthymia

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100
Q

list the types of bipolar disorders

A
  1. bipolar I disorder
  2. bipolar II disorder
  3. cyclothymic disorder
  4. BDNOS
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101
Q

what is bipolar disorder I?

A

1 or more manic or mixed episode followed by a major depressive episode

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102
Q

what is bipolar disorder II?

A

1 or more major depressive episode followed by 1 or more hypomanic episode

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103
Q

what is cyclothymic disorder?

A

2 or more years of episodes of hypomania and depression (less than major depression)

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104
Q

what is BDNOS?

A

doesnt meet criteria for bipolar I/II or cyclothymic

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105
Q

what are manic episodes?

A

last more than 1 week with the following sx:

physical–> irritable, risk taking, pressured speech, decreased sleep, functional impairment

psychological–> grandiosity, flight of ideas or racing thoughts, goal directed actions

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106
Q

what are hypomanic episodes?

A

same sx as mania but less severe–> last about 4 days

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107
Q

what is the natural history of bipolar disorders?

A

early onset, lifelong relapse, high rates of depression and suicide

108
Q

what is the tx for bipolar disorders?

A

usually need a mood stabilizer before antidepressant to decrease risk of rapid cycling

109
Q

what are two other types of mood disorder?

A

mood disorder due to general medical condition

substance induced mood disorder (i.e medication, drug of abuse, toxin etc)

110
Q

what is normal depression?

A

normal reaction to a life event, normal functioning should return in less than a year

usually returns within weeks or months

111
Q

what is the lifetime prevalence of the following anxiety disorders?

  1. panic disorder
  2. agorophobia
  3. specific phobia
  4. social phobia
  5. PTSD
  6. OCD
  7. BAD
A
  1. 1-2%
  2. 1-2%
  3. 7-11%
  4. 3-13%
  5. 8%
  6. 2.5%
  7. 5%
112
Q

what is the lifetime prevalence of major depression and bipolar disorder?

A

major depression:
10% men
20% women

bipolar:
1-2%

113
Q

what is the hypothesized abnormality underlying schizophrenia?

A

due to functional EXCESS of dopamine

114
Q

based on the hypothesized abnormality underlying schizophrenia, what is the most appropriate pharmacological intervention?

A

use a dopamine receptor antagonist to block synaptic transmission of dopamine

115
Q

what is the hypothesis behind the cause of depression?

A

due to a functional DEFICIENCY of biogenic amines (i.e NE, serotonin (5-HT) and probably dopamine

116
Q

list 4 classes of drugs that can be used in the treatment of depression

A
  1. tricyclic antidepressants (TCAs)
  2. serotonin reuptake inhibitors (SRIs)–selective –> SSRI
  3. monoamine oxidase inhibitor (MAOIs)
  4. noradrenergic and specific serotonergic antidepressants (NaSSAs)
117
Q

MOA of tricyclic antidepressants?

A

inhibit reuptake of noradrenaline (NA) and serotonin (5-HT)

118
Q

what are the three classes of side effects associated with tricyclic antidepressants? what are specific examples of each?

A
  1. anticholinergic (because blocks NE)–> urinary retention, constipation, dry mouth etc…
  2. Antiadrenergic (because blocks NE)–> block peripheral alpha-1 receptors leading to decrease in venoconstriction (postural hypotension in the elderly)
  3. antihistaminic–> can be good or bad; i.e useful in helping to fall asleep
  4. cardiotoxic–> main reason these have fallen out of use
119
Q

what is the main reason tricyclic antidepressants aren’t used as much anymore?

A

cardiotoxicity

120
Q

MOA of serotonin reuptake inhibitors?

A

used to treat depression

selectively inhibit the reuptake of serotonin (5-HT)

121
Q

side effects of SSRIs?

A

agitation, GI (nausea), sleep (increase or decrease) sexual dysfunction (in 20-60% of cases)

122
Q

name two examples of TCAs

A

nortriptyline

amitriptyline

123
Q

name two examples of SSRIs

A

fluvoxamine

fluoxetine

124
Q

MOA of MAOIs?

A

monoamine oxidase breaks down monoamines by oxidizing them

the old MAOIs–> irreversible inhibition of MAO-A and MAO-B

the new MAOIs–> reversible inhibition of MAO-A

125
Q

side effects of the old MAOIs?

