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Flashcards in Psychiatry (finished) Deck (871):
1

What are some differential diagnoses for dementia?

Delirium, reversible dementias (e.g. brain lesion, endocrine, vitamin deficiencies), pseudodementia (memory problems in severe depression in the elderly)

2

What investigations should you do in dementia?

Basic obs + physical examination, blood tests to rule out organic causes (FBC, U+E, glucose, TFTs, LFTs, B12 + folate, calcium, VDRL), MMSE, collateral history, septic screen, consider imaging

3

When should you do imaging in dementia?

If unusual presentation/neurologiacl signs, first onset of psychotic symptoms later in life (especially olfactory or visual hallucinations), if planning to start anti dementia medication

4

What therapies are relevant in dementia?

Behavioural approaches, reminiscence therapy, validation therapy, meultisensory therapy, cognitive stimulation therapy

5

How is dementia managed?

Adaptations for patients to keep them safe, social support, support for their carers, optimise physical health, psychological therapies, psychotropic medications

6

What medications can you use for dementia?

Anticholinesterase inhibitors e.g. donepezil/rivastigmine

7

How do anticholinesterase inhibitors work in dementia?

Prevent acetylcholinesterase destroying the acetylchoilne, which increases NT levels in the synapse and compensates fo rthe overall cholinergic loss

8

What is the pathology in Lewy Body dementia?

Lewy bodies are eosinophilic intracytoplasmic neuronal structures, composed of alpha-synuclein with ubiquitin. They are seen in the brain stem, in the cingulate gyrus and in the neocortex

9

What are the features of lewy body dementia?

Fluctuating confusion with marked variation in levels of alertness, vivid visual hallucinations (often of people or animals) and spontaneous (new) Parkinsonian signs. Need 2 of these.

10

What are features suggestive, but not diagnostic, of lewy body dementia?

Repeated falls, syncope, transient losses of consciousness, short term memory being less affected

11

Why shouldn't you prescribe antipsychotics in lewy body dementia?

Extreme antipsychotic sensitivity can cause death

12

What are the features of dependency?

Tolerance, compulsion, withdrawal, problems controlling use, continued use despite harm, salience (primacy), reinstatement after abstinence, narrowing of the repertoire

13

What are the features of dependent personality disorder?

REPORT + 3 of SUFFER: Subordinate, Undemanding, Feels helpless and alone, Fears abandonment, Encourages others to make decisions, Reassurance needed

14

What are the differentials of dependent personality disorder?

Reliance on others because of cognitive impairment, anxiety disorder

15

What are the core symptoms of depression?

Low mood, anergia, anhedonia (diagnosis requires 2 of these)

16

At what time of day does depression tend to be worse?

The morning

17

What are the cognitive symptoms of depression?

Feeling worthless, useless and unlovable, dwelling on the past leading to guilt, pessimistic view of the future, loss of self confidence, suicide may seem the only option, poor concentration and memory, thinking may feel slowed

18

What are the most worrying features in depression?

Suicidality, psychotic symptoms, severe self-neglect or ceasing to eat and drink

19

What are the biological symptoms of depression?

Altered sleep pattern: initial insomnia and early morning waking, less commonly hypersomnia (may coexist with hyperphagia and weight gain), decreased appetite for food and sex, constipation, aches and pains, dysmenorrhoea, all tend to emerge as the severity of depression increases

20

What are the psychotic symptoms in depression?

Emerge in very severe depression: auditory hallucinations (unpleasant derogatory voices), rarely visual hallucinations of scenes of destruction or evil spirits, nihilistic delusions (world has ended, person is dead), persecutory delusions (person feels they deserve persecution, punishment), guilt may progress to delusions of hainvg committed a terrible crime

21

What are the non-medical options for depression?

Will often resolve spontaneously so can do 'watchful waiting'; support at home, consider inpatient if significant risk of suicide or self harm, give advice on sleep hygiene, exercise, self help, address social stressors, light box for SAD

22

What is ECT?

Electroconvulsive therapy; uses electrodes to produce generalised tonic-clonic seizure while the patient is anaesthetised. Some people experience a degree of memory loss after but it is a fast and life saving treatment in severe or psychotic depression e.g. if has stopped eating

23

What investigations should you do in depression?

Collateral history, physical examination, blood tests as indicated (TFTs, FBC as anaemia causes fatigue, glucose or HBA1c as diabetes causes fatigue), Rating scales to measure or monitor severity and response (Beck Depression Inventory, Hospital Anxiety and Depression Scale), CT/MRI is not routine but can be done if cerebral pathology suspected

24

How do antidepressants work?

Increase the overall levels of monoamines at the synapse by either decreasing reuptake or breakdown. Over time, serotonin and central beta-adrenergic receptors become downregulated in depression, which is thought to account for the 4-6 week delay for antidepressant effect.

25

When are antidepressants indicated?

Moderate-severe depression ideally with psychotherapy

26

Which antidepressant tends to be the first choice and why?

Selective serotonin reuptake inhibitors, as they have milder side effects and are safer in overdose than others

27

How long should antidepressant treatment continue for?

Until the patient is no longer depressed and then a further 6 months

28

What are the main risks of antidepressant treatment?

All can cause hyponatramemia or some degree of sexual dysfunction. Most lower the seizure threshold. Avoid in mania or hypomania and patients shouldn't drink due to increased sedation, and shouldn't drive if feeling drowsy. Risk of serotonin syndrome if over treated

29

What is serotonin syndrome?

Happens when there is an excess of serotonin: restlessness, sweating, myoclonus, confusion, fits - can be life threatening

30

What is the mechanism of action of SSRIs?

Enhance serotonergic neurotransmission by blocking the reuptake of serotonin in the presynaptic nerve terminal

31

What is the mechanism of action of tricyclic antidepressants?

Inhibit reuptake of NA and 5-HT.

32

Why are tricyclics becoming less popular?

Because they can be lethal in overdose due to cardiotoxicity, so need to be avoided where there is a risk of suicide.

33

What is the mechanism of action of monoamine oxidase inhibitors?

Inhibit the metabolism of monoamines thus increasing synaptic levels

34

Why are MAOIs becoming less popular?

Risk of hypertensive crisis due to build up of noradrenaline when eating tyramine rich foods e.g. mature cheese, yeast extracts, fermented soya beans. Also can't be combined with others.

35

How is treatment resistant depression defined?

Failure to respond to 2 adequate trials of different drugs for 6-8 weeks (happens in up to 30% of patients)

36

How is treatment resistant depression managed?

Check diagnosis and adherence, then can try adding: lithium, tri-iodothyronine (T3), levothyroxine (T4), buspirone (anxiolytic which acts on 5-HT 1alpha receptors; no action alone but synergistic with SSRIs)

37

What should you bear in mind when stopping an antidepressant?

They're not addictive but they can ause discontinuation symptoms: flu-like, electric shocks

38

What is CBT?

Views psychologica problems as a result of the patient's distorted perceptions of themselves/the world/the future, and works to challenge negative automatic thoughts to build an alternative set of more realistic beliefs about themselves.

39

What is psychodynamic therapy?

Where the developing relationship between the therapist and patient is the key issue; patient applies unconscious templates of relationships from past experiences to the therapst (transferences) and putting words to the feeligns with the therapist enables the patient recognise their hidden beliefs and re-evaluate them

40

What does interpersonal therapy focus on?

Main themes of: unresolved loss, psychosocial transitions, relationship conflict, social skills deficit

41

What is the average age and limit age to make eye contact/follow a face?

1-4 weeks; 3 months

42

What is the average age and limit age to smile responsively?

4-6 weeks; 8 weeks

43

What is the average age and limit age to reach for objects?

4 months; 6 months

44

What is the average age and limit age to have good head control when sitting?

4 months; 6 months

45

What is the average age and limit age to turn to a voice?

7 months; 9 months

46

What is the average age and limit age to have tuneful babble?

5-6 months; 10 months

47

What is the average age and limit age to sit unsupported?

7-8 months; 10 months

48

What is the average age and limit age to have a pincer grip?

9-10 months; 15 months

49

What is the average age and limit age to walk independently?

11-3 months; 18 months

50

What is the average age and limit age to build two cubes?

13-15 months; 19 months

51

What is the average age and limit age to say a first word?

8-18 months; 2 years

52

What are the features of dissocial PD?

REPORT + 3 of FIGHTS: Forms but cannot maintain relationships, Irresponsible, Guiltless, Heartless, Temper easily lost, Someone else's fault

53

What are the differentials of dissocial PD?

Acute psychotic episode, manic episode

54

What is the heritability of anorexia nervosa?

About 50%

55

What are the aetiological factors in eating disorders?

Genetics, Psychological theories (perfectionism and low self esteem are risk factors), socail pressure to be thin, personal history (of obesity or AN in bulimia), experiences of child abuse, parental overprotection and family enmeshment in AN and disturbed family dynamics, parental weight concern and high parental expectations in BN

56

What are the theories behind AN?

Successful weight loss enhances patient's sense of achievement, autonomy, perfectionism. AN provides the ability to control something when life feels uncontrollable. Can also be a way to avoid separation from family or becoming an independent sexual being: maintains dependency on close family and a peri-pubertal physique.

57

What is the prognosis in anorexia?

After 10 years, 50% have no eating disorder and 10% have died. Suicide accounts for 1/3 deaths. The remaining 40% have ongoing problems and crossover to BN is common.

58

What are the poor prognostic factors in anorexia?

Very low weight, bulimic features, later onset, longer illness duration

59

What is the prognosis for bulimia?

After 10 years, 70% have recovered completely and only 1% have died

60

What are the poor prognostic factors in bulimia?

Severe bingeing or purging, low body weight, comorbid depression

61

When do eating disorder patients need urgent medical treatment?

BMI 1kg/week, purpuric rash, cold peripheraies, core body temp

62

What is refeeding syndrome and what causes it?

Characterised by electrolyte imbalance (principally low serum phosphate, potassium and magnesium). Due to sudden intracellular movement due to switch from fat to cabohydrate metabolism, and associated increased insulin secretion. Recognised cause of mortality in early stages of treatment of nutritional decompensation

63

What is the median number of ECT treatments needed in the UK?

7

64

What are the side effects of ECT?

Muscle pain, confusion or dizziness, but most commonly headache and memory problems

65

Does ECT damage the brain?

No evidence of structural damage

66

What kind of cognitive impairment follows ECT?

Post ictal confusion for 20 minutes then anterograde and retrograde amnesia in some - compounded by cognitive effects of depression and the effects on cognitive function are cumulative

67

What is the mode of action of ECT?

Not really known but probably involves the hippocampus and prefrontal cortex/ACC

68

What are the indications for ECT?

Severe depression wth psychosis and psychomotor retardation, alternative treatments have failed, rapid response required, dangerous self neglect, resistant psychotic depression

69

What are the RELATIVE contraindications to ECT?

Pregnancy, retinal detachment, cerebral tumour, history of CVA

70

What are the contraindications to ECT?

Raised ICP, recent cerebrovascular accident, unstable vascular aneurysms, recent MI with unstable rhythm; treatment of other medical conditions should be optimised before if possible

71

What are the features of elective mutism?

Often begins around the time of starting school, child is commonly very talkative at home but painfully shy and completely silent elsewhere

72

What is the management for elective mutism?

Reassurance, reduce stressors, sometimes behavioural management

73

What are the features of emotionally unstable PD?

REPORT + 3 of AEIOU - Affective instability, Explosive behaviour, Impulsive, Outbursts of anger, Unable to plan or consider consequences

74

What are the features of borderline PD?

REPORT + 3 of SCARS: Self image unclear, Chronic empty feelings, Abandonment fears, Relationships are intense and unstable, Suicide attempts and self harm

75

What are the differentials for borderline PD?

Adjustment disorder, depression, psychosis (patients ocasionally experience fleeting psychotic features)

76

What are the features of impulsive type EUPD?

REPORT + 3 of LOSEIT: Lacks impulse control, Outbursts or threats of violence, Sensitivity to being thwarted or criticised, Emotinla instability, Inability to plan ahead, Thoughtless of consequences

77

What are the differentials for impulsive type PD?

Affective disorder, adjustment disorder, adult ADHD

78

What is the definition of encopresis?

Inappropriate defecation after age 4, when bowel control is expected

79

What is the most common cause of encopresis?

Constipation (overflow incontinence)

80

What are some causes of constipation in children?

Dehydration, painful defecation e.g. anal fissure, fear of punishment, toilet fears (e.g. monsters in toilet), Hirschsprung's disease

81

What are some reasons for incontinence other than constipation?

Diarrhoea, learning disabilities, occasionally hostility (e.g. angrily defecating in parent's shoe), feeling defeated by transition from potty to toilet e.g. if punitive toilet training, stress (secondary incontinence)

82

How should encopresis be managed?

Laxatives + stool softeners if constipated; treat other causes; reassure, address stress and review toilet training, star charts

83

What is the prognosis for encopresis?

60-90% become continent within a year

84

How common is enuresis?

Poor bladder control affects up to 10% of 5 year olds and 1% of adolescents

85

How is enuresis classified?

Primary (never mastered toilet training) or secondary (dryness achieved for at least 1 year but has been lost)

86

Which kinds of enuresis are more common in boys and girls?

Nocturnal enuresis in boys, diurnal in girls

87

What are the causes of primary enuresis?

Delayed maturation of the bladder's nervous innervation, more generalised developmental delay, stress and excessively relaxed or strict toilet training

88

What are the causes of secondary enuresis?

Usually stress e.g. new school

89

How is enuresis managed?

Refer organic causes to paediatrics (epilepsy, UTI, ocnstipation, diabetes), restrict fluids before bed, reassure that the problem is common and no one's fault, star charts to celebrate each dry night, blel and pad, medication e.g. imipramine (TCA) or desmopressin (synthetic ADH)

90

How is epilepsy defined?

