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Year 3 > Block 33 Week 2 > Flashcards

Block 33 Week 2 Flashcards

1
Q

ECT’s effect in NA?

A
  • ·increased plasma catecholamines, especially adrenaline
  • increased cerebral plasma tyrosine hydroxylase activity
  • increased cerebral noradrenaline
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2
Q

ECT’s effect on beta receptors (chronic)

A

decreased beta-adrenoceptor density

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3
Q

Acute impact of ECT on serotonin?

A

· increased cerebral serotonin concentration

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4
Q

chronic impact of ECT on serotonin?

A

· increase in post-synaptic 5-HT2 receptors

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5
Q

ECT’s impact on GABA?

A
  • acute increase in the release of GABA – may be responsible for the neuronal hypometabolic rate subsequent to ECT
  • acute increase in GABA-B binding
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6
Q

ECT’s acute impact on dopamine?

A
  • · increased cerebral dopamine concentration
  • increased cerebral concentration of dopamine metabolites
  • increased behavioural responsiveness to dopamine agonists
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7
Q

ECT’s chronic impact on dopamine?

A
  • increased D1 receptor density
  • increased second-messenger potentiation at dopamine D1 receptors
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8
Q

embryological shunt from PA to aortic arch?

A

The ductus arteriosus is the embryological structure that allows blood to shunt from the pulmonary arteries back into the aortic arch, therefore bypassing the pulmonary circuit.

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9
Q

adult remanent of the ductus arteriosus?

A

The remnant of this in the adult is called the ligamentum arteriosum and functions as an anchor for the aortic arch.

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10
Q

bulbus cordis ->

A

forms part of te ventricules

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11
Q

common cardinal vein ->

A

SVC

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12
Q

truncus arteriosus ->

A

aorta

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13
Q

GAD - drug treatments?

A
  • if drug treatment required, use SSRI - usually sertraline
  • if ineffective, offer alternative SSRI or SNRI
  • if not tolerated, use pregabalin
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14
Q

interventions for mild to moderate panic disorder?

A
  • low intensity interventions:
  • individual non-facilitated self-help
  • individual facilitated self-help.
  • info about support groups
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15
Q

intervention for moderate to severe panic disorder?

A
  • CBT
  • AD if disorder long-standing or the person hasn’t benefitted from psych treatment
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16
Q

pharmacological management of panic disorder?

A
  • AD - only drug that should be used in the longer term management of panic disorder
  • offer an SSRI
  • 2) imipramine or clomipramine may be considered.
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17
Q

inform patient started on AD of:

A
  • risks including transient increase in anxiety at the start of treatment)
  • and of the risk of discontinuation/withdrawal symptoms if the treatment is stopped abruptly or in some instances if a dose is missed or, occasionally, on reducing the dose of the drug.
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18
Q

mild functional impairment OCD management?

A
  • low intensity psych treatments - including CBT and ERP
  • if this doesn’t work: offer SSRI or more intensive CBT
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19
Q

moderate functional impairment OCD?

A
  • SSRI or more intensive CBT
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20
Q

Severe functional impairment OCD Tx?

A

should be offered combined treatment with an SSRI and CBT (including ERP).

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21
Q

SSRIs in OCD?

A
  • for adults with OCD, SSRIs should be used as the intial pharm treatment: fluoxetine, fluvoxamine, paroxetine, sertraline or citalopram.
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22
Q

DSM-5 criteria for depression

five of the following symptoms, for at least two weeks, one of which should be low mood or loss of interest/pleasure:

A
  • Low mood
  • Loss of interest or pleasure
  • Significant weight change
  • Insomnia or hypersomnia(sleep disturbance)
  • Psychomotor agitation or retardation
  • Fatigue
  • Feelings of worthlessness
  • Diminished concentration
  • Recurrent thoughts of death or suicidewithout a specific plan, or a suicide attempt or specific plan for committing suicide
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23
Q

DSM depression criteria: in addition the following must be present

A
  • Symptoms cause significant distress and impair normal function
  • Symptoms or episode not caused by another condition of substance
  • Episode no better explained by other mental health illnesses
  • No episodes of mania or hypomania
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24
Q

Mild depression =

A

few or no extra symptoms beyond the five to meet the diagnostic criteria

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25
Q

Moderate depression =

A

symptoms and impairment between mild and severe

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26
Q

Severe depression =

A

most or all the symptoms (see above) causing marked functional impairment with or without psychotic features

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27
Q

which antidepressants to avoid in those with high suicide risk or history or overdose?

A

Avoid tricyclics and venlafaxin

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28
Q

examples of SSRIs?

A
  • Sertaline
  • paroxetine
  • citalopram
  • fluoxetine
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29
Q

How SSRIs work?

A
  • Block reuptake and enhance the serotonergic neurotransmission
  • first lines for depression
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30
Q

SNRIs e.g.s?

A
  • Venlafaxine
  • duloxetine
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31
Q

SNRI mechanism?

A
  • block both serotonin and NA reuptake in the synapse
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32
Q

AD - bupropion?

A

inhibiting the reuptake of dopamine and norepinephrine at the presynaptic cleft.

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33
Q

TCA AD examples?

A
  • amitriptyline
  • Clomipramine
  • nortryptiline, proptriptyline
  • Imipramine
  • Trimipramine
  • Desipramine

end in ine

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34
Q

how to TCA AD like amitryptiline work?

A
  • inhibits the reuptake of norepinephrine and serotonin at the presynaptic neuronal membrane
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35
Q

MAOI - monoamine oxidase inhibitors?

A
  • Moclobemide
  • Isocarboxazid
  • Phenelzine
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36
Q

MAO catabolizes?