A

food and drug interactions

DONT MISS WITH SSRIs (or other classes of antidepressant)

126
Q

side effects of new MAOIs?

A

drug interactions (demerol and NSAIDs)

DONT MIX WITH SSRIs or other drug classes

127
Q

name two MAOIs

A

phenelzine

tranylcypromine

128
Q

MOA of noradrenergic and specific serotonergic antidepressants (NaSSAs)?

A

block pre-synaptic adrenergic and serotonergic receptors: alpha-1 adrenergic, alpha-2 adrenergic, 5-HT2a, 5-HT2c and 5-HT3

129
Q

why is there a lag time in effectiveness seen in noradrenergic and specific serotonergic antidepressants (NaSSAs)?

A

the 3-4 lag time is thought to be due to the time it takes for down regulation of these receptors

130
Q

name a noradrenergic and specific serotonergic antidepressants (NaSSAs)

A

mirtazapine

131
Q

what is the hypothesis behind the cause of mania (bipolar disorder?

A

due to a functional EXCESS of biogenic amines, thought to be at the 2nd messenger level (specifically the phosphoinositide system)

132
Q

name 3 classes of drugs that can be used in the treatment of mania/bipolar disorder

A
  1. lithium
  2. anticonvulsants
  3. atypical anti-psychotics
133
Q

MOA of lithium in the treatment of bipolar?

A

thought to interfere with phosphoinositide second messenger system and thereby dampen down overactive neurotransmission

134
Q

why must you consider renal function when administering lithium to a patient?

A

Li+ and Na+ compete at an ionic level

anything that affects electrolytes or kidney function can make Li+ toxic

*hyponatremia promotes reuptake of Li+ and can lead to toxicity–> Na+ losing diuretics (thiazide) can do this (enhances proximal tubule Li+ reabsorption)

135
Q

what are the symptoms of lithium toxicity?

A

tremor

edema

hypothyroidism

136
Q

what test should you run on a patient before administering lithium to treat bipolar?

A

electrolytes

kidney function

ECG

TSH

betahCG

137
Q

what is the MAO of anticonvulsants (in this case to treat bipolar)?

A

enhance GABA, an inhibitory neurotransmitter

138
Q

what specific anticonvulsants are used to treat bipolar?

A

valproate

carbamazepine

lamotrigine

139
Q

how do atypical anti-psychotics treat bipolar?

A

dampen dopaminergic activity?

140
Q

what is the hypothesis behind the cause of anxiety/anxiety disorders?

A

due to CNS excitation of hyperactivity

multifactorial

may involve NA, 5-HT and/or GABA

141
Q

list 3 types of drugs used in the treatment of anxiety disorders

A
  1. benzodiazepines
  2. antidepressants
  3. beta blockers
142
Q

MOA of benzodiazepines in the treatment of anxiety disorders?

A

enhances the effects of GABA (inhibitory NT)–> open Cl- channels so neurons become hyperpolarized and less excitable

143
Q

name another substance that potentiates benzodiazepines

A

EtOH

144
Q

why can benzodiazepines becomes addicting?

A

withdrawal sx mimic anxiety

145
Q

MOA of antidepressants in the treatment of anxiety?

A

may treat “anxious depression” via 5-HT receptor down regulation effects

146
Q

for which anxiety disorders are SSRIs indicated?

A

panic and OCD

147
Q

MOA of beta blockers in the treatment of anxiety?

A

inhibit epinephrine mediated sympathetic actions on beta receptors

only effective for physiologic sx of anxiety (tremor, palpitations etc)

PRN

non-selective beta blockers are toxic for asthmatics

148
Q

what is a big difference in side effects in benzodiazepines and beta blockers in the treatment for anxiety?

A

benzos are sedating

beta blockers are non sedating

149
Q

name 4 factors that influences psychotherapy outcomes

A
  1. patient characteristics –> i.e motivation, capacity for interpersonal functioning, intelligence
  2. therapeutic alliance–> i.e positively valued and productively collaborative relationship between patient and therapist
  3. patient expectations–> i.e patients belief in therapy improves outcomes, if patient sees relevance in therapy, there is an improved outcome and shared rationale on treatment
  4. modality/brand of therapy–> i.e adherence to the modality of therapy (i.e therapist doing what is required for that therapy)
150
Q

what do short term psychotherapies target?

