What distinguishes features of unipolar depression from its symptoms?

;Features are
facts about who gets depression and how often, symptoms are behaviours and feelings
used to diagnose it.;Features include prevalence, age groups, and types (mild,
major, postnatal, SAD). Symptoms are affective (low mood), cognitive (poor
concentration), social (withdrawal), and physical (sleep changes). Exams test
features and symptoms separately.
What is the prevalence of unipolar depression in the UK?;About 3.5 million
people.;Nearly 19 % of British adults report an episode of depression. It is more
common in women (30 %) than men (15 %), and in lower-income households. Exams may
ask for these statistics.
Which demographic groups are at higher risk for depression?;Women, divorced or
separated people, lower-income households, and people aged 50-54.;Women report
depression at 30 %, men at 15 %. Divorced or separated report 27 %, singles 20 %,
and stable relationships 16 %. Lower-income groups have higher rates. The highest-
risk age group is 50-54.
Define mild versus major depression and their effects.;Mild depression slightly
affects daily life, major depression significantly disrupts eating, sleeping, and
functioning.;Mild depression might cause low motivation but still allow basic
routines. Major depression can lead to hospital admission if self-harm risk rises.
Exams expect definitions based on impact on daily activities.
What is postnatal depression and how does it differ from baby blues?;Postnatal
depression is severe feelings of anxiety and negative thoughts that begin 2–3 weeks
after birth, affecting 1 in 10 mothers, baby blues are brief mood changes lasting a
couple of weeks.;Baby blues involve mild sadness and worry right after birth, but
symptoms resolve in two weeks. Postnatal depression includes panic attacks,
overwhelm, and negative thoughts toward the baby, requiring treatment.
What is Seasonal Affective Disorder (SAD)?;A type of depression that lasts during
winter due to less daylight.;SAD can cause mood drops, oversleeping, overeating,
and social withdrawal from autumn until spring. Mild cases are called winter blues.
Exams may ask to connect SAD to reduced sunlight affecting melatonin and serotonin.
What codes does ICD-10 assign to depression?;F32.0 for mild, F32.1 for moderate,
F32.2 or F32.3 for severe.;ICD-10 requires four symptoms for mild, six for
moderate, and eight for severe. Three key symptoms: depressed mood, loss of
interest, and decreased energy. Exams want you to understand these codes and
criteria.
How does DSM-5 define Major Depressive Disorder (MDD)?;At least five of nine
symptoms for two weeks, including depressed mood or loss of interest.;Symptoms
include weight change, sleep change, psychomotor change, fatigue, feelings of
worthlessness or guilt, poor concentration, and recurrent thoughts of death. One
key symptom (depressed mood or anhedonia) must be present.
What are the four categories of depression symptoms?;Affective : low mood,
worthlessness, Cognitive : poor concentration, indecisiveness, Social : withdrawal
from activities and relationships, Physical : appetite changes, aches, sleep
disturbances.;Exams expect examples such as pessimism, difficulty concentrating,
giving up hobbies, and unexplained pains. Link intensity and duration to diagnosis.
How long must symptoms persist for a DSM-5 diagnosis of MDD?;At least two
weeks.;ICD-10 also requires two weeks, though it can be shorter if symptoms are
severe and there is risk of harm. A short period risks false positives, a longer
one risks false negatives.
What key change did DSM-5 make regarding bereavement and depression?;It removed the
bereavement exclusion, allowing diagnosis of MDD soon after a loved one’s
death.;DSM-IV prevented diagnosing MDD within two months of bereavement. DSM-5’s
removal increases the chance of timely treatment but raises false-positive risk by
medicalising normal grief.
How do DSM-5 and ICD-10 differ on key symptoms?;DSM-5 has two key symptoms
(depressed mood, loss of interest), ICD-10 has three (depressed mood, loss of
interest, decreased energy).;For ICD-10, two key symptoms must be present for mild
or moderate depression, all three for severe. ICD-10’s extra key symptom reduces
false positives but increases false negatives. Exams ask you to compare these
differences.
