Clinical Psychology & Mental Health - Unit 3

what are the symptoms of major depressive disorder (mdd)?

persistent sadness/emptiness, hopelessness, anhedonia, weight/appetite changes, sleep disturbances, psychomotor changes, fatigue, worthlessness, suicidal thoughts

what is anhedonia?

a markedly diminished interest in almost all activities

what is insomnia?

difficulty falling asleep, staying asleep, or early morning awakening

what is hypersomnia?

excessive sleeping (often as an escape mechanism)

what are some psychomotor changes?

agitation (restlessness), retardation (slowed movements/speech/thinking)

what is seen in mdd with anxious distress?

co-occurring anxiety symptoms (tension, worry about losing control)

what is seen in mdd with melancholic features?

severe anhedonia (worse in morning), early awakening, excessive guilt, weight loss

what is seen in mdd with atypical features?

mood reactivity, increased appetite (weight gain), hypersomnia, leaden paralysis, rejection sensitivity

what is seen in mdd with psychotic features?

hallucinations, delusions (often with themes of guilt/disease/nihilism)

what is seen in mdd with catatonia?

psychomotor immobility, stupor, excessive purposeless activity

what is seen in mdd with peripartum onset?

during pregnancy or within four weeks postpartum

what is seen in mdd with seasonal pattern?

regular seasonal occurrence (typically fall/winter with spring/summer remission)

what is persistent depressive disorder (dysthymia)?

chronic depression lasting more than two years with fewer symptoms than mdd

what is premenstrual dysphoric disorder?

severe mood symptoms during the luteal phase of the menstrual cycle

what is disruptive mood dysregulation disorder?

childhood disorder with severe irritability and temper outbursts

what is substance/medication-induced depressive disorder?

depression directly caused by intoxication, withdrawal, or medications

what disorders should be screened for before diagnosing mdd?

bipolar disorders, adjustment disorder with depressed mood, bereavement, medical conditions (hyperthyroidism, vitamin deficiencies, anemia)

why should bipolar disorders be screened for before diagnosing mdd?

must screen for past manic/hypomanic episodes to avoid triggering mania with antidepressants

what is adjustment disorder?

a time-limited reaction to identifiable stressors

what is bereavement?

normal grief that involves waves of sadness with positive memories (differs from mdd cause not persistent)

what is the leading cause of disability worldwide?

depressive disorders

what are some gender disparities in depressive disorders?

women are 2x more likely after puberty, men have higher completed suicide rates

what are some age patterns in depressive disorders?

can occur at any age, but average onset is in the mid-20s

what are some socioeconomic factors of depressive disorders?

higher rates in lower SES groups, unemployment and financial stress as both cause and consequence

what are some cultural variations in depressive disorders?

more psychological symptoms reported in western cultures, more somatic complaints in non-western cultures, stigma varies

what is the monoamine hypothesis?

a neurotransmitter theory that states deficiencies in serotonin, norepinephrine, and/or dopamine caused depression

what is the beyond simple depletion theory?

states depression is caused by receptor sensitivity, neurotransmitter synthesis, and breakdown issues

how can glutamate and GABA cause depression?

excitatory/inhibitory balance

how can hippocampus structure cause depression?

atrophy is linked to memory problems and stress response dysregulation

how can prefrontal cortex structure cause depression?

reduced activity affects executive function and emotion regulation

how can amygdala structure cause depression?

hyperactivity leading to heightened emotional responses

how can the default mode network in the brain cause depression?

increased connectivity is associated with rumination

how does beck’s cognitive triad explain depression?

negative view of self (worthlessness), world (worldwide rejection), and future (never improving)

how do cognitive distortions explain depression?

all-or-nothing thinking, overgeneralization, mental filter (focusing only on the negatives), catastrophizing

what is learned helplessness?

believing that actions don’t affect outcomes, leading to passive resignation

what is rumination?

having a repetitive focus on symptoms and causes without problem-solving

how can a loss of reinforcement explain depression?

reduced positive experiences → withdrawal

how can deficits in social skills cause depression?

poor interpersonal skills → rejection → depression

how do avoidance patterns affect depression?

withdrawal maintains and worsens depression

what is avoidance?

a coping mechanism where individuals evade thoughts, feelings, or situations that cause discomfort

what are some social/environmental factors affecting depression?

life stressors (major losses, failures), interpersonal factors (conflict, isolation, lack of support), childhood adversity, chronic stress

how does beck’s cognitive-behavior model explain depression?

negative schemas are activated by stress → cognitive distortions → depression

how does hopelessness theory explain depression?

negative attributional style (negative events stem from internal, stable or global causes) → hopelessness → depression

how does behavioral activation describe depression?

depression is a consequence of avoidance and reduced activity

what is the interpersonal model for depression?

four problem areas: grief, role disputes, role transitions, interpersonal deficits → depression occurs in the interpersonal context and affects relationships

what is the biological/medical model for depression?

depression is a brain disease that requires medical intervention — focus on neurotransmitters, brain circuits, and genetic vulnerability

what are some integrative models for depression?

diathesis-stress (genetic vulnerability + environmental triggers), gene-environment interaction (certain genes increase sensitivity to stress)

what are structured clinical interviews (SCID, MINI)?

interviews with standardized questions to ensure a comprehensive assessment

what are unstructured clinical interviews?

interviews that are flexible and rapport-building, but may miss symptoms

what is the beck-depression inventory (BDI-II)?

a self-report measure with 21 items that’s widely used and has good reliability

what is the PHQ-9?

a self-report measure with 9 items (brief) that tracks DSM criteria and is primarily used in primary care

what is the hamilton depression rating scale?

a self-report measure that is clinician-administered and considered a gold standard in research

what is the columbia scale?

a suicide risk assessment that systematically assesses any ideations, plans, and attempts

what is safety planning?

the collaborative creation of coping strategies and resources to prevent suicide

how can cognitive-behavioral therapy (cbt) treat mild-moderate depression?

identifies and changes negative thought patterns and behaviors using thought record, behavioral experiments, and activity scheduling

how can interpersonal therapy (ipt) treat depression interpersonal triggers?

uses three phases (initial - assessment, middle - working on problem area, termination) to focus on current relationships and life circumstances

how can behavioral activation treat depression?

a simple delivery that increases rewarding activities to improve mood by activity monitoring, scheduling pleasant events, and reducing avoidance

what is the first-line medication treatment for depression?

selective serotonin reuptake inhibitors (SSRIs)

how do SSRIs treat depression?

block the reuptake of serotonin at the synaptic cleft, which increases serotonin availability, affecting neuroplasticity and mood regulation

what is fluoxetine/prozac?

a common SSRI with a long half-life (4-6 days), is activating and good for depression with fatigue, and has less withdrawal symptoms

what is sertraline/zoloft?

a common SSRI with a mild dopamine reuptake inhibition, has lower drug interactions, is good for depression with anxiety, and is often the first choice in cardiac patients

what is paroxetine/paxil?

a common SSRI that is anticholinergic (inhibit acetylcholine), sedating, good for insomnia, has the worst withdrawal symptoms, and can cause weight gain

what is escitalopram/lexapro?

a common SSRI that is the most selective, has few side effects, fast onset, and good tolerability in the elderly

what is citalopram/celexa?

a common SSRI with a QT prolongation risk at higher doses, so doses are limited, but have generic availability, making them cost-effective

what are common side effects of SSRIs?

nausea, sexual dysfunction, long-term weight gain, activation/anxiety (initial), emotional blunting

when is improvement expected for SSRIs?

initial improvement by two weeks

how long are SSRIs taken?

4-6 weeks

what are SNRIs?

serotonin-norepinephrine reuptake inhibitors

how do SNRIs treat depression?

dual reuptake inhibition — affects both serotonin and norepinephrine systems, leading to a broader spectrum of action  

what is venlafaxine/effexor?

a common SNRI that is dose-dependent (low = SSRI, high = SNRI), may increase blood pressure, is good for treatment-resistant depression, and can cause withdrawal syndrome

what is duloxetine/cymbalta?

a common SNRI that is FDA-approved for chronic pain, is good for depression with pain symptoms and useful in diabetic neuropathy, and has more balanced dual action at all doses

what is desvenlafaxine/pristiq?

a common SNRI that causes more consistent blood levels, has less drug interactions, and a similar efficacy to venlafaxine (parent compound)

what is levomilnacipran/fetzima?

a common SNRI that focuses more on norepinephrine activity, may improve energy and motivation, and is less studied than other SNRIs

what are common side effects of SNRIs?

similar to SSRIs + increased blood pressure, sweating, and constipation

what is bupropion/wellbutrin?

an atypical antidepressant that inhibits the reuptake of norepinephrine and dopamine, causes no sexual dysfunction, can cause weight loss, seizure disorders, eating disorders, and is good for fatigue, comorbid ADHD, and smoking cessation

what is mirtazapine/remeron?

an atypical antidepressant that causes rapid sleep improvement, appetite stimulation, and no sexual dysfunction, can cause weight gain and sedation, and is used on depression with insomnia, poor appetite, and in elderly patients

what is trazodone?

an atypical antidepressant that is a serotonin antagonist and reuptake inhibitor, can cause priapism and orthostatic hypotension, and is used in low doses for insomnia 

what is vilazodone/viibryd and vortioxetine/trintellix?

atypical antidepressants that are serotonin partial agonist reuptake inhibitors, may have cognitive benefits, causes less sexual dysfunction, but is newer, more expensive, and has limited long-term data

what is the second/third-line medication treatment for depression?

tricyclic antidepressants (TCAs)

how do tcas treat depression?

block the reuptake of serotonin and norepinephrine, as well as block histamine, acetylcholine, and alpha1 receptors

what is amitriptyline?

a common tca that is very sedating and used for chronic pain and migraines

what is nortriptyline?

a common tca that is better tolerated than amitriptyline

what is imipramine?

a common tca that is used for panic disorder

what is desipramine?

a common tca that is noradrenergic (targets norepinephrine) and the least sedating

what are some side effects of tcas?

anticholinergic (dry mouth, constipation, urinary retention), sedation, weight gain, cardiac effects

what are monoamine oxidase inhibitors (MAOIs)?

medications reserved for treatment-resistant depression cases

how do maois treat depression?

inhibit enzymes that break down monoamines, increasing serotonin, norepinephrine, and dopamine

what is phenelzine/nardil?

a maoi that is an irreversible inhibitor

what is tranylcypromine/parnate?

a maoi that is irreversible and more activating  

what is a selegiline patch/emsam?

a maoi that is transdermal and has fewer dietary restrictions at low doses

what are the dietary restrictions when taking maois?

avoiding tyramine-rich foods (aged cheese, cured meats, fermented foods) to prevent a hypertensive crisis

how do maois interact with other drugs?

fatally interacts with other serotonergic drugs and many over-the-counter medications

what is ketamine/esketamine/spravato?

a rapid-acting treatment (improvement within hours to days) that is an NMDA receptor antagonist, increasing glutamate, which releases BDNF, causing synaptogenesis, has temporary effects, dissociative side effects, abuse potential, and is used in treatment-resistant depression and acute suicidality

what is a standard depression treatment plan?

start with SSRI/SNRI, switching strategies if no improvement, consider augmentation options, target treatment resistance

how should SSRIs/SNRIs be chosen?

consider side effects matching needs, family history to previous responses, comorbidities, and drug interactions

what are some switching strategies?

direct switch (to a similar medication), cross-taper (different classes of medication), wash-out period (to-and-from maois)

what are some augmentation options for bipolar disorder?

atypical antipsychotics (aripiprazole, quetiapine), lithium, thyroid hormone T3, a second antidepressant

what happens if it seems like the depression is treatment-resistant?

the diagnosis is reassessed, dosage and duration are reoptimized, and ect/tms/ketamine is considered

how can electroconvulsive therapy (ect) treat depression?

controls seizures for neuroplastic changes, is used for psychotic depression, catatonia, during pregnancy, after medications fail, can cause (temporary) memory loss and headaches, 6-12 sessions

how can transcranial magnetic stimulation (tms) treat depression?

magnetic pulses are used to stimulate the prefrontal cortex, a non-invasive treatment with no memory loss, daily sessions