Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Patient Semester 2 > Mental Health > Flashcards

Mental Health Flashcards

1
Q

Incidence of schizophrenia?

A

approx 1% develop it at some point
affects men and women in equal proportions, men tend to have an earlier onset, and women have a second incidence peak in mid-late 40s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Biological basis of schizophreia?

A

MRI scans show sufferers have enlarged ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Genetic risk factors for schizophrenia?

A

there are multiple genes in creating a predisposition to schizophrenia. higher rates between families

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Environmental risk factors for schizophrenia?

A

Prenatal problems, obstetric complications, urban/city birth, stressful life events, drug abuse
- related to dopamine production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How to genetic and environmental risk factors combine to turn into schizophrenia?

A

cause gene expression impairments, leading to neurochemical and metabolic changes. altered connectivity leads to impaired information processes and then the symptoms: altered behaviour, altered cognition and altered emotion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Positive symptoms of schizophrenia?

A

Delusions, hallucinations, disorganised speech

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Negative symptoms of schizophrenia?

A

reduced emotion, motivation, interests, thought/speech and pleasure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cognitive deficits from schizophrenia?

A

Problems with attention, memory (working and verbal), executive function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mood symptoms of schizophrenia?

A

depression/anxiety, hostility/aggression, suicide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which brain circuits/areas cause the positive symptoms of schizophrenia?

A

mesolimbic and striatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which brain circuits/areas cause the negative symptoms of schizophrenia?

A

mesocortical and prefrontal cortex, nucleus accumbens reward circuits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which brain circuits/areas cause the cognitive symptoms of schizophrenia?

A

dorsolateral prefrontal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which brain circuits/areas cause the aggressive symptoms of schizophrenia?

A

orbitofrontal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which brain circuits/areas cause the affective symptoms of schizophrenia?

A

ventromedial prefrontal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

DSM-V criteria for schizophrenia?

A

A: at least two of: delusions, hallucinations, disorganised speech, grossly disorganised or catatonic behaviour, negative symptoms for at least one month. certain delusions or hallucinations mean no other symptoms from A need to be present.

B: social/occupational dysfunction

C: duration of at least 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Impact of increased dopamine in subcortical pathways?

A

psychotic symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do agonists of dopamine do, and exmaple?

A

induce psychotic symptoms e.g. amphetamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What do antipsychotics do?

A

dopamine antagonists D2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does too much dopamine at the D2 receptors relate to the symptoms?

A

D2 receptors are inhibitory - so increased dopamine leads to too much inhibition, causing symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Consequences of NMDA receptor hypofunction?

A
  • can be genetic or non-genetic, triggers psychosis in early adulthood
  • important in the balance of GABA (inhibitory) and glutamate (excitatory)
  • hypo NMDA leads to less GABA, which leads to more glutamate. this activates cell bodies to increase dopamine, which can cause psychosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Examples of typical antipsychotics

A

haloperidol, chlorpromazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do typical antipsychotics work?

A

high affinity for dopamine D2 receptors

  • only effective against positive symptoms, not negative ones
  • blockade of D2 receptors can lead to motor control impairments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Examples of atypical antipsychotics

A

Clozapine, olanzapine, risperidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do atypical antipsychotics work?

A

higher affinity for 5HT2 (serotonin) receptors over D2

  • effective against positive symptoms, and more effective than typicals against negative symptoms
  • significant side effects of weight gain etc
  • less motor impairments than typicals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does evidence suggest about the difference in efficacy vs side effects between antipsychotic types?

A

differences in efficacy were small, and smaller than the differences in side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is EPS?

A

Extrapyramidal symtpoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the balance between receptor occupancy and dose for antipsychotics?

A

certain receptor occupancy percentage needed to treat psychosis, but too much causes EPS. different drugs require different doses to reach the threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the % D2 occupancy required for antipsychotic efficacy?

A

65%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

At what % D2 occupancy does hyperprolactinaemia begin to occur?