A

acute problems like anxiety, depression, and some longer term problems

151
Q

name 3 types of short term psychotherapy

A
  1. CBT
  2. interpersonal therapy
  3. mindfulness based cognitive therapy
152
Q

what do longer term psychotherapies target?

A

changes in character

153
Q

what id dialectical behavioral therapy used for?

A

long term psychotherapy

for borderline personality disorder

based on mindfulness

154
Q

list the types of psychodynamic therapies

A

long term psychotherapy

  1. classical psychoanalysis
  2. existential
  3. humanistic
  4. focus on the relationship issues as motivation
  5. accept the significance of present day influence of early life experiences (freud)
  6. use freud’s topographic theory of the mind
    - ego–> skills, knowledge, identity, filters/protects psyche
    - superego–> conscience, mortality, judgement
    - Id–> unconscious libidinal drives (represses libidinal urges which are basis of motivation)
155
Q

what are some phenomena that may arise in the interaction between patient and therapist?

A
  1. projection/transference
  2. projective identification (counter-transference)
  3. splitting
  4. denial
  5. suppression
156
Q

what is projection/transference?

A

from patient to therapist

i.e you remind me of my mother so i hate you

157
Q

what is projective identification/counter transference?

A

from therapist to patient

i.e i remind him of his mother, am i now acting like his mother?

158
Q

what is splitting?

A

phenomenon in psychotherapy

patient projects positive attributes to one person/group and negative to another–> or switches between extremes over time with the same person

159
Q

what is denial (in the context of the psychotherapeutic relationship?

A

sacrificing reality in exchange for decrease in emotional distress

i.e ignore lump in breast and refuse mammogram

160
Q

what us suppression (in the context of the psychotherapeutic relationship)?

A

putting something out of your ming without sacrificing reality in order to function better

i.e dont ignore the lump in breast, book mammogram, but then forget about it and distract self with regular tasks

161
Q

what is cognitive behavioral therapy?

A

assumed mutual influence of thought, action and mood–> by challenging automatic thoughts, behavior and mood can change

automatic thoughts are in the periphery of awareness–> pathology is associated with cognitive distortions in different disorders

162
Q

what are some of the cognitive distortions that CBT aims to address?

A
  1. jumping to conclusions
  2. emotional reasoning
  3. all or nothing
163
Q

how do patients address cognitive distortions in CBT?

A
  1. links the thoughts, feelings and actions in a way that makes the patient more aware of them
  2. then they can influence and challenge them
  3. this implicitly produces mindfulness of thoughts and emotions/reactions
  4. this skill produces resiliency to relapse
164
Q

list the major risk factors for mood disorders

A
  1. women
  2. ages 25-30 are at highest risk
  3. marital status–> married or never married individuals have a lower risk compared to widowed, divorced or separating couples
  4. income–> people that make less than $20 000 are at higher risk
  5. risk does NOT vary with race
  6. may be genetic factors–> specific cause has not been found
  7. several personality disorders may predispose people to getting a mood disorder
  8. specific life events–> death of a loved one, assault, serious marital problems
  9. physical trauma in early life seems to increase risk
165
Q

what are the major risk factors for bipolar disorder 1 and 2?

A
  1. not much of a difference between men and women but may be slightly higher in men
  2. ages 18-27 seem to have highest risk
  3. BP seems to be higher risk in people who are part of a higher socioeconomic class
  4. early age of onset and number of ill relatives seems to increase the family risk of bipolar but other variables such as type of relative does not seem to
  5. stressful life events and social rhythm disruptions seem to play a role in reoccurrence but not initial incidence
166
Q

what are the major risk factors for anxiety disorders in general?

A
  1. gender–> with exception of OCD, women have twice the risk for most anxiety disorders
  2. age–> in general, phobias, OCD and separation anxiety show up in early childhood while social phobia and panic disorder are often diagnosed during the teen year
  3. personality factors–> children’s personalities may indicate higher or lower risk for future anxiety disorders
  4. family history and dynamics–> anxiety disorders tend to run in families; genetic factors may play a role in some cases but family dynamics and psychological influences are also often at work
  5. anxiety was associated with a lack of social connections and a sense of a more threatening environment
  6. traumatic events–> trigger anxiety disorders in individuals who are susceptible to them because of psychological, genetic or biochem factors (i.e PTSD)
  7. medical conditions–> although there has been no causal relationship found, certain medical conditions have been associated with increased risk of panic disorder (migraines, obstructive sleep apnea, mitral valve prolapse, IBS, chronic fatigue syndrome, premenstrual syndrome
167
Q

what are specific risk factors for generalized anxiety disorder?