Recurrent (2 or more) seizures, unprovoked by an immediate identifiable cause

91

What kinds of epilepsy carry a particularly increased risk of psychiatric disorder?

Temporal lobe or treatment resistant

92

What psychiatric problems are commonly comorbid with epilepsy?

Cognitive impairment, psychotic symptoms, learning diabilityies, depression (50%), suicide rates are 4x higher than in general population

93

What are the 4 kinds of extrapyramidal side effects?

Dystonia, akathisia, parkinsonism, tardive dyskinesia

94

When is the onset of dystona (EPSE)?

Early, sometimes within hours

95

What are the symptoms of dystonia?

Involuntary, painful, sustained muscle spasm, e.g. torticollis (neck twists to one side), oculogyric crisis (eyes twist up and can't look down)

96

What is the treatment for dystonia?

Anticholinergic e.g. procyclidine

97

What is the onset of akathisia?

Hours to weeks

98

What are the symptoms of akathisia?

An unpleasant subjective feeling of restlessness; often have to pace about/jiggle legs to cope

99

What is the treatment for akathisia?

Decrease dose/change antipsychotic; add propranolol or benzodiazepines

100

What is the onset of parkinsonism as an EPSE?

Days to weeks

101

What are the symptoms of parkinsonism as an EPSE?

Triad of resting tremor, rigidity (experienced as stiffness) and bradykinesia. Patients may have a mask-like facies and a shuffling gait

102

What is the treatment for parkinsonism?

Decrease dose/change antipsychotic; try and anticholinergic e.g. procyclidine but review frequently and do not prescribe prophylactically

103

What is the onset of tardive dyskinesia?

Months or years

104

What are the symptoms of tardive dyskinesia?

Rhythmic involuntary movements of the mouth, face, limbs, trunk which are very distressing. May grimace, or make chewing and sucking movements with their mouth and tongue.

105

What is the treatment for tardive dyskinesia?

Stop antipsychotic or reduce dose if possible (though problems may initially worsen). Avoid anticholinergics as they often make it worse. Switch to an atypical or clozapine. Often irreversible.

106

What is flumazenil?

A compettive antagonist of benzodiazepines at the gABA-BDZ receptor

107

What is flumazenil used for?

Reverses the CNS depressant effects of benzodiazepine overdose; intravenous use and half life of 1 hour only

108

What is the treatment for benzodiazepine overdose?

Flumazenil

109

What are the headings for a formulation?

Case synopsis (history/MSE), differential diagnosis, risk, aetiology (predisposing, precipitating, perpetuating), investigations (biological, psychological, social), management (biologica, psychological, social and short, intermediate and long term), prognosis for current episode and long term (include positive and negative prognostic factors to support your view)

110

What is the function of the frontal lobes?

Weigh all reasonable information to produce a more reasonable plan of action rather than just going with impulses

111

What are the 3 main categories of symptoms of frontal lobe syndrome?

Executive dysfunction, social behaviour and personality change, apathy

112

What are the features of executive dysfunction in frontal lobe syndrome?

Poor judgement, poor reasoning and problem solving, poor planning and decision making

113

What are the features of social and personality change in frontal lobe syndrome?

Loss of social awareness: irresponsible/disinhibitied/inappropriate behaviour, impulsivity, euphoric or 'fatuous' mood, lability, repetitive or compulsive behaviours

114

What are the features of apathy in frontal lobe syndrome?

Lack of motivation/initiative, decline in self care

115

What clusters of symptoms do patients get in frontal lobe syndrome?

Either apathetic OR disinhbited, impulsive, aggressive and socially irresponsible

116

What investigations should you do in frontal lobe syndrome?

MRI brain may help to identify atrophy or space occupying lesion, formal occupational therapy and neuropsychological testing will give insight into functional impairment

117

How is frontal lobe syndrome managed?

Unless the cause can be treated, managemetn is through rehabilitation and supporting the family

118

State the categories of frontal lobe testing

Set shifting, Go-no-go task, verbal fluency (FAS testing, animals in a minute), abstract reasoning (proverbs, cognitive estimates), primitve reflextes

119

How do you test set shifting?

Place one hand flat with your palm up. With the other, make a sequence of 3 movements onto it: a fist, a slice (karate chop) and a slap. Get the patient to do it with you, and once they have mastered it they should be able to manage 3 cycles on their own.

120

How do you test with a go-no-go task

"When I touch my nose, you raise your finger like this" (point at the ceiling). "And when I raise my finger, you touch your nose like this" (touch your nose, all with the same index finger). Then start with either move and see what the patient does. LEave your finger in place while waiting for a response. Make a sequence of a few moves before stopping.

121

How do you do FAS testing?

Get the person to give you all the owrds they can beginning with a certain letter exculuding proper nouns and similar words (e.g. superlatives and adjectives). Give them a minute with F, then A, then S. Less than 15 should raise concerns.

122

How do you do the animals in a minute test?

Get them to name all the animals they can in a minute; less than 15 should raise concerns

123

What does set shifting test?

The ability to shift from one action to another, which is a key part of sequencing and monitoring behaviour

124

What does the go-no-go task test in frontal lobe testing?

The ability to inhibit an inappropriate response (to copy) but also tests set shifting

125

What do verbal fluency tests tell you?

They primarily tes the ability to initiate the retriebal of words held in semantic memory.

126

How do you do a proverb test in frontal lobe testing?

Give an example of how proverbs have a hidden meaning e.g. too many cooks = jobs aren't done well when too many people are involved. See if it makes sense to them. Then ask them for the hidden meaning of: birds of a feather flock together, a stitch in time saves nine, people in glass houses shouldn't throw stones

127

Other than frontal lobe syndrome, in which conditions would you see concrete interpretation of proverbs?

Schizophrenia, autism, learning disability

128

What are some questions of cognitive estimates you can ask?

How fast can a racehorse run? What's the best paid job in this country? How many camels are there in Holland? How many eyelashes are on your lower eyelid?

129

Why do primitive reflexes get tested in frontal lobe testing?

Because the frontal lobes inhibit primitive reflexes, so if damaged the reflexes may re emerge

130

How do you test primitive reflexes?

Hed the patient to hold their hands out and stroke across the patient's palm towards their thumb (grasp reflex); Ask the patient if you can touch their face and then either lightly tap the patient's lips or stroke down their philtrum (suck/pout reflex), or stroke the patient's cheek with your finger (rooting reflex)

131

When do frontotemporal lobar degenerations tend to begin?

Age 40-60

132

What is the cause of frontotemporal lobar degeneration?

Generally sporadic but up to 40$ show autosomal inheritance

133

What is the pathology in all 3 forms of frontotemporal lobar degenerations

Cortical atrophy

134

What is the pathology in Pick's disease?

Neurons contain 'Pick bodies', rounded collections of hyperphosphorylated tau protein

135

What does FTLD-U stand for?

Frontotemporal lobar degeneration with tau negative ubiquinated inclusions

136

What is the pathology in FTLD-U and what other conditions is it similar to?

Tau negative inclusions; similar to motor neurone disease

137

What are the clinical forms of frontotemporal lobar degeneration?

Frontotemporal dementia (frontal lobe syndrome with prominent disinhibition and social/personality changes), semantic dementia (progressive loss of understanding of verbal and visual meaning), progressive non fluent aphasia (begins with naming difficulties and progresses to mutism)

138

What is the prognosis for frontotemporal lobar degeneration?

Death is usually within 5-10 years

139

What are the features of generalised anxiety disorder?

Anxiety which is not triggered by a specific stimulus but which is continuous and generalise. Past mistakes and future imagined catastrophies occupy the mind. Symptoms can occur at any time and severe cases also have panic attacks

140

What is needed to diagnose generalised anxiety disorder?

Symptoms must be present for at least 6 months, although intensity may fluctuate

141

What is the differential diagnosis for generalised anxiety disorder?

Hyperthyroidism, substance misuse, excess caffeine, depression, anxious (avoidant) personality disorder, dementia (anxiety may be an early feature), schizophrenia (anxiety may occur before delusions/hallucinations)

142

When can you diagnose mixed anxiety and depressive disorder?

Where there are low level depressive and anxiety symptoms that present equally together and neither jusitifies a diagnosis alone

143

What symptoms does taking hallucinogens cause?

Visual illusions and hallucinations, synaesthesia, depersonalisation and derealisation, may become acutely anxious

144

What is behavioural toxicity?

Where a person taking drugs suffers accidental harm due to acting on a drug induced belief e.g. being able to fly

145

What are 4 examples of hallucinogens?

LSD, phenylcyclidine, ketamine, magic mushrooms

146

What does LSD stand for?

Lysergic acid diethylamine

147

What is LSD also known as?

Acid

148

What is the mode of action of LSD?

Affects dopamine and serotonin transmitter systems

149

How is LSD usually sold?

Impregnated on tabs

150

What happens when LSD is ingested?

Up to 12 hours of 'trips' with perceptual changes and euphoria

151

What are the symptoms of a 'bad trip' on LSD?

Experiences become frightening/unpleasant; sudden flashbacks can occur even years later

152

What are the risks associated with LSD?

Anxiety, depression, psychosis

153

What is penylcyclidine?

Increasingly popular drug that comes as a liquid or powder which can be added to a joint and smoked. Associated with violent outbursts and ongoing psychosis.

154

What is phenylcyclidine also known as?

PCP, 'angel dust'

155

What is ketamine?

A powerful veterinary anaesthetic that prevents the brain's awareness of pain

156

What are the risks associated with ketamine?

Because it is an anaesthetic people can severely harm themselves while hallucinating e.g. pulling out teeth

157

What is ketamine also known as?

Speical K

158

What are the greatest risks with magic mushrooms?

Mistakenly eating poisonous mushrooms

159

What are the two categories of brain injury?

Open (skull is penetrated causing local cerebral damage) or closed (no penetration but brain damage is caused by acceleration/deceleration and shearing forces)

160

How is the severity of a head injury classed?

Mild/moderate/severe according to GCS, duration of coma,a nd duration of post-traumatic amnesia

161

In what kind of head injury is it more common for consciousness to be impaired to the point of delirium/coma?

Closed

162

What memory impairments can occur with a head injury?

Post traumatic amnesia (from time of injury to recovery of normal memory; longer lasting = greater risk of complications), and retrograde amnesia (memory loss before the injury - from the last clear memory until the injury occurred, not a good predictor of outcome)

163

What kinds of cognitive impairment are more likely in open and closed head injuries?

Open - focal, closed - global

164

What typical cognitive problems do head injuries cause?

Attention/concentration, memory, speed of processing, problem solving

165

What kind of head injury is most likely to cause personality changes?

Frontal - previous personality traits may be exaggerated

166

How common is depression and anxiety in head injury survivors?

50%; can persist and suicide risk may be increased

167

What is post concussional syndrome?

May follow a head injury with LOC; symptoms occur in at least 50% of those with a mild head injury and a significant proportion persist for at least a year.

168

What are the symptoms of post concussional syndrome?

People become preoccupied with their symptoms. MOOD: depression, anxiety, irritability. COGNITIVE: poor concentration and memory. SOMATIC: headache, dizziness, fatigue, insomnia, noise sensitivity.

169

What influences the likelihood of post concussional syndrome?

Premorbid personality and highly comorbid with anxiety and depression

170

How can you manage post concussional syndrome?

Speacialst head injury service (rehab and support), psychotropic drugs might be needed but be careful as they lower the seizure threshold, education and reassurance in mild injury can help and prevent it

171

What are the features of histrionic PD?

REPORT and 3 of ACTORS: Attention seeking, Concerned with own appearance, Theatrical, Open to suggestion, Racy and seductive, Shallow affect

172

What are the differentials for histrionic PD?

Hypomanic/manic episode, substance misuse

173

What causes HIV encephalopathy?

Direct effect of the virus on the brain

174

How common is HIV encephalopathy?

Affects 10% of HIV patients; incidence has halved since itnroduction of HAART but prevalence has increased due to increased survicval rates

175

What are the features of HIV dementia?

Early apathy and withdrawal progress to a subcortical dementia with neurological features like ataxia, tremors, seizures, and myoclonus. MRI may show atrophy and diffuse white matter signal changes

176

What is the inheritance of Huntington's disease?

Autosomal dominant

177

What are the 2 main problems that Huntington's disease causes?

Dementia and chorea

178

What is the cause of Huntington's disease?

A trinucleotide CAG repeat in the Huntingtin gene on chromosome 4

179

When does Huntington's disease start?

Onset is usually in middle age but longer CAG repeats cause eariler and more severe presentations (lengthening occurs with each inheritance so onset is younger in subsequent generations ('anticipation'))

180

What is the pathology in Huntington's disease?

Deposits of abnormal Huntingtin protein cause atrophy of the basal ganglia and the thalamus as well as some cortical neuron loss, mostly frontal

181

What do investigations show in Huntington's disease?

MRI/CT may show caudate nucleus atrophy; EEG may be flat

182

What are the clinical features of Huntington's disease?

-Personality + behavioural changes, sometimes with aggression
-Depression, irritability or euphoria are common
-Subcortical dementia later
-Chorea affects limbs, trunk, face, and speech muscles, and produces a wide based lurching gait

183

What is the prognosis for Huntington's disease?

Currently no cure - death occurs within 15 years

184

What are the uses of hypnotics?

Short term use - to help induce sleep

185

How long does it take hypnotics to take effect?

Usually effective after half an hour - 1 hour; initial insomnia

186

What are the 2 classes of hypnotics?

Benzodiazepines, Z drugs

187

What are the 3 Z drugs?

Zopiclone, Zimorane, Zalepon

188

What is the mechanism of action of Z drugs?

Act via GABA-BDZ receptors

189

What are the side effects of Z drugs?

Rebound insomnia, dependence and neuropsychiatric disturbance

190

What side effect may be more prominent with zopiclone than BDZs?

Impaired driving performance

191

What are the local complications of IV drugs?

Abscess, cellulitis, DVT, emboli which can cause gangrene requiring amputation

192

How does IV drug use cause abscess?

Injected particles form a nidus of infection under the skin

193

How does IV drug use cause DVT?

Repeated injection into the femoral veins damages the valves which slows venous return and facilitates blood clotting in the legs

194

What are the systemic complications of IV drug use?

Septicaemia, infective endocarditis, blood borne infections, increased risk of overdose

195

How does IV drug use cause septicaemia?

Either due to direct infection of bacteria, or spread from abscesses or cellulitis

196

How does IV drug use cause endocarditis?

Injected organisms settle on the mitral valve

197

Which blood borne infections in particular are IVDUs at risk of?

Hep B and C, HIV, syphilis

198

Why are IVDUs at increased risk of overdose?

Because there is less dose titration than in smoked drugs

199

What are the differentials for learning disability?

Autism spectrum disorders, epilepsy, adult brain injury or progressive neurological conditions, psychiatric problems, educational disadvantage/neglect

200

What investigations should you do for learning disability?

-IQ test
-Functional assessment of skills, strengths and weaknesses
-Detailed developmental history from parents
-FBC, U+E, LFT, TFT to exclude reversible disturbances
-Additional blood tests for known causes of learning disability
-Investigations for associated physical illness e.g. EEG for epilepsy
-Genetic testing if appropriate

201

What are the antenatal causes of learning disability?

Genetic e.g. PKU
During pregnancy: alcohol, drugs, medications, smoking, infection e.g. rubella

202

What are the perinatal causes of learning disability?

Neonatal hypoxia, birth trauma, hypoglycaemia, prematurity

203

What are the postnatal causes of learning disability?

Social deprivation, malnutrition, lead, infections e.g. meningitis, head injury

204

How should learning disability be managed?

-Support to access and use mainstream services
-Involve MDT
-Treat physical and psychiatric comorbidity
-Educational support
-Psychological therapy
-Help with ADLs
-Address carers' needs

205

How does management of psychiatric problems differ in those with learning disabilities?

-Presentation may be different due to cognitive, language and communication difficulties
-Specialist criteria e.g. DC-LD may be needed to improve diagnostic accuracy
-Usual treatment principles apply but may be more sensitive to medication so slower dose titration and careful monitoring essential

206

How does behavioural therapy help with learning disability?

ABC: what are the antecedents, behaviour and consequences?
Avoid antecedents
Reinforce positive behaviours
Precent reinforcement of negative behaviours (e.g. using distraction techniques)
Helping people to understand the consequences of their behaviour

207

Describe the features of 'mild learning disability'

-IQ 50-69
-Language reasonably good but development may be delayed
-Problems may go undiagnosed though may struggle through school/be labelled with behavioural problems
-With appropriate support, many Iive and work independently

208

Describe the features of 'moderate learning disability'

-IQ 35-49
-Language and cognitive abilities less developed
-Reduced self care abilities and limited motor skills need support
-May need long term accommodation with family or in a staff supported group home
Simple practical work should be achievable in a supported setting

209

Describe the features of 'severe learning disability'

-IQ 20-34
-Marked impairment of motor function
Little/no speech during early childhood; some may develop during school years
-Simple tasks can be performed with assistance
-Likely to require their family home or a 24h staffed home

210

Describe the features of 'profound learning disability'

-IQ

211

What are the complications of all levels of learning disabilities?

-Increased morbidity, mortality and epilepsy
-Compounded by less frequent involvement in health screening and preventative interventions
-30-50% have additional mental health problems and associated autism spectrum disorders
-Mood and anxiety disorders are more common across the spectrum
-Increased risk of schizophrenia in those with mild learning disability

212

What is diagnostic overshadowing (re learning disabilities)

Tendency to attribute everything to the learning disability itself

213

How common is fragile X syndrome?

1/4000 boys, 1/8000 girls

214

What causes fragile X syndrome?

Mutation on the FMR1 gene on the X chromosome

215

What are the physical characteristics of fragile X syndrome?

-Elongated face
-Prominent ears
-High arched palate
-Large testes
-Hyperextensible joints

216

What are the problems associated with fragile X syndrome?

-Autistic type behaviour
-Anxiety
-Depression
-Hyperactivity
-Expressive language deficits

Can be a carrier, in which case they have milder problems

217

How common is foetal alcohol syndrome?

0.6/1000; 9/1000 spectrum disorder

218

What are the physical characteristics of foetal alcohol syndrome?

-Wide palpebral fissure
-Smooth philtre
-Thin top lip

219

What are the problems associated with foetal alcohol syndrome?

-Behavioural difficulties
-Foetal growth retardation
-Neurological abnormalities

220

How common is Down syndrome?

1/700

221

What is the cause of Down syndrome?

Trisomy 21 (most commonly) but also translocations or mosaicism of chromosome 21

222

What are the physical characteristics of Down syndrome?

-Upward slanting palpebral fissures
-Protruding tongue
-Hypotonia
-Epicanthic folds
-Single palmar crease

223

What are the problems associated with Down syndrome?

-Congenital heart abnormalities
-Epilepsy
-Early onset Alzheimer's
-Thyroid problems
-Depression
-Leukaemia

224

What is the most common genetic cause of learning disability?

Down syndrome

225

What are some specific syndromes causing learning disability?

Fragile X, foetal alcohol syndrome, Downs

226

What are the 'minor' adverse effects of lithium?

Fine tremor
Mild GI upset
Metallic taste in mouth

227

What are the 'persistent' adverse effects of lithium?

-Polyuria and polydipsia
-Hypothyroidism
-Lethargy
-Weight gain
-Persistent tremor
-T wave flattening on ECG
-Mild cognitive impairment
-Change in hair texture
-Mild leucocytosis

228

What are the features of lithium toxicity?

-Dysarthria
-Ataxia
-Coarse tremor
-Marked GI upset
-Impaired consciousness
-Epileptic seizures

229

What blood level correlates to lithium toxicity?

>1.2 mmol/L

230

What can trigger lithium toxicity?

-Salt balance changes due to dietary variation, dehydration, diarrhoea, vomiting
-Drugs interfering with lithium excretion e.g. NSAIDs, diuretics, ACE inhibitors
-Accidental or deliberate overdose

231

How should you manage lithium toxicity?

Stop lithium and transfer for medical care (rehydration, osmotic diuresis)

232

What are the functions of the frontal lobe?

-Executive function
-Personality/social behaviour
-Initiative/motivation
-Speech production (Broca's area: dominant lobe)
-Motor cortex
-Suppression of primitive reflexes

233

What happens if there is damage to the motor cortex?

Contralateral spastic hemiparesis

234

What are the functions of the temporal lobe?

-Auditory, olfactory, gustatory perception
-Understanding of speech (Wernicke's area: dominant lobe)
-Memory
-Emotional regulation

235

What are the functions of the parietal lobe?

-Somatosensory perception
-Integration of sensory perception allowing awareness and movement of body
-Communication between Broca's and Wernicke's areas (dominant lobe)
-Calculation

236

What are the functions of the occipital lobe?

Visual perception and interpretation

237

What are the consequences of damage to the frontal lobe?

-Poor judgement/planning
-Inappropriate behaviour/impulsivity
-Apathy/decline in self care
-Expressive dysphasia
-Telegraphic speech (short words and sentences)
-Contralateral spastic hemiparesis
-Primitive reflexes re emerge

238

What are the consequences of damage to the temporal lobe?

-Auditory impairment/agnosia
-Auditory, olfactory, gustatory hallucinations
-Receptive dysphasia
-Speech fluent but nonsensical with mistakes, additional sounds/words/neologisms
-Amnesic syndrome
-Lability

239

What are the consequences of damage to the parietal lobe?

-Contralateral sensory impairment
-Apraxias
-Agnosias
-Contralateral sensory neglect
-Receptive dysphasia
-Dyscalculia

240

What are the consequences of damage to the occipital lobe?

-Contralateral visual defects
-Visual agnosia
-Cortical blindness

241

What is the differential diagnosis for mania?

-Organic causes
-Schizophrenia
-Schizoaffective disorder
-Cyclothymia
-Puerperal disorders

242

What are the organic causes of mania-like symptoms?

-Drug induced states (amphetamines, cocaine)
-Dementia
-Frontal lobe disease
-Delirium
-Cerebral HIV
-Myxoedema madness (paradoxical state of frenzied activity in extreme hypothyroidism)

243

What is cyclothymia?

Persistent mood instability with many episodes of low mood (mild) and mild elation. None of the episodes are sufficiently severe or prolonged to meet criteria for even mild depression or hypomania

244

What investigations should you do in mania?

-Collateral history
-Physical examination
-Bloods: FBC, TFTs, CRP (to exclude infection and thyroid problems), others as indicated
-Urine drug screen
-CT/MRI brain to exclude organic causes if indicated

245

Which 3 drugs count as mood stabilisers?

Lithium, valproate, carbamazepine

246

How can mania be treated pharmacologically?

Mood stabilisers, antipsychotics, other anticonvulsants

247

What is the mechanism of action of mood stabilisers?

Uncertain, but anticonvulsants may act on sodium channels or GABA.

248

How should lithium be monitored?

-Check levels a week after starting or changing the dose
-Monitor weekly until a steady therapeutic level achieved then every 3 months
-Monitor U+Es and TFTs every 3-6 months as can cause renal impairment and hypothyroidism
-Beware as lithium citrate and carbonate have different amounts of lithium

249

What's the therapeutic range of lithium?

0.6-1.0 mmol/l

250

What is valproate and what is it used for?

Anticonvulsant - but treats acute mania and prophylactic in BPAD

251

How is valproate administered and what is the active drug?

Valproic acid is the active drug but it's usually given as the sodium or semi-sodium salt in hope of decreasing adverse effects

252

How is valproate monitored?

Doesn't needed to be - no generally accepted therapeutic range and dose related toxicity isn't usually a problem

253

What is carbamazepine?

An anticonvulsant

254

What are the risks of carbamazepine and how is it monitored?

Can cause toxicity at high doses. It induces liver enzymes that metabolise many drugs including itself so you need to closely monitor levels and check for drug interactions

255

How do lithium and carbamazepine compare for mania?

Carbamazepine is less effective than lithium but is second line for BPAD prophylaxis

256

How are antipsychotics used in mania?

Used in the manic phase and can be continued as prophylaxis after mood has settled. Generally atypical are chosen over typical as fewer side effects (e.g. olanzapine, risperidone, quetiapine)

257

Which other anticonvulsants than valproate/carbamazepine are used in mania?

Lamotrigine is effective in prophylaxis especially in BPAD II.
Topiramate and gabapentine are being assessed for effectiveness as mood stabilisers

258

What are the first steps in treating acute mania?

Stop all meds that could have induced symptoms: antidepressants, drugs of abuse, steroids, dopamine agonists.
Monitor food and fluid as mania can lead to exhaustion

259

How should you treat acute mania/hypomania in a patient who is not currently on any treatment?

Give an antipsychotic or a mood stabiliser.
Short course of benzodiazepines often added for sedation as the sleep deprivation can worsen mania and cause collapse.
If symptoms are severe or there is a poor response, combine mood stabiliser and antipsychotic

260

How should you treat acute mania/hypomania in a patient who is currently on treatment?

Optimise treatment. Check compliance, adjust dose, consider adding another agent. A short term benzodiazepine can help.

261

When should you consider ECT in a patient with acute mania?

If unresponsive to medication or there is a risk of life threatening over activity and physical exhaustion

262

Why is long term treatment needed for mania?

Because further episodes are very likely

263

How should you treat mania long term?

Use mood stabilisers and add other drugs when symptoms arise/facing stress that could cause relapse (benzodiazepines or antipsychotics)

264

How should you treat depression in BPAD?

Tricky - antidepressants can switch mood to mania, so only give them with a mood stabiliser or antipsychotic 'cover'. Monitor closely and stop if getting manic

265

How should you withdraw treatment in mania/BPAD?

You can withdraw if symptom free for a sustained period but needs to be slow and cautious. Patient should be aware of the risk of relapse and be fully involved in the decision

266

What are the 3 types of BPAD?

Type 1, Type 2 and rapid cycling

267

What is type 1 BPAD?

Manic episodes interspersed with depressive episodes

268

What is type 2 BPAD?

Mainly recurrent depressive episodes with less prominent hypomanic episodes

269

What is rapid cycling BPAD?

4 or more affective episodes in a year. More common in women and may respond better to sodium valproate

270

What are the core symptoms of mania?

-Elevated mood (can be replaced by irritability/aggression)
-Mood may be labile
-Boundless energy and overactivity
-Increased enjoyment and interest

271

What are the biological symptoms of mania?

-Dramatically reduced sleep
-Voracious appetite for food and sex
-Reckless, disinhibited, inappropriate behaviour
-Risky sexual liaisons
-Drugs/alcohol may become new interests

272

What is needed for a clinical diagnosis of a manic episode?

Symptoms lasting at least one week and preventing work and ordinary social activities

273

What is hypomania?

Less severe manic symptoms which don't entirely disrupt ability to function.

274

What are the cognitive symptoms of mania?

-Inflated self esteem and confidence
-Optimistic, hopeful, future full of opportunity
-Exciting ideas, racing thoughts, concentration dissolves
-Despite being distractible, they feel they're thinking more clearly than ever
-Speech becomes pressured and topics change rapidly (flight of ideas)

275

What are the psychotic symptoms of mania?

-If severe, optimism develops into grandiose delusions of an important mission, fame, special powers
-Persecutory delusions may arise if they believe others to be jealous
-Auditory hallucinations reflect the elevated mood: prime ministers/saints talking to them

276

When can you diagnose BPAD?

When a patient has suffered a manic episode and any other affective episode, whether depressed, hypomanic, manic, or mixed (elements of depression and mania all at once)

277

What are some relapse prevention strategies in mania?

-Develop a routine
-Ensure good quality sleep
-Promote a healthy lifestyle
-Avoid excessive stimulation or stress (not easy)
-Address substance misuse
-Ensure drug compliance

278

What effect does CBT have on manic patients?

-Reduces relapse rates
-Shortens episodes of illness
-Decreases length and number of hospitalisations

279

What does CBT do in mania?

Identifies relapse indicators, psychoeducation, identifies excessively positive thoughts in mania and helps patients to test them out regain a sense of perspective

280

What kinds of therapy can be used in mania?

CBT, psychodynamic therapy

281

What social interventions are needed in mania?

Family support and therapy, aid return to education or work

282

What are the predisposing factors for medically unexplained symptoms?

Being female, genetics, shorter duration of formal education, childhood experience

283

What are the 3 underlying theories of medically unexplained symptoms/

Somatisation
Psychiatric illness
Cognitive models

284

Explain the somatisation theory of medically unexplained symptoms

Unconscious expression of psychological distress through physical symptoms

285

Explain the 'psychiatric illness' theory of medically unexplained symptoms

Depression and anxiety symptoms can be psychological and physical; physical symptoms may be the presenting symptoms

286

Explain the 'cognitive models' of medically unexplained symptoms

Person's interpretation of normal physiology can create anxiety and perpetuate symptoms. Misinterpretation of normal experiences, selective attention to the problem, repeated checking/constantly seeking reassurance can maintain anxiety, reassurance reinforces the behaviours and prevents patients knowing symptoms are benign.

287

What is the differential disorder for medically unexplained symptoms?

-Organic
-Anxiety + depression
-Hypochondriasis
-Schizophrenia, persistent delusional disorder, affective psychosis (hypochondriacal delusions and somatic hallucinations)
-Factitious disorder
-Malingering

288

What is factitious disorder?

Deliberate production of of symptoms to receive medical treatment (if extreme = Munchausen's)

289

What is malingering?

Feigning symptoms to obtain external reward

290

What are some recognised medically unexplained syndromes?

Fibromyalgia
IBS
Non-ulcer dyspepsia
Dizziness, tinnitus
Non cardiac chest pain, palpitations
Gulf War syndrome
Pain: headache, pelvic pain, lower back pain

291

What are the features of somatisation disorder?

Rare, disabling, chronic
10x more common in women
Multiple medically unexplained symptoms that affect any system of the body
Symptoms are difficult to treat - constantly moving target

292

How do you manage medically unexplained symptoms?

-Therapeutic assessment
-Explain and reassure (Reattribution Model)
-Avoid over investigation, unnecessary referrals, physical medication
-Emotional support
-Encourage normal function
-Antidepressants
-Treat forbid illness
-CBT
-Graded exercise

293

Explain the reattribution model for medically unexplained symptoms

Ensure they feel understood
Broaden the agenda to psychological causes
Make the link with symptoms

294

What are the components of the MSE?

APPEARANCE AND BEHAVIOUR
-General appearance
-Body language
-Other movements
-Rapport
-Other e.g. responding to hallucinations

SPEECH
-Rate
-Volume
-Tone
-Flow
Note: dysarthria, dysphasia, clang associations, punning, neologisms

MOOD
-Subjective
-Objective
-Labile
-Flat/blunted

THOUGHT
-Preoccupations and worries
-Delusions
-Overvalued ideas
-Obsessions (-> compulsions)
-Thoughts of harm to self/others

PERCEPTION
-Illusions
-Hallucinations
-Depersonalisation
-Derealisation

COGNITION
-Orientation
-Attention
-Concentration
-Memory
-If concerned do MMSE

INSIGHT

295

What are the questions in an MMSE?

-What is the year? season? date? day? month?
-Where are we now? County? Town? Hospital? Floor?
-Name 3 unrelated objects and ask the patient to name all 3; repeat until the patient learns them
-Count backwards from 100 by 7s
-Ask what the 3 things were
-Show the patina two simple objects and ask to name them
-Repeat the phrase 'no ifs, ands, or buts'
-Take the paper in your right hand, fold it in half, and put it on the floor
-Please read this and do what it says (written instruction - close your eyes)
-Make up and write a sentence about anything (needs to contain a noun and a verb)
-Copy a picture of 2 intersecting pentagons

296

Can you take mood stabilisers in pregnancy?

They are teratogenic but the risk needs to be weighed against the harm of manic relapse. Women of childbearing age should be given contraceptive advice and given a folate supplement if using valproate . Closely monitor the foetus if used in pregnancy.

297

What risk does lithium carry in pregnancy?

Epstein's anomaly (atrialization of the right side of the heart)

298

What risk do valproate and carbamazepine have in pregnancy?

Spina bifida

299

What are the side effects of lithium?

GI effects (nausea, vomiting)
Polyuria, polydipsia
Arrhythmia
Hypothyroidism
Weight gain

300

What are the side effects of carbamazepine?

Rash
Leucopenia
Dizziness, ataxia
Drowsiness, fatigue
Nausea, vomiting
Oedema, fluid retention
Weight gain
Hyponatraemia
Enzyme induction may decrease levels of other drugs, making them ineffective e.g. OCP

301

What are the side effects of valproate?

GI effects, nausea, vomiting, diarrhoea
Liver failure
Thrombocytopenia
Hair loss
Weight gain

302

Why are the side effects of lamotrigine?

Skin rashes which may be life threatening
Headache, tiredness
Nausea
Dizziness
Insomnia
Arthralgia and back pain

303

What are the main pathological features and course of MS?

Episodes of inflammation and demyelination occurring at different sites and different times within the white matter tracts of the CNS. May be relapsing remitting and then progressive; less commonly progressive from the start.

304

What 2 main psychiatric problems are MS patients at risk of?

Depression and cognitive impairment/dementia

305

How common is depression in MS?

50%; risk of suicide is also substantially increased

306

Why are MS patients at risk of depression?

Disability, pain, MS medication (steroids, anti-spasticity drugs, interferon); also some symptoms overlap and mood changes can occur as part of MS (emotional lability, pathological crying)

307

How do you treat depression in MS?

Same as primary depression but mania is also common

308

How common is dementia in MS?

Memory and concentration problems are common. Dementia affects up to 60% in the late stages.

309

What is neonatal abstinence syndrome?

Babies born to opiate dependent mothers who suffer withdrawal symptoms

310

What are the symptoms of neonatal abstinence syndrome?

Starts within hours of birth an dam last several weeks
High pitched cry
Restlessness
Tremor
Hypertonia
Convulsions
Loose stools, vomiting
Sweats, fever
Tachypnoea

311

What is the treatment for neonatal abstinence syndrome?

Paediatric opiate preparations, anti convulsants, supportive measures

312

What are the effects of opiates on foetuses?

-Neonatal abstinence syndrome
-IUGR
-Low birth weight
-Prematurity
-Sudden infant death syndrome increased

313

What is neuroleptic malignant syndrome?

A rare but potentially fatal side effect of antipsychotics - sympathetic overactivity

314

What are the features of neuroleptic malignant syndrome?

Fever
Sweating
Rigidity
Confusion
Fluctuating consciousness
Labile BP
Tachycardia
Elevated CPK
Leukocytosis

315

What are the risk factors for neuroleptic malignant syndrome?

-High potency typical antipsychotic drugs
-Recent or rapid dose increase/reduction
-Abrupt withdrawal of anticholinergics
-Psychosis
-Organic brain disease
-Alcoholism
-Agitation

316

What is normal pressure hydrocephalus?

A relatively rare but potentially reversible cause of dementia. Usually affects older adults.

317

What are the causes of normal pressure hydrocephalus?

Meningitis and head injury. Up to 50% are idiopathic.

318

What is the pathophysiology of normal pressure hydrocephalus?

CSF absorption in the subarachnoid space is impaired with normal communication with the ventricles. CSF accumulates in the ventricles (hydrocephalus) although CSF pressure remains fairly normal as CSF production adjusts. Distortion of periventricular white matter tracts produces the classic symptom triad.

319

What are the symptoms of normal pressure hydrocephalus?

Dementia (subcortical)
Unsteady gait
Urinary incontinence

320

What is the treatment for normal pressure hydrocephalus?

Ventriculo-atrial shunt may allow CSF drainage from the brain ventricles to the heart

321

What makes the prognosis worse in normal pressure hydrocephalus?

Unknown cause

322

What is OCD?

Where people cannot ignore unpleasant, intrusive thoughts and may try to relieve them with rituals (compulsions)

323

How common is OCD?

1% of the population in any year; affects men and women equally

324

What is the aetiology of OCD?

-Relatives are at 3x risk but mode of transmission unknown
1/4 have premorbid anankastic personality traits (rigidity, orderliness)
-Stress may precipitate OCD symptoms
-Basal ganglia are implicated since they are involved in diseases which increase risk
-Anti basal ganglia antibodies found in those who get OCD post strep
-Linked with a deficit in frontal lobe inhibition - intrusive or ritualistic thoughts may be harder to suppression OCD

325

Which diseases increase risk of OCD?

Sydenham's chorea, Tourette's, encephalitis lethargica

326

What are obsessions?

Recurrent unwanted intrusive thoughts, images, or impulses, that enter the patient's mind despite attempts to resist. Patient recognises them as irrational an their own

327

What is a compulsion?

Used to neutralise tension/discomfort in OCD. A repeated, stereotyped, and seemingly purposeful ritual. Irrational and lacks an obvious link to thought. Can take hours and severely affect quality of life

328

What are the differentials for OCD?

Anxiety disorders
Depression
Anankastic personality disorder
Schizophrenia
Organic causes rarely e.g. sydenham's chorea

329

How do you manage OCD?

Education and self help
CBT: exposure and response prevention
-Prevent compulsive behaviour by allowing the tolerated anxiety to habituate
-Hierarchy of feared situations used
-Works will with motivated patients
SSRIs, or clomipramine

330

What is the prognosis for OCD?

Tends to be chronic, and symptoms are worse at times of stress. Often disabling. Commonly comorbid with depression

331

How common is depression in the elderly?

15% of those in the community and 30% of those in hospital

332

What are the common etiological factors for depression in older people?

-Multiple bereavements
-Social isolation
-Poverty
-Physical illness
-Chronic pain

333

What features of depression may be more obvious in older people?

-Physical symptoms e.g. constipation
-Agitation or retardation
-Memory problems (and pseudo dementia)

334

What are the risks of depression in older people?

-High risk of completed suicide especially in men
-Self neglect, poor food and fluid intake

335

Why should you follow up older people with pseudo dementia?

They're more likely to get dementia down the line

336

How do you manage depression in older people?

-Problem solving: socialisation, daytime activities
-Psychological therapies: CBT, psychodynamic, group, family, couple
-Antidepressants - SSRIs usually 1st line
-ECT if psychotic or life threatening

337

Why do you need to be careful with SSRIs in the elderly?

Can cause hyponatraemia, so check sodium levels

338

When are anxiety disorders more common in older people?

-Prevalence and incidence fall with age probably due to under reporting
-Women
Isolated
Suffered adverse life events

339

How do you manage anxiety disorders in the elderly?

CBT but SSRIs can help

340

What are some common causes of psychotic symptoms in the elderly?

Delirium, dementia, secondary to sensory impairment, late-onset schizophrenia

341

What are some risk factors for late onset schizophrenia?

Being a woman, isolated, single, widowed, childless, sensory deficits

342

Which kinds of symptoms are more prominent in late onset schizophrenia?

Positive symptoms rather than negative

343

How should you manage late-onset schizophrenia?

Reduce sensory impairment
Exclude organic cause/Lewy Body dementia
Then low dose antipsychotics

344

What is Charles Bonnet syndrome?

Complex visual hallucinations, secondary to visual impairment alone

345

What are some common opiate drugs?

Morphine, heroin, pethidine, codeine, dihydrocodeine

346

What is the mechanism of action of heroin?

Opiate agonist, stimulating brian and spina lord receptors that are normally acted upon by endogenous endorphins

347

What are some features of IV heroin use?

Intense rush/buzz with euphoria warmth and wellbeing
Sedation and analgesia follow
Some become dizzy and vomit
Respiratory depression and bradycardia
Some can die from respiratory depression or aspiration of vomit in OD
'Pinpoint pupils'

348

What are some side effects of heroin use?

Constipation, anorexia and decreased libido

349

When does withdrawal from heroin typically begin and peak?

~6 hours after injecting heroin, peaks at 36-48 hours

350

What are the features of opiate withdrawal?

Extremely unpleasant but rarely life threatening
Dysphoria, nausea, insomnia, agitation
As effects on opiate receptors are reversed, everything runs - diarrhoea, vomiting, lacrimation, rhinorrhoea
Feverish with abdominal cramps and aching joints and muscles
Piloerection -> goose flesh
Yawning and dilated pupils

351

How should you manage opiate misuse?

Harm reduction
Substitute prescribing
Support withdrawal
Otherwise same as alcohol

352

What are some harm reduction strategies for opiates?

Sterile needles via needle exchange
Information and advice on drug safety
Offer vaccination and testing for blood borne viruses, free condoms, sexual health services especially if doing sex work

353

What is a substitute prescribed in opiate misuse?

Methadone (liquide)
Buprenorphine (sublingual tablet

354

What is the difference between methadone and buprenorphine?