A

serotonin, NA, dopamine

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37
Q

serotonin modulatiors e.g.s?

A
  • vilazodone
  • trazadone
  • nefazodone
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38
Q

how do serotonion modulators work?

A
  • inhibition of presynaptic reuptake of serotonin
  • agonism of post synpatic serotonin receptors
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39
Q

indications for AD?

A
  • depressive disorders
  • premenstrual dysphoric disorder
  • anxiety
  • OCD
  • phobias
  • PTSD
  • TCAs - chronic pain
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40
Q

side effects of antidepressants?

A
  • sexual problems
  • tooth decay and oral health
  • diabetes
  • SIADH
  • GI bleeding
  • mania
  • serotonin syndrome
  • neuroleptic malignant syndrome
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41
Q

TCAs specific side effects?

A
  • antimuscarinic effects
  • serotonin syndrome
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42
Q

mood stabiliser in depression?

A

lithium

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43
Q

how does lithium work?

A
  • promotes GABA - facilitates GABA release preysnaptically and upregulates GABA-B receptors post synaptically
  • Mania, bipolar, recurrent depression, aggressive or self harm behaviour
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44
Q

Side effects of lithium?

A
  • excessive urination
  • polydipsia
  • fine tremor
  • metallic taste
  • nausea and diarrhoea
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45
Q

ECT =

A
  • electric current delivered to the patient’s brain which induces a generalized clonic seizure
  • causes changes in the release of neurotransmittters and hormones
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46
Q

indications of ECT?

A
  • treatment resistant depression
  • severe major depression
  • bipolar depressive and mania
  • schizophrenia
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47
Q

side effects of ECT?

A
  • nausea
  • headache
  • fatigue
  • confusion
  • slight memory loss
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48
Q

depression management: advice?

A

provide advice on the nature and course of depression, recovery and sources of info including self help materials

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49
Q

self help materials in depression?

A
  • royal college of psychiatrists which provides patient information
  • MIND
  • Depression UK
  • mental health foundation
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50
Q

depression management: improving wellbeing?

A
  • provide advice on activities to imptove wellbeing such as
  • physical activity: walking, jogging, swimming, dance
  • Maintaining a healthy lifestyle through diet, alcohol intake, and sleep.
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51
Q

depression management: social support?

A
  • social support for family/ carers supporting the person
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52
Q

Which antidepressants pose a high risk for overdose?

A
  • avoid TCAs except lofepramine and venlafaxine (SNRI) due to risk of death from overdose
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52
Q
A
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53
Q

First line AD for depression?

A
  • SSRIs are the first line
  • If the person has a chronic physical health condition, sertraline or citalopram may be preferred first-line
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54
Q

antidepressants start to work within ? weeks

A

4

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55
Q

which drugs interact with antidepressants increasing the risk of GI bleeding?

A

NSAIDS interact w SSRIs and SNRIs

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56
Q

Other drugs that interact with AD?

A
  • warfarin
  • heparin
  • aspirin
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57
Q

Tx options for depression?

A
  • CBT
  • SSRI
  • SNRI
  • TCA
  • CBT with either an SSRI or TCA
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58
Q

BPD: features of mania?

A
  • Elevated mood
  • Extreme irritability and/or aggression
  • Increased energy
  • Restlessness
  • Pressure of speech
  • Increase libido and disinhibition
  • Distractibility, poor concentration
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59
Q

psychotic features that can be present in mania?

A

delusions (fixed belief contradictory to reality or rational argument) or hallucinations

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60
Q

hypomania?

A

features of mania but usually not as severe. there are no psychotic features

depression

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61
Q

depression is characterised by?

A
  • characterised by persistently low mood and loss of pleasure/ interest in everyday activities
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62
Q

What are the features of depression?

A
  • Low mood
  • Loss of interest or pleasure
  • Significant weight change
  • Insomnia or hypersomnia(sleep disturbance)
  • Psychomotor agitation or retardation
  • Fatigue
  • Feelings of worthlessness
  • Diminished concentration
  • Suicidal thoughts
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63
Q

CMHTs assess patients who are referred and?

A

patients are then allocated a key worker who co-ordinates their treatments

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64
Q

Crisis teams involve?

A
  • psychiatrists
  • MH nurses
  • social workers
  • support workers
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65
Q

Roles of crisis teams (4)?

A
  • can visit the patient’s home or them in hospital if they’re being discharged
  • assist with self help strategies
  • administer medications
  • provide practical help e.g. with money or housing
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66
Q

Early intervention teams can?

A

support you if you experience psychosis for the first time

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67
Q

What are EIT?

A
  • they are MDTs set up to identify and reduce treatment delays at the onset of psychosis and promote recovery by reducing the probability of relapse following a first episode of psychosis
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68
Q

who are assertive outreach teams for?

A
  • for those with complex mental health needs e.g. for those with severe long term mental illnesses and those who have been in hospital many times
  • complex needs such as violent behaviour, drug or alcohol use and mental illness, those detained under the mental health act or serious self harming
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69
Q

AOTs are also known as?

A
  • also known as the complex care team or programme of assertive community treatment
  • AOTs review the care plan every 6 months
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70
Q

exposure to ? play a role in the onset of depression?

A

poverty and violence

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71
Q

Cultural factors in depression?

A
  • cultures vary in their conceptualisation of mental health
  • symptoms they recognize as signs of depression, and their openness towards discussing feelings of depression.
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72
Q

How may different cultures interpret the symptoms of depression?

A
  • For instance, some cultures might interpret symptoms of depression in a more somatic or physical way, focusing on complaints like fatigue orpain, while others may focus more on the emotional or cognitive symptoms.
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73
Q

fear of ? may stop people from seeking help for depression

A

stigma

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74
Q

cultural factors also influence the types of ?

