100% satisfaction guarantee Immediately available after payment Both online and in PDF No strings attached
logo-home
Summary 7PAGMBMH Basic Mental Health: Mental Health Disorders for Formulation £30.00   Add to cart

Summary

Summary 7PAGMBMH Basic Mental Health: Mental Health Disorders for Formulation

 15 views  0 purchase

Summary consisting of 80 pages. Topics include: depression, bipolar disorder, OCD, GAD, anxiety disorders, schizoaffective disorder, psychotic disorders, borderline personality disorder, anorexia nervosa, bulimia nervosa, binge eating disorder, alcohol use disorder, psychiatric assessment and MSE s...

[Show more]

Preview 8 out of 82  pages

  • January 21, 2023
  • 82
  • 2021/2022
  • Summary
All documents for this subject (2)
avatar-seller
patrycjak
Table of Contents
Depression................................................................................................................................................2
Bipolar disorder......................................................................................................................................13
OCD........................................................................................................................................................21
GAD........................................................................................................................................................27
Additional - Anxiety disorders.................................................................................................................32
Additional - Schizoaffective.....................................................................................................................35
Psychotic disorder – General and schizophrenia......................................................................................35
Borderline Personality Disorder – Emotionally unstable PD.....................................................................46
Anorexia Nervosa...................................................................................................................................52
Bulimia Nervosa.....................................................................................................................................61
Binge Eating Disorder.............................................................................................................................66
Alcohol Use Disorder...............................................................................................................................68
Formulation – Psychiatric assessment & MSE structure/content.............................................................75




BASIC MENTAL HEALTH – FORMULATION/MH DISORDERS
KCL
PATRYCJA_KUSACZUK@ICLOUD.COM


1

,Depression
Signs/symptoms – clinical features
 Depressed mood
 Negative thinking
 Lack of enjoyment (anhedonia)
 Reduced energy
 Slowness
 ALL LEAD TO DECREASED SOCIAL AND OCCTUPATIONAL FUNCTIONING

Appearance  Dress and grooming neglected
 Facial features – turning downward of the corners of the mouth, vertical furrowing of the centre of
the brow
 Reduced blinking rate
 Shoulder bent and the head inclined forward so the direction of gaze in downward
 Gestures and movements are reduced
Mood  Mood is one of misery
 Mood does not improve substantially in circumstances where ordinary feelings of sadness would be
alleviated
 Low mood is pervasive
 Mood experiences is often experienced as different from ordinary sadness
 Mood is often worse in the morning, improving as the day wears on – diurnal variation of mood
Depressive  Worthlessness – failing in what they do, and that other people see them as a failure, no longer feel
cognitions confident, discount ay success as a chance happening for which they can take no credit
 Pessimism – concern future prospects, patients expect the worst, they foresee failure in work, the
ruin of finances, misfortune for family, and an inevitable deterioration in health
 Guilt – unreasonable self-blame about minor matters, blame themselves for their misery and
incapacity and attribute it to personal failing and moral weakness
 Hopelessness – often accompanied by the thought that life is no longer worth living and that death
would come as welcome release
Goal-directed  Lack of interest and enjoyment (anhedonia) is frequent
behaviour  No enthusiasm for activities and hobbies
 No zest for living and no pleasure in everyday thing
 Withdraw from social encounters
 Reduced energy – lethargic, find everything an effort, leave tasks unfinished
 ANHEDONIA – important symptoms because it can distinguish between moderate severity and
milder disorders
Psychomotor  Walks and acts slowly
changes  Slowing of thought is reflect in speech – significant delay in answering, pauses in conversation
 Agitation – inability to relax, such as movements in their legs
 Anxiety – frequent
 Irritability – responds with undue annoyance to minor demands and frustrations
Biological  Sleep disturbance – early morning waking but delay in falling asleep (2-3 hours before usual wake
symptoms up), lies feeling unrefreshed, restless and agitated
 Diurnal variation in mood
 Loss of appetite – decrease but can be increased
 Loss of weight – due to lack of appetite, but can gain weight if they eat more than usual, eating
typically brings temporary relief of distressing feelings
 Constipation, fatigue, aching discomfort
 Loss of libido
 Women (amenorrhoea)
Other  Depersonalisation
features  Obsessional symptoms
 Panic attacks
 Dissociative symptoms – e.g., loss of function of a limb
 Poor memory