What reliability issues arise in diagnosing depression across countries?;British
psychiatrists diagnosed depression twice as often as American ones, showing
cultural and reliability differences.;Cooper et al. (1972) had psychiatrists watch
the same films. Brits labelled patients depression, Americans labelled
schizophrenia. ICD-10 and DSM-5 convergence has improved reliability, but cultural
context still affects diagnosis.
Why can thyroid problems or other disorders complicate valid depression
diagnosis?;They cause negative affect similar to depression
symptoms.;Hypothyroidism can cause fatigue and low mood. Distinguishing depression
requires ruling out medical causes. Exams may ask how differential diagnosis
ensures valid identification of depression.
How do cultural differences interfere with diagnosing depression?;Different
cultures value emotional expression differently, changing how symptoms are
displayed.;In Asian cultures emotional restraint is praised, so emotional symptoms
might be hidden. In some Arabic cultures overt emotional expression is expected.
Clinicians must understand cultural norms to avoid misdiagnosis.
What objections exist to DSM-5’s removal of the bereavement exclusion?;It may lead
to false positives, diagnosing healthy grief as MDD and prescribing unnecessary
medication.;Normal grief can include sadness and sleep issues, but if diagnosed as
MDD, healthy people get medication, feel “sick”, and risk side-effects. Exams may
ask to discuss medicalisation of sadness.
How did Kraepelin contribute to understanding depression?;He introduced the term
depression in the 1890s and distinguished it from other disorders like
schizophrenia.;Emil Kraepelin’s work led to modern diagnostic categories. His
classification of melancholia persisted through DSM editions and ICD. Exams might
ask for historical context like this.
What is the PHQ-8 and what does it measure?;A questionnaire scoring depression
symptoms out of 24, a score of 10 or more indicates clinical depression.;Developed
by Kroenke et al. (2008), PHQ-8 omits the suicidal-ideation question found in PHQ-
9. It is used in clinics to screen for depression severity.
What family and adoption study supports a genetic link to depression?;Gershon
(1990) found two-to-three times higher depression rates in first-degree relatives,
Wender et al. (1986) showed similar findings in adoption studies.;Gershon reviewed
ten family studies: parents or siblings of depressed people have double or triple
risk. Wender et al. found adopted-away children of depressed parents still had
higher rates, showing genetics over environment.
What is the monoamine hypothesis of depression?;It says low levels of serotonin,
noradrenaline, and dopamine lead to depression.;Serotonin regulates the other two.
Low serotonin causes noradrenaline and dopamine to drop, leading to lack of
pleasure, alertness, and energy. Genetic factors affecting the 5-HTT gene can
reduce serotonin uptake, increasing risk after stress.
How does the 5-HTT gene relate to depression risk?;Variants of 5-HTT lead to lower
serotonin transporter function, increasing risk after stressful life events.;People
with the short allele of 5-HTT show lower serotonin uptake. The diathesis-stress
model says gene vulnerability plus stress triggers depression. Exams expect you to
mention specific gene–environment interaction.
Explain MAO-A’s role in the monoamine hypothesis.;MAO-A removes monoamines
(serotonin, noradrenaline, dopamine) from the synapse, too much MAO-A lowers these
neurotransmitters, causing depression.;MAO-A is like Pac-Man, eating up
neurotransmitters. If MAO-A is over-active, the brain is starved of mood-regulating
chemicals. MAO-A inhibitors (MAOIs) block this enzyme, raising monoamine levels.
What post-mortem findings support the monoamine hypothesis?;Mann (2003) found
reduced serotonin levels and increased serotonin receptor sites in brains of people
who committed suicide.;In suicide victims low serotonin suggests deficiency, and
extra receptors imply the brain tried to compensate. Exams want you to cite this
study to show biological evidence.