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

At what % D2 occupancy do EPS start to occur?

A

78%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which antipsychotic has least risk of EPS?

A

Clozapine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which antipsychotic has most risk of EPS?

A

Haloperidol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are some of the theories about antipsychotic induced weight gain?

A
  • antagonism of histamine H1 receptors, serotonin 5HT2c receptors, dopamine D2
  • affecting hormonally controlled systems e.g. leptin
  • significant individual variation implies genetic involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Ways to manage antipsychotic induced weight gain?

A
  • warn patients before starting high risk drugs
  • early hunger, snacking and early weight gain are all indicators
  • standard weight management
  • consider swapping or stopping
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Which other psychotropic drugs have a greater risk of weight gain?

A
  • TCAs
  • Mirtazapine
  • Lithium
  • Valproate
  • Carbemazepine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Which other psychotropic drugs have a lower risk of weight gain?

A
  • SSRIs
  • Duloxetine
  • Agomelatine
  • Lamotrigine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which antipsychotics have the highest risk of prolactin increase?

A

Haloperidol, risperidone, paliperidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

When was the Mental Health Act 1983 amdended?

A

2007

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Examples of disorders of mood?

A

Depression, anxiety, elation, anger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Examples of disorders of perception?

A

Hallucinations, sensory perceptions, illusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Examples of disorders of thinking?

A

Delusions, obsessions, abnormal thought streams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Diagnostic process for mental illness?

A
  • Patient interview/observation essential
  • May speak to family/carers
  • Blood tests/scans used to rule out a physical cause
  • Two main diagnostic criteria, DSM-V and ICD-10
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What countries does the Mental Health Act apply to?

A

England and Wales

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What does the mental health act outline?

A

When people with a mental disorder might be admitted to hospital, assessed and treated against their own will for their own health and safety, and/or the protection of others
Also specifies rights of those with mental health disorders, enshrining respect, communication, participation and least restriction principles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What must decisions taken under the Mental Health Act minimise?

A

undesirable of metnal disorder, by maximising safety and wellbeing, and promoting recover of the patient and protecting others from harm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is an informal mental health patient?

A

One who comes into hospital voluntarily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What does a Section 2 cover?

A

hospital admission of patients against their will, considered to have a disorder requiring inpatient care for the patients or others’ safety

mainly used for assessment and treatment - usually for people not known to services

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How long does Section 2 last?

A

28 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How is a Section 2 carried out?

A

Application for admission made by an Approved Mental Health Professional (AMHP) within 14 days of interviewing the patient (including views of the relatives). Nearest relatives can also apply for admission.

Two doctors must assess the patient to confirm sectioning, one of which is an approved doctor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Who manages patient care once the patient is admission?

A

The responsible clinician

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is a Section 3 for?

A

Appropriate treatment for a mental health disorder

52
Q

How long does a Section 3 last?

A

Up to 6 months, can be renewed

53
Q

Who is a Section 3 for?

A
  • patients in the community who are known to services/have a previous section
  • already in hospital having undergone assessment/treatment under section 2 (apply for section 3 before the section 2 expires)
54
Q

What professions can AMHP be?

A

Social worker, mental health nurses, psychologists, occupational therapists

55
Q

Who can block a sectioning?

A

Nearest relative (though this too can be appealed in court)

56
Q

How long can medication be given to sectioned patients with capacity against their will?

A

Up to 3 months

57
Q

What happens if a sectioned patient continues to refuse medication after 3 months, with or without capacity?

A

Responsible clinician must get a recommendation that treatment must continue - from a Second Opinion Appointed Doctor (SOAD).

completion of a T3 form

58
Q

What happens if a sectioned patient with capacity consents to medication after 3 months?

A

T2 form is filled out and proceed

59
Q

Who else must a SOAD consult to continue giving a sectioned patient drugs against their will?

A

Two other non-doctor professionals involved in the patients care, e.g. nurse and pharmacist

60
Q

What treatment cannot be given without consent under any circumstances?