A

most common anxiety disorder amongst elderly

usually begins in childhood and becomes a chronic ailment (particularly when left untreated)

depression commonly accompanies this anxiety disorder and depression in adolescence may be a strong predictor of GAD in adulthood

168
Q

what are specific risk factors for panic disorder?

A

age–> usually first occurs in late teens or in mid-30s

gender–> women have twice the risk; panic attacks are very common after menopause

169
Q

what are specific risk factors for OCD?

A

equally in men and women

most cases develop in childhood or adolescence although can occur throughout the life span

170
Q

what are specific risk factors for social phobias?

A

age–> usually onset during early teen years

gender–> women are more likely though equal numbers seek treatment

171
Q

what are specific risk factors for PTSD?

A
  1. pre-existing emotional disorder–> hx of depression (i.e) before a traumatic event
  2. drug or alcohol abuse
  3. family history of anxiety
  4. history of abuse (particularly that which threatens family integrity such as spousal or child abuse–> studies suggest up to one third of people who experience this type of abuse develop PTSD)
  5. early separation from parents
  6. lack of social support
  7. poverty
  8. sleep disorders–> insomnia and excessive daytime sleepiness even within a month after the traumatic event are important predictors for the development of PTSD
172
Q

what are demographic risk factors for suicide?

A

male

not married

low education

poverty

173
Q

what mental disorders increase risk for suicide?

A

affective/mood disorders

alcohol and drug use disorders

personality disorders

schizophrenia

174
Q

why might mood and anxiety disorders commonly co-occur?

A

comorbidity may be due to several factors including similarities in underlying neurochemistry or anatomy, genetic predisposition and similar risk factors

individuals with greater neuroticism are at greater risk for both anxiety and mood disorders (people with higher neuroticism have the tendency to experience negative emotional states such as anger, anxiety and depression)

175
Q

describe the characteristics of normal and clinical anxiety

A

anticipation of a future threat

characterized by:
muscle tension

vigilance in preparation for danger

cautious or avoidant behaviors

176
Q

describe the characteristics of normal and clinical fear

A

emotional response to a real or perceived threat

characterized by:

  • surges of autonomic arousal
  • thoughts of immediate danger
  • escape behaviours
177
Q

how does clinical fear and anxiety differ from normal?

A
  • excessive in relation to the degree of threat
  • persistent
  • characterized by significant distress and/or impairment in social and occupational functioning
178
Q

what are 3 fundamental features of anxiety and related disorders?

A
  1. unwanted emotions (panic attacks, chronic hyperarousal, excessive fear)
  2. unwanted thoughts (obsessions, excessive worries, intrusive recollections)
  3. unwanted actions (avoidance, escape, distraction, compulsions)
179
Q

what anxiety disorders are characterized by panic attacks?

A

they can occur in all anxiety disorders

180
Q

what are panic attacks?

A

they can occur in all anxiety disorders

discrete period of intense fear and discomfort

abrupt onset

peaks within 10 min

peak intensity averages about 20 min length

can occur during waking hours or during sleep

four or more symptoms are required to define a panic attach

attacks with fewer than 4 symptoms are called “limited symptom” panic attacks

181
Q

are all phobias learned?

A

no, some are innate

however there is a role for learning in some phobias (i.e pavlovian conditioning, operant conditioning, and maladaptive beliefs)

182
Q

what are some protective factors for phobias?

A

learning to associate a stimulus with LACK of harm–> acquisition of “fearless familiarity”

protects against fear acquisition

example is positive experiences with dogs protects against development of dog phobia

183
Q

what are some of the neuroanatomical structures that have been implicated in anxiety disorders?

A
  1. amygdala–> processing of emotional significance of stimuli
  2. HPA axis
  3. prefrontal cortex–> assignment of meaning to stimuli, working memory
  4. hippocampus–> contextual learning for fear conditioning
  5. frontal-striatal circuits–> implicated in OCD
184
Q

name 3 parts of the fronto-striatal complex

A

putamen

dorsal caudate

nucleus accumbens

185
Q

how is the striatal complex implicated in OCD?