A

treatment sought by the patient, wirh some cultures relying more on traditional/ alternative medicines

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75
Q

cultural identifity influences the degree to which a person?

A
  • cultural identity influences the degree to which a person shows physical symptoms of depression
  • in other words, some cultures are more comfortable reporting depressive symptoms that are physical in nature rather than mental.
  • For example, research shows that many depressed Chinese people complain of bodily discomfort, feelings of inner pressure, and symptoms of pain, dizziness, and fatigue
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76
Q

Depression and the western world?

A
  • depressed individuals might not readily seek out psychiatric or mental health care for depressive symptoms.
  • Because the public discourse regarding depression is more prevalent in Western societies, it is more socially acceptable to have depression, and more people are willing to seek help.
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77
Q

stigmatisation of mental illness in other cultures?

A
  • mental illnesses may be denied out of shame of being identified as craxy
  • Others may find the label “depression” morally unacceptable, shameful, and experientially meaningless
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78
Q

? of people w MH problems are cared for within primary care

A

90

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79
Q

PC uses ? of total expenditure on MH

A

10

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80
Q

Which proportion of GP appoinments are mental health related?

A

40%, has risen since the pandemic started

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81
Q

assessments for disturbed, suicidal or agitated people?

A
  • psychosocial needs - social needs like home environment, recent life events, history leading to the thoughts of self harm
  • psychological and physical needs - MH disorders, miuse of recreational drugs and/or alcohol
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82
Q

factors that increase the person’s risk of depression/ self harm?

A
  • hopelessness
  • features of depression
  • features suggestive of suicidal intent - evidence of planninf, changes to will, precautions taken to prevent rescue
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83
Q

Features that make a person higher risk of suicide/ self harm?

A
  • features associated with risk - male sex, physical health problems, low SES, high-risk employment (such as farmers or healthcare professionals)
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84
Q

management of a person at risk of suicide/ self harm?

A
  • prevent access to means of self harm
  • written and verbal info for the person and their family
  • ensure all members of MDT are kept informed
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85
Q

what does counselling involve?

A
  • involves the patient talking about their feelings and emotions with a trained therapist
  • the therapist can help the patient gain a abetter understanding of their feelings and thought processes
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86
Q

counselling is ideal for people who are?

A

coping with a current crisis such as anger, bereavement, interftility etc

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87
Q

what is behavioural activation?

A
  • talking therapy that aims to help people with depression take simple, practical steps towards enjoying life again.
  • The aim is to give you the motivation to make small, positive changes in your life.
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88
Q

BA also involves teaching the person…

A

problem-solving skills to help them tackle problems that are affecting their mood

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89
Q

problem solving therapy is aimed at?

A

improving an individual’s ability to cope with stresful life experiences

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90
Q

what is the underlying assumption of problem solving therapy?

A
  • The underlying assumption of this approach is that symptoms of psychopathology can often be understood as the negative consequences of ineffective or maladaptive coping.
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91
Q

PST aims to help individuals adopt a ?

A

realistically optimistic view of coping, understand the role of emotions more effectively, and creatively develop an action plan geared to reduce psychological distress

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92
Q

PROBLEM SOLVING THERAPY

interventions in PST?

A

psychoeducation, interactive problem solving exercises and motivational homework assigments

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93
Q

First line in mania Tx?

A

Antipsychotics such ashaloperidol,olanzapine,quetiapine, andrisperidone

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94
Q

Mania - if there’s inadequate resp to AP then ? can be added?

A

lithium or valproate

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95
Q

how should AP be discontinued?

A

the dose should be reduced gradually over at least 4 weeks to minimise the risk of recurrence.

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96
Q

Mania - benzodiazepines?

A
  • Use of benzodiazepines (such as lorazepam) may be helpful in the initial stages of treatment for behavioural disturbance or agitation.
  • Benzodiazepines should not be used for long periods because of the risk of dependence.
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97
Q

Mania - lithium?

A
  • used for the treatment of acute episodes of mania or hypomania in bipolar disorder.
  • Lithium is also used for the long-term management of bipolar disorder to prevent recurrence of acute episodes.
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98
Q

Mania - lithium is considered the ?

A

gold standard

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99
Q

Mania - valproate?

A
  • used for the treatment of manic episodes associated with bipolar disorder if lithium is not tolerated or contra-indicated.
  • Valproate is also used for the long-term management of bipolar disorder to prevent recurrence of acute episodes
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100
Q

BPD - carbamazepine?

A
  • LT management
  • to prevent reoccurence of acute episodes in patients unresponsive to lithium therapy.
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101
Q

Mood stabilisers in BPD?

A
  • Valproate
  • lamotrigine
  • carbamazepine
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102
Q

BPD psych therapies - individal psychoeducation?

A

trained to identify and cope with early warning signs of mania and/or depression.

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103
Q

BPD psych therapies - Interpersonal and social rhythm therapy?

A
  • focuses on the role of interpersonal factors (i.e. interpersonal relationships, role conflicts)
  • and circadian rhythm stability (i.e. sleep-wake cycle, work-life balance) in the context of bipolar.
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104
Q

BPD psych tehrapies - group psychoeducation?

A
  • high frequency and intensity sessions to help patients become experts in their own condition.
  • Aims to improve mood stability, medication adherence and self-management.
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105
Q

BPD psych therapies - family focused therapies?

A
  • psychoeducation for families with one individual suffering from bipolar.
  • Looks at risks, communication and problem-solving within the family to prevent relapses.
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106
Q

Inital management of bipolar?

A
  • offer a psychological intervention
  • if the person develops moderate or severe bipolar depression offer fluoxetine with olanzapine or quetiapine on its own
  • if this doesn’t work consider lamotrigine on its own
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107
Q

what should be used for moderate to severe bipolar disorder?

A

lithium

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108
Q

Bipolar Tx options summary?

A
  • antipsychotics
  • lithium - gold standard but requires close monitoring
  • antieplieptics - prevent depression relapses
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109
Q

the use of ? is restricted in BPD?

A
  • antidepressants restricted due to the risk of inducing mania or rapid cyclinc - SSRI floxetine commonly used
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110
Q

What is primary insomnia?

A
  • sleep disorder not directly caused by any underlying medical, psychiatric or environmental factors
  • It is a standalone condition characterized by difficulties falling asleep, staying asleep, or experiencing non-restorative sleep.
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111
Q

what is secondary insomnia?

A
  • secondary insomnia is linked to an underlying cause or condition.
  • It may arise due to various factors such as medical conditions (e.g., chronic pain, respiratory disorders), mental health disorders (e.g., anxiety, depression), substance abuse, or certain medications.
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112
Q

primary insomnia typically presents as?

A

persistent difficulties with sleep initation, maintenance or poor sleep quality without an underlying cause

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113
Q

secondary insomnia presents as?

A

may have identifiable tiggers or pattens related to specific medical or psychological conditions

114
Q

first line for primary insomnia?

A

CBT-I, improvement with this supports diagnosis of primary insomnia

115
Q

secondary insomnia - Treatment ?

A

addressing the underlying cause or condition leads to improved sleep.

116
Q

techniques for self management of insomnia?

A
  • developing a sleep/wake routine - getting up at the same time everyday
  • ‘start the day well routine’ e.g. showering and brushing teeth
  • exercising in the afternoon or early evening
  • ‘end the day well routine’ - dinner, taking a bath, changing into sleepware
  • regular bedtime
  • relaxation exercise
  • meditation
117
Q

Things to avoid in insomnia?

A
  • working or studying the hour and a half before bed
  • thinking abour work the next day
  • naps
  • exercising too late in the day
  • too much caffeine
  • alcohol in the 4 hours before the routine starts
  • don’t use phones, TVs, computers in the hour before bed
  • staying in bed if you can’t sleep - if you go to bed at your bedtime but can’t fall asleep after 15 minutes, get up and do something relaxing until you begin to feel sleepy
118
Q

when are hypnotics used in insomnia?

A
  • hypnotics are used if sleep hygiene measures fail, daytime impairment is severe causing significant distress, and insomnia is likely to resolve soon (for example due to a short term stressor)
  • they can only be used short term if other methods failed and be used as an adjunct to CBT
119
Q

groups of people hypnotics can not be used in?

A

-preg/ breastfeeding women
- older people

120
Q

drugs for insomnia that can cause withdrawal symptoms?

A
  • benzodiazepines and z drugs can cause withdrawal symptoms when used long term
121
Q

chronic insomnia can be caused by?

A

injudicious prescribing of hypnotics

122
Q

hypnotics - tolerance developsw ithin?

A

3 to 14 days of continous use

123
Q

LT use of hypnotics like z drugs and benzodiazepines can cause?

A

rebound insomnia and withdrawal syndrome

124
Q

why are hypnotics avoided in the elderly?

A

bc they’re at greatest risk of becoming ataxic and confused leading to falls and injury

125
Q

benzodiazepines used as hypnotics?

A
  • nitrazepam and flurazepam
126
Q

What are the Z drugs?

A

Zolpidem tartrateandzopicloneare non-benzodiazepine hypnotics - act at the benzodiazepine receptor

127
Q

which hypnotic can be used in the elderly?

A
  • Clomethiazole
  • bc its freedom from hangover
  • can’t be used routinely though
128
Q

sleep disorders affect upto ? of the population

A

1/3

129
Q

PSD are divided into ?

A

dyssomnias or parasomnias

130
Q

symptoms of sleep disorders?

A
  • difficulty falling asleep,
  • difficulty remaining asleep,
  • abnormal behaviour during sleep
131
Q

What are dyssomnias?

A
  • The sleep itself is largely normal but the client sleeps too little, too much, or at the wrong time.
  • So, the problem is with the amount (quantity), or with its timing, and sometimes with the quality of sleep.
132
Q

What are parasomnias?

A
  • Something abnormal occurs during sleep itself, or during the times when the client is falling asleep or waking up (e.g., bad dreams.
  • The quality, quantity, and timing of the sleep are essentially normal.
133
Q

PSD: primary insomnia characeristics?

A

—Difficulty initiating or maintaining sleep
—Persists for 1 month or longer

134
Q

primary insomnnia is often due to?

A

—Major Depressive Episode, Manic Episode, or anxiety disorder
—Commonly misused substances, as well as some prescription medicines.
—Breathing-related problems

135
Q

Tx of primary insomnia?

A

—Vigorous daytime exercise, not exercising before sleep
—Metronome or ticking clock- slow, 60 beats per minute or slower, beat of human heart
—Relaxation exercises, practice regularly but condensed to 5 minutes

136
Q

PI - decrease?

A
  • decrease stimulation and inc soothing environments e.g. ear plugs
  • practice good sleep habits
137
Q

What to reduce in insomnia?

A

caffeine - esp minimal in afternoon and evening

138
Q

Management of short term insomnia (<4 weeks)?

A
  • identify and manage causes
  • advise the person to not drive if they feel sleepy - don’t inform DVLA unless a primary sleep disorder is confirmed
  • advise good sleep hygiene
139
Q

Hypnotics are only used in STI if?

A
  • only if daytime impairment severe
140
Q

When hypnotics are used in STI, they are?

