Exam 4-psychopathology Flashcards
Patho of Depression
Patho: monoamine-deficiency theory posits that the underlying pathophysiological basis of depression is a depletion of the neurotransmitters serotonin, norepinephrine or dopamine in the central nervous system.
Patho of Bipolar
Patho: characterized by dysregulation in the dopamine and serotonin systems and by pathology in the brain systems involved in regulating emotion; hereditary
Social anxiety
Fear and avoidance in social situations
Etiology: increased activity in limbic and frontal cortical areas
•Reduction of serotonin and GABA in amygdala
•Role of oxytocin ? - antianxiety effects and promotes social attachment, trust and
empathy
Clinical Manifestations:
•Speaking, reading and eating in public, going to parties, speaking to authority figures,
engaging in informal socialization
•More common in children
Patho:
General anxiety
Fear and worry about life events
•Marital relationships, jobs, money, health, social status
•More common in women, onset typically in early 20s but lessens with age
Etiology: •High family concordance
•Abnormal norepinephrine and serotonin systems in amygdala (particular on right
side?)
Clinical Manifestations: restlessness, muscle tension, irritability, easily fatigued, difficulty
concentrating, difficulty sleeping
Patho:
Post traumatic disorder
Etiology: Exposure to a threat of death, serious injury or sexual violence
•Symptoms develop hours to years after event
Clinical Manifestations: 4 diagnostic clusters: re-experiencing, avoidance, negative cognitions and mood, arousal
Patho: stress alterations in neural structures (amygdala and prefrontal cortex) and neurotransmitters
•Change how memories are stored, retrieved and extinguished
Substance use disorder-Etiology
Etiology:
Genetics-Up to 70 genes assocaited, early exposure increases misuse
Psychological-ADHD, anxiety, depression, bipolar
Biological- how body processes/perceives substance
Socio-cultural-peer pressure
Environmental-stress, parental drug use
Dopamine
Regulates: mood and muscle movement and plays a vital role in the brain’s pleasure and reward systems.
Mood: Increased levels increases pleasure
Anxiety: increased levels decreased anxiety
Norepinepherine
Regulates: concentration; increases alertness and arousal, and speeds reaction time.
Mood: improves/increases mood
Anxiety: responsible for how the person reacts to stress and anxiety and is associated with the fight-or-flight response.
Serotonin
Regulates: thought to regulate mood, happiness, and anxiety.
Mood: low levels lead to depression
Anxiety: decreases anxiety
How does genetics contribute to mood d/o
•Family and twin studies show strong association with mood disorders
•Bipolar is linked with chromosomes 18 and 22
•Large variation in symptoms suggests developmental and environmental factors
contribute to etiology
•Role of exposure to uncontrollable psychosocial stress in precipitating disorders
How does neurochemical contribute to mood d/o
•Monoamine hypothesis of depression:
deficits in monoamine neurotransmitters and
metabolites in CSF is underlying cause of
depression
•Dopamine: reduced = fatigue, low energy,
motivation
•Norepinephrine: depletion planning and
concentration
•Serotonin: ? depletion precedes depression
How does neuroendocrine contribute to mood d/o****
it changes the HPA dysregulation
How does neuroanatomical contribute to mood d/o
•Decreased serotonin receptor and transporter binding
sites
•Norepinephrine receptor alterations
•Smaller amygdala àrecurrent depressive episodes
•Smaller hippocampus, from chronic stress?
•Decreased prefrontal cortex cerebral blood flow
•Decreased glucose metabolism
Substance use d/o
•Mental and physical dependence that results from long-term exposure to
substances
•Nicotine, alcohol, illicit substances including: cannabis, sedatives, hypnotics, anxiolytics,
inhalants, opioids, hallucinogens and stimulants
Patho of BASAL GANGLIA with substance use d/o
- All addictive substances produce pleasurable surge of dopamine
- Acts in basal ganglia (reward center of brain)
***responsible for the formation of habitual substance taking
Patho of AMYGDALA with substance use d/o
plays a role in stressful feelings like anxiety, irritability, and unease, which characterize withdrawal after the drug high fades and thus motivates the person to seek the drug again. This circuit becomes increasingly sensitive with increased drug use.
Patho of PREFRONTAL CORTEX with substance use d/o
•Make stopping difficult
•Support conditioning – associate rewarding high with other cues in life (e.g., friends,
drinking, a place…)
Clinical manifestations of depression
5+ symptoms for 2+ weeks
Depressed or irritable mood Loss of interest and pleasure >5% weight loss/gain in a month Insomnia or hypersomnia Psychomotor agitation or retardation Fatigue or loss of energy Feelings of worthlessness or guilt Poor concentration or indecisiveness Thoughts of suicide or death
Clinical manifestations of manic episodes
3+ symptoms for about a week
Elevated mood Irritable mood Inflated self-esteem Decreased need for sleep Excessive talking Racing/crowded thoughts Distractibility Increased goal-directed activity Excessive risky activity
Manifestations of anxiety
arousal, tenseness, increased autonomic activity (heart rate, blood pressure, respirations), avoidance behavior
What does anxiety co-occur with?
depression
Patho of SUD (substance use d/o)
•As body adapts to substance à scale back sensitivity to dopamine à reduced euphoria (tolerance) à increased use of substance
- Each substance has a different effect on the brain
- All addictive substances produce pleasurable surge of dopamine
- Acts in basal ganglia (reward center of brain)
- Other centers of brain – amygdala and prefrontal cortex
- Make stopping difficult
- Support conditioning – associate rewarding high with other cues in life (e.g., friends, drinking, a place…)
Physical dependence:
refers to the physiologic effects of multiple episodes of
substance abuse.
Psychological dependence:
is characterized by craving of the substance to avoid a dysphoric state.