What evidence challenges the monoamine hypothesis?;Thase et al. (2002) found
increased noradrenaline in severe depression, Kirsch (2008) showed antidepressants
barely outperform placebo in mild cases.;Thase’s findings contradict expected low
noradrenaline. Kirsch meta-analysis on SSRIs versus placebo suggests minimal effect
except in severe cases, questioning direct neurotransmitter causation.
What genetic and environmental model helps explain depression?;Rosenthal’s
diathesis-stress model.;It says genes create vulnerability (e.g. 5-HTT variants),
but stress (e.g. trauma, loss) triggers depression. Genes alone do not guarantee
illness. Exams expect you to explain this interaction.
List two strengths of the biological explanation for depression.;1. Family and
adoption studies show genetic links. 2. Antidepressant effectiveness supports
monoamine involvement.;Gershon and Wender provide strong genetic evidence. SSRIs
and MAOIs lessen depressive symptoms, consistent with neurotransmitter models.
Exams want you to link theory to treatment.
List two weaknesses of the biological explanation for depression.;1. Correlation
does not prove causation. 2. It ignores social and psychological factors like
poverty or trauma.;Low neurotransmitter levels could result from depression, not
cause it. Biological models reduce complex experiences to chemicals, overlooking
environment and cognition.
What are the main types of antidepressant drugs?;MAOIs, tricyclics, SSRIs, and
SNRIs.;MAOIs (e.g. phenelzine) inhibit monoamine oxidase, tricyclics (e.g.
amitriptyline) boost serotonin and noradrenaline, SSRIs (e.g. Prozac) block
serotonin reuptake, SNRIs (e.g. venlafaxine) block noradrenaline reuptake.
How do MAOIs treat depression?;They inhibit monoamine oxidase A, preventing removal
of monoamines, thus raising serotonin, noradrenaline, and dopamine.;MAO-A
inhibitors like isoniazid were first used. They increase synaptic monoamine levels,
improving mood. Exams expect pros (effective for resistant cases) and cons
(hypertensive crisis with tyramine-rich foods).
What side-effects do MAOIs and tricyclics have?;MAOIs can cause irreversible high
blood pressure, tricyclics can cause constipation, blurred vision, memory loss, and
risk of overdose leading to psychosis or coma.;MAOIs require a strict diet (no
cheese, wine). Tricyclic side-effects come from anticholinergic actions and cardiac
toxicity in overdose.
What are SSRIs and why are they preferred?;Selective serotonin reuptake inhibitors
block serotonin reuptake, boosting synaptic serotonin with fewer side-effects than
older drugs.;Prozac is a famous SSRI. SSRIs cause headaches, nausea, weight gain,
sexual problems but have lower overdose risk. NICE recommends SSRIs as first-line
treatment.
What are SNRIs and when are they used?;Serotonin-noradrenaline reuptake inhibitors
block reuptake of both serotonin and noradrenaline, used also for anxiety and
OCD.;Venlafaxine and duloxetine are SNRIs. They help patients with mixed anxiety-
depression symptoms and those not responding to SSRIs.
What prescribing guidelines exist for antidepressants?;NICE (2014) recommends SSRIs
first, if ineffective try another SSRI, then tricyclics or MAOIs. Only one
antidepressant at a time.;Prescribers avoid combining MAOIs with tricyclics within
two weeks. Thirty per cent of patients fail to respond to one drug but may respond
to another. Exams expect you to know the trial-and-error approach.
Why do antidepressants take weeks to work?;Because they first change serotonin
levels but need several weeks for downstream changes like neurogenesis in the
hippocampus to occur.;SSRIs increase serotonin immediately, but receptor
sensitivity changes, gene expression, and neuron growth take weeks, explaining
delayed symptom relief. Exams want you to link increased BDNF and neurogenesis to
the delay.
