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18 Cards in this Set
- Front
- Back
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Explain what's included in each DSM axis:
- axis 1 - axis 2 - axis 3 - axis 4 - axis 5 |
- axis 1: severe mental disorders that are episodic/transient (states!) eg. mood disoders, schizophrenia
- axis 2: pervasive, persistent conditions that are present from birth (traits!) e.g. mental retardation & personality disorders - axis 3: non-psychiatric or "medical" disorders that can affect behaviour, mood or thinking (e.g. HIV, epilepsy, Hothyroidism) - axis 4: Psychosocial stressors - axis 5: Global assesment of functioning scale from 1-100. Most ppl around 70-100. |
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Most psychiatric etiologies are unkonwn. As a result, how do psychologist identify/group diseases?
How does this affect treatment? |
Use symptom clusters in the hope that symptom clusters will reflect conditions with similar etiologies (however may be many etiologic paths to the same clinical presentation)
Tx: symptom-based, can't treat the etiology when you don't know it! |
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What are the 2 fear pathways?
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1. The "low road" - is fast but has low stimulus discrimination
sensory organ --> thalamus --> amygdala --> Hypothalamus 2. The "high" road: slower but has better discrimination and can inhibit signals from low road organ --> thalamus --> sensory cortex --> frontal cortex --> amygdala --> hypothalamus |
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Why does the brain have 2 fear pathways?
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The low road has persisted through evolutionary development of the more sophisticated high road. This is b/c it is ++ adaptive; time = survival so having a fast system has been preserved
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Where are fear-inducing stimuli stored (2 areas)? What is the cognitive experience like for activity in each of these areas?
What happens when you are re-exposed to fear-inducing stimuli? |
THe amygdala and hippocampus!
Amygdala = general fear/anxiety Hippocampus = conscious explicit memories of fearful stimuli Rexposure to stimuli causes reactivation of stored amygdala fear-association |
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When the amygdala is activated, this causes a general feeling of fear or anxiety? Why is this? (ie why is it general and not specific?)
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General b/c it is subcortical and thus subconscious. Compare to visceral sensations of upset stomach (unable to localize!)
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What are 4 forms of pathological anxiety?
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1. Inappropriate response to a stimuli
2. Unprecipitated attacks of anxiety (panic attacks) 3. Chronic state of arousal (generalized anxiety) 4. Excessive fear of objects (phobias) |
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What is the role of CCK in panic attacks?
Why is this significant/what does it suggest? |
CCK is a peptide NT that is abundant in the Bstem, Hcampus and amydala. When you give CCK - 2 receptor agonists you can provoke panic attacks = evidence for amygdala involvement in panic!
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List the 3 common pharmacological treatments for panic and the NT they work on
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1. TCA: increase NE in cleft which eventually down regulates their receptors
2. Benzodiazepines - stimulate GABAergic inhibitory effects generally (diazepam) 3. SSRI's - increase 5HT in the cleft and down regulate it's receptors |
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Explain how the fear response is conditioned in humans? How can this lead to agoraphobia?
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Any stimuli present at the time of a panic attack can become a conditioned fear stimuli. The stimuli can be generalized until a person has agoraphobia and is house-bound.
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How are avoidance bahaviours created?
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Escaping a fearful situation relieves the fear and this creates avoidance bahaviours.
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How do you treat someone with debilitating anxiety/fears?
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Exposure therapy: have pt expose themselves to their feared object or place. Must remain exposed until anxiety has reduced to 1/2 it's peak. Repeat this until the anxiety response has been extinguished.
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Why is extinguishing not the same as erasing?
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Extinguishing does not erase the fear it just established cortical inhibition of the fear. Experimental removal of cortex = fear returns. Previously conditioned triggers are also more readily relearned
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Describe the processes involved in the epigenetic programming of fear and anxiety responses.
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Offspring of attentitive moms were found to be less fearful & have lower HPA axis activation, a trait that persists into adulthood. This is b/c their DNA is modified in such a way that they express fewer cortisol receptors and thus have a much smaller effect for the same amount of cortisol released
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According to the DSM, to be depressed, a pt must have 5 or more of the following symptoms during the same 2week period, and these must represent a change from previous functioning. What are the symptoms (name at least 5/9)
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1. Depressed mood most of the day, nearly every day
2. Markedly diminished pleasure in all or almost all activities 3. Wt loss when not dieting 4. insomnia or hypersomnia 5. Psychomotor agitation or retardation 6. fatigue/loss of energy 7. Feelings of worthlessness or excessive guilt 8. Diminshed ability to think or concentrate 9. Recurrent thoughts of death |
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"Social environments leave lasting molecular scars that can be circumvented but not directly reversed by antidepressant treatment"
How do the meds do this? Ie what happens with chronic social defeated mice? |
Chronic social defeat leads to DNA methylation and this down regulates BDNF (less hippocampal neurogenesis).
Adepres meds --> DNA acetylation --> down regulates HDAC5 --> reverses the down regulation of BDNF allowing increased or normal neurogenesis in the hippocampus |
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Antidepressant drugs will increase dendritic arborization and BDNF expression in hippocampal neurons. Why is this helpful?
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Deficient hippocampal neurogenesis impairs ability to learn new fea-context associations, including positive ones. Restoring the Hcampal Ngenesis thus allows for nrew contextualization of experiences that can gate the generalized fear traces in the amygdala.
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In addition to anti-depressants, what else will increase neurogenesis in the hippocampus?
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EXERCISE!! wooo!!
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