A

ECT

61
Q

What must be done every time a dose is administered to a T3 patient?

A

Consent sought - even if it’s not given

62
Q

What is vital with all T2 and T3 forms?

A
  • all individual medicines that are likely to be used to treat the disorder in question are listed (including PRN), according to BNF classification
  • if a class is specified, the number included and which are excluded should be specified
  • RoA and max dose should be specified for all medicines
  • should be kept with prescription charts
63
Q

What is a CTO?

A

Community treatment order

Can impose certain conditions when they are discharged following section 3

64
Q

Who organises CTOs and how?

A

Responsible clinician

Must apply to the NHS trust, and gain AMHP approval

65
Q

How long do CTOs last?

A

6 months, can be renewed

66
Q

Consequences of breaching a CTO?

A

That or their health deteriorates again, can be brought back into hospital

67
Q

Role of the Medicines Management in mental health hospitals?

A
  • medicines reconciliation completed by pharmacists/technicians (24-72 hour goal)
  • Ward rounds/daily patient reviews and make interventions
  • Counsel patients on medicines
  • Prescribing roles and non-medical prescribing
  • Audits and research
  • Discharge prescriptions (often handled by external pharmacy)
68
Q

Key differences of mental health pharmacists compared to general hospital?

A
  • Different nature - more professionals, longer
  • Legal activity surrounding mental health
  • Holistic patient care, tailored treatment choices
  • Nature of mental illness - insight and stigma

no one size fits all approach

69
Q

What physical health problems can increase the risk of someone developing a mental health problem?

A
  • obesity and T2D (irrespective of weight)
  • positive correlation between number of physical health problems and risk of developing mood disorder
  • smoking associated with anxiety and schizophrenia
  • adoption of the smoking habit likely in affective and alcohol misuse disorders
70
Q

Which mental health problems increase the risk of someone developing a physical health problem?

A
  • psychoses, bipolar and major depression increase the risk of obesity, diabetes, COPD and CVD
  • depression is an independent risk factor for stroke
  • patients with depression have less favourable outcomes after cardiac events (perhaps mediated by adherence)
  • people with schizophrenia may have higher rates of:
    epilepsy, obesity, eczema, hypothyroidism, dermatitis, viral hepatitis, diabetes, hypertension, COPD, fluid/electrolyte disorders
71
Q

Why are people with mental health conditions at higher risk of physical health issues?

A
  • more likely to live unhealthy lifestyles before diagnosis
  • result of mental health medications (esp. antipsychotics)
  • more likely to experience disparities in care compared to those without mental illness
  • less likely to access appropriate services to identify and address problems with physical health
72
Q

What behaviours are mental health patients more at risk of that increases likelihood of physical health problems?

A
  • smoking
  • substance misuse
  • unsafe sexual acitivty
  • poor dental health
  • consume less fruit and veg
  • consume only one deal per day
  • little physical activity
  • consume high fats/salt/sugar
73
Q

What disparities in care arise in physical care for mental health patients?

A
  • less likely to be prescribed ACEi/AT2, BBs, antihypertensives and statins
  • lower than average cardiac care of schizophrenia and SMI patients (weak link to mortality)
  • preventative care often inferior for schizophrenics compared to general population
  • only 36% of schizophrenic patients with evidence of IGT have intervention. 59% intervention for smoking and 25% for hypertension
  • lithium patients have inadequate renal monitoring
74
Q

What are the four pathways that norardrenaline controls?

A

Alertness, arousal, sensory perception, motor tone

75
Q

What happens at a noradrenaline synapse?

A
  • Tyrosine -> DOPA -> dopamine -> noradrenaline
  • activation of receptors on postsynaptic membrane
  • reuptake into presynaptic neurone (MAO breaks it down to inactivate)
76
Q

What happens at a serotonin synapse?