2

,Symptoms needed to meet the criteria for ‘depressive episode’ – ICD-10

A  Depressed mood Mild depressive disorder
 Loss of interest and enjoyment  At least 2 of A
 Reduced energy and decreased activity  At least 2 of B
B  Reduced concentration Moderate depressive disorder
 Reduced self-esteem and confidence  At least 2 of A
 Ideas of guilt and unworthiness  At least 3 of B
 Pessimistic thoughts
 Ideas of self-harm Severe depressive disorder
 Disturbed sleep  All 3 of A
 Diminished episode  At least 4 of B

Core Symptoms Severity  Mild
 Hypothmia (Low mood)  Moderate
 Anhedonia (Loss of interest in  Severe
previously pleasurable activities) Special features  With melancholic symptoms
 Anergia (Low energy)  With atypical symptoms
 With prominent anxiety
Associated Symptoms  With psychotic symptoms
 reduced concentration and attention  With agitation
 reduced self-esteem and self-  With retardation or stupor
confidence The course Single or recurrent episodes
 ideas of guilt and unworthiness Aetiological factors  Organic
 bleak and pessimistic views of the  Family history of mood disorder
future  Personal history of mood disorder
 ideas or acts of self-harm or suicide;  Childhood experiences
 disturbed sleep  Personality
 diminished appetite  Social support
 Life events




A. Five (or more) of the following symptoms have been present during the same 2-week period and represent a change
from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or
pleasure.
Note: Do not include symptoms that are clearly attributable to another medical condition.
1. Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad,
empty, hopeless) or observation made by others (e.g., appears tearful). (Note: In children and adolescents, can
be irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as
indicated by either subjective account or observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a
month) or decrease or increase in appetite nearly every day. (Note: In children, consider failure to make
expected weight gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of
restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not
merely self-reproach or guilt about being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or
as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a
suicide attempt or a specific plan for committing suicide.
B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of
functioning.
C. The episode is not attributable to the physiological effects of a substance or to another medical condition.
3

, Note: Criteria A–C represent a major depressive episode.
Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a natural disaster, a serious medical
illness or disability) may include the feelings of intense sadness, rumination about the loss, insomnia, poor appetite,
and weight loss noted in Criterion A, which may resemble a depressive episode. Although such symptoms may be
understand- able or considered appropriate to the loss, the presence of a major depressive episode in addition to the
normal response to a significant loss should also be carefully considered. This decision inevitably requires the exercise
of clinical judgment based on the individual’s history and the cultural norms for the expression of distress in the context
of loss
D. The occurrence of the major depressive episode is not better explained by schizoaffective disorder, schizophrenia,
schizophreniform disorder, delusional disorder, or other specified and unspecified schizophrenia spectrum and other
psychotic disorders.
E. There has never been a manic episode or a hypomanic episode.
Note: This exclusion does not apply if all of the manic-like or hypomanic-like episodes are substance-induced or are
attributable to the physiological effects of another medical condition.