Methadone is a full agonist at opiate receptors with longer half life than heroin (so withdrawal is longer but milder)
Buprenorphine is a partial agonist at the u receptor, blocking euphoric effects and preventing withdrawal

355

How long are opiate addicts on substitutes for?

Wean off slowly over a period of months or weeks

356

What medications can you give to support opiate detox?

Antidiarrhoeals (loperamide)
Antiemetics (metoclopramide)
Non opiate painkillers

357

What is anorgasmia?

The inability to achieve orgasm

358

What are some management strategies for anorgasmia?

Self exploration, masturbation, sensate focus therapy

359

What is premature ejaculation?

Where ejaculation occurs just after or even before penetration

360

What are some management strategies for premature ejaculation?

Usually improves with practice but can also try squeezing the glans penis to postpone orgasm (the 'stop-start technique') and serotonergic antidepressants e.g. SSRIs

361

What is delayed ejaculation?

Delayed or absent male orgasm. Can be caused by a physical problem e.g. SSRIs or psychological e.g. fear of conception.

362

What is the management for delayed ejaculation?

Psychotherapy, advice on varying sexual techniques, and medication review

363

What is dyspareunia?

Painful intercourse

364

What are some physical causes of dyspareunia?

Women: infection, episiotomy, endometriosis, tumour, vaginal dryness
Men: urethritis, prostatitis

365

What are some psychological reasons for dyspareunia?

May reflect failure of arousal but also associated with past abuse or relationship problems

366

What is vaginismus?

Painful, involuntary spasm of the vaginal muscles when penetration is attempted

367

How is vaginismus treated?

Education
Relaxation
Self-exploration
Insertion of 'trainers' (cylindrical plastic objects) of increasing sizes to accustom the patient to penetration

368

What is panic disorder?

A disorder where anxiety is intermittent and without an obvious trigger

369

What is a panic attack?

A sudden onset attack of extreme anxiety with accompanying physical symptoms. Patient fears they will die, lose control, become incontinent or go mad. The alarming thoughts provide further panic until the patient gains reassurance or engages in safety behaviours

370

What are some of the physical symptoms of a panic attack?

Breathing difficulties/choking feeling
Chest discomfort/tightness
Palpitations
Tingling ('pins and needles') or numbness in hands, feet, or around the mouth
Depersonalisation/derealisation
Shaking
Dizziness/faints
Sweating

371

How long do panic attacks last?

372

What do you need for a diagnosis of panic disorder?

Recurrent panic attacks, preferably several within a month, with the person being relatively free from anxiety in between episodes.

373

What are the differentials for panic disorder?

Other anxiety disorders e.g. GAD/agoraphobia
Depression
Alcohol or drug withdrawal
Organic causes

374

What are the features of paranoid PD?

REPORT + 3 of SUSPECT:
Sensitive
Unforgiving
Suspicious
Possessive and jealous of partners
Excessive self importance
Conspiracy theories
Tenacious sense of rights

375

What are some differentials for paranoid PD?

Schizophrenia
Persistent delusional disorder

376

What are paraphilias?

Disorders of sexual preference although the definition of 'normal' varies with culture and over time. Occur almost exclusively in men.

377

When do paraphilias need treatment?

If they cause harm or distress

378

What is fetishism?

Sexual arousal and gratification that rely on an object rather than a person e.g. shoes, rubber, leather

379

What is sadism?

Where inflicting pain causes arousal

380

What is masochism?

Where humiliation or suffering causes arousal

381

How can the unwanted arousal in a paraphilia be extinguished?

By 'covert sensitisation' - pairing the arousal with aversive images

382

Other than covert sensitisation, how can paraphilias be managed?

Avoid activities that reinforce the paraphilia e.g. fantasising, looking at related pornography. Anti androgens can be used in severe or dangerous situations but these rely on patient's motivation and cooperation.

383

What is Parkinsons' disease?

An idiopathic movement disorder where degeneration of dopaminergic cells in the substantia nigra causes depletion of dopaminergic tracts leading to the basal ganglia

384

What is the classic triad of symptoms in Parkinsons?

Tremor (pill rolling)
Rigidity (stiffness)
Bradykinesia (slowed movement)

385

What are the symptoms of Parkinsons other than the classic triad?

Stooped posture
Shuffling gait
'Mask like' facies
Recurrent falls
Constipation
Urinary problems

386

How common is depression in Parkinsons

Occurs in up to 45% and can be difficult to diagnose as symptoms overlap

387

How should you treat depression in Parkinsons?

As primary depression

388

How common is dementia in Parkinson's and what are its consequences?

Up to 80% eventually develop dementia. Linked to increased mortality, carer stress and nursing home admission.

389

What is an early symptom of dementia in parkinson's disease?

Bradyphrenia

390

What distinguishes parkinson's disease dementia from Lewy body dementia?

Presence of PD before cognitive impairment (other way round in Lewy body)

391

Which medication may help in Parkinsons' disease dementia?

Acetylcholinesterase inhibitors

392

How common are psychotic symptoms in Parkinson's, what's a risk factor for them, and what's an important consequence?

Affect up to 40%
Risk factor is PD dementia
Strongest predictor of nursing home placement

393

What kind of psychotic symptoms do people get in Parkinsons?

Visual hallucinations, often of animals/people

394

What may cause psychotic symptoms in Parkinson's?

Dopaminergic anti-Parkinson's drugs - so need to balance too much dopamine (psychotic symptoms) and too little (Parkinsonism)

395

How should you manage psychotic symptoms in Parkinson's?

Dopaminergic drugs can be slowly withdrawn or cautious doses of atypical antipsychotics tried but both may exacerbate Parkinsonism - if patient and family are coping may be better not to change anything

396

What distinguishes a personality disorder from traits?

The 3 Ps:
Pervasive
Persistent
Pathological

397

What is required for the diagnosis of personality disorder by the ICD10?

REPORT:
Relationships affected
Enduring
Pervasive
Onset in childhood/adolescence
Results in distress
Trouble in occupational/social performeance

398

Can a personality disorder have an organic cause?

No - must not be attributable to brain damage or disease or another psychiatric disorder

399

What are the 3 broad ICD clusters for personality disorder?

Cluster A - 'odd or eccentric' - paranoid, schizoid
Cluster B - 'dramatic, erratic or emotional' - histrionic, emotionally unstable, dissocial
Cluster C - 'anxious and fearful' - anankastic, anxious and dependent

400

Which PDs are more common in men and in women?

Men have overall higher rates esp cluster A, dissocial or anankastic ties.
Histrionic or emotionally unstable borderline PDs are commoner in women

401

How common is PD?

Community - 10%
Primary care - 20% (mostly cluster C)
Mostly cluster B:
Psych OP - 30%
Psych inpatient - 40%
Prison - 50%

402

What are some possible causes of personality disorder?

Genetics - determines 50% of personality
Family history, including of depression and alcohol dependency
Childhood temperament (temperament at 3 is predictive of personality traits in adulthood); difficult temperament
Early attachment difficulties
Traumatic, neglectful or chaotic upbringing

403

How should you investigate PD?

Second interview and collateral history - do traits amount to a disorder?
Psychology/psychotherapy assessment

404

Which psychotherapies are useful in PD?

CBT
Dialectical behavioural therapy
Cognitive analytical therapy
Metallisation
Therapeutic communities
Psychodynamic and psychoanalytical psychotherapy

405

What medications are useful in PD?

Occasionally used to improve certain symptoms and facilitate psychosocial treatments
Antipsychotics - reduce impulsivity and aggression
Antidepressants - general effects in reducing impulsivity and anxiety
Mood stabilisers - used for labile affect but effects are unimpressive

406

What is the prognosis for PD?

Disrupt relationships, education and employment
Some are associated with child abuse and domestic violence
Persistent but may change in severity over time

407

Why might cluster B personality disorders become less common with increasing age?

Due to maturation, 'burning out' and the high mortality rate in the group (due to suicides and accidents)

408

What are the 3 main theories to explain personality disorders?

Cognitive + psychoanalytical theraoes
Psychological defences
Neurotransmitter theories

409

What are the cognitive/psychoanalytical explanations for PD?

Quality of early relationships and nature of childhood environment influences expectations about self and world
Behaviour is motivated by combination of beliefs and desires (cognitive > beliefs, psychoanalytical > desires)
Expectations are filled and perpetuated e.g. aggressive people tend to spark hostility in others

410

What are psychological defences and why do they cause PD?

Unconscious strategies to manage uncomfortable feelings - can be adaptive but become pathological when people become overly reliant on them, causing conflict with others or never addressing their underlying emotions.

411

What are some examples of psychological defences?

Acting out
Splitting
Projection
Fantasising
Reaction formation

412

What is acting out?

Impulses are expressed through actions without conscious awareness of the underlying emotion

413

What is splitting?

Other people are thought of in polarised terms and either idealised or denigrated; this protects 'good people' from hostility by directing it at 'bad people'

414

What is projection?

Uncomfortable feelings are 'put onto' someone else and then experienced as belonging to them

415

What is fantasising?

Using imagination to escape from the painfulness of reality

416

What is reaction formation?

Behaving in a way that is opposite to unacknowledged and unacceptable desires

417

What are the neurotransmitter theories of PD?

Evidence of lower serotonin levels in dissocial PD, and serotonin has been implicated in regulation of impulsivity and aggression. Other monoamines have less attention ut may be implicated in predicting certain patterns of behaviour - dopamine for novelty seeking and noradrenaline for persistence and dependency to rewards

418

What are the 5 broad personality factors?

OCEAN:
Openness to experience
Conscientiousness
Extraversion
Agreeableness
Neuroticism

419

What are the traits coming under 'openness to experience'

Curiosity
Imagination and appreciation of art
Adventure and emotion

420

What traits come under 'conscientiousness'?

Ability to plan and be self disciplined to achieve goals

421

What is extraversion?

Predisposition to experience positive (social) events

422

What traits come under 'agreeableness'?

Tendency to be cooperative, trusting and kind

423

What traits come under 'neuroticism'?

Predisposition to negative emotions e.g. anxiety, anger, or depression

424

What is a phobic anxiety disorder?

Where intermittent anxiety occurs in specific but ordinary circumstances - patients characteristically avoid feared situations and the seriousness of the phobia depends on resultant disability.

425

What are the 3 most common examples of phobic anxiety disorders?

Agoraphobia
Social phobia
Specific phobias

426

What is agoraphobia?

Fear of being unable to escape to a safe place (usually home)

427

What are the things someone might be afraid of in agoraphobia?

Open places, situations that are confined and difficult to leave without attracting attention e.g. buses, queuing, supermarkets, crowds, parks

428

Describe the typical onset of agoraphobia?

20s-30s; mat be gradual or precipitated by a sudden panic attack.

429

What is the pattern of anxiety in agoraphobia?

Prospect of leaving home causes anxiety which increases with distance from home/difficulty in returning - present of a dependable companion/car may increase range

430

What are the differentials for agoraphobia?

Depression, social phobia, OCD, schizophrenia

431

What is social phobia?

Fear of bring scrutinised or criticised by others

432

What is the typical onset of social phobia?

Late teens, M=F

433

What are some of the things patients are anxious about in social phobia?

Embarrassing themselves in public. Can tolerate an anonymous crowd but small groups feel intimidating. Sometimes specific worries e.g. eating in public

434

What might a person with social phobia do to improve symptoms?

Self medicate with drugs or alcohol, which perpetuates the problem as it offers psychological avoidance

435

What do patients with social phobia complain about most?

Embarrassing symptoms: blushing, trembling, sweating, urinary frequency

436

What are some of the differentials for social phobia?

Shyness, agoraphobia, anxious (avoidant) PD, poor social skills/autistic spectrum disorder, benign essential tremor, schizophrenia/psychosis

437

What is 'specific phobia'?

Anxiety restricted to a single, specific situation e.g. spiders.

438

What are some features of specific phobia?

Often develop in childhood although sometimes later, usually after a frightening experience. Result in avoidance and, in severe cases, disability. Rarely confused with another disorder but should exclude comorbid depression

439

What is the relationship between childbirth and BPAD?

Puerperium increases risk of relapse in women with BPAD eightfold

440

What are the 'postnatal blues'?

50-75% of mothers, a few days after birth, feel weepy, irritable, and muddled. Mood is labile and may have trouble sleeping. Distressing but normal.

441

How should postnatal blues be managed?

No treatment (explain and reassure) but if severe may progress to postnatal depression

442

How common is postnatal depression?

1/10 mothers in the first year after birth

443

What are some risk factors for postnatal depression?

Personal/family history of PND, or depression, younger maternal age, recent lie events, marital discord, poor social support

444

What are the features of postnatal depression?

Very similar to normal depression but fatigue, irritability or anxiety may be marked. expressive cognitions relate to the baby - guilt, feeling a failure. May have recurrent intrusive thoughts of harming the baby.

445

How should postnatal depression be managed?

As for depression but use medication with care in breastfeeding - low dose amitriptyline is probably safe, avoid lithium if possible, and be aware that neuroleptics can cause lethargy.
Hospital admission if severe/suicidal/infanticidal ideation, preferable to mother and baby unit to enable bonding.

446

What is the prognosis for postnatal depression?

Most respond well within a month. Lasts >1 year for some. Early treatment is important as it can affect attachment and therefore baby's personality and development

447

How common is puerperal psychosis?

1/500-1000 births

448

When does puerperal psychosis usually start?

Usually a fortnight later

449

What are the risk factors for puerperal psychosis?

Personal/family history including BPAD, puerperal infection, obstetric complications

450

What are the features of puerperal psychosis?