A
  • short acting benzos like loprazolam
  • z drugs zopiclone, zolpidem, and zaleplon
  • 3 to 7 day course
141
Q

hypnotics should not be used for more than?

A
  • 2 weeks
  • Review after 2weeks and consider referral for cognitive behavioural therapy if symptoms persist
142
Q

first line for LTI?

A

CBT-I

143
Q

Managing LTI - refer to?

A
  • Refer to psychological services IAPT (Improving Access to Psychological Therapies) for a cognitive or behavioural intervention.
  • Advise good sleep hygiene and regular exercise in addition to cognitive and behavioural interventions.
144
Q

LTI - pharmacological therapy?

A

generally not recommended for the long-term management of insomnia

145
Q

what can be used in those > 55 with peristent insomnia?

A

modified release melatonin

146
Q

if insomnia persists despite PC management, ? is needed?

A

refer to sleep clinic or specialist

147
Q

primary hypersomnia is when?

A

the person sleeps too much, is drowsy at times when they should be alert

148
Q

Characteristics of primary hypersomnia?

A

—Excessive sleepiness
—Persists for 1 month or longer

149
Q

primary hypersomnia is often due to?

A

—Major Depressive Episode, Dysthymic Disorder with atypical features
- Use of substances is less likely to produce hyersomnia than insomnia, but it can happen (e.g., sleeping pills overdose)

150
Q

tx of primary hypersomnia?

A

exercise when becoming sleepy

151
Q

what is nacrolepsy?

A

sleeping at the wrong time

152
Q

characteristics of nacrolepsy?

A

—Sleep intrudes into wakefulness, causing clients to fall asleep almost instantly
—Sleep is brief but refreshing
—May also have sleep paralysis, sudden loss of strength, and hallucinations as fall asleep or awaken.

153
Q

Tx of narcolepsy?

A

Stimulants, sometimes antidepressants with less success.

154
Q

Breathing related sleep disorder -characteristics?

A
  • Sleep disruption (excessive sleepiness or insomnia)
  • Due to sleep-related breathing condition (e.g., Obstructive Sleep Apnea Syndrome)
155
Q

Mild cases of BRSD - Tx?

A

weight loss, sleeping on one’s side, and avoiding hypnotics and alcohol

156
Q

serious cases of BRSD Tx?

A

CPAP

157
Q

Characteristics of circardian rhythm sleep disorder?

A

—Persistent or recurrent pattern of sleep disruption leading to excessive sleepiness or insomnia, due to mismatch between sleep-wake schedule required by a person’s environment and his/her circadian sleep-wake pattern (e.g., shift work, jet lag).

158
Q

Tx of circadian rhythm sleep disorder?

A

—Darken bedroom and use soundproofing
—Limit caffeine and hard to digest food.
—Ensure all family members learns shift
—To help jet lag, exposure to sun helps

159
Q

types of parasomnias?

A
  • nighmares
  • sleep terrors
  • sleep walking
160
Q

Nightmares - characteristics

A

(1) Repeated awakenings from bad dreams
(2) When awakened client becomes oriented and alert

—Usually occurs in early morning when REM sleep dominates.

161
Q

? may induce nightmares

A

stress

162
Q

dreams in nightmares are?

A

clearly remembered

163
Q

Sleep terrors?

A
  • (1) Abrupt awakening from sleep, usually beginning with a panicky scream or cry
  • (2) Intense fear and signs of autonomic arousal
  • (3) Unresponsive to efforts from other to calm persons
164
Q

sleep terrors involve ? of the episode

A
  • amnesia for episode
  • no detailed dream recalled
165
Q

Sleep terrors usually affect?

A
  • usually affects children, isn’t a nightmare
  • usually happens in early evening
  • probably due to brain wave upset, fever or medications
166
Q

characteristics of sleepwalking?

A

(1) Rising from bed during sleep and walking about.
(2) Usually occurs early in the night.
(3) On awakening, the person has amnesia for episode

167
Q

sleep walking runs in families and begins between the ages?

A
  • 6-12
  • may be stress related
168
Q

tx of sleepwalking?

A
  • relaxation techniques
  • Biofeedback training
  • Hypnosis.
  • May need to sleep on the ground floor, have outside doors securely locked, and have car keys unavailable
169
Q

Abnormal behaviours that don’t meet the criteria for more specific parasomnias?

A
  • sleep talking
  • sleep paralysis
  • sleep behaviour disorder
170
Q

sleep talking involves?

A
  • having no memory of it in the morning
  • REM sleep, pronunciation is clear and understandable;
  • in deep sleep (delta) apt to be mumbled and unintelligible
171
Q

sleep paralysis?

A
  • to perform voluntary movement during the transition between waking and sleep.
    Usually associated with extreme anxiety, and sometimes fear of impending death.
172
Q

sleep behaviour disorder?

A

characterized by agitated and violent behavior.

173
Q

characteristics of substance induced sleep disorder?

A

—Evidence must be present that the sleep disturbance is a direct physiological consequence of substance use.
- Substance use that produces a sleep disorder severe enough to warrant independent clinical attention

174
Q

what is an eating disorder?

A
  • eating disorder is a MENTAL DISORDER defined by abnormal eating habits that negatively affect a person’s PHYSICAL or MENTAL health
175
Q

mental illness with the highest mortality rate?

A

EDs

176
Q

what is anorexia nervosa?

A
  • people maintain a low body weight as a result of wanting to either be thin or due to a fear of being fat - preoccupation with weight
177
Q

women: men ratio in anorexia?

A

10:1

178
Q

when does anorexia typically occur?

A
  • typical onset during early to mid adolescence
  • estimated yearly incidence 0.1 in 1000 per year in females
179
Q

what are the main RF for anorexia?

A
  • Female gender
  • Living in Western society
  • Family History
  • Severe life stresses
180
Q

RF for anorexia - premorbid experiences?

A

sexual abuse, dieting behaviour in family, occupational or recreational pressure to be slim, criticism about weight or eating behaviours.

181
Q

RF for anorexia - personal characteristics?

A

perfectionism, low self-esteem, obsessional traits, anxiety, borderline personality disorder.

182
Q

clinical features of anorexia?

A
  • refusal to maintain normal BMI
  • Weight below 85% predicted (<17.5kg/m2)
  • Dieting/restricting eating habits
  • Rapid weight loss
  • Disproportion about weight or shape.
  • Denial of problem, resistant to intervention
  • Social withdrawal; few interests
  • Enhancing weight loss with excessive exercise, laxatives & self-induced vomiting.
183
Q

Physical features of anorexia - general?

A
  • Fatigue, fainting, dizziness and intolerance of cold.
184
Q

Physical features of anorexia - GI?

A
  • GI symptoms such as constipation, dysphagia and abdominal pains
185
Q

physical features of anorexia - sexual characteristics?

A
  • Delay in secondary sexual characteristics if pre-pubertal
  • Lanugo hair - fine thin hair all over the body
  • Primary or secondary amenorrhoea
186
Q

examination for anorexia?

A
  • height, weight, BMI
  • core temperature
  • peripheral circulation and oedema
  • pulse, BP
  • test muscle power - sit up test and squat test
187
Q

examination findings in anorexia ?

A
  • laguno hair
  • hypotension, bradycardia
  • peripheral oedema
  • scanty pubic hair
188
Q

anorexia findings - acrocyanosis?

A

hands or feet are red/ purple

189
Q

Ix for anorexia?

A
  • ESR & TFTs (screen for other causes of weight loss)
  • U&E’s- particularly in those who are vomiting, taking laxatives, diuretics or water loading
  • ECG- may show bradycardia or a prolonged QTc
190
Q

MARISPAN - factors suggestive of severe anorexia which are a guide for urgent referral ?

A
  • raised urea, creatinine or transaminases indicate end organ damage
191
Q

Psychological management of anorexia in under 18s?

A
  • first line Anorexia-nervosa-focused family therapy (FT-AN)
  • CBT or adolescent-focused psychotherapy
192
Q

Psychological management of anorexia in over 18s?

A
  • 1st: CBT-ED: 40 sessions over 40 weeks
  • Maudsley Anorexia Nervosa Treatment for Adults: 20 sessions
  • Specialist supportive clinical management
  • Eating-disorder-focused focal psychodynamic therapy
193
Q

physical management of anorexia - weight related?

A
  • Managing weight gain and also maintain a healthy weight - aiming for average 0.5kg -1kg gain a week
  • When in refeeding phase consider daily U&Es and ECGs until electrolytes have stabilised
194
Q

anorexia - bisphosphonates?

A
  • Bisphosphonates if diagnoses of osteopenia/osteoporosis
195
Q

anorexia - dentist assessment?

A
  • Advise regular dentist assessment if regularly purging
196
Q

anorexia - MDT approach when?

A

there is comorbid physical or mental illness

197
Q

feeding against will?

A
  • last resort
  • should only be done in the context of the Mental Health Act 1983 or Children Act 1989.
198
Q

complications of anorexia - electrolyte?

A
  • Hypokalaemia, hyponatremia
  • Hypotension
  • Hypoglycaemia
199
Q

cardiac complications of anorexia?

A

mitral valve prolapse, peripheral oedema, sudden death

200
Q

renal complications of anorexia?

A
  • Renal calculi
  • AKI or CKD
201
Q

psychological/ neuro complications of anorexia?

A
  • Anxiety and mood disorders
  • Pseudoatrophy on brain imaging
202
Q

what is bulimia nervosa characterised by?

A
  • characterised by repeated binges followed by compensatory weight loss behaviours
203
Q

bulimia - compensatory weight control mechanisms can be?

A
  • Self induced vomiting
  • Fasting/restricting intake
  • Intensive exercise
  • Abuse of laxatives, diuretics, thyroxine or amphetamines.
204
Q

lifetime female prev of bulimia?

A

2%

205
Q

bulimia occurs across all?

A

socioeconomic groups

206
Q

Female: male ratio in bulimia?

A
  • female:male 10:1 although incidence in men is increasing
  • common in adolescent and young adulthood
207
Q

RF for bulimia

A
208
Q

core features of bulimia?

A
  • regular binge eating, loss of control eating during binges
  • attempts to counteract the binges
  • BMI > 17.5kg/m2
  • Preoccupation with weight, body shape and body image
  • Preoccupation with food & diet.
209
Q

physical symptoms of bulimia?

A
  • bloating & fullness
  • lethargy
  • heartburn & reflux
  • abdominal pain
  • sore throat & dental problems
210
Q

what is common with bulimia?

A
  • mood disturbances, anxiety, low self esteem and self harm are common with bulimia
  • depressive symptoms are more common than anorexia nervosa
211
Q

examination in bulimia?

A
  • Salivary glands (especially the parotid) may be swollen.
  • Oedema if there has been laxative or diuretic abuse
212
Q

bulimia - Russel’s sign?

A
  • Russell’s sign - calluses develop on the back of the hand due to repeated abrasions against the teeth when inducing vomiting
  • Erosion of dental enamel.
213
Q

Ix in bulimia?

A
  • usually normal but serum potassium is often low
  • Renal function and electrolytes should be checked in view of frequent self-induced vomiting
214
Q

Psych management of bulimia?

A
  • immediate referral to communit based specialist eating disorder service for assessment and management
215
Q

bulimia management in under 18s?

A
  • Bulimia-nervosa-focused family therapy first line
  • CBT-ED (if above not effective or not an option)
216
Q

bulimia management in over 18s?

A
  • Encouragement to follow an evidence-based bulimia-focused guided self-help programme, with direct encouragement from healthcare professionals
  • CBT-ED
217
Q

medical management of bulimia?

A
  • If vomiting or taking large quantities of laxatives should have fluid & electrolyte balance assessed weekly.
  • Regular dental reviews & dental hygiene
  • Reduce laxatives slowly
  • Screen for osteoporosis
218
Q

Bulimia - prognosis?

A

80% make full recovery without Tx

219
Q

bulimia - metabolic complications?

A
  • Metabolic abnormalities (hypochloraemic, hypokalaemic metabolic alkalosis) following excessive vomiting
220
Q

bulimia - electrolyte imbalanceS?

A
  • Electrolyte imbalances leading to cardiac arrhythmias, renal impairment, muscular paralysis
221
Q

? of bulimia patients go on to develop anorexia

A

10-15%

222
Q

bulimia complications - ? from hypocalcaemia?

A

tetany

223
Q

? has the highest mortality rate - deadliest psychiatric condition

A

anorexia

224
Q

causes of death with EDs?

A
  • suicide - always screen for mood disturbances and also suicide risk
  • medical complications - heart failure, fatal arrhythmias, severe dehydration/ malnourishment, multi-organ failure
225
Q

screening questionnaire for EDs?

A

SCOFF questionnaire

226
Q

SCOFF questionnaire?

A
  • do you make yourself Sick because you feel uncomfortably full?
  • do you worry that you have lost Control over how much you eat?
  • have you lost more than One stone in a 3-month period?
  • Do you believe yourself to be Fat when others say you’re too thin?
  • Would you say Food dominates your life? (2+ indicate likely case of anorexia or bulimia)
227
Q

MSE in EDs?

A

to look for depressive symptoms

228
Q

Physical examination in EDs?

A

look at distribution of body hair, emaciation, vitamin deficiency, reduced peripheral circulation.

229
Q

binge ED is characterised by?

A
  • Characterised by frequent and recurrent binge eating episodes with associated negative social and psychological problems, without episodes of purging
230
Q

features of binge ED?

A
  • eating fast in a short space of time,
  • making themselves uncomfortably full,
  • eating large amounts when not hungry,
  • subjective loss of control over how much is eaten.
  • Binges may be planned in advance involving purchase of special binge foods
  • Eating alone or secretly due to embarrassment over the amount of food consumed
  • Dazed mental state during the binge
  • Feelings of shame, guilt or disgust following a binge.
231
Q

Psych management of binge ED?

A
  • Encouraged to follow an evidence-based self-help programme. Healthcare professionals should provide direct encouragement and support.
  • CBT-BED
  • Interpersonal psychotherapy, modified dialectical behaviour therapy
232
Q

Pharmacological management of EDs?

A

SSRIs

233
Q

physical management of EDs?

A

monitor weight & offer support.

234
Q

refeeding syndrome can occur after?

A
  • Eating disorders, elderly, after severe illness, major surgery & children.
  • Anyone who has had a period of starvation.
  • Only occurs AFTER commence refeeding.
235
Q

refeeding syndrome occurs ? days after commencing reeding?

A

4 days - 2 weeks

236
Q

RS: ppts develop?

A
  • Patients develop fluid & electrolyte disorders, specifically hypophosphatemia, along with neurologic, pulmonary, cardiac, neuromuscular & haematologic complications.
237
Q

what is the first visible sign of RS?

A

peripheral oedema

238
Q

most common cause of death from RS?

A

cardiac arrythmias

239
Q

other risks of RS?

A

confusion, coma, convulsions & cardiac failure.

240
Q

diagnosis of refeeding syndrome?

A
  • biochemical abnormalities and clinical findings
  • most usual change is decrease in phosphate
241
Q

Monitoring for RS?

A
  • Urea, Cr, Na, K, Ca and Mg should be measured daily for 5 days, on day 10 and then day 14
  • electrolyte changes will normally occur 72 hrs into refeeding
242
Q

Weight monitoring in RS?

A
  • Hydration & nutritional status, daily weight - sharp increase in weight in oedema which is a sign of refeeding syndrome
243
Q

RS pharm management?

A
  • Decrease calories until phosphate normalised
  • Oral phosphate supplements, or IV if not tolerated
244
Q

diabulimia is?

A

deliberate manipulation of insulin levels by T1D to control their rate

245
Q

Features in history that indicate medical risk are:

A
  • excess exercise with low weight
  • blood in vomit
  • inadequate fluid intake in combination with poor eating
  • rapid weight loss
  • factors which disrupt ritualised eating habits (journey/ holiday/exam).
246
Q

what is often chronically low in purging?

A

potassium

247
Q

potassium levels in purging are often controlled w?

A
  • Regular feeding with control of purging is usually sufficient for re-establishment of normal levels.
  • If potassium replacement is required, because it is usually caused by a loss of gastric secretion, it should be done with oral replacement with a salt and water
248
Q

What can occur from initial reefeding?

A
  • Rebound hypophosphataemia can occur on initial refeeding as it is sequestered by carbohydrate metabolism.
  • It can be lethal.
249
Q

initial refeeding with foods with high phosphorous content such as ?

A

milk-based products (>2 pints/day) may be helpful.

250
Q

what do patients need to be assessed for with RS?

A
  • dehydration leads to a medical crisis through circulatory and renal failure
  • all patients should be assessed fully for dehydration
  • fluid intake, signs of decompensation (dizziness/ fainting)
251
Q

Physical exam for RS?

A

should include assessment of skin turgicity, ocular pressure and lying and standing blood pressure.

252
Q

If a patient is at medical risk but does not consent to treatment they must be:

A
  1. assessed for capacity
  2. treated under the appropriate legal criteria.
253
Q

Capacity is related to a patient’s ability to:

A
  • understand information relevant to the specific decision;
  • be able to understand the nature of their illness and understand the implicationsof non-treatment
  • be able to rationally weigh up the pros and cons of treatment;
  • thus make an informed decision regarding their management and communicate their
    decision.
254
Q

new MCA (2005) means

A
  • under the new MCA (2005) people lacking capacity may be treated if it’s in their best interest
255
Q

treating people without capacity:

A
  • needs to be the least restrictive option
  • is not depriving them of their liberty
  • there is no advanced refusal or objection by a done or court of protection.
256
Q

anorexia and MH act?

A
  • Treatment of people with severe anorexia nervosa who are not consenting to treatment for their mental disorder will in most cases require use of the MHA as it involves deprivation of liberty and compulsory refeeding.
257
Q

for people lacking capacity, emergecy treatment can be performed under ?

A
  • For people lacking capacity, emergency medical treatment can be performed under Common Law.
  • Non-emergency treatment for a physical condition not related to the eatingdisorder may be performed under the MCA 2005.
258
Q

16-18 year olds who are refusing Tx?

A
  • treatment for 16-18 year olds who are refusing treatment - parental conset cannot be used as authority to treat
259
Q

Physical signs of malnutiriton and purging?

A
260
Q

anorexia subtypes?

A
  • restricting type
  • binge eating/ purging type
261
Q

Restricting type of anorexia?

A
  • during the current episode of anorexia, the person hasn’t engaged in binge eating or purging behaviour - self induced vomiting or the misuse of laxatives, diuretics, enemas
262
Q

binge eating/ purging type of anorexia?

A
  • the person has reg engaged in purging behaviour or binge eating
263
Q

purging type of bulimia?

A
  • person has engaged in self induced vomiting, laxatives, diuretics or enemas
264
Q

non purging BN?

A
  • person has used other inappropriate compensatory behaviours like fasting or excessive exercise
  • but hasn’t regularly engaged in self-induced vomiting, laxatives etc
265
Q

short term consequences of EDs - CARDIAC

A
  • T wave inversions, ST depression, supraventricular beats and ventricular tachycardia
  • superior mesenteric artery syndrome
266
Q

long term consequences of EDs?

A
  • pubertral delay/ arrest
  • growth retardation/ short stature
  • anxiety, depression
267
Q

anorexia vs bulimia?

A
  • In anorexia, there is an intense fear of gaining weight, even if the person is underweight. The experience of body shape or weight is disturbed and affects self-image excessively.
  • In bulimia nervosa, recurrent bouts of binge eating alternate with inappropriate compensatory behaviour to prevent weight gain, such as laxatives, vomiting or fasting.
  • Young people who binge eat consume large amounts of food even if they are not hungry.
268
Q

serious underweight BMI?

A
  • A BMI below the <2nd centile (or percentage median BMI <80%) indicates serious underweight.
269
Q

Head and neck examination findings in ED (3)?

A
  • Eyes. Petechiae on the sclerae may be due to vomiting.
  • Parotid glands. Parotid gland swelling occurs in malnutrition.
  • Teeth. Dental caries may be caused by increased acid exposure due torepeated vomiting.
270
Q

EDs in males ?

A
  • later age of onset
  • typically higher rates of obesity pre-onset
  • Often a fixation on body shape or type rather thanweight. e.g. ‘to be muscular’
  • More likely to see excessive exercise
271
Q

Poor prognosis associated with:

A

–Early age of onset
–Depression during illness
–Disturbed family relationships
- Duration of illness (>3 years / more than 1 inpatient admission)

272
Q

adolescent focused therapy?

A
  • Individual approach
  • Focus on patients identifying, tolerating and managing their emotions
273
Q

3 phases of adolescent focused therapy?

A
  • Alliance and mutual understanding of AN
  • Enhancing independence from parents
  • Develop strategies to deal with the tasks of adolescence
  • AFT less effective and takes longer than FBT
274
Q

family based therapy/ maudsley model - 4 phases?

A

1 - Acknowledging state of starvation, focus on refeeding, emphasis on parental control
2 – Continued focus on weight gain, starting to shift responsibility
3 – Weight maintenance, focus on family relationships, develop family strengths
4 – Relapse prevention, endings

275
Q

Family therapy?

A
  • views the problems as relational not individual
  • externalisation of the ED
  • non-blaming, unifies the family and shares responsibility
  • family is best positioned to find their own solutions
276
Q

CBT-E?

A
277
Q

Developmental theories of ED?

A
  • features preceding the onset of EDs which are present in childhood
  • childhood perfectionism
  • individuals with both constrained (anorexia) and disinhibited (bulimia) eating share the personality trait of high harm avoidance.
  • impulsivity & binge eating
  • compulsivity and anorexia
278
Q

Genetic predisposition in ED?

A
  • genetic predisposition - relatives of those diagnosed with an eating disorder are up to 6x more likely to develop an ED
279
Q

Lateral hypothalamus is resp for?

A

initating hunger cues ca

280
Q

ventromedial hypothalamus is resp for?

A

sending signals of satiation, telling the organism to stop eating.

281
Q

serotonin’s effect on eating?

A

inhibitory effect on eating behaviour

282
Q
A

Year 3 (45 decks)

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