NUSC-3P14 exam 2

biological factors of suicidal ideation

biological factors of suicidal ideation

reduced serotonin, 5-HT, & 5-HIAA (serotonin receptors) & gene altering factor - (reduced SKA2 (spindle & kinetochore associated complex subunit 2)) & (reduced PKA (protein kinase A) which regulates neural pathways)

psychological factors of suicidal ideation

• Sigmund Freud’s theory (depressed = cannot let go of an object or person / aggression turned inwards leads to rage against an object or person)

• Karl Menninger suicidal hostility (wish to kill/be killed/die)

• Aaron Beck (central emotional factor is hopelessness)

• combination of suicidal fantasies, significant loss, guilt, etc.

• cluster suicides/copycats

biological factors of MDD (genetic)

no specific genes but many genes w/ small effects; twins are more likely to be at risk (50% more w/ monozygotic twins); family hx effects chances of MDD too

biological factors of MDD (hormonal)

CRH is released from hypothalamus in response to perceived psychological stress, it induces the secretion of pituitary corticotropin which stimulates release of cortisol into plasma. MDD patients’ cortisol levels do not decrease after output so they have prolonged stress due to high blood cortisol

biological factors of MDD (biochemical)

depletion/dysregulation of serotonin, norepinephrine, &/or dopamine in the CNS. Deficient glutamate results in interference w/ normal neurotransmission which affects cognition, attention, & mood.

biological factors of MDD (inflammation)

high levels of C-reactive protein & interleukin-6 activates HPA which impairs the central serotonin system

biological factors of MDD (diathesis/stress model theory)

some individuals are more vulnerable to stress & early life trauma leads to neural loss in adulthood from CRF having a neurotoxic effect on the hippocampus

psychological factors of MDD

• cognitive theory - positive thoughts lead to positive emotions; past life experiences/childhood trauma cause MDD; how one sees the world (based on early life experiences)

• learned helplessness - self blame/guilt (when they actually have no control over the situation) & anxiety mix to cause depression

psychotic features

disorganized thinking, delusions, & hallucinations

melancholic features

severe apathy, weight loss, & suicidal ideation

atypical features

over eat, over sleep, slower psychomotor

catatonic features

extreme psychomotor retardation, non responsive & withdrawn

postpartum onset

after the birth/delivery (psychosis is common)

season features or seasonal affective disorder

hypersomnia, weight gain, craving for carbohydrates, begins in early winter or fall

electroconvulsive therapy

consists of a controlled electric current passing through part of the brain to stimulate the brain (causes a controlled therapeutic seizure which lasts 20-90 seconds). It allows for transfer of messages between the nerve cells which corrects biochemical changes in the brain.

transcranial magnetic stimulation

consists of an electromagnetic coil placed against the scalp which creates a magnetic field that stimulates certain areas of the brain which have decreased activity. Does not require implantation of electrodes or sedation & does not cause seizures.

vagus nerve stimulation

involves an implanted pulse generator & lead wire which stimulates the vagus nerve which leads to stabilization of abnormal electrical activity in the brain

deep brain stimulation

is when a neurosurgical procedure is done to implant electrodes into a specific brain region which are connected to a subcutaneous implantable pulse generator that controls stimulation. Continuous electrical stimulation is provided (though it does not have to be continuous)

therapies

light therapy (SAD), exercise & outdoor activity/time outside, reflexology, application of pressure on hands & feet, massage, meditation, guided imagery & relaxation, yoga, herbal remedies

BD 1

lifetime hx of mania w/ depressive episodes; episodes of mood disturbance w/ mixed features; rapid cycling (4+ episodes of mania or depression w/i 1 year)

BD 2

hx of hypomanic episodes & major depressive episodes w/ no hx of full mania

cyclothymic disorder

recurrent episodes of hypomania & mild/moderate depressive symptoms

biological factors of BD (genetic)

individuals w/ a parent w/ BD have a 15-30% chance of developing BD & 3 times the chance of developing other mental health disorders & monozygotic twins have a ~70% chance of developing BD

biological factors of BD (biochemical/neurobiological)

CNS transmitters (serotonin, norepinephrine, & dopamine) have issues interacting w/ hormones & receptor sites (neurotransmitters are unable to reach the correct synapses)

brain structure & function factor of BD

dysfunction (possibly due to loss of grey-matter) in prefrontal cortical region, hippocampus, & amygdala causing emotional dysregulation

neuroendocrine factors of BD

hypothyroidism is associated w/ BD (often undetected); low levels of estrogen results in a 4x greater chance of developing BD

environmental factors of BD

BD is more prevalent in upper socioeconomic classes; children who have genetic & biological risks of developing BD are most vulnerable when their social determinants are compromised & stress in adults is a common trigger for mania or depression

psychological factors of BD

when overwhelmed, faulty ego uses mania via pleasurable impulses such as sex or feared impulse such as aggression. critical/overactive super ego gets replaced w/ euphoria from mania

BD nonpharmaceutical treatment

support groups, health teaching/promotion (healthy lifestyle), omega-3 fatty acids (crucial to CNS functioning), & milieu management

milieu management

seclusion room which provides relief/comfort for patients unable to control their behaviour

biological factors of SZ (genetic)

errors in genetic coding; gene mutation & inherited mutations; abnormal function of individual gene/dysfunction of entire molecular networks

biological factors of SZ (nongenetic)

prenatal stressors; intrauterine infection (rubella); prenatal malnutrion; LBW (<2.5kg); preeclampsia; Rh incompatibility

biological factors of SZ (neurobiological/neurochemical)

• dopamine theory (hyperactivity of dopamine D2 receptor (causes positive symptoms) & hypoactivity of dopamine D1 receptor (causes negative symptoms))

• glutamate hypothesis (NMDA glutamate receptor alteration causes all the different types of symptoms of SZ & GABA dysfunction causes cognitive symptoms of SZ)

psychosocial/environmental factors of SZ

early life (obstetric complications, high prevalence of SZ & winter birthdays, prenatal/postnatal infection, maternal malnutrition, & maternal stress); childhood (head injuries & child abuse); & later life → substance use (alters dopamine activity), migration/urbanization, social adversity, crises, loss, & trauma

thought insertion

one’s thought is not one’s own but inserted into their mind by an external source/entity

thought broadcasting

one’s thought is projected/perceived by others

delusion of grandeur

conviction of being a powerful/important person

somatic delusion

involve bodily function/changing (rotting, disease, etc.)

delusion of persecution

being conspired against/being singled out for harm by others

delusion of reference

belief that events/objects/people have significant relevance to oneself

ideas of reference

sense that events & actions of others (e.g., talking, whispering, smiling) relate to oneself