A
  • Tryptophan -> 5-hydroxytryptophan -> 5-hydroxytryptamine -> serotonin
  • activation of postsynaptic receptors
  • reuptake into presynaptic neurone
  • inactivation
77
Q

What effect does noradrenaline have on the postsynaptic receptors?

A

Protein kinase activation, protein phosphorylation

78
Q

What effect does serotonin have on the postsynaptic receptors?

A

Opens ion channels

79
Q

What are the 6 pathways that serotonin regulates?

A

Sleep, food intake, thermoregulation, sexual behaviour, pain, motor tone

80
Q

Difference between unipolar and bipolar depression?

A

Unipolar is only depressive (either episodes or persistent)

81
Q

Examples of unipolar depression

A

Major depressive disorder
Dysthymia (persistent mild depression)
Seasonal affective disorder
Postnatal depression

82
Q

What is bipolar depression?

A

Alternating periods of depresion and mania

83
Q

Causes of depression?

A

Life events, childhood experience, genetics, chemical imbalance, medication side effects, physical conditions, diet

84
Q

Neurotransmitters involved in depression?

A

Serotonin, noradrenaline, Ach, Glutamate

85
Q

Treatments for depression?

A

CBT
Antidepressants
Exercise
ECT

86
Q

Which part of the brain and neurotransmitter gives rise to loss of pleasure, interest and motivation?

A

Dorso-lateral PFC

Dopamine

87
Q

Which part of the brain and neurotransmitter gives rise to sadness and suicide?

A

Ventro-medial PFC

serotonin, noradrenaline, dopamine

88
Q

Which part of the brain and neurotransmitter gives rise to fatigue and loss of energy?

A

Dopamine, noradrenaline and serotonin

89
Q

Which part of the brain and neurotransmitter gives rise to problems with sleep, appetite and libido?

A

Nucleus accumbens and hypothalamus

Serotonin, noradrenaline and dopamine

90
Q

Which part of the brain and neurotransmitter gives rise to problems with attention, concentration and problem solving?

A

Dorso-lateral PFC

Dopamine (D1), Ach, Serotonin, noradrenaline, GABA, histamine

91
Q

What are the classes of antidepressant drugs?

A
  • TCAs
  • SSRIs
  • NaRIs
  • SNRIs
  • MAOIs
  • Atypical
  • Ketamine
92
Q

What types of psychotherapy can help with depression?

A

Talking therapy
Counselling
CBT

93
Q

What kinds of physical interventions can help with depression?

A

ECT
Electromagnetic therapy
Deep brain stimulation
Vagal stimulation

94
Q

What is the main issue with MAOIs as depression treatment?

A

A lot of interactions with both foods and drugs - some quite severe

Can’t consume tyramine - found in cheese etc. Very dangerous response (precursor for MAO synthesis). Large hypertensive response, often enough to cause haemorrhages

95
Q

How long do antidepressant drugs take to have an effect?

A

2-4 weeks

96
Q

How long does psychotherapy take to have an effect on depression?

A

weeks, months, years

97
Q

How long do physical interventions take to have an effect on depression?

A

Immediate

98
Q

What is the monoamine hypothesis?

A

Antidepressants correct the depletion of neurotransmitters in the brain, immediately. The effect of the antidepressant on the depression takes several weeks.

Important to consider secondary changes that the corrected monoamine levels have, as these may be what causes the changes in behaviour

99
Q

Reasons why antidepressants take time to work other than the monoamine hypothesis?

A
  1. Some antidepressants initiate neurogenesis, which takes time
  2. initiation of SSRI can initially cause autoreceptor activation, which reduces cell firing, so less serotonin released at all. after a while, autoreceptor gets down regulated so normal cell firing is restored and the SSRI can prevent reuptake of a normal amount of serotonin
100
Q

What are the DSM symptoms of depression?

A

Core (must have at least one of these):

  • low mood
  • loss of pleasure

Other (must have at least 4):

  • Loss of energy
  • Worthlessness, guilt
  • Recurrent thoughts of death or suicide
  • Reduced ability to think or concentrate
  • Psychomotor agitation or retardation
  • Insomnia/hypersomnia
  • Weight changes
101
Q

When to start pharmacological treatment for depression?