What are common side-effects of SSRIs?;Headaches, weight gain, lethargy, nausea,
sexual dysfunction, and possible worsening of depression.;Some patients feel
emotionally “numb” and withdraw SSRI use to feel any emotion. Discontinuation can
cause flu-like symptoms. Exams ask for side-effects and their impact on compliance.
What is the discontinuation syndrome of antidepressants?;Symptoms like anxiety,
mood swings, flu-like sensations, or tremors when stopping an antidepressant
abruptly.;It is not withdrawal because SSRIs are not addictive. The body must adapt
to reduced serotonin. Longer half-life drugs like Prozac cause fewer
discontinuation symptoms.
What evidence suggests over-prescription of antidepressants?;Kirsch (2008) found
SSRIs no better than placebo in mild depression, in the UK over 40 million
prescriptions per year, suggesting many get pills with no benefit.;In the US one in
ten has been prescribed antidepressants, one in six of those are not depressed.
This implies medicalisation of normal mood swings.
What is Electro-Convulsive Therapy (ECT) and when is it used?;ECT induces seizures
under anaesthesia to treat severe, treatment-resistant depression.;It is rare due
to ethical concerns and side-effects such as memory loss. Exams might ask for its
mechanism: resets neurotransmitter systems quickly but with cognitive costs.
What genetic study supports depression risk apart from monoamine genes?;Elliot
Gershon (1990) family studies and Wender et al. (1986) adoption studies.;Gershon
showed two-to-three times higher depression in first-degree relatives. Wender found
adopted-away children with depressed parents still had higher rates, supporting
heredity over environment.
What is the cognitive explanation of depression?;It says negative thinking patterns
about self, world, and future drive depression.;Beck’s cognitive triad: depressed
patients have negative views about themselves (“I’m worthless”), the world
(“Everything is against me”), and the future (“Things will never improve”). Ellis’s
ABC model says an activating event leads to beliefs which cause emotional
consequences, dispute challenges irrational beliefs.
How does Beck’s Cognitive Triad explain depression?;Negative thoughts about self
(“I am worthless”), the world (“Nobody cares about me”), and the future (“Things
will never get better”) create and maintain low mood.;Patients believe they are
failures, see the world as hostile, and expect more failure. These beliefs cause
depressed feelings and behaviours. CBT helps identify and rewire these thoughts.
What is Ellis’s ABC model for depression?;Activating event, belief about event,
consequence (emotional or behavioural), dispute challenges irrational beliefs. For
example, A : friend cancels plans, B : “They hate me”, C : sadness and
withdrawal.;The therapist disputes the belief (“Are you sure they hate you?”)
leading to a new emotional outcome.
What evidence supports cognitive explanations of depression?;Lewinsohn et al.
(2001) found negative thinking in non-depressed participants predicted later
depression after life events.;Researchers assessed participants without depression
and tracked them for a year. Those with more negative thoughts were more likely to
become depressed following stress, suggesting cognition precedes mood disorder.
What are two strengths of cognitive explanations?;1. They offer valid links between
thoughts and mood. 2. They guide effective CBT treatments that reduce relapse
rates.;By focusing on faulty thinking, cognitive models can directly improve mood.
CBT’s success (Stiles et al. 2006) supports the validity of cognitive theory.
What are two weaknesses of cognitive explanations?;1. They cannot fully explain
negative symptoms. 2. Cognitive dysfunction may result from mood, not cause
it.;Cognitive deficits like poor memory could be an effect of depression. Socio-
economic factors or biology may cause depression independent of thoughts.
What is the structure of a CBT session for depression?;Identify problems, set
goals, challenge negative thoughts, set homework to test beliefs.;Therapist and
client collaborate: list negative thoughts, examine evidence, create alternative
thoughts, plan behavioural experiments such as socialising to test “People don’t
like me”. Homework reinforces changes.