Usually rapid onset with insomnia, restlessness, and perplexity, settling into 1 of 3 patterns:
1) delirium
2) affective (psychotic depression or mania)
3) schizophreniform
Symptoms fluctuate dramatically and quickly

451

What should you exclude in puerperal psychosis?

Underling delirium state or substance misuse

452

How should puerperal psychosis be managed?

Antipsychotics, antidepressants, or lithium and benzodiazepines to control agitation depending on presentation. If severe, ECT can be life saving. Admission is usually required, preferably to mother and baby unit.

453

What is the prognosis for puerperal psychosis?

Most recover in 6-12 weeks and overall risk of recurrence is 1/3

454

What are prion diseases?

Transmissible spongiform encephalopathies, which are rare, and often cause rapidly progressive neurological symptoms

455

What is the pathology in prion diseases?

The normal prion protein changes into an abnormal insoluble form which seems to act as a template for further transformation of normal to abnormal prion. Accumulations of abnormal prion protein are linked to spongiform and amyloid change sin the cerebrum, basal ganglia and cerebellum. Cause of conversation is not well understood in most patients

456

How are prion diseases managed?

No specific treatment currently

457

What is the cause, features and onset of sporadic CJD?

No known cause. 40-60 year olds.
Various near signs: extra-pyramidal, pyramidal, cerebellar, myoclonus, dementia

458

What is the cause, features and onset of variant CJD?

Eating BSE infected beef. Mostly 20s.
Prominent psych symptoms: dementia, depression, irritability, psychosis, behavioural changes, ataxia and sensory symptoms.

459

What are the lab/imaging features of sporadic CJD?

EEG: typically triphasic sharp wave complexes.
MRI: may be high signal in anterior basal ganglia.
CSF: raised 14-3-3 protein
Brain biopsy may help diagnosis

460

What are the lab/imaging features of variant CJD?

EEG: less typical changes
MRI: the pulvinar sign - high signal in post thalamus (sometimes)
CSF: raised 14-3-3 protein less common
Brain or tonsil biopsy may help

461

How soon does death come in sporadic CJD?

6-12 months

462

How soon does death come in variant CJD?

May be >1 year

463

What are the 'extra' history categories you need to include in a psychiatric history?

Pst psychiatric history
Personal history: birth and early development, family background and early childhood, education, occupation, psychosexual and relationships
Forensic history
Premorbid personality
Collateral

464

What are the diagnostic criteria for PTSD?

Must follow a traumatic event, which is often experienced as life threatening. Must be an event of exceptionally threatening or catastrophic nature likely to cause pervasive distress in anyone.

465

Who is at higher risk of PTSD?

Women, genetic factors, neurotic traits, personal or family history of psychiatric problems, childhood abuse, poor attachment

466

What can exacerbate PTSD?

Survivor guilt, continual exposure to trauma/stressors

467

What aspects of the trauma increase the risk of it causing PTSD?

Degree of exposure, proximity and human design

468

How many people experiencing extreme trauma get PTSD?

~10%

469

What is the pathology yin PTSD?

Amygdala (emotional processing) is hyperactive and the hippocampus (memory storage) is atrophied

470

What are the features of PTSD?

Often a latency period but usually starts within 6 months
Re-experiencing (flashbacks, nightmares)
Difficulties remembering the entire episode voluntarily
Avoidance (of reminders of the event)
Hyperarousal (persistent inability to relax, hyper vigilance, enhanced startle reflex, insomnia, poor concentration, irritability)
Emotional detachment
Decreased interest in activities
Powerful emotions including loss of control, anger, shame, uncontrollable crying
Overlap with depression/other anxiety disorders
May self medicate with alcohol/drugs

471

How should PTSD be managed?

Be flexible and sensitive
Psychological: CBT, eye movement desensitisation and reprocessing
Pharmacological: SSRIs

472

What is eye movement desensitisation and reprocessing?

Original trauma is deliberately re-experienced in as much detail as possible. While doing this they fix their eyes on the therapist's finger as it passes from side to side in front of them quickly. Effective - and eye movements can be replaced by any left-right stimulus. Thought to aid memory processing.

473

What is the prognosis in PTSD?

Majority of patients recover but some suffer for many years. Chronicity can lead to enduring personality change. Symptoms can resurface at anniversaries associated with the trauma

474

How should you assess risk in the perinatal scenario?

Look for unusual or guarded responses to questions about the birth and baby's development
Screen for delusions
Screen for thoughts of harm to self or baby
Don't leave alone with the baby if psychotic, severely depressed or agitated but don't try to separate them unless the risk is high

475

How should you assess risk in schizophrenia?

Greater risk to themselves than to others!
Risk to self: suicide, self neglect, social decline, victimisation by others
Risk to others: response to persecutory elusions or command hallucinations
Risk from others: increased risk of being victims of (violent) crime

476

What is the risk of suicide in schizophrenia?

10% lifetime risk (10x that of the general population)

477

Who is especially vulnerable to the risk of suicide in schizophrenia?

Intelligent young men with good premorbid functioning

478

When is suicide risk highest in schizophrenia?

In the early years after diagnosis, following first admission, or where there are depressive symptoms

479

How much of UK violent crime is committed by schizophrenics?

480

What factors increase the risk of violence in schizophrenia?

Past history of violence
Substance misuse
acute psychotic symptoms
Non concordance with treatment
Access to weapons
Specific threats to a victim
Comorbid personality disorder (dissocial, Emotionally unstable, or paranoid) or psychopathy

481

What aspects of a suicide attempt cause it to be regarded as higher risk?

Careful planning (duration/detail)
Final acts in anticipation of death e.g. writing wills
Isolation at the time of the act
Precautions taken to prevent discovery
Writing a suicide note
Definite intent to die (rather than to change or temporarily escape a situation)
Believing the method to be lethal even if it wasn't
Violent method (shooting, hanging, jumping in front of a train)
Ongoing wish to die/regretting that attempt failed

482

What factors should you consider when assessing risk in suicide/self harm?

Ask about suicidal thoughts and plans
Ask about the story - planning, the act, precautions, method, purpose, certainty, discovery
Now: how do they feel about it, has anything changed, any regrets
Future: how do they see it, anything that would make it easier, what would they do next time they feel stressed/upset
Risk factors: past psych history, support, depression/hopelessness, drug and alcohol use, current problems e.g. relationships, work, ill health, losses

483

What are the features of schizoid PD?

REPORT + 3 of ALL ALONE
Anhedonic
Limited emotional range
Little sexual interest
Apparent indifference to praise/criticism
Lacks close relationships
One-player activities
Normal social conventions ignored
Excessive fantasy world

484

What are the differentials for schizoid PD?

Asperger's, agoraphobia, social phobia, psychosis, depression

485

What are the etiological factors in schizophrenia?

Genetics
Obstetric complications
Substance misuse
Social disadvantage
Urban life and birth
Migration and ethnicity
Expressed emotion
Premorbid personality
Adverse life experience

486

How do genetics influence schizophrenia risk?

Lifetime risk is 1% for general pop but 10% if a first degree relative is affected (48% if both parents).
Probably multiple susceptibility genes which may overlap with other disorders

487

How do obstetric complications relate to schizophrenia risk?

Maternal prenatal malnutrition and viral infections increase risk, as do pre-eclampsia, low birth weight and emergency C section. May reflect underlying genetic abnormality of hypoxic brain damage.

488

How does substance misuse relate to schizophrenia risk?

Cannabis, amphetamines, cocaine, LSD can all produce psychotic symptoms. Cannabis doesn't cause schizophrenia but increases overall risk. Enzyme COMT (catechol-O-methyl-transferase) breaks down dopamine. Two alleles for COMT, val and met, and the val allele increases risk for schizophrenia in cannabis users. Top elf cannabis is important - skunk is most dangerous for those who are vulnerable as has higher concentrations of THC. Adolescents are very vulnerable as brains ae still developing

489

How does social disadvantage influence schizophrenia risk?

Higher prevalence among adults of low SES isn't reflected in their status at birth - 'downward drift' due to disease

490

How does urban life and birth influence schizophrenia risk?

Prevalence is twice as high in urban areas compared to rural. May be due to drift or stress specific to the urban environment.

491

How does migration and ethnicity influence schizophrenia risk?

1st and 2nd gen immigrants have 3 fold risk. Seems to vary with ethnicity - black caribbean and african have highest rates. Not fully understood and not explained by preferential migration, diagnostic bias, higher rates in country of origin or lower social class.

492

How does expressed emotional influence schizophrenia risk?

Close contact with highly critical or over involved relatives doubles risk of relapse in the 9-18 months after discharge. The high expressed emotion does not CAUSE schizophrenia.

493

How doe premorbid personality influence schizophrenia risk?

Premorbid schizoid personality precedes schizophrenia in up to 1/4 of cases. Schizotypal disorder is more commonly associated with schizophrenia, probably due to shared genetic basis.

494

How do adverse life experiences influence schizophrenia risk?

Sexual or physical abuse in childhood or adulthood increases risk - and psychological treatments to address these may be an important part of management.

495

What are the differentials for schizophrenia?

Organic
Acute and transient psychotic episode
Mood disorder
Schizoaffective disorder
Persistent delusional disorder
Schizotypical disorder

496

What are the physical causes of psychosis?

Substance misuse (intoxication or withdrawal)
Dementia
Delirium
Epilepsy (especially temporal lobe)
Medication side effect (steroids, dopamine agonists)
Other: brain tumour, stroke, HIV, Wilson's disease, porphyria, neurosyphilis

497

What is an acute and transient psychotic episode?

Appears identical to schizophrenia but resolves completely within a few months. Can be stress related.

498

When can you diagnose schizoaffective disorder?

Where schizophrenic and affective symptoms develop together and are ~ balanced

499

What is persistent delusional disorder?

Delusions with few (if any) hallucinations

500

What is schizotypal disorder?

Lifelong state of eccentricity with abnormal thoughts and affect which is regarded as a personality disorder in DSM. Suspicious, cold and aloof with rather odd ideas but without showing definite symptoms of schizophrenia (though some eventually do develop it)

501

What investigations should you do in schizophrenia?

Full physical examination and investigations to exclude an organic cause and assess physical health before starting treatment.

Bloods: FBC, TFTs, U+E, LFT, CRP, fasting glucose.

Consider HIV testing nd syphilis serology. Check lipids before starting long term antipsychotics.
MSU
Urine drug screen
CT scan if suspected organic pathology
EEG if epilepsy suspected
Symptom rating scales to assess severity and monitor response to treatment
OT assessment of ADLs
Social work assessment of housing, finances, and carer's needs
Collateral history

502

What are the three phases of clinical symptoms in schizophrenia?

At-risk mental state/prodrome
Acute phase
Chronic phase

503

What are the features of the prodrome of schizophrenia?

Low grade symptoms: social withdrawal, loss of interest in work, study and relationships, without frank psychotic symptoms. May deny vague psychotic symptoms for fear of their significance.

504

What are the features of the acute phase of schizophrenia?

Delusions and hallucinations
Behaviour may be withdrawn, overactive or bizarre
Loosening of associations
Disjointed speech that is hard to follow and senseless
Poverty of thought and thought blocking

505

What are the diagnostically significant hallucinations in schizophrenia?

Voices discussing/arguing about them
Voices giving a running commentary
Thought echo

506

What are the diagnostically significant delusions in schizophrenia?

Delusional perception
Passivity (controlled by outside force)
Thought interference: thought withdrawal, insertion, or broadcasting

507

What are the symptoms of the chronic phase of schizophrenia?

Apathy
Blunted affect
Anhedonia
Social withdrawal
Poverty of thought and speech
Lack for attention to personal hygiene and care
Limited repertoire of daily activities
Social isolation
May have residual and less prominent positive symptoms e.g. may still have persecutory delusional thoughts but less distressed/affected by them

508

What is the mechanism of action of antipsychotics?

Dopamine antagonists - block post synaptic D2 receptors

509

What are the typical antipsychotics?

Chlorpromazine, haloperidol

510

What are the main advantages and disadvantages to typical antipsychotics?

Cause EPSEs at therapeutic doses, but are effective, cheap and can be used as depots

511

What is an example of a depot antipsychotic?

Flupentixol decanoate

512

What are the advantages of atypical antipsychotics?

Cause fewer EPSEs and generally don't increase prolactin levels

513

What is the mechanism of action of atypical antipsychotics?

Block dopamine and serotonin 5-HT2 receptors

514

What are some examples of atypical antipsychotics?

Olanzapine, risperidone, quetiapine, aripiprazole, amisulpride, clozapine

515

Which atypical antipsychotic is available as a depot?

Risperidone

516

When should you consider using an atypical antipsychotic in schizophrenia?

As 1st line treatment in newly diagnosed schizophrenia, if unacceptable side effects from typical, or if relapse occurs on a typical

517

Can you use more than one antipsychotic at once?

Should be avoided as this increases risk of and widens side effect profile

518

What should you monitor when a patient is on antipsychotics?

BMI and waist circumference
Blood pressure
FBC, LFT, U+E, glucose, HbA1c, lipids
Some may need prolactin if hyerprolactinaemia suspected or likely (e.g. risperidone) or ECG may be needed in middle aged or elderly and in those on a high dose or using clozapine (QTc interval)

519

Which therapies can be useful in schizophrenia?

CBT - should be offered to all
Family therapy
Concordance therapy

520

How is CBT helpful in schizophrenia?

Particular emphasis on reality testing - encouraged to think about evidence for and against beliefs and consider alternative explanations. Improves self esteem, problem solving, and helps patients to cope with delusions and hallucinations

521

How is family therapy helpful in schizophrenia?

Can reduce relapse rates. Effects of high expressed emotion can be ameliorated through communication skills training, education, problem solving and helping to expand social network as well as taking time out from family.

522

What does concordance therapy do in schizophrenia?

Helps patients to consider the pros and cons of management and understand their treatment

523

What are the social approaches to schizophrenia management?

Social skills training
Rehabilitation - access to education, training, employment, skills like budgeting and cooking, housing, social activities, developing personal skills

524

What is the prognosis in schizophrenia?

1/4 recover and experience no further difficulties after a single episode.
2/3 remain liable to relapse or continue to have symptoms.
1/10 will be seriously ill and continuously disabled.

525

What are the negative prognostic factors in schizophrenia?

Male
Early insidious onset
>3 months duration of untreated psychosis
Low premorbid IQ
Negative symptoms prominent
Poor social support/social withdrawal
Not concordant with medication
Family history of schizophrenia
No precipitating features
Substance misuse, especially cannabis

526

What is the mortality in schizophrenia?

>2x that of general population; significantly higher in males than females due to increased rates of accidents and suicide. Poor physical health contributes.

527

What are the 5 subtypes of schizophrenia?

Paranoid
Catatonic
Hebephrenic
Simple
Residual

528

What are the features of paranoid schizophrenia?

Most common form - main symptoms are prominent delusions and hallucnations

529

What are the features of catatonic schizophrenia?

Psychomotor disturbance
Stupor
Excitement - extreme + apparently purposeless motor hyperactivity
Posturing - assuming and maintaining bizarre or inappropriate positions
Rigidity - rigid posture against efforts to be moved
Waxy flexibility
Automatic obedience to any instructions
Perseveration - inappropriate repetition or words or movements

530

What is waxy flexibility?

Where the limbs have minimal resistance to being placed in odd positions which are maintained for unusually lengthy periods (cataplexy)

531

What are the features of hebephrenic schizophrenia?

Onset 15-25 years
Predominant feature is disorganised and chaotic mood, behaviour and speech
Affect is shallow or inappropriate
Behaviour feels aimless
Delusions and hallucinations not prominent

532

What are the features of simple schizophrenia?

Negative features only, without ever having had positive symptoms

533

What are the features of residual schizophrenia?

Prominent negative symptoms only after delusions/hallucinations have subsided

534

What are some of the neurodevelopment theories of schizophrenia?

Enlarged ventricles with overall smaller and lighter brains seen.
No gloss at post mortem - changes may occur before adulthood
Brain changes also suggested by lower pre morbid IQ and particular deficits in learning, memory and executive function.
Changes may be imperceptible at first but progress as the brain matures through ongoing myelination and synaptic pruning
Maturation with other risk factors, like cannabis, may allow functional and connectivity abnormalities to evolve until overt symptoms emerge

535

What are the neurotransmitter theories of schizophrenia?

Dopamine hypothesis: result of dopamine overactivity in certain areas of the brain/
Positive symptoms are from excess dopamine in mesolimbic tracts.
Negative symptoms are due to dopamine under activity in mesocortiyal tracts.
Other theories: serotonergic overactivity, glutamate dysregulation

536

What is the evidence for the neurotransmitter theories of schizophrenia?

All known effective antipsychotics are dopamine antagonists
Antipsychotics work better against positive rather than negative symptoms
Dopaminergic agents like cocaine, amphetamine, L-dopa and bromocriptine all can induce psychosis, symptomatically indistinguishable from schizophrenia

537

Why do we know that dopamine isn't the full explanation for schiworehani?

Because otherwise antipsychotics would cure all psychoses

538

What are the psychological theories of schizophrenia?

Cognitive models propose subtle defects of thinking such as the tendency to jump to conclusions without adequately examining contra indicatory evidence, leading to delusions
Fear of madness ma prompt defences of denial and rationalisation, resulting in a delusional system to explain persecutory voices.

539

Why are benzodiazepines sedative?

Because they enhance the inhibitory effect of GABA transmission

540

What are the effects of benzodiazepines?

Feeling of calm and mild euphoria
Slurred speech
Ataxia
Stupor (even coma) at higher doses

541

What are the withdrawal effects of benzodiazepines?

Like alcohol e.g. seizures

542

How can you treat benzodiazepine overdose?

Flumazenil, a benzo antagonist

543

Why are barbiturates not used so much as benzodiazepines now?

Because they are more dangerous - cause cardiovascular and respiratory collapse

544

What are some reasons for self harm?

Avoiding more dangerous self harm or suicide
Self punishment
Suicide attempt
Substituting psychological distress for physical pain
Overcoming numbness
To change intolerable situations e.g. relationship issues

545

How common is self harm and for whom is it more common?

Lifetime risk is 7-13%.
More common in children and teens. Women are more likely to present in A&E than men.

546

What are the aetiological factors behind self harm?

Associated with affective and personality disorders
Substance abuse and borderline or dissociative PD due to impulsivity
Past childhood abuse and domestic violence
culture of self harm among some adolescents

547

Why does a traumatic or neglectful childhood cause self harm?

Because childhood should provide a 'validating experiment' where the child's experiences are taken seriously and they are helped to manage intense emotion. This provides the basis to 'mentalise' - to reflect on and process emotional experiences. Where this doesn't happen the person may cope with self harm instead

548

How is self harm helpful as a coping mechanism?

Attacking only a pert of the body (representing the condemned self), which secures survival of the person

549

What are the states in managing self harm?

Physical treatment
Risk assessment
Immediate interventions
Follow up
Coping strategies

550

What is the prognosis for self harm?

1/6 will do it again within a year. The risk of completed suicide is 50-100x that of the general population.

551

What are some causes of new onset low libido?

Depression
Medication
Relationship problems
Childbirth

552

What are the stages of sensate therapy?

1) Intercourse is banned
2) Non-genital caressing; focus on pleasure and relaxation
3) Genital touching to achieve arousal and subsequently orgasm
4) In time intercourse occurs naturally

553

What conditions do you need to exclude in hypersexuality?

Mania
Substance misuse
Organic brain disorders e.g. frontal lobe syndrome

554

What are the side effects of antipsychotics?

Extrapyramidal
Hyperprolactinaemia
Weight gain
Sedation
Increased risk of diabetes
Dyslipidaemia
Anticholinergic side effects
Arrhythmias
Seizures
Neuroleptic malignant syndrome

555

What are the extrapyramidal side effects?

Dystonia
Akathisia
Parkinsonism
Tardive dyskinesia

556

What are the features of hyperprolactinaemia?

Galactorrhoea
Amenorrhoea
Gynaecomastia
Hypogonadism
Sexual dysfunction
Increased risk of osteoporosis

557

Which antipsychotics in particular cause weight gain?

Olanzapine and clozapine

558

What kind of dyslipidaemia do antipsychotics cause?

Raised triglycerides and cholesterol

559

What are the anticholinergic side effects of antipsychotics?

Dry mouth
Blurred vision
constipation
Urinary retention
Tachycardia

560

How to antipsychotics cause seizures?

They lower the seizure threshold

561

Which antipsychotic in particular causes seizures?

Clozapine

562

What is neuroleptic malignant syndrome?

A rare but life threatening syndrome usualy triggered bya new antipsychotic or dose increase

563

What is the presumed mechanism of neuroleptic malignant syndrome?

Thought to be an idiosyncratic response to dopamine antagonism

564

What are the symptoms of neuroleptic malignant syndrome?

Muscle stiffness and rigidity
Altered consciousness
Disturbance of autonomic nervous system (fever, tachycardia, labile BP)

565

What are the lab features of neuroleptic malignant syndrome?

Raised creatine kinase and white cell count

566

How do you treat neuroleptic malignant syndrome?

Stop antipsychotics immediately and get urgent medical treatment, often in ICU

567

What causes death in neuroleptic malignant syndrome?

Lots of causes, including renal failure secondary to skeletal muscle breakdown (rhabdomyolysis)

568

What are some causes of sleep disorders?

Poor sleep routine or environment
Changes to sleep patterns
Physical illness
Medications
Trauma
Unhelpful psychological associations
Alcohol, drugs and stimulants
Stress, worry, anxiety
Mood disorders
Anxiety disorders
Psychotic problems

569

What are some consequences of sleep disorders?

Struggling to deal with everyday life
Feeling of loneliness
Low mood
Negative thoughts
Psychotic episodes

570

How should sleep disorders be managed?

Sleep hygiene
Healthy diet and exercise
Regulate light exposure
Keep a sleep diary
Try to reduce stress and worry
Therapies: CBT, stimulus control therapy, relaxation therapy, sleep restriction therapy
Medication: benzos, Z drugs, melatonin, antihistamine
Sleep clinic

571

What are some telltale physical signs of solvent use?

Blistering and redness around the mouth and nose

572

What are the effects of solvent use?

Bit like being drunk
Euphoria
Disinhibition
Ataxia
Nausea and vomiting
Dizziness
Thinking becomes muddled and some people hallucinate
Coma can occur and result in death if vomit is aspirated
Hangover can occur afterwards with severe headache and fatigue

573

What are the ICD-10 characteristics of somatisation disorder?

At least 2 years of multiple physical symptoms with no physical explanation
Persistently refuses to accept advice from doctors that there is no physical explanation
Social and family functioning is impaired as a result of the illness

574

What kinds of somatic complaints are most common?

GI and skin

575

Who gets somatisation disorder?

Mostly women, and usually starts before 30

576

What is thought to be the explanation behind somatisation disorder?

Experience of pain is generated by the mind not the body - it's thought that people with somatisation disorder misinterpret normal bodily sensations or relatively mild discomfort as pain. This then causes them worry and stress which may exacerbate their symptoms.

577

What is the mechanism of action of stimulants?

Potentiate the effects of neuro transmitters (dopamine, noradrenaline, and sometimes serotonin)

578

What are the general effects of stimulants?

Increase energy, alertness and euphoria whilst decreasing the need for sleep.
They increase confidence and impulsivity while impairing judgement, leading to risky behaviour.

579

What are the side effects of stimulants?

Cardiac arrhythmias
Hypertension
Stroke
Anxiety, panic and drug induced psychosis can occur,
Often an unpleasant crash after the substance wears off: a period of dysphoria and lethargy

580

How do you treat stimulant misuse?

Mostly harm reduction - but you can offer short term benzos in an inpatient setting to help with withdrawal anxiety

581

What particular risks are associated with cocaine in comparison to other stimulants?

Fomication - the sensation of insects crawling on or below the skin ('cocaine bugs')
Powerful vasoconstrictor so snorting it damages the nasal mucosa, causing necrosis and septal perforation

582

What is cocaine?

A concentrated smokable form of cocaine, made by heating cocaine in a baking soda solution until the water evaporates, leaving rocks of crack which are heated and smoked

583

What are the effects of crack cocaine?

Almost immediate and intense high
Lasts 5-10 minutes
On-off effect makes it highly addictive

584

What is speedballing/snowballing?

Use of crack with heroin to produce a bigger rush

585

How can you treat IV amphetamine dependency?

With dexamphetamine, aiming for stabilisation and detoxification (not everywhere does this)

586

What is Khat and what is a particular risk of it?

Mild stimulant popular in East African communities. Chewable leaves. Can cause florid psychosis

587

What is the mechanism of action of ecstasy?

Chemical structure and action are like a cross between a stimulant and a hallucinogen (although hallucinations are rare). It is a serotonin release and reuptake inhibitor

588

What are the effects of ecstasy?

Stimulant but also causes a sense of empathy and closeness to others. Users become chatty, dance relentlessly, and show bruxism (tooth grinding)

589

What are the side effects of ecstasy?

Nausea, vomiting, sweating

590

What causes death in ecstasy use?

Hyperthermia and dehydration

591

What is the morbidity and mortality in stroke?

Mortality is 30% in the first year and up to 70% within 3 years.
1/3 of survivors return to independent living, often with ongoing disability

592

How common is depression in stroke and what causes it?

Affects up to 1/3 and can impair rehab.
May relate to consequences of the stroke or to adverse life events before the stroke occurred. Can also relate to the site of the lesion.

593

Define intoxication?

A transient state of emotional and behavioural change following drug use. Dose dependent and time limited.

594

Define harmful use

A pattern of use likely to cause physical or psychological damage

595

Define dependency (ICD 10)

A cluster of psychological, cognitive and behavioural symptoms in which the use of a substance takes on a much higher priority than other behaviours that once had greater value

596

Define withdrawal

A transient state occurring while readjusting to lower levels of the drug in the body

597

In which groups is alcohol misuse most common?

Young males are the heaviest drinkers but alcohol misuse is increasing in women. 2:1 M:F for alcohol disorders but 4:1 M:F for substance misuse disorders.
Substance misuse is highly comorbid with mental illness

598

What are 4 subtypes of depression?

Seasonal affective disorder
Atypical depression
Agitated depression
Depressive stupor

599

What are the features of seasonal affective disorder?

Low mood in the winter
Reversed biological symptoms of overeating and oversleeping

600

What are the features of atypical depression?

No seasonal variation but reversed biological symptoms. May retain mood reactivity.

601

What are the features of agitated depression?

Depression with psychomotor agitation instead of retardation e.g. restlessness, pacing, hand wringing

602

What are the features of depressive stupor

Psychomotor retardation so profound that the person grinds to a halt - they become mute and stop eating, drinking, or moving

603

What are some social causes of suicide?

Live events and stress (especially bereavement and other losses, childhood adversity may predispose)
Social class (I and V are at highest risk)
Social isolation: divorced, widowed, single, unemployed, living alone
Occupation: stressful job and access to lethal means e.g. vets, pharmacists, doctors, farmers

604

How many of those who die by suicide have a major mental illness at the time of death?

9/10

605

What is the strongest predictor of suicide risk?

Previous attempt - 10-15% lifetime risk

606

What is the lifetime risk of suicide in those with previous self harm?

3-5%

607

What is the lifetime risk of suicide in depression?

15%

608

What are some risk factors for suicide within depression?

Older, single
Previously self harmed
Recurrent suicidal thoughts
Insomnia/weight changes
Extremely hopeless, worthless, guilty

609

When in the course of depression does suicide risk increase?

As a severely depressed person begins to recover

610

What is the lifetime risk of suicide in schizophrenia?

10%

611

What are some risk factors for suicide within schizophrenia?

Young ambitious patients early in their illness with insight into the severity of their diagnosis. Also those with command hallucinations.

612

What is the lifetime risk of suicide in alcohol misuse?

3-4%

613

What physical health problems can cause suicide?

Chronic, painful, terminal illnesses

614

Which systemic conditions can cause depression?

Addison's disease (hypoadrenalism)
B12 deficiency
Corticosteroids
Cushing's syndrome (hyperadrenalism)
Hypo/hyperparathyroidism
Hypothyroidism
SLE

615

Which systemic conditions can cause mania?

Corticosteroids
Cushing's syndrome
Hypothyroidism ('myxoedema madness')

616

Which systemic conditions can cause anxiety?

Hypoglycaemia
Hyperthyroidism
Phaeochromocytoma

617

Which systemic conditions can cause psychosis?

Acute porphyria
Corticosteroids
Cushing's syndrome
Hypothyroidism (rare)
SLE

618

Which systemic conditions can cause dementia?

Addison's disease
B12 deficiency
Cushing's syndrome
Folate deficiency
Hypo/hyper parathyroidism
Hypothyroidism

619

What is Seligman's theory of affective disorders?

Learned helplessness - depressed people learn they can't change their situation and give up

620

What is Beck's model of affective disorders?

Negative thinking can depress mood, which generates negative thoughts. This causes a downward spiral into depression. Negative cognitive triad of views on the self, world and future leading to feeling worthless/guilty, helpless and hopeless. This is a positive triad in mania.

621

What are the psychoanalytical theories of affective disorders?

Early experiences, particularly the quality of early relationships, determines the risk of later depression. Mental states are a kind of internal drama:
Depression = a cruel relationship between a harsh, critical judge and a helpless, inadequate agent
Mania = the agent rebels and denies vulnerability, defending against depression

622

What is the monoamine hypothesis of depression?

Depression is the result of a brain monoamine neurotransmitter deficiency.
Noradrenaline affects mood and energy
Serotonin (5HT) affects sleep, appetite, memory and mood
Dopamine affects psychomotor activity

623

What is the evidence for the monoamine hypothesis of affective disorders?

Drugs that deplete monoamines e.g. reserpine cause depression, and anti depressants increase 5HT and NA levels.
Findings in depression suggest deficiency: low plasma tryptophan (5HT precursor), low CSF 5-HIAA (5HT metabolite) in suicide victims, and low CSF homovanillic acid (dopamine metabolite)

624

What doesn't the monoamine hypothesis of affective disorders explain?

The 4-6 week delay in mood elevation by antidepressants despite their more rapid chemical effects.

625

What is the neurochemical theory of mania?

May be related to dopamine overactivity. Drugs that induce manic episodes are dopamine agonists/increase dopamine and antipsychotics which treat mania are dopamine antagonists

626

What is the endocrine theory of affective disorders?

Cortisol, the main stress hormone, is thought to mediate between stressful life events and biological change sin depression, possibly by damaging hippocampal neurones.
In 50% of depressed patients, dexamethasone fails to suppress cortisol secretion.

627

Why isn't dexamethasone suppression test useful in diagnosing depression?

Because non suppression also occurs in mania, schizophrenia and old age.

628

What are the 3 main 'learning theories' behind substance dependence?

Classical/Pavlovian conditioning
Operant (Skinnerian) conditioning
Social learning theory (vicarious learning)

629

How does classical conditioning explain substance dependence?

Cravings become conditioned to 'cures' e.g. needles for heroin users. The cue itself can then trigger a craving, causing drug seeking behaviour.

630

How does operant conditioning explain substance dependence?

Depends on repetitive behaviours having predictable outcomes. Behaviours that are rewarded are repeated (positive reinforcement). Behaviours are also repeated if they relieve unpleasant experiences (negative reinforcement). Therefore, a drug will be used again if it relieves unpleasant feelings, either by ending withdrawal or providing temporary escape from a painful unconsciousness.

631

How does social learning theory explain substance dependence?

We learn by copying the behaviours of others - therefore substance misuse can result from peer pressure

632

How does neurobiology explain substance dependence?

All drugs of abuse affect the dopaminergic 'reward' pathway - this starts in the ventral tegmental area and projects into the prefrontal cortex and limbic system (the 'emotional' brain).
The prefrontal cortex has a role in motivation and planning.
Dopamine release in the nucleus accumbens is central to the sensation of pleasure, which is important in reward.

633

What is a tic?

A repetitive, involuntary, and purposeless movement or vocal utterance

634

How can tics be categorised?

Simple e.g. blinking, throat clearing
Complex e.g. self hitting, swearing

635

How common are tics?

Affect 10% of children and more common in boys

636

What are some risk factors for tic disorder?

Being a boy, family history, OCD often comorbid, stress or stimulant medications often worsen them

637

When do tics often recede?

When concentrating on something else - can also be voluntarily suppressed at the cost of internal tension, which is relieved by their expression

638

How are tics treated?

Reassurance and stress management
Clonidine - adrenergic agonist
Haloperidol - antipsychotic

639

What is Gilles de la Tourette syndrome?

Multiple motor tics with at least one vocal tic. Tends to worsen in adolescence and persists into adulthood.

640

What is transient global amnesia?

Acute global memory loss lasting 1-24 hours

641

What causes transient global amnesia?

Transient ischaemia affecting memory structures, but can also be caused by physical or emotional stress

642

Who gets transient global amnesia?

Usually >50 but otherwise healthy

643

What are the features of transient global amnesia?

Anterograde memory is particularly affected but retrograde can also be affected
Patients are bewildered - 'where am I'
Patients do not forget their identity in contrast to psychogenic amnesia
Consciousness and cognition are otherwise normal with no signs of neurological disease

644

What do you need to exclude in transient global amnesia?

Intoxication, head injury, stroke, epilepsy

645

What is the prognosis in transient global amnesia?

Good, but episodes can sometimes recur

646

What causes vascular dementia?

Infarcts caused by thrombo embolus or arteriosclerosis

647

What are the risk factors for vascular dementia?

Same as stroke - older, male, smoking etc

648

What is the pathology in vascular dementia?

Arteriosclerosis/embolus
Cortical ischemia
Infarction

649

How does an infarct in vascular dementia appear on CT?

As multiple lucencies

650

What is the clinical presentation of vascular dementia?

Stepwise progression - each 'step' represents a sudden deterioration as an infarct occurs
Many tiny infarcts cause a smoother, more subtle course
One strategically located stroke can cause dementia (=strategic infarct dementia)
Symptoms reflect sites of lesions so presentation may be 'patchy' with personality or some areas of cognition spared
Neuro signs e.g. hemiparesis or aphasia may be present
May be episodes of confusion especially at night

651

What is Wernicke's encephalopathy?

Caused by acute thiamine (b1) deficiency, presents classically with a triad of confusion, ataxia and ophthalmoplegia. A medical emergency which needs to be treated with parenteral thiamine in order to avoid Korsakoff's syndrome

652

What is Korsakoff's syndrome?

An irreversible anterograde amnesia (and some retrograde amnesia). Patient can register new events but can't recall them within a few minutes. May confabulate to fill gaps in memory.

653

What is Wilson's disease?

An autosomal recessive disorder of copper metabolism in which copper deposition leads to pathology of the liver, brain, cornea and othe rorgans

654

What are the features of Wilson's disease?

Kayser-Fleischer rings in the eyes
Motor disturbance e.g. tremor, dysarthria
Psychiatric symptoms in a young person can be the first sign - depression, psychosis, personality change
Treat with chelating agents

655

Define 'acute stress reaction'

A state of shock following traumatic events

656

How long does an acute stress reaction last?

Starts within minutes of the trauma and resolves spontaneously within hours (1-3 days max)

657

What are the symptoms of an acute stress reaction?

-Anxious but may seem dazed
-May have amnesia for the event
-May have depersonalisation and derealisation
-Often disorientated and agitated but can be irritable, panicky, or even aggressive

658

How is acute stress reaction managed?

-Exclude injury
-Support and reassurance
-Benzos can alleviate short term distress but don't prevent later PTSD

659

Does 'debriefing' after a trauma help prevent PTSD?

NO - may increase the likelihood of alter PTSD

660

How common is ADHD?

2% children

661

How many more boys than girls get ADHD?

3x more common in boys

662

What is the cause of ADHD?

Unknown but genetics are important - dopamine and noradrenaline deficiencies + frontal lobe abnormalities

663

How is ADHD diagnosed clinically?

-Should present by age 6
-Must be persistent and pervasive across different situations
-Hyperactivity
-Inattention
-Impulsive and reckless
-Risky behaviour
-Tend to be clumsy and accident prone
-May be disobedient (through impulsivity - not deliberate)
-Socially disinhibited

664

What is ADHD associated with?

Learning disability and conduct disorder

665

DDx for ADHD?

-Depression/anxiety (can cause agitation)
-Mania (very rare in childhood)
-Conduct disorder

666

What investigations can you do in ADHD?

Questionnaires e.g. Conner's Rating Scales, classroom observation, educational psychology assessment

667

How is ADHD managed?

-FAMILY: education, advice on parenting + boundaries
-BEHAVIOURAL MANAGEMENT
-FAMILY THERAPY
-STIMULANT MEDICATION e.g. methylphenidate, dexamphetamine
-DIETARY CHANGES - no good evidence but parents report benefit from more oily fish/excluding certain foods

668

How does stimulant medication work in ADHD?

Increases monoamine pathway activity, improving concentration and allowing learning and maturation

669

What are the adverse effects of stimulant medications in ADHD?

Appetite suppression, insomnia, growth retardation

670

How can you limit growth retardation when using stimulant medication in ADHD?

Drug holidays - weekends and school holidays - should limit it to 1cm finally

671

Are stimulant medications addictive in ADHD?

No

672

What's the prognosis for children with aDHD?

-Often suffer low self esteem, peer rejection, educational under-achievement + harsh parenting
-Symptoms often improve in adolescence
-Up to 50% of adults have ongoing problems and 30% retain the diagnosis
-If untreated is a risk factor for later dissocial personality disorder, criminality and substance misuse

673

What is an adjustment disorder?

Where a person's reaction to a life change is greater than usually expected for the situation but not severe enough to diagnose an anxiety or depressive disorder

674

What is the timing of an adjustment disorder?

Symptoms start within a month of the stressor and resolve within 6 months

675

How is adjustment disorder managed?

Support, reassurance and problem solving

676

Is depression more common in women or men?

Women

677

What is the aetiology of mood disorders?

-GENETICS: relatives with depression or BPAD (even adopted children), serotonin transporter gene promoter region S allele rather than L allele
-Adverse childhood experiences
-Vulnerability factors e.g. unemployment, lack of a confiding relationship
-LIFE EVENTS: death of a spouse > divorce > marital separation > jail term > death of close relative (particularly 'loss events')
-Puerperium, sleep deprivation and flying across time zones can trigger mania
-PHYSICAL CAUSES - illnesses and medications

678

What are some illnesses causing depression?

Cushing's, hyperthyroidism, stroke, MS, Parkinson's, hyperparathyroidism, chronic pain

679

What are some medications causing depression?

Beta blockers, anti hypertensives, cocaine

680

What are some illnesses causing mania?

Cushing's, head injury, MS

681

What are some medications causing mania?

Steroids, antidepressants, stimulants

682

What is the prognosis for depression?

-About 50% of patients will have at least one more episode
Each episodes lasts about 8-9 months but treatment can reduce this to 2-3 months
-Psychotic depression has a poorer prognosis but better response to ECT
-Up to 15% of those with major depression eventually take their own lives

683

What is the prognosis for mania?

-Usually shorter than depressive episodes: a fortnight-5 months
-Recovery is usually complete between episodes
-Remissions become shorter with age and depressions become more frequent
-15% of people with BPAD kill themselves, but long-term treatment with lithium reduces this to the same elves as in the general population

684

What is the aetiology of alcohol misuse?

-GENETICS: 25-50% predisposition is inherited, ethnic groups (acetaldehyde dehydrogenase in Asians)
-OCCUPATION: publicans, journalists, doctors, armed forces, entertainment; stressful work and socially sanctions drinking
-SOCIAL BACKGROUND: difficult childhood with parental separation, education achievement commonly poor, juvenile delinquency
-PSYCHIATRIC ILLNESS: assoc with personality disorders, mania, depression and anxiety disorder (esp social phobia)

685

What investigations should you do in alcohol misuse?

-FBC: alcohol causes macrocytic anaemia due to B12 deficiency
-LFTs: GGT rises with heavy alcohol use, raised transaminases suggest hepatocellular damage
-ECG for chest pain
-Urine drug screen if suspicious
-Hepatitis screen if IVDU

686

What is the current recommended alcohol limit?

14 units a week with some drink-free days; now the same for men and women

687

What are the stages in the States of Change model?

1) Precontemplation
2) Contemplation
3) Preparation
4) Action
5) Maintenance
6) Relapse

688

What is motivational interviewing?

A kind of counselling which aims to empower the person to change; helps them to recognise the gap between where they are now an where they want to be, based on a supportive but challenging therapeutic relationship

689

What is the aim of detoxification?

Allows metabolism and excretion of the substance while minimising discomfort

690

What medications can you use in alcohol detox?

-Long acting benzo (e.g. chlordiazepoxide) - replaