NEUR 1202 > Mid term 2 > Flashcards

Mid term 2 Flashcards

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1
Q

Psychoses

A

psychological disorder, loss of contact with reality

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2
Q

Schizophrenia

A

psychotic, most common (1 in 100), comorbid with depression, anxiety and substance abuse.

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3
Q

comorbid

A

additional disease or condition which co-occurs with the primary diagnosis.

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4
Q

diagnose

A

mental illness is diagnosed based on subjective reports of behavioral changes.

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5
Q

DSM 3

A

multiaxial system; 1: clinical syndrome (schi)
2; personality disorder
3; medical conditions
4; psychosical (rape)
5; global assessment of functioning scale.

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6
Q

DSM 5

A

single axis scale; 1-3 merged, 4 was replaced with the ICD coding system, and 5 was eliminated.

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7
Q

why were DSM 5 changed made?

A

Destigmatize disorders, increase worldwide consistence, consistency with the ICD.

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8
Q

3 categories of symptoms schi

A

Positive; negative, disorganized (erratic behavior, motor, emotion)

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9
Q

delusions

A

are strongly held beliefs despite overwhelming evidence to the contrary.

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10
Q

2 types delusion

A

Bizarre; implausible,
non-bizarre; false, somewhat plausible, surveillance.
*the most common are persecutory delusions,

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11
Q

Hallucinations

A

perception in the absence of an actual sensory stimulus. Any of the senses.

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12
Q

negative symptoms A’s

A

Apathy; lack of desire to get started, problem with day-today function.
Anhedonia: without pleasure
Autism: oneself,
Affect Flatten: reduction in range and intensity of emotion.

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13
Q

Alogia

A

a poverty of speech.

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14
Q

schi, diagnosis

A

5; delusions, hallucinations, disorganized speech, disorganized or catatonic behavior, negative symptoms.

Must have one of the first three.
Must demonstrate 2 for 6 months.

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15
Q

why were the 5 types of schi eliminated from DSM 5?

A

low reliability, poor validity, and did not predict patterns of disease progression or therapeutic potential.

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16
Q

Problems with the diagnostic model

A
  1. honest reporting
  2. application of criteria inconsistent between medial professionals
  3. not direct link to ideal therapeutic plan
  4. does not predict therapeutic response
  5. diagnosis is only possible once symptoms have manifested.
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17
Q

Biomarker

A

objectively measurable indicator of a biological process which can be used as a predictor of an organisms physiological state.

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18
Q

How can biomarkers be used

A

prognostic; identify ppl at high risk for developing disease prior to symptoms.
Diagnostic: identification of disease
Theranostic; identify the appropriate therapy and predict therapeutic response.

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19
Q

Saccades

A

Fast jumping eye movements between fixation points. eye tracking deficit, 98 % accurate, biomarker

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20
Q

schi genes

A

the amount of DNA shared with an affected family member is directly related to one’s risk of developing schi.

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21
Q

schi stress

A
  1. stressors increase risk

2. and the initial psychotic break leading to diagnosis is almost always preceded by a stressful event.

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22
Q

schi neuroanatomical

A

reduction in brain weight, enlargement of the ventricles, this suggests a neurodegenerative component to schi

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23
Q

Neurodegeneration

A

Process which leads to neuronal damage and or death

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24
Q

reduced brain weight

A
  1. frontal, temporal volume= cognitive and language deficits.
  2. basil ganglia; reduced emotional control and motoric changes
  3. hippocampus; learning and memory deficits.
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25
Dopamine hypothesis; schi
that symptoms are due to excess dopamine. * antipsychotic drugs blck D2 receptors and stop symptoms. * And drugs that release dopamine, may produce psychosis similar to schizophrenia. * The problem is that antipsychotics are only partially effective,
26
relative activity of dopaminergic pathways
Hyperactivity: mesolimbic connections VTA, NA, hippocampus, overstimulate D2 receptors. positive symptoms. Hypoactivity: mesocortical VTA, PFC, under stimulate the D1 receptors, negative symptoms.
27
GABA, Glutamate;
contribute to imbalance in dopamine signalling between the basal ganglia and the PFC
28
Antipsychotic
Haldol; improve positive symptoms, block D2, Atypical; Seroquel, improve both positive and negative symptoms,
29
side effects; anti psychotics
Hyperprolactinemia: breast development, milk production. Extrapyramidal symptom; spasms, rigidity, tardive dyskinesia. Neuroleptic malignant syndrome.
30
Tardive dyskinesia
similar to Parkinson's disease, often permanent.
31
Neuroleptic malignant syndrome
muscle stiffness, dif, breathing, can be fatal.
32
schi
40-60% quit medication within a year, symptoms can return in a week.
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Big problem
not beliefs, hallucination, BUT social interactions, what others say, or what they think someone is thinking. Therapies dont address this.
34
4 f's hypothalamus
feed, fight, flee, fuck
35
pleasure
positive feedback, strengthens memory that associates the two, thus increasing the likelihood that you will repeat the behavior.
36
ICSS
operant conditioning, rat has electrode in brain, learns that bar press will stimulate brain region. *rat will press lever and exclude everything else when the mesocorticolimbic dopamine system is stimulated.
37
mesocorticolimbic dopamine system
VTA ventral tegmental area, axons from here go to hippocampus and NA, dopamine release at these structures.
38
Dopamine in areas
NA; pleasure Hippocampus; learned association PFC; cognitive control, seek/avoid.
39
Addiction
is the compulsive engagement in rewarding stimuli despite adverse consequences.
40
substance use
moderate, does not interfere with daily function.
41
substance abuse
rely on a drug, central place in life.
42
chronic drug use
physiologic changes, psychological stressors lead it to become compulsive.
43
substance dependence
physical/psychological dependence. drug seeking behavior tolerance withdrawal.
44
Cocaine
blocks dopamine reuptake transporter, dopamine accumulates in the synapse,
45
cocaine tolerance
1. dopamine receptors are removed from post-synaptic membrane 2. dopamine release from pre-synaptic terminal is reduced. this reduces the effect, creating tolerance.
46
DSM 5
*addiction not a diagnostic term substance use disorder, addictive disorders
47
Wanting and liking
wanting increases with use, becomes learned, with cues (needle), Liking decreases with use,
48
Ibogaine
one dose help eliminate craving, withdrawal, mimics serotonin, stimulate serotonergic system, psychedelics also help neurogenesis,
49
Default mode network
high level activity when not focused on task. 1. integration center, organize information 2. self, thinking about thinking, ponder events, or future,
50
Default mode network and addiction
DMN is overactive in addiction, craving, rumination, psychedelic drugs reduce this activity, helps break negative thinking loops,
51
Diurnal
humans active during the day, sleep at night.
52
Adenosine
hypnogenic molecule, neuronal processes use energy (ATP), accumulate adenosine, sleep allows metabolic processes to catch up and reduce adenosine levels.
53
Serotonin
precursor melatonin, also hypnogenic
54
Coffee
Caffeine is psychoactive, prevents adenosine from binding to certain neurons in the brain, it can efficiently cross the blood brain barrier.
55
Chronotype
sleep time, night owl, sleep unaffected by day coffee drinking, the opposite is the case for morning larks, caffine disrupts their sleep.
56
melatonin
regulate circadian rhythm, pineal gland, Dracula hormone.
57
Day melatonin
light to suprachiasmatic nucleus, inhibit the release of melatonin. This is reversed at night, release melatonin. *And melatonin production changes over the lifespan.
58
sleep
reduce motor activity, diminished response to external stimuli, stereotyped posture, reversible.
59
awake
neurons fire, desynchronized, beta rhythm. Non-rem; delta waves, low frequency high amplitude. REM; similar to awake, high freq, low amp, paradoxical sleep.
60
non-REM
low body temp, low blood flow, able to move, dreaming less vivid, may have night terrors.
61
REM sleep
no temp regulation, paralyzed, sprawled, dreaming,
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Parasomnia
abnormal behavior during sleep, sleep walk, Both rem and non rem, sleep paralysis; during rem sleep.
63
Dyssomnias;
dif getting enough sleep at the right time; narcolepsy. Insomnia; 1/3, depression, treatment; melatonin,
64
narcolepsy
short onset of rem sleep, spend more time in rem sleep, few bursts of cyclic alternating patterns (CAP)
65
hypocretin
hypothalamus, promote wakefulness, supress rem sleep. narcolepsy; poor receptor hypocretin, reduced grey matter hypothalamus, and reduced hypocretin in CSF.
66
march
more than doubles risk of developing narcolepsy with cataplexy.
67
EEG
electroencephalogram used to measure electrical output. specific brain areas.
68
motivation
not it brain, our inference of why someone engages in a...
69
sex
announced at birth, genitalia,
70
differences in sex development; intersex
a set of conditions in which genotypic sex and phenotypic sex do not align.
71
brain and hormone
organizing effect; hormones permanently alter the development activating effect; hormone short term effect on behavior.
72
Estradiol
masculinizing effects on the brain
73
dimorphic
frontal cortex, hypothalamus, amygdala, medial preoptic area--sexually dimorphic nucleus
74
hypothalamus
ventromedial region; mating posture. testosterone causes rats to mount medial preoptic area; copulation in males,
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amygdala
male sexual motivation, amygdala size positively correlates with sex drive.
76
sex orientation
how sexual attraction manifests itself. Kinsey scale, spectrum of sex orientation
77
homosexuality
included in DSM until 1968
78
older brother effect
a man's likelihood of being homosexual increases by 33% for each older brother he has.
79
gender identity
subjective feeling of maleness or femaleness, independent of biological sex.
80
neurodevelopmental disorder
development of the CNS is impaired and symptoms appear during the early developmental period. Autism most common.
81
autism
deficit; communication and social interaction | 2. restrictive repetitive behaviors.
82
echolalia
repeating words over, over,
83
theory of mind
ability to attribute mental states to others and to realize that other individuals have their own entirely separate mental state.
84
ASD anatomical differences
Corpus callosum; smaller in sections, limited connection between brain regions, inability to integrate complex ideas. caudate; increased volume and activity, associated with repetitive behavior. Amygdala; increased volume and social withdrawal. frontal and temporal; perception of social interaction, interpret face expression, theory of mind, decresed activity in these regions.
85
cld too much testosterone cause ASD?
1. amniocentesis correlates intrauterine testosterone levels during development 2. females with ASD experience polycyctic ovarian syndrome which is caused by high testosterone.
86
De novo mutation
glitches in the genetic code that occur spontaneously in a sperm or egg, and are not inherited. cause; parental age,
87
how does psychiatric assessment differ from standard medical
it is subjective, no xray can find the problem.
88
TED
brain disorder, brain changes b4 behavior, early intervention
NEUR 1202
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