A
  • moderate or severe depression
  • a past history of moderate or severe depression
  • subthreshold depressive symptoms present for at least 2 years
  • subthreshold depressive symptoms or mild depression persisting after other interventions
102
Q

What is a big reason for patients stopping their antidepressant treatment?

A

not being warned properly of the side effects

103
Q

Which class of antidepressants is first line?

A

SSRI

104
Q

Examples of SSRIs?

A

Fluoxetine, Sertraline, Citalopram, Escitalopram, Paroxetine

105
Q

Main side effects of SSRIs?

A

GI effects, hyponatraemia (low sodium)

Can have increased bleeding risk (DDIs)

106
Q

Examples of SNRIs?

A

Venlafaxine (more common), duloxetine

107
Q

When is venlafaxine contra-indicated?

A

uncontrolled hypertension

108
Q

Benefits of mirtazapine?

A

Considered quite well tolerated

109
Q

Main side effects of mirtazapine?

A

Sedation and weight gain

can also cause blood disorders

110
Q

Examples of TCAs?

A

Amitriptyline, Clomipramine, Nortriptyline, Lofepramine, Dosulepin

111
Q

Main side effects of TCAs?

A

Antimuscarinic side effects.
Cardiotoxicity
Shouldn’t be used in high suicide risk

112
Q

When should reboxetine not be used?

A

In the elderly (rarely used anyway)

113
Q

What is Agomelatine?

A

Melatonergic agonist (also 5HT2C antagonist)

114
Q

Main risks with agomelatine?

A

Hepatotoxicity - cases of liver injury incl fatal liver failure reported

115
Q

What monitoring needs to be done to agomelatine?

A

LFTs baseline, 3 weeks, 6 weeks, 3 months, 6 months

116
Q

What is Vortioxetine?

A

Serotonin based drug

117
Q

When is Vortioxetine recommended for use?

A

By NICE for adults who have not responded to 2 antidepressants in the current episode

118
Q

First step when initiating antidepressant therapy?

A

Monotherapy - SSRI first or better tolerated other, can switch if needed (incl between classes)

then try older, less well tolerated antidepressants

119
Q

What to do if inital antidepressant monotherpy doesn’t worK?

A

combinations/augmentation

120
Q

Things to consider before changing antidepressant due to lack of effect?

A
  • how long has the patient been taking it
  • have they been taking it properly
  • try increasing dose
  • 4-6 weeks for full effect
121
Q

Things to consider before changing antidepressant due to side effects?

A
  • which options would be better tolerated?
122
Q

Why is specialist input required for combinations of antidepressants?

A
  • interactions
  • serotonin syndrome
  • increased risk of or combined side effects
123
Q

What is augmentation with antidepressants?

A

addition of something else e.g. lithium or antipsychotic

124
Q

Place of St Johns Wort in depression therapy?

A
  • while it is effective, it is not recommended
  • causes lots of drug interactions
  • different potencies
125
Q

How to stop antidepressant treatment?

A
  • should continue for 6 months after remission (may need to be longer, up to 2 years)
  • reduce dose slowly
126
Q

Role of the pharmacist in depression therapeutics?

A
  • advice on choice of medication
  • review patient history
  • counselling for side effects and adherence
  • monitoring for efficacy and side effects
127
Q

What are the main counselling points for antidepressants?

A
  • Patient choice
  • Doses – vary for adult and elderly – check appropriate
  • Timing of doses
  • Increased agitation, anxiety at start – feeling worse before feeling better
  • Suicide risk? History, younger patients (under 30)
  • Time to benefit
  • Duration of treatment
  • Not addictive, but can get discontinuation symptoms
  • Not to stop abruptly. Discuss with prescriber first.
  • Side effects
  • Take regularly

Patient Semester 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions