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MRCPsych Part B - Al-Rashid Hospital > Liaison Psychiatry 1.3 > Flashcards

Liaison Psychiatry 1.3 Flashcards

1
Q

Prevalence of CFS

A

0.5%

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2
Q

M:F ratio of CFS

A

1:3

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3
Q

Who is CFS more common in

A

Females
Lower occupational status
Lesser educational background

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4
Q

Mean age of onset of CFS

A

29-35 years

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5
Q

Mean illness duration of CFS

A

3-9 years

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6
Q

CFS criteria

A

Persistent or relapsing unexplained chronic fatigue of new onset, lasting at least 6 months and not the result of organic disease or continuing exertion, not alleviated by rest.

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7
Q

Which sx are required for CFS?

A 
Four or more of the following, present for >6 months:
Impaired memory/concentration
Sore throat
Tender cervical/axillary lymph nodes
Muscle pain
Pain in several joints
New headaches
Unrefreshing sleep
Malaise after exterion
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8
Q

Exclusion criteria for CFS

A

Major psychiatric disorders including psychotic depression, bipolar, schizophrenia, dementia, ED, alcohol or substance abuse.
Does not include non-psychotic disorders.

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9
Q

Predictors of poor outcome of CFS

A 
Claiming a disability related benefit
Low sense of control
Strong focus on physical sx
Being passive with reduced activity
Membership of self-help grous
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10
Q

How many patients with CFS are unable to work?

A

33%

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11
Q

Which sx of CFS may indicate another serious illness

A 
Significant weight loss
Clinically significant lymphadenopathy
Localising neurological signs
Features of inflammatory arthritis, connective tissue disease or cardiorespiratory disease
Sleep apnoea
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12
Q

When does onset of CFS typically occur?

A

After an episode of viral infection

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13
Q

Predisposing factors of CFS

A

Neuroticism
Childhood inactivity
Childhood illness

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14
Q

Precipitating factors of CFS

A

Infectious mononucleosis
Q fever
Lyme disease
Serious life events

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15
Q

Perpetuating factors of CFS

A 
Strong belief in physical cause
Activity-avoidance
Poor self-control
Primary/secondary gains
Low self-perception of cognitive ability
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16
Q

Metabolic findings in patients with CFS

A

Abnormality in HPA-axis and serotonin pathway suggest altered physiological response to stress.

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17
Q

How many patients with CFS have low cortisol?

A

33%

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18
Q

What do family studies of CFS suggest?

A

Mutation of cortisol transporting globulin

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19
Q

Effective treatment of CFS?

A

CBT

Graded exercise therapy

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20
Q

Components of CBT for CFS

A

Explanation of aetiological model
Motivation for CBT
Challenging and changing of fatigue related cognition
Achievement and maintenance of basic amount of physical activity
Gradual increase in physical activity
Rehab e.g. rigorous self-monitoring

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21
Q

How long can CBT last for in patients with CFS who initially respond?

A

5 years

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22
Q

How is timing of treatment important in CFS?

A

Patients improve if medications are added to CBT but now when CBT is added to medication

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23
Q

What is graded exercise therapy based on?

A

Physiological model of deconditioning

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24
Q

What is affected by inactivity?

A

Muscle strength
Autonomic response
Perception of exercise related sensations

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25
Q

What is the aim of graded exercise therapy?

A

Gradually increase exercise and thus reduce unwanted consequences of inactivity.

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26
Q

Improvement rate of CBT for CFS

A

70%

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27
Q

Improvement rate of graded exercise therapy for CFS

A

55%

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28
Q

Antidepressant treatment for CFS

A

Should not be used

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29
Q

When should antidepressants be considered for CFS?

A

Depressive sx

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30
Q

What factors must be taken into account if antidepressants are used for CFS?

A

Polonged inactivity increases risk of autonomic side effects such as postural hypotension
Sedation may worse fatigue

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31
Q

What is pacing?

A

People with CFS are encouraged to achieve a balance between rest and activity

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32
Q

What is the aim of pacing?

A

Prevent vicious circle of overactivity and setbacks while setting realistic goals for increasing activity

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33
Q

Disadvantages of pacing

A

No evidence

May prolong illness by encouraging avoidence

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34
Q

Prognosis of CFS

A

1-5 years

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35
Q

How many patients improve over 5 years with CFS?