A
  1. anterolateral OFC (motor control, response inhibition)–> putamen–> back and forth from thalamus
  2. dorsolateral PFC (working memory, executive function)–> dorsal caudate–> back and forth with thamalus
  3. ACC/ventromedial PFC (error monitoring, doubting)–> nucleus accumbens–> back and forth from thalamus
186
Q

what are dysfunctional beliefs?

A

extreme, irrational or rigidly held beliefs

i.e
GAD–> worry helps me prepare for danger

panic disorder–> if my heart races i could be having a heart attack

social anxiety disorder–> people are hypercritical and i can’t meet their expectations

PTSD–> i was raped by my neighbour in my own apartment; that means I am never, ever safe, no matter where I am

*twin studies show that dysfunctional beliefs are shaped by environmental factors interacting with genetic factors

187
Q

what are first line treatments for anxiety disorders?

A

CBTs and SSRIs

188
Q

give examples of SSRIs used to treat anxiety disorder

A

fluoxetine

sertraline

paroxetine

clomipramine

189
Q

what does the limbic system do?

A

learning, memory, executive function

190
Q

what is the modern definition of the limbic system?

A

definition I: a collection of cortical and subcortical structures that regulate learning, memory and executive function –> these processes involve but are NOT limited to: hippocampus, entorhinal cortex, frontal lobes

definition II: a collection of structures that regulate emotion–> best understood by its RESULTS

  1. experiences or feelings of emotional state
  2. expression of behaviors (anger, joy, fear)
191
Q

what is executive function?

A

planning of appropriate actions

192
Q

define emotional state

A

best defined as a subjective, internal physiological response

193
Q

why are emotions important?

A

emotions are critical for survival–> disorders of emotion kill

play a role in memory–> so closely coupled, can’t understand one without the other

plays a role in decision making–> from how a rat avoids danger to the finest of human achievement

emotion provides context

194
Q

what structure’s comprised Broca’s “limbic lobe”?

A

cingulate gyrus, amygdala, hippocampus

195
Q

the cingulate gyrus, hippocampal formation, mammillary body and anterior thalamic nuclei all communicate with one another as part of the limbic system… through which pathways do they each communicate?

A
  1. cingulate gyrus –> cingulum–> hippocampal formation
  2. hippocampal formation–> fornix–> mammillary body
  3. mammillary body–> mammilo-thalamic fasciculus–> anterior thalamic nuclei
  4. anterior thalamic nuclei–> internal capsule–> cingulate gyrus
196
Q

how are the amygdala and frontal cortex related?

A

amygdala can affect the frontal cortex and the frontal cortex should normally inhibit the amygdala–> hypothesized that this inhibition is dysfunctional in some anxiety disorders

197
Q

how does the amygdala communicate with the papez circuit?

A

via the hippocampal formation

also communicates with the frontal cortex and the hypothalamus

198
Q

how does the hippocampus manage to be informed of all sensations?

A

because of all the brain regions it communicates with

199
Q

what types of functions can the hippocampus access and regulate?

A

behavior, autonomic function and endocrine function

in addition to learning and memory

200
Q

describe the connections to the amygdala

A
  1. ACTUAL stimulus input from the THALAMUS
  2. PERCEIVED stimulus from the CORTEX
  3. RECALLED stimulus from the hippocampus
201
Q

what part of the amygdala (a nucleus) is the most sexually dimorphic and why? why part of the brain does this nucleus communicate with?

A

medial nucleus of the amygdala
regulates social behavior

lots of receptors for androgens etc… (amygdala knows the gender of the person, how old they are, and so knows how this info may act in the limbic system)

communicates with the thalamus

202
Q

what nucleus of the amygdala performs the diagnosis of real or perceived or recall stimuli? what other part of the brain does this nucleus communicate with?

A

basolateral nucleus
integrates sensory info

“always asking pesky questions”

communicates with cortex, hippocampus and hypothalamus

203
Q

what nucleus in the amygdala mediates fight or flight? what regions does this nucleus communicate with?

A

central nucleus
mediates fight or flight

well conserved across all mammals–> only two synapses removed from affecting paraventricular nucleus of the hypothalamus and thus release of cortisol from adrenal gland

communicates with hypothalamus (PVN), frontal cortex and brainstem

204
Q

list the nuclei of the hypothalamus

A
  1. medial preoptic (MPN)
  2. suprachiasmatic (SCN)
  3. supraoptic (SON)
  4. dorsomedial (DMN)
  5. ventromedial (VMN)
  6. arcuate nucleus (AN)
  7. mammillary bodies (MB)
  8. paraventricular nucleus (PVN)
205
Q

what does the paraventricular nucleus of the hypothalamus do?

A

regulates release of cortisol from adrenal gland

regulation by the hypothalamus is mediated by a chain of sequentially released hormones–> HPA axis

206
Q

what are the consequences of acute elevations in cortisol? what happens if these become chronic and maladaptive?

A

under acute conditions, are adaptive

  1. mobilize energy //myopathy, diabetes
  2. increased vascular tone //hypertension
  3. suppress digestion //ulceration
  4. suppress reproduction //amenorrhea, impotence
  5. immune suppression //increased disease risk
  6. sharpen cognition //neuron death
207
Q

how is memory and cortisol related?

A

“events that are emotionally arousing [or produce an increase in cortisol] may be worth remembering”

therefore, successful behavioral and emotional responses require proper integration across memory, motor and hormone response system

208
Q

what is the pathway of first, activation, and second, dampening or arousal, in the threat response pathway?

what happens if this second part of the pathway is disfunctional (ie in a misguided fear situation)

A

first response–> path of panic
stimulus–> thalamus–> amygdala… reticular and autonomic relays cause panic (adrenaline, HR up, BP up); communication with PVN in hypothalamus causes release of cortisol

mediating response–> path of reason
thalamus also communicates with sensory cortex–> frontal cortex–> inhibits amygdala

careful appraisal by sensory and frontal cortexes dampen the amygdala’s reaction and logic prevails… panic is removed and cortisol levels return to normal

**if logic fails, the amygdala will continue to arouse and cause fear and panic–> left unchecked, chronic elevations in cortisol result in a myriad of disorders

209
Q

the extent to which a stimulus produces a threatening or panic feeling depends on what?

A

depends on to the extent to which the amygdala is engaged

panic may be overcome by the frontal cortex (higher order reasoning) as well as several other limbic structures

210
Q

what is the difference between temperament and character?

A

temperament–> basic biological disposition toward certain behaviors; genetically coded influences of nature

character–> crystallized influence of environment/nurture; characteristics acquired during upbringing

211
Q

what is a pneumonic to describe the 5 personality dimensions?

A

OCEAN

Openness to experience
Conscientiousness
Extraversion 
Agreeableness
Neuroticism (emotional stability)
212
Q

what is the prevalence of personality disorders in the US population?

A

about 10%

213
Q

what % of those with BPD have a hx of self-injurious acts?

A

70-75%

214
Q

what is a mnemonic for remembering the major depressive disorder criteria?

A

SAD SAP ECG

Suicidal thinking/behavious
Anhedonia (losing pleasure in stuff)
Depressed mood

Sleep changes
Appetite changes
Psychomotor changes

Energy loss
Concentration loss or indecision
Guilt

215
Q

list the component of the mental status examination (MSE)

A
  1. appearance and demeanor
  2. behaviour and movements
  3. speech (how they sound)
  4. mood (subjective) and affect (objective)
  5. thought process (flow of thinking)
  6. though content including violent ideation
  7. perception (5 senses)
  8. cognition (with folstein/MoCA if appropriate)
  9. insight and judgement
216
Q

how are fear and anxiety different?

A

fear is an emotional response to a SPECIFIC EXTERNAL threat (i.e seeing a snake)

anxiety is an emotional response to a NON SPECIFIC INTERNAL threat that may not actually even occur (i.e what if i go walking in the forest and come across a snake?)

threat processing is central to fear/anxiety disorders

217
Q

what is the Bed nucleus of the stria terminalis (BNST)?

A

extension of the amygdala

while the amygdala is involved with the response to an immediate, known threat, the BNST likely fulfills a similar role when responding to a non-specific, internal threat

can also mediate freezing, activation of the autonomic nervous system, endocrine output and brain arousal systems, although main inputs are from higher cortical and hippocampal regions rather than sensory cortex or thalamus (like amygdala would be)

218
Q

what neural structures mediate avoidance behaviors?

A

connections between the amygdala and the ventral striatum (nucleus accumbens)

avoidance causes negative reinforcement of anxiety–> if you avoid the threat, you will learn the avoidance as a good way of being safe

219
Q

what is the centre of the stress response circuit?

A

amygdala (“fear centre”)

220
Q

what are the major monoamine neurotransmitters? what disease is associated with low monoamine levels?

A
  1. catecholamines (dopamine, NE, epinephrine)
  2. indoleamines (serotonin, melatonin)

according to the monoamine theory of depression (1950s), believe that depression is caused by decreased levels of monoamines (esp. NE, serotonin–> wasnnot clear which was primarily affected)

221
Q

what amino acid is serotonin formed from?

A

tryptophan (in the raphe nucleus)

222
Q

what amino acid is NE formed from?

A

tyrosine (in the locus ceruleus)

223
Q

what is the “catecholamine theory of depression”?

A

1965

believes depression is related to decreased catecholaminergic (ME) transmission

animal models of altered catecholamine metabolism show abnormal exploratory behavior, conditioned avoidance and reward seeking behavior (animal version of depression?)

interference with serotonin metabolism caused irritability, insomnia, hyperactivity and hypersexual behaviours (animal version of mania?)

224
Q

what is the serotonin theory of depression?

A

low levels of 5HT metabolite 5HIAA reported in the CSF of depressed patients

tryptophan depletion studies caused relapse of depression in patients who had previously responded to SSRIs

225
Q

what are the problems with the monoamine theory of depression?

A

biochemical effects of antidepressants are almost instantaneous, but clinical effects take several weeks

5-HT or NE/DA depletion do not induce depression in healthy subjects

antidepressants are not effective in all patients

newer theories suggest depression may be related to dysfunction in specific neural circuits–> while function of these circuits involves monoamines, a deficit in neurotransmitters is not the primary pathology

226
Q

what neural circuits may be dysfunctional in depression?

A

may result from dysfunctional connectivity including the frontal cortex, hippocampus and amygdala

structural imaging studies have reported decreased size of frontal and cingulate cortices

amygdala volume reduced although amygdala activity is increased (at baseline)

hippocampal volume reduced in depressed patients with smaller volume associated with greater lifetime depressive episodes

227
Q

in what ways do anxiety and depression symptoms overlap?

A

sleep disturbance

fatigue

concentration

228
Q

in what % of patients with depression would you expect to see dysfunction in the HPA axis?

A

50%

excess secretion of cortisol and failure to suppress cortisol release on dexemethasone test suggests impaired feedback regulation of HPA axis

in endocrine disorders you get increased depression risk (i.e cushings)

229
Q

what is the heritability of depression, based on twin studies?

A

35-50%

230
Q

what receptor do SSRIs block?

A

SERT transport pump

interferes with recycling of serotonin back to the presynaptic neurons thereby increasing 5HT availability in the synapse

231
Q

what specific side effect is associated with the SSRI sertraline?

A

diarrhea

232
Q

what specific side effect is associated with the SSRI paroxetine?

A

constipation

233
Q

what are some CNS side effects associated with SSRI use (increased serotonin side effects)?

A

initial agitation

initial worsening of anxiety

tremors

insomnia

headache

suicidal ideation

serotonin syndrome

234
Q

what are some reproductive side effects associated with SSRI use (increased serotonin side effects)?

A

sexual dysfunction

235
Q

what are some endocrine side effects associated with SSRI use (increased serotonin side effects)?

A

hyponatremia

236
Q

what are some hematologic side effects associated with SSRI use (increased serotonin side effects)?

A

bleeding (platelets need serotonin to function properly)

237
Q

what is serotonin syndrome?

A

triad of clinical changes

  1. autonomic–> fever, shivering, mydriasis
  2. cognitive–> agitation, hypervigilance
  3. neuromuscular–> hyperreflexia, rigidity, myoclonus

**CLONUS (spontaneous, induced, ocular) is the most important finding in establishing the diagnosis of serotonin syndrome

  • may be confused with neuroleptic malignant syndrome or anticholinergic toxicity but there are important differences
  • increased serotonin results in decreased dopamine
238
Q

what are SNRIs?

A

serotonin and norepinephrine reuptake inhibitors

239
Q

name 4 SNRIs

A

venlafaxine
duloxetine
desvenlafaxine
levomilnacipran

240
Q

how do SNRIs work?

A

blocks SERT and NET (transporter pumps)–> interferes with recycling of NTs back to their respective presynaptic neurons

autoreceptors are stimulated until they downregulate (same as in SSRIs)

241
Q

what are SEs of SNRIs?

A

overlap with SSRIs but can also get possible noradrenergic effects:
sweating
increased BP or HR
urinary retention

242
Q

what is an NDRI?

A

norepinephrine dopamine reuptake inhibitor

243
Q

name an NDRI

A

bupropion (only one available at this time)

244
Q

how do NDRIs work?

A

block NET and DAT transporter pumps–> effect is the same as with SNRIs but there is more available neurotransmitter in the synaptic space

**because dopamine modulates the reward center, this med plays a useful role in smoking cessation

245
Q

in what other way (other than depression) can NDRIs be used?

A

bupropion–> smoking cessation

246
Q

what is a mnemonic to remember NDRI side effects?

A

SHARES

Seizure
Headache
Agitation 
Rash
Emesis
Sleep disturbance
247
Q

when are NDRIs a particularly good option?

A

if there have been issues with sexual dysfunction in antidepressant treatment for that patient

248
Q

what type of drug is vortioxetine? how does it work?

A

multimodal–> serotonin stimulator/modulator

blocks reuptake of serotonin (SSRI function)

is a 5HT3 antagonist (which can influence the release of 5HT, NE, DA, histamine and ACh)

5HT1a agonist

5HT1b partial agonist

other 5HT receptor subtype effects are either much weaker, receptor density in critical areas is minimal or roles are unclear

**5HT neurons interact with GABA and glutamate receptors but because of the different effects on the different receptors (vs SSRIs) it may be better to fine tune the glutamate system in the hippocampus and PFC

249
Q

what are NaSSAs?

A

noradrenergic serotonin specific antidepressants

250
Q

name a NaSSA

A

mirtazapine

251
Q

how does mirtazapine work?

A

is a NaSSA

primary mechanism is alpha-2 antagonism–> 5HT/NE disinhibition means increased release of both

blocks 5HT3–> antiemetic effect

blocks 5HT 2a/2c–> sleep restoring, antiolytic, antidepressant effects (via increasing NE/DA release in PFC)

blocks histamine–> hypnotic and antiolytic effect, particularly at low doses (but responsible for weight gain)

252
Q

what are SARIs?

A

serotonin agonist and reuptake inhibitor

253
Q

name a SARI

A

trazodone

254
Q

how is trazodone primarily used? what is its MOA?

A

a SARI

primarily used as a sedative versus an antidepressant

at lower doses, it blocks histamine (at 5HT2a)

higher doses are required for the antidepressant effect when the SSRI function begins to kick in

255
Q

what type of drug is amitriptyline?

A

TCA and SNRI–> most studied in pain

256
Q

what type of drug is desipramine?

A

TCA and NRI

257
Q

what type of drug is clomipramine?

A

TCA and SRI –> most studied in OCD

258
Q

how do the MOAs of MAO-A versus MAO-B drugs differ (both are MAOIs)?

A

MAO-A metabolizes NE, 5HT, tyramine

MAO-B metabolizes dopamine preferentially

259
Q

how do MAOIs work?

A

enhance monoamine function by interfering with the metabolism of these NTs

260
Q

what other function do mood stabilizing drugs perform?

A

(except lithium)

are also antiepileptic drugs

261
Q

are benzos recommended for long term use?

A

generally recommended for SHORT term use

262
Q

which benzo is the safest in liver dysfunction?

A

still metabolized by the liver but LORAZEPAM is the safest in the case of liver dysfunction

263
Q

for which disorders does the evidence support CBT effectiveness?

A

most unipolar depression disorders

most anxiety disorders

psychotic illness with a focus on medication compliance

264
Q

in what disorders is CBT less useful?

A

chronic disorders such as eating disorders, personality disorders, chronic depression

265
Q

what is interpersonal therapy?

A

equally as effective as CBT

focuses more on relationships than self talk–> maybe less helpful with socially avoidant depression patients

266
Q

in what patients does dialectic behavior therapy tend to be effective?

A

chronically parasuicidal patients with borderline personality disorder

B&B Part 2 (5 decks)

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