What is psychoanalysis and how is it applied to depression?;A therapy focusing on
unconscious conflicts using free association, dream analysis, and
transference.;Psychoanalysis aims to uncover childhood traumas. Free association
has the client speak freely, dream analysis interprets symbols, transference
reveals feelings toward parents projected onto the analyst. These methods seek deep
insight into depressive causes.
List two strengths of Beck’s cognitive model for depression.;1. Face validity:
negative thoughts align with common-sense of depression. 2. Guided development of
CBT, which shows lower relapse rates than drugs.;Beck’s model matches patients’
reported thoughts, and CBT’s efficacy (Hollon et al. 2005) supports its accuracy.
List two weaknesses of Beck’s cognitive model for depression.;1. Relies on self-
report measures like the BDI, risking subjective bias. 2. Does not explain why some
develop negative schemas and others do not.;Self-reports can reflect demand
characteristics. Origins of schemas are vague—Beck attributes them to childhood but
provides little mechanism for variation among individuals.
What is learned helplessness and how does it relate to depression?;People believe
they have no control over negative events, leading to passivity and
depression.;Seligman & Maier (1967) showed dogs exposed to unavoidable shocks later
did nothing to escape. In humans repeated failures or trauma can produce a mindset
of no control, called learned helplessness or fatalistic thinking. This cognitive
style predisposes individuals to depression.
What is Beck’s negative schema and how does it form?;A deep-seated belief formed in
childhood, for example “I’m unlovable”, arising from critical or traumatic
experiences.;Schemas develop from parental criticism, abuse, or bullying. When
triggered by similar situations in adulthood they cause negative thoughts and
depressed mood. CBT aims to identify and modify these schemas.
How are Beck’s schemas and Seligman’s explanatory styles similar?;Both describe
learned negative patterns of interpreting events that lead to depression.;Beck’s
schemas are core beliefs that filter perceptions negatively. Seligman’s explanatory
style describes attributing negative events to stable, global, internal causes.
Both frameworks highlight cognition’s role in depression.
What role does the Beck Depression Inventory (BDI) play in cognitive models?;It
quantitatively measures negative thoughts and depressive symptoms through a 21-item
self-report.;Each item scored 0–3 covers hopelessness, guilt, and physical
symptoms. Clinicians use the BDI to assess severity and track response to CBT,
supporting cognitive hypotheses about symptom change.
What role does the PHQ-8 play in cognitive assessment of depression?;It screens for
depression severity using eight questions about mood, failures, and
concentration.;Developed by Kroenke et al. (2008), a score of 10 or above suggests
clinical depression. Its focus on thoughts and feelings aligns with cognitive
models and helps detect patients needing treatment.
What objections exist to Beck’s cognitive explanation of depression?;1. Origins of
negative schemas are unclear—why do some develop them after trauma and others do
not? 2. Negative cognitions might result from early undetected depression rather
than cause it.;The Lewinsohn et al. (2001) study may reflect participants already
in prodromal stages. The model is descriptive of thought patterns but does not
explain aetiology.
What face validity supports Freud’s psychodynamic explanation for
depression?;Traumatised or neglected children often develop depression as adults,
matching Freud’s view of an over-active superego and inverted anger.;Freud’s idea
that repressed anger toward caregivers turns inward explains guilt and low self-
worth in depressed individuals. Psychoanalysis’s continued use in some settings
reflects its resonance with clinical observations.
What objections exist to Freud’s psychodynamic explanation for depression?;1. Fewer
than 10 % of abused children develop depression, challenging predictive claims. 2.
Many traumatised children externalise anger rather than internalise it as Freud
predicts.;Freud’s model fails to account for variability—anger at neglect often
leads to externalising behaviours or resilience, not depression. His theory relies
on unobservable constructs with limited empirical support.
How are cognitive and psychodynamic explanations complementary?;Cognitive models
explain present thought patterns, psychodynamic models explore childhood origins of
those patterns.;Beck’s schemas may arise from Freud’s unconscious conflicts. Early
trauma forms schemas, which manifest as negative thoughts. Combining both provides
a fuller understanding and treatment options.
How do cognitive and biological explanations interact in understanding
depression?;Biological changes such as low serotonin can trigger negative thinking,
and faulty cognitions can worsen stress responses and neurotransmitter
imbalance.;Rayner et al. (2016) found over-active prefrontal areas related to guilt
and brooding in depressed patients, linking brain function to negative thoughts.
This supports an integrated biopsychosocial view.
What is the role of ECT compared to pharmacotherapy for severe depression?;ECT
works faster for treatment-resistant cases but risks memory loss, whereas
pharmacotherapy is slower with fewer cognitive side-effects.;ECT induces seizures
to reset neurotransmitters rapidly, often improving mood within weeks.
Pharmacotherapy takes weeks to alter neurochemistry but has lower risk of cognitive
impairment. Exams ask for advantages, risks, and when to use ECT.
Why is CBT considered a longer-term curative treatment compared to
antidepressants?;CBT changes underlying thought patterns, reducing relapse risk,
whereas antidepressants only relieve symptoms and have high relapse rates upon
discontinuation.;Hollon et al. (2005) found 31 % relapse in CBT patients versus 76
% in drug-only patients over 12 months. This shows CBT’s curative effect, while
drugs are palliative.
What is behavioural activation and why is it used in CBT for
depression?;Encouraging depressed patients to engage in pleasurable or meaningful
activities to improve mood.;Patients plan activities that provide a sense of
accomplishment or joy, such as exercise or hobbies. Increased engagement breaks
withdrawal and negative cycles, raising activity levels and positive reinforcement.
What is cognitive defusion in third-wave CBT and how does it help?;Teaching
patients to observe thoughts as mental events rather than facts, reducing their
grip.;In mindfulness-based CBT patients learn to notice “I am having the thought
that I’m worthless” rather than believing it. This reduces rumination and the
emotional impact of negative thoughts.
What are the four assumptions of CBT according to Kendall & Hammen (1998)?;1.
Patients’ interpretations differ from reality. 2. Thoughts, behaviours, and
feelings are interrelated. 3. Treatment needs to change thoughts and world-views.
4. Treatment must tackle both cognition and behaviour.;These guide CBT: identifying
distortions, challenging them, and implementing behavioural experiments to
reinforce new thoughts, improving mood comprehensively.
What is the NICE first-line recommendation for mild to moderate depression?;CBT is
the first-line treatment, offered free through IAPT in the UK.;NICE guidelines
suggest CBT over drugs for mild to moderate cases. IAPT aims to increase access to
CBT in the NHS, reflecting government support.
What is a SMART goal in CBT treatment planning?;A goal that is Specific,
Measurable, Achievable, Relevant, and Time-bound.;Example : increase social outings
from zero to two per week within four weeks. SMART goals help track progress and
keep therapy focused on concrete changes.
What is the role of homework in CBT for depression?;Homework practice helps clients
apply cognitive and behavioural skills in real life, reinforcing therapeutic
gains.;Activities include thought records, behavioural experiments, or scheduling
pleasurable activities. Completing homework strengthens new patterns and
accelerates progress.
What role does social support play in depression prognosis?;Strong social networks
buffer stress, reduce isolation, and improve adherence to therapy, leading to
better outcomes.;Clients with supportive families or friends recover faster and
have lower relapse rates. CBT can include family sessions to strengthen social
support and coping strategies.
How does exercise function as an adjunctive treatment for depression?;Regular
exercise increases endorphins and BDNF, improving mood and complementing
pharmacotherapy or CBT.;Guidelines suggest 30 minutes of moderate activity most
days. Exercise reduces symptoms, enhances neurogenesis, and can prevent relapse
when combined with other treatments.
What is self-efficacy and its role in depression recovery?;Belief in one’s ability
to manage tasks leads to active coping and reduced depression risk.;Increasing
self-efficacy through mastery experiences such as completing tasks counteracts
feelings of helplessness. CBT interventions include setting small, achievable goals
to build confidence.
How does rumination perpetuate depression and how does CBT address it?;Rumination
is repetitive negative thinking that reinforces depressive mood. CBT teaches
clients to notice and interrupt rumination, replacing it with active problem-
solving.;Therapists use techniques like thought-stopping and scheduling problem-
solving sessions to break the cycle of rumination, reducing the intensity and
duration of depressive episodes.
What is the Beck Depression Inventory (BDI) used for?;To measure severity of
depressive symptoms and track changes during treatment.;The BDI is a 21-item self-
report questionnaire probing hopelessness, irritability, guilt, and physical
symptoms. Clinicians use it to assess improvement in cognitive and affective
domains over time.
What is psychoanalytic transference and how does it aid depression treatment?;The
client projects feelings about important individuals onto the analyst, revealing
unconscious conflicts.;When a depressed patient reacts to the analyst with anger or
dependency mirroring past relationships, the analyst interprets these reactions to
uncover unresolved issues, facilitating insight and emotional resolution.
What is dream analysis in psychoanalytic treatment of depression?;Interpreting
symbolic content of dreams to uncover repressed conflicts behind depressive
symptoms.;Freud argued that dreams disguise unconscious material. By decoding
symbols—for example being chased indicating fear of loss—the therapist helps
clients connect dreams to past traumas fuelling their depression.
What are two strengths of psychoanalysis for depression?;1. It addresses deep-
rooted childhood conflicts that may underlie schemas. 2. It has face validity for
clients with early trauma linked to depression.;Free association and transference
can reveal hidden conflicts, providing comprehensive understanding. Its focus on
unconscious material can complement surface-level CBT work.
What are two weaknesses of psychoanalysis for depression?;1. It takes years and
requires high client motivation, which depressed patients often lack. 2. Empirical
support is limited and it is less structured than CBT.;Depressed clients may
struggle with introspection and long-term commitment. Modern modifications aim to
be more directive, but traditional psychoanalysis remains lengthy and costly.
What evidence shows CBT reduces relapse more than drug therapy?;Hollon et al.
(2005) found 31 % relapse in CBT group versus 76 % in drug therapy group after 12
months.;Three groups : CBT only 31 % relapse, drug only 76 % relapse, continued
drug 47 % relapse. This demonstrates CBT’s curative effect compared to drugs’
palliative nature.
What is the Recovery Movement’s critique of depression treatment?;They argue drugs
cause dependency, prioritise pharmaceutical profits, and overlook patient
empowerment and lifestyle changes.;Recovery advocates encourage people to
understand and challenge negative thoughts, focus on strengths, and adopt coping
strategies instead of relying solely on medication. They highlight over-
prescription and side-effects, promoting holistic approaches.
What is comorbidity with substance abuse and how does it affect depression
treatment?;Substance use can mask depression symptoms, reduce drug efficacy, and
requires integrated treatment plans.;Patients abusing alcohol or drugs need
detoxification before depression treatment. CBT must address both disorders, and
drug interactions may limit pharmacotherapy options.
What role does poverty play in depression risk?;Chronic stress from poverty,
limited access to care, and social isolation raise depression risk.;Financial
hardship can cause chronic stress and reduced healthcare, increasing vulnerability.
Biological explanations ignore these social determinants, making them reductionist.
What is treatment-resistant depression?;Depression that does not improve after two
or more adequate trials of different antidepressants.;Such patients may need ECT,
combination therapies, or specialised psychotherapy. Exams ask for definition and
alternative treatment options.
What is double depression?;When a person with dysthymia (persistent mild
depression) experiences an episode of major depression.;Double depression is
chronic low mood punctuated by severe episodes. Treatment often requires a
combination of medication and psychotherapy.