A

17-65%

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36
Q

How many patients with CFF recover over 5 years?

A

<10%

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37
Q

How many patients with CFS worsen over 10 years>

A

10-20%

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38
Q

Mortality of CFS?

A

Not associated with increased mortality

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39
Q

How many patients with CFS have depression

A

23%

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40
Q

How many patients with CFS have a history of depression

A

50-75%

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41
Q

Impact of CFS on CNS

A

Upregulation of serotonin

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42
Q

What sx does CFS not have which depression does?

A

Absence of lack of motivation, guilt, anhedonia

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43
Q

HPA axis in CFS

A

Downregulation

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44
Q

HPA axis in depression

A

Upregulation

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45
Q

Sleep disturbance in depression

A

Reduced REM latency

Increased REM density

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46
Q

Lifetime prevalence of panic disorder in those with CFS

A

17-25%

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47
Q

Lifetime prevalence of GAD in those with CFS

A

2-30%

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48
Q

Overlapping sx between anxiety and CFS

A

Decreased cerebral blood flow
Sympathetic overactivity
Sleep abnormalities

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49
Q

Rate of somatisation in CFS

A

28%

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50
Q

How does examination impact rate of somatisation of CFS?

A

If examiner attributes sx to physical cause, rate of somatisation decreases and vice versa.

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51
Q

How many patients with fibromyalgia meet criteria for CFS?

A

20-70%

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52
Q

How many patients with CFS meet criteria for fibromyalgia?

A

35-70%

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53
Q

Which conditions do sx of CFS overlap with?

A

Fibromyalgia
Multiple chemical sensitivity
IBS
Temporomandibular joint disorder

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54
Q

What has replaced the diagnostic criteria for pain disorder in DSM IV in DSM V?

A

Somatic Symptom and Related Disorders (SSD)

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55
Q

What is SSD diagnosis made on?

A

The basis of positive sx and signs rather than absence of a medical explanation for somatic complaints.

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56
Q

What are the positive sx and signs of SSD?

A

Distressing somatic sx plus abnormal thoughts, feelings and behaviours in response to these sx

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57
Q

Which DSM IV disorders have been removed?

A

Somatization disorder
Hypochondriasis
Pain disorder
Undifferentiated somatoform disorder

58
Q

How do psychiatric illnesses increase pain intensity?

A

Via shared mehcnaism through central pain modulating system

59
Q

What is the most common presenting somatic sx in medial OP?

60
Q

What is the most common mental disorder in patients suffering from pain disorders?

A

Depression - 10-15%

61
Q

How many depressed adults complain of pain?

62
Q

When is CBT effective for chronic pain?

A

Cognitive restructuring
Relaxation training
Time-based activity pacing
Graded homework assignments to decrease avoidance and encourage more active lifestyle

63
Q

Who first introduced the term atypical facial pain?

A

Frazier and Russell in 1924

64
Q

What is atypical facial pain?

A

Atypical in distribution, unilateral, poorly localised, lasts most of the day and described as severe ache, crushing or burning.

65
Q

What is the definition of persistent idiopathic facial pain?

A

Facial pain that is present daily and persists most of the day.
Pain is confined at onset to limited area on one side of the face, deep ache, poorly localised.

66
Q

Exclusion criteria for persistent idiopathic facial pain?

A

Associated sensory loss or physical signs

Abnormalities in lab or imaging studies

67
Q

BAP guidelines on use of antidepressants in pain management

A

Lack of evidence that SNRIs are more effective than SSRIs for pain sx associated with depression.

68
Q

What are primary organic neuropsychiatric disorders due to in HIV?

A

Viral CNS damage

69
Q

What are secondary organic neuropsychiatric disorders due to in HIV?

A

Opportunistic infections

Drugs

70
Q

What are reactive neuropsychiatric disorders in HIV due to?

A

HIV-associated acute stress reaction

71
Q

Prevalence of any mental disorder in the lifetime of HIV positive patients?

72
Q

When does HIV associated acute stress reaction occur?

A

When informing someone of seropositivity of when a transition to full clinical AIDs occurs from state of infection.

73
Q

Sx of HIV associated acute stress reaction?

A 
Brooding about the future
Panic attacks
Social isolation
Rage
Feelings of isolation
74
Q

Duration of HIV associated acute stress reaction

A

Appear within minutes of hours of patient being informed

Remit within 2-3 days

75
Q

How many patients with HIV show adjustment disorder?

76
Q

How many patients with HIV show anxiety disorder?

77
Q

Which psychiatric disorder is most common in HIV patients?

A

Depression

78
Q

How many patients with HIV report being depressed at some point?

79
Q

M:F ratio of depression in HIV patients

A

More common in women

80
Q

Reasons for high incidence of depression in HIV patients

A 
Psychological impact
Neuripathological deficits
Homosexuals
Lower socioeconomic groups
Some sx of depression also occur in HIV e.g. weight loss, sleep disorder
81
Q

Risk factors of suicide in patients with HIV

A

Having friends who died from AIDS
Recent notification of HIV seropositivity
Difficult social issues due to homosexuality
Inadequate social and financial support
Presence of dementia or delirium

82
Q

Treatment of depression in HIV patients

A

SSRIs or TCAs

83
Q

Dosing of SSRIs for depression in HIV

A

25% of usual recommended dosage when starting

84
Q

Which TCAs to use in depression in HIV?

A

Secondary amines

85
Q

Risk of TCAs used in patients with AIDS

A

May suffer severe anticholinergic effects

86
Q

What therapy is helpful for depression in HIV

A

Interpersonal psychotherapy

87
Q

What might cause psychosis during late stages of HIV?

A

Direct neurotoxicity
Iatrogenic
Substance misuse

88
Q

Difficulties in px antipsychotics to patients with AIDs

A

Prone to EPSEs and NMS

89
Q

What is the most frequent reason for psychiatric hospitalisation of patients with HIV?

A

Mania
Depression
Psychosis (in that order)

90
Q

Causes of mania in HIV

A

Illicit drug use

Iatrogenic

91
Q

What iatrogenic things can cause mania in HIV?

A 
Didanosine
Ganciclovir
Procarbazine
Estavudine 
Steroids
Zidovudine
92
Q

What is mania in advanced HIV associated with?

A

Cognitive impairment

Reduced survival

93
Q

Difficulties in treating mania in HIV patients

A

Lithium and Valproate can induce neurological reactions and toxicity

94
Q

What needs to occur if a patient with HIV is started on Carbamazepine?

A

Control of patients haemopoietic function as other medications can trigger toxic effects in bone marrow

95
Q

Which organic mental disorder is most frequently observed in patients with HIV?

96
Q

What is ‘mild cognitive/motor disorder’ in HIV?

A

AIDs dementia where ADLs are intact

97
Q

How many patients with AIDs have dementia?

98
Q

Incidence of dementia syndrome within first 2 years of diagnosis of AIDs?

A

7% per year

99
Q

How many patients with AIDs develop dementia?

100
Q

Risk factors for developing HIV-associated dementia

A

Older age
Decreased body mass
Decrements in haematocrit
History of IV drug abuse

101
Q

Early cognitive sx of HIV-dementia

A

Forgetfulness
Loss of concentration
Mental slowing
Reduced performance on sequential mental activities
Apathy
Reduced spontaneity and emotional responsivity
Social withdrawal

102
Q

Early emotional sx of HIV-dementia

A

Depression
Emotional lability
Agitation
Psychotic sx

103
Q

Early motor sx of HIV dementia

A 
Loss of balance and coordination
Clumsiness
Leg weakness
Postural tremor
Hyperreflexia
Ataxia
Slowing of rapid alternating movements
Frontal release signs
Dysarthria
Saccades
104
Q

Cognitive tests in early HIV dementia

A

Slowing in verbal or motor responses or difficulty in recalling a series of objects after >5 mins

105
Q

Sx in late HIV dementia

A 
Global deterioration of cognitive function
Severe psychomotor retardation
Mutism
Paraparesis
Bowel/bladder incontinence
Myclonus
Seizues
Pedal parasthesias and hypersensitivities due to concurrent sensory neuropathy
106
Q

Predictive markers for HIV Dementia

A

B2-microglobulin and neopterin levels in CSF

CD41 cell counts

107
Q

Indirect factors leading to HIV dementia

A

Cytokines - TNF
Parts of HIV itself - gp41, gp120, Tat, Rev, Nef
Excitatory aminoacids - quinolinic acid

108
Q

What can be used to differentiate HIV Dementia from depression?

