Exam Four Flashcards

How the Placebo Effect Works

expectancy

spontaneous remission/regression to the mean (small proportion)

classical conditioning

neurotransmitter system implicated

non-specific physiological regulatory mechanism

specific physiological events

Spontaneous Remission

getting better without intervention

Regression to the Mean

an extreme result is likely to be followed by a more average one

Nocebo Effect

expectation of a negative outcome may lead to the worsening of symptoms

ethics limit studies

Setting Effects

how the environment influences responses

Advantages of Pharmacotherapy

focus on physical issues and comfort from that

tend to be less expensive

tend to work faster

easier to avoid stigma (more discreet)

Advantages of Psychotherapy

work through issues and be aware

address root of issue

less likely to relapse

Disadvantages of Pharmacotherapy

side effects (some of which are dangerous or stop people from wanting to use them)

may be costly over time

increased risk of relapse when discontinued

may turn short-term problem into a long-term problem (physical dependence)

medicalizing problems making them appear out of patient's hands

Disadvantages of Psychotherapy

talking does not work for everyone

difficult to develop a trusting therapeutic relationship (may make people less likely to go back or find another therapist)

some negative potential outcomes

The Complex Issue of Combination Therapy

not always best

insurance plans/availability/accessibility

cost effective/more is not always better

psychotherapy may influence side effects

core symptoms vs. real world relationships

some drugs impair cognition and thus CBT

not mutually exclusive

Role of Client Choice

small, significant effect in favor of clients who received a preferred treatment

Diagnostic and Statistical Manual (DSM-5)

used to diagnose psychological disorders

focuses on symptoms

revised every 10-15 years

Why Stigma of Mental Illness is a Big Deal

deter people from getting help

Major Depressive Disorder (MDD)/Unipolar Depression

debilitating condition characterized by overwhelming sadness, feelings of worthlessness, and loss of interest in normally pleasurable activities

most common disabling psychiatric illness in the adult population

Drug Research Issues

drugs more effective in clinical trials than in real world settings

community sample advantages

trend towards using e-technology

patient variability/not all equal

comorbidity

challenging to determine if changes in the brain are due to condition or drug

Comorbidity

having multiple conditions

Depression Demographics

women more common than men and have different symptoms

more common in young people and the elderly

more common in LGBTQ+ people

Depression Symptoms in Women

sadness

guilt

hopelessness

Depression Symptoms in Men

rage

aggression

irritability

substance abuse

Reason for Increase in MDD Prevalence

greater awareness

less stigma

societal changes (social media)

over-diagnosis

COVID

increased availability of pharmaceutical treatments

Biological Factors in MDD

genetics

neurochemistry/monoamines

neuroanatomy/smaller brain structures

overactive stress response

chronic inflammation

obesity

gut bacteria

Monoamine Theory

low levels of serotonin, dopamine, and norepinephrine involved in depression

problem because there is a lack of consistent data showing lower levels in depressed populations and therapeutic lag

Therapeutic Lag

taking time to show therapeutic effects even when drug works quickly

Psychological Factors in MDD

cognitive beliefs

interpersonal factors

stressful life events

Social Factors in MDD

poverty

adverse work conditions

trauma

drug use

lack of social support

Negative Cognitive Triad

psychological factor in depression from Aaron Beck

negative views about the world

negative views about the future

negative views about onself

Neurogenic/Neurotrophic/Glucocorticoid Theory of Depression

depression as a disorder of cellular plasticity and survival

depression as a stress-induced, reversible, structural disorder of the brain, involving neuronal atrophy and neuronal loss secondary to reduced expression of certain neurotrophic factors that are essential to maintenance of neuronal health and survival

based on the ideas that existing neurons repair and remodel themselves and neurogenesis

prolonged stress can lead to hyperactive HPA which is linked to hippocampal atrophy and reduced neurogenesis and dendritic branching and spines and impaired immune system

Brain-Derived Neurotrophic Factor (BDNF)

central during brain development, cellular survival, and synaptic changes in adults

when low, dendritic branching and spines reduced

chronic stress reduces it and antidepressants increase it

functional polymorphisms is gene play a role in predisposition to depression

Neurogenesis

the creation of new neurons

especially in the hippocampus and the frontal cortex

Limbic System

brain’s emotional system

includes structures such as the hippocampus and amygdala

Hippocampal Volumes in People with Depression

reduced volume

longer the depressive episode, greater the shrinkage

shrinkage reversible with antidepressants

Drug Treatment for Depression Based on Neurogenic Hypothesis

drugs may exert their effects by increasing growth and survival of newly formed neurons in the hippocampus

Therapeutic Lag in Depression

2-4 weeks/4-6 for maximum effects

time to reach steady state and promote BDNF and neurogenesis

Symptoms of Major Depressive Disorder

sadness, despair, depressed mood

loss of interest or pleasure in activities

guilt, anxiety, low self-esteem

lack of motivation, fatigue, loss of energy

diminished ability to concentrate

changes in appetite or weight

disrupted sleep patterns

recurrent thoughts of death or suicide attempts

to be diagnosed, must have at least five or more symptoms that last for at least two weeks, have at least one of the first two symptoms, and impaired functioning

Three Most Commonly Prescribed Medications

blood pressure

cholesterol

antidepressants

Monoamine Oxidase Inhibitors (MAOIs)

class of antidepressant drugs that inhibit the enzyme that breaks down serotonin, dopamine, norepinephrine, etc.

monoamine agonist because they increase activity

common side effect: tyramine build up leading to severe increase in blood pressure, heart attack, and stroke

Tricyclic Antidepressants (TCAs)

class of antidepressant drugs that block reuptake of serotonin and norepinephrine and block postsynaptic acetylcholine, norepinephrine, and histamine receptors

serotonin and norepinephrine agonist

postsynaptic acetylcholine, norepinephrine, and histamine antagonist

common side effect: cardiotoxic with low therapeutic index

Selective Serotonin Reuptake Inhibitors (SSRIs)

class of antidepressant drugs that block reuptake of serotonin

serotonin agonist

Atypical/Mixed Antidepressants/Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs)

class of antidepressant drugs where most block reuptake of serotonin and norepinephrine 

drugs that block dopamine reuptake also included in this group

serotonin and norepinephrine agonist

Tyramine

byproduct of fermentation

metabolized by MAO

Wine and Cheese Effect

tyramine build-up from taking MAOIs

can lead to severe increase in blood pressure, heart attack, and stroke which can be potentially fatal

Useful TCA Side Effects

sedating effects of amitriptyline and doxepin for agitation and insomnia

stimulating effects of desipramine and nortriptyline for motivational issues

Serotonin Discontinuation Syndrome/Withdrawal

60% show upon antidepressant discontinuation

produce dependence but not addiction

onset within days and persists 3-4 weeks

psychological symptoms may be confused with relapse

variability in frequency and symptoms across antidepressants

FINISH Symptoms of Serotonin Discontinuation Syndrome

flulike symptoms (fatigue, lethargy, chills, headache)

insomnia (sleep disturbances, vivid dreams)

nausea (gastrointestinal symptoms, vomiting, diarrhea)

imbalance (dizziness, vertigo, ataxia)

sensory disturbances (sensation of electric shocks)

hyperarousal (anxiety, agitation, crying spells)

Serotonin Syndrome

occurs with high doses or when SSRIs or other antidepressant drugs are combined with other serotonergic drugs

lasts 24-48 hours after discontinuation of drug(s)

symptoms: cognitive alterations (disorientation, confusion, hypomania, visual hallucinations), behavioral alterations (agitation, restlessness), autonomic nervous system functions (fever, chills, sweating, diarrhea, hypertension, tachycardia), and neuromuscular activity (ataxia, enhanced reflexes, muscle spasms)

Depression that Responds Best to Medication

severe depression and symptoms

Neonatal Abstinence Syndrome

type of withdrawal in newborns whose mothers took antidepressants during pregnancy

high pitched crying, tremors, disturbed sleep

Real World Efficacy of Antidepressants Worse Because

more monitoring/control in clinical trials

Determinants of Antidepressant Drug Choice

side effect profile

possibly mixing with other drugs

experience with certain drugs/free samples

symptom variability and severity

Clinical Considerations for Emergent Suicidal Thoughts

appropriate monitoring of patients

adjust doses or change drug

adding cognitive therapy to medications

consider alternative treatments

Combination of Pharmacotherapy and Psychotherapy

moderately increase acute response (10-20%)

retains the benefits of both

Effects of Antidepressants During Pregnancy

mixed results

linked to spontaneous abortion, preterm birth, low birth weight, and some specific effects such as cardiac development

Risk of Suicidal Thoughts on Antidepressants

complex

risk increases but is very low (2-4%)

suicides increase when number of people using antidepressants drops (seen in multiple countries)

more likely that suicidal behavior leads to treatment than treatment leads to suicidal behavior

Alternate Treatments for MDD

psilocybin

ketamine

electroconvulsive therapy

transcranial direct current stimulation