Definitions
 Linking word by sound rather than meaning - Clang Association
 Continuous, rapid speech that changes focus from moment to moment based on association, distractions, or plays on
words - Flight of ideas
 Attention is drawn to irrelevant stimuli - Distractibility
 Perception in the absence of a stimulus – Hallucination
 A belief, out of keeping with the individual's cultural origins, that is held with strong conviction despite superior
evidence to the contrary - Delusion
 Excessive or incongruous displays of emotion - Labile affect
 Abnormally increased arousal, responsiveness to stimuli, and screening of the environment for threats – hypervigilance
 unintentional and purposeless motions that stem from mental tension and anxiety of an individual – psychomotor
agitation
 Habitual sleeplessness; inability to sleep - Insomnia
 Lack of enjoyment taken from things previously enjoyed - Anhedonia
 Loss of appetite for food - Anorexia
 Lack of restraint manifested in disregard for social conventions, impulsivity, and poor risk assessment – Disinhibition
 Abnormal lack of energy - Anergia
 A psychological state that is normal, neither elated nor depressed - Euthymic
 A state of depression - Hypothymia
 A mild form of mania marked by elation and hyperactivity – Hypomanic
 Affect is dulled in tone and reduced in intensity. The person is observed to be unengaged and emotionally-unreactive –
Blunted affect
 Delusion that things, including self, do not exist; a sense that everything is unreal - nihilistic delusion

Classification
 Depressive disorders in DSM-5
 No general agreement about the best method of classifying depressive disorders.
 A number of approaches have been tried based on the following: presumed aetiology, symptomatic picture, course

Assessment
Clinical screening for bipolar depression
 Have you ever had a period of time when you were feeling so good, ‘high’, excited, or hyper that other people thought
you were not your normal self, or you were so hyper that you got into trouble?
 If yes, was this most of the day and nearly every day and for at least four days?
 YES + YES  Investigate for bipolar disorder
 NO or NO  bipolar disorder unlikely

- Hamilton Depression Rating Scale (HDRS)25
- Montgomery-Asberg Depression Rating Scale (MADRS)
- The main difference between these two scales is that MADRS is more sensitive to change and does not emphasise
somatic symptoms as much as does HDRS.

Aetiology – prevalence, onset, course, co-morbidity, impairment
 Genetic
o Family and twin studies

4

,  Depression tends to run in families and the risk in first-degree relatives is high
 Heritability of major depression has been estimated at 37% (Bienvenu et al., 2011)
 Twin studies also suggested that susceptibility to major depression and GAS involves similar genes but
different environmental risk factors (Hettema et al., 2005)
o Mode of inheritance
 Female preponderance of depression is well established – possible that genetic factors play a
somewhat greater aetiological role in woman
 Seems likely that genetic liability to depression results from the combined action of multiple genes of
modest, or small effect in a context od gene-environment interaction
o Molecular genetics
 Monoamine theory of depression suggests that allelic variation in gene coding for monoamine
synthesis or metabolism or specific receptors may contribute to the risk of mood disorders
 Personality
o What is recognised as a personality characteristic may in fact represent a milder form of an illness
o Some personality features might influence the way in which people respond to adverse circumstances and
thus make depressive disorder more likely – e.g., a cognitive style characterised by a strong need for approval
is associated with increased risk of depression after adverse life events (Mazure and Maciejewski, 2003)
o Certain kinds of personality development and depressive disorder may share common genes – e.g.,
neuroticism predisposes to major depression, but twin studies suggest that neuroticism and major depression
have genes in common (Fanous and Kendler, 2004)
 Early environment
o Parental deprivation
 Childhood deprivation of maternal affection through separation or loss predisposes to depressive
disorder in adult life
 Family discord and lack of adequate car predispose to depression even in families where separation
does not occur (Brown, 2009)
o Relationship with parents
 Non-caring and overprotective parenting styles are associated with non-melancholic depression in
adulthood (Parker and Hadzi-Pavlvic, 1992)
 Mothers with post-natal depression may manifest a rearing style that is characterised b neglect and
emotional indifference – this could lead to longer term deleterious effects on self-esteem and
attachment style in the child thus increasing the risk of depression in the subsequent generation
(Ramchandani et al.., 2009)
 Precipitating factors
o Recent life events
 Sixfold excess of adverse life events in the months before the onset of depressive disorder
 An excess of similar events also precedes suicide attempts, and the onset of anxiety disorders and
schizophrenia
 In general, ‘loss’ events are associated with depression and ‘threat’ events are associated with anxiety
 Life events are important antecedents of all forms of depression, but appear to be relatively less
important in established melancholic-type disorders and where there is a strong family history of
depression
o Vulnerability factors and life difficulties
 Events immediately preceding a depressive disorder act as the ‘last straw’ for a person who has been
subjected to a long period of adverse circumstances
 Good evidence for poor social support, measured as a lack of intimacy or social integration, is
associated with an increased risk of depression (Brown, 2009)
o The effects of physical illness
 Medical illnesses and their treatment can act as non-specific stressors which can lead to mood
disorders in predisposed individuals
 Sometimes they can play a more direct role in causing the mood disorder – e.g., brain disease, certain
infections, including HIV and endocrine disorders
 The resulting mood disorders are known as organic mood disorders
 Psychological approaches
o Cognitive theories
 Depressed patients characteristically have recurrent and intrusive negative thoughts
 Beck (1967) proposed that these depressive cognitions reveal negative views of the self, the world
and the future and persist because of illogical ways of thinking called cognitive distortions
 Arbitrary inference – drawing a conclusion when there is no evidence for it and even some evidence
against it
5

,  Selective abstraction – focusing on a detail and ignoring more important features of a situation
 Overgeneralisation – drawing a general conclusion on the basis of a single incident
 Personalisation – relating external events to oneself in an unwanted way
 These cognitions are dysfunctional beliefs or schemas
 Early experience  formation of dysfunctional assumptions  critical incidents  assumptions
activated  negative automatic thoughts  symptoms of depression  negative automatic
thoughts
 Neurobiological approaches
o Monoamine hypothesis
 Suggests depressive disorder is due to an abnormality in a monoamine neurotransmitter system at
one or more sites in the brain
 Three monoamine transmitters have been implicated – serotonin (5-HT), noradrenaline, and
dopamine
 5-HT function – decreased plasma tryptophan contributes to impairments of brain 5-HT function in
depressed patients, blunted neuroendocrine response, low brain 5-HT function is not sufficient to
cause depression because tryptophan depletion fails to alter mood in those who are not vulnerable to
mood disorder, low brain 5-HT functions appear to interact with other vulnerability factors to cause
depressive symptoms
 Noradrenaline function – evidence that brain or CSF concentrations of noradrenaline are altered in
depressed patients (Anand and Charney, 2000), increasing noradrenaline functions increases ACTH,
cortisol and growth hormones
 Dopamine function – dopamine neurons play a key role in incentive behaviour and reward; these
processes are disrupted in depression due to melancholic states
 Role of monoamines in depression – unmedicated depressed patients have abnormalities in various
aspects of monoamine function, some abnormalities may persist into clinical recovery suggesting that
they are related to vulnerability to illness rather than the acute depressive state
o Amino acid neurotransmitters
 Decreased levels of glutamate in the anterior brain regions in depressed patients (Arnone et al., 2015)
 Brian levels of GABA are also lowered in depression
o Endocrine abnormalities
 Endocrine pathology and depression
 About 50% of patient with Cushing’s syndrome suffer from major depression which usually
remits when the cortisol hypersecretion is corrected
 Depression also occurs in Addison’s disease, hypothyroidism and hyperparathyroidism
 Endocrine changes may account for depressive disorder that occur premenstrually, during
the menopause and after childbirth
 HPA axis
 Increase in cortisol secretion is associated with enlargement of the adrenal gland and
increased cortisol response to ACTH
 About 50% of depressed inpatients do not show the normal suppression of cortisol secretion
induced by administering 1mg of the synthetic corticosteroid dexamethasone
 CRH may play a direct role in the aetiology of depression – CRH levels may be increased in
the CSF of depressed patients, therefore it is possible that hypersecretion of CRH could be
involved in the pathophysiology of the depressed state
 Thyroid function
 Circulating plasma levels of free thyroxine appear to be normal in depressed patients but
levels of free triiodothyronine may be decreased
 25% of depressed patients have a blunted thyrotropin=stimulating hormone (TSH) response
to intravenous TRH – also found in alcoholism and panic disorder
 Abnormalities in thyroid function that are found in depressed patients may eb associated
with changes in central TRH regulation (Bunevicius and Prange, 2010)
o Depression and the immune system
 Immune activation with increases in the release of certain pro-inflammatory cytokines – known to
provoke the HPA axis activity and therefore changes in immune regulation may play a role in HPA axis
dysfunction in depression
o Sleep changes in depression
 Impaired sleep continuity and duration
 Decreased deep sleep
 Decreased latency to the onset of rapid eye movement (REM) sleep
 An increase in the proportion of REM sleep in the early part of the night

6

, o Brain imaging in mood disorder
 Structural brain imaging
 Changes in brain volume – enlarged lateral ventricles, decreased hippocampal volume,
decreased volume of basal ganglia structure, decreased grey matter in the anterior brain
areas, including frontal cortex, orbitofrontal cortex, and cingulate cortex
 White matter hyperintensities – in depression increased deep white matter hyperintensities
are associated with late onset of depressive disorder, greater illness severity and poorer
treatment response, apathy, psychomotor slowness and retardation, the presence of
vascular risk factors
 Cerebral blood flow and metabolism
 Growing consensus that the abnormalities in functional brain imagine in depression support
a circuitry model in which mood disorders are associated with abnormal interaction between
several brain regions rather than major abnormality in a single structure
 Neuropsychological changes in mood disorder
o Impairment in attention, learning, memory, and executive function

Biological and psychological mechanisms in mood disorders
- MONOAMINE HYPOTHESIS
 Depression is caused by reduced levels of serotonin, noradrenalin and dopamine in the limbic system
 Evidence for theory
o Most commonly prescribed antidepressants are selective serotonin reuptake inhibitors (SSRI’s) and
noradrenaline reuptake inhibitors (NRI’s)
o Drugs work by increasing activity in serotonin and noradrenalin systems, and both are effective at
alleviating the symptoms of major depression
o Neuroimaging and post-mortem studies of depressed patients’ brain scans show that they have fewer
serotonin receptors, and their receptors tend to be less sensitive compared to healthy controls
 Evidence against the theory
o SSRI’s alter serotonin function immediately, but people need to take them for several weeks before
they see an improvement in symptoms
o Observed deficits in serotonin function might reflect changes in the brain that occur as a consequence
of chronic depression, rather than being a cause of it
o We know that neurotransmitters do not function in isolation, and we have to consider the
interactions between different neurotransmitters (glutamate, GABA, acetylcholine) in order to
understand mood disorders properly
o Current biological theories of mood disorders on abnormal function in different regions of the brain,
rather than the activity levels of different neurotransmitters

Abnormal brain function in depression
- Network of brain structures was implicated in major depression
- These regions are included within the medical prefrontal cortex (MPFC) and the limbic system, and the connections
between the two
- In mood disordered patients we can see reduced grey matter volume (a structural deficit) and glucose metabolism (a
marker of brain activity) in specific regions of the MPFC, particularly the left anterior cingulate cortex (ACC)
 Important because the MPFC normally inhibits activity in the limbic system, so one indirect consequence of
reduced activity in the MPFC would be increased activity in the limbic system
 This is exactly what we see in mood disorders – activity in the limbic systems increased in major depression
patients when they are in the middle of a major depressive episode, and the level of increased activity in these
regions is associated with the magnitude of emotional processing biases in depressed patients
- Antidepressants normalise activity in these regions
- CBT may work in a different way, by increasing activity in the MPFC and therefore indirectly increasing inhibition of the
limbic system
- Antidepressants and CBT can normalise an overactive limbic system, but their mechanism of action is very different
 Top-Down action for CBT – the MPFC changes first and then influences activity in the limbic system
 Bottom-Up action for antidepressants – the limbic system changes first, and then activity in the MPFC changes
afterwards

Environmental factors
- A number of environmental factors have been posited which may have more or less relevance at different points in
development
 Parenting
7

, o The more negative the parenting, the worse the depression
o But we cannot conclude that parenting causes depression
 Standard of living / social economic status
 Childhood abuse
 Bullying
 Life events
o Life events have been consistently associated with depression
 Multiple stressful events lead to Kindling
o A major life stressor is needed to trigger the initial depressive episode
o Once the person has recovered from this episode, their threshold for experiencing a subsequent
episode is lowered
o This continues until at some point a very minor stressor is sufficient to cause a major depressive
episode
o After that, an environmental trigger may not be needed, and it can occur spontaneously
o There is a declining relationship between life stress and major depressive episodes over time: the first
episode is almost always linked to a major stressor, but recurrences can occur independent of life
stress

Gene-Environment interactions
- Individuals with a heritable risk for mood disorder are more likely to report symptoms of depression, but only after a
stressful life event
- In the absence of a stressful life event, there is no relationship between heritable risk for depression and experiencing
the symptoms of depression
- Gene and environment cannot be disentangled as easily as we would like, because people at increased heritable risk for
depression also tend to have more stressful environments

Explanation using the biopsychosocial model

Biological Psychological Social
 Female  Childhood Abuse/Trauma  Young children (>3 under
 Unclear about genetic  Insecure attachment as a child age 15)
loading  Personality traits - Anxiety or Eating disorder  Financial worries
 HPA axis abnormalities  PTSD  Work changes
 Need to rule out physical  Depression in childhood  Separation from partner
causes, medication use and  High levels stress and anxiety  Single parent
illicit drug use.  Ongoing stress  Financial worries
 Non concordance with  Co-morbidity (including substance abuse and  Good structure in daily
treatment personality disorder) routine
 Older age at onset  Insidious onset  Employment
 Chronic physical illness  Chronic residual symptoms  Good social support –
 Concordance with  Insight sister/partner/friends
treatment  Seeking support
 Exercise  Engagement in psychological therapy – CBT /
 Acute onset Psychotherapy
 First degree relative with  Emotional, Social, physical, sexual traumas
depression increases risk 3-  Financial worries
fold  Health problems
 Unemployment

BIOLOGICAL: An important genetic contribution to mood disorders is made by multiple gens of small individual effect. This
genetic contribution may be expressed directly through modification of relevant cortical circuitry, or indirectly through effects
on personality and psychological coping mechanisms.

SOCIAL: Adverse early life experiences also shape personality and limit subsequent attachment behaviour and ability to access
social support. In addition, adverse early life experience may affect development of the HPA axis and neurobiological responses
to stress in adulthood.

SOCIAL: Depressive disorders are often triggered by current life events, particularly in people who lack social support. The
impact of life events is modified by early life experience, personality, and genetic inheritance. The interaction of these factors
determines the resilience or vulnerability of an individual to a life event, and the subsequent risk of clinical mood disturbance.
8

The benefits of buying summaries with Stuvia:

Guaranteed quality through customer reviews

Guaranteed quality through customer reviews

Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.

Quick and easy check-out

Quick and easy check-out

You can quickly pay through credit card for the summaries. There is no membership needed.

Focus on what matters

Focus on what matters

Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!

Frequently asked questions

What do I get when I buy this document?

You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.

Satisfaction guarantee: how does it work?

Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.

Who am I buying these notes from?

Stuvia is a marketplace, so you are not buying this document from us, but from seller patrycjak. Stuvia facilitates payment to the seller.

Will I be stuck with a subscription?

No, you only buy these notes for £30.00. You're not tied to anything after your purchase.

Can Stuvia be trusted?

4.6 stars on Google & Trustpilot (+1000 reviews)

80364 documents were sold in the last 30 days

Founded in 2010, the go-to place to buy revision notes and other study material for 14 years now

Start selling
£30.00
  • (0)
  Add to cart