A

Neuropsychological tests

Brain imaging

109
Q

What cognitive functions are preserved in HIV dementia?

A

Naming

Vocab

110
Q

What does brain imaging show in HIV dementia?

A

Cerebral atrophy, widened cortical sulci, enlarged ventricles
High intensity T2 signal abnormalities in periventricular white matter and centrum semiovale

111
Q

What in brain imaging would suggest primary CNS lymphoma?

A

Contrast-enhancing mass lesions

112
Q

What in brain imaging would suggest cerebral toxoplasmosis?

A

Multiple bilateral ring-enhancing lesions

113
Q

What can CSF help to exclude in HIV?

A

Cryptococcal meningitis
CNS TB
CMV encephalitis
Neurosyphilis

114
Q

What does CSF show in HIV dementia?

A

Increase of total proteins
Increase of IgG fraction and mononuclear pleocytosis index
HIV core antigen p24 or HIV RNA

115
Q

What does HIV RNA in CSF correlate with?

A

Severity of dementia

116
Q

What can help diagnosis of cryptoccocal meningitis?

A

CSF indian ink staining, cryptococcal antigen tires and fungal cultures

117
Q

Treatment of HIV infection

A

Zidovudine

118
Q

What is Zidovudine?

A

Reverse transcriptase inhibitor

119
Q

What medication has been found to improve cognitive sx in patients with AIDs?

A

Methykphenidate 10-90mg/day

120
Q

What secondary organic brain diseases can occur in HIV?

A

Progressive multifocal leucoencephalopathy
Cerebral toxoplasmosis
Cryptococcal meningitis
Primary CNS lymphoma

121
Q

What is progressive multifocal leucoencephalopathy?

A

Papovavirus infection affecting white matter diffusely.

122
Q

Sx of progressive multifocal leucoencephalopathy?

A

Rapid dementia
Blindness
Ataxia
Hemiparesis

123
Q

Treatment of progressive multifocal leucoencephalopathy?

124
Q

What is cerebral toxoplasmosis?

A

Reactivation of latent cerebral infection by Toxoplasma gondii

125
Q

What is Toxoplasma gondii?

A

Opportunistic intracellular protozoan

126
Q

Sx of cerebral toxoplasmosis?

A

Rapid development of marked alteration in mental state

127
Q

Where do lesions tend to be in cerebral toxoplasmosis?

A

Basal ganglia

128
Q

How is diagnosis of cerebral toxoplasmosis made>

A

Structural neuroimaging tests

129
Q

Treatment of cerebral toxoplasmosis?

A

Pyrimethamine and Sulphadiazine

130
Q

What is cryptococcal meningitis?

A

Caused by yeast-like fungus cryptococcus neoformans

131
Q

Sx of cryptococcal meningitis?

A 
Headache
Meningism
Photophobia
Nausea
Fever
Deirium
132
Q

Treatment of cryptococcal meningitis?

A

Amphotericin B IV

133
Q

What is primary CNS lymphoma?

A

Late complication of HIV

EBV-assocaited

134
Q

How many patients with HIV develop primary CNS lymphoma?

135
Q

Sx of primary CNs lymphoma?

A 
Epileptic seizures
Personality change
Changes in attention
Headache
Focal deficits without fever
136
Q

Name some antiretrovirals used in HIV

A 
Zidovudine
Stavudine
Didanosine
Zalcitabine
Efavirenz
137
Q

Side effects of Zidovudine

A 
Confusion
Agitation
Insomnia
Mania
Depression
138
Q

Side effects of Stavudine and Zalcitabine

A

Peripheral neuropathy

139
Q

Side effects of Didanosine

A

Peripheral Neuropathy

Mania

140
Q

Side effects of Efavirenz

A

Neuropsychiatric side effects:

33% depression, 2% psychosis

141
Q

How many patients on Efavirenz develop neuropsychiatric side effects?

MRCPsych Part B - Al-Rashid Hospital (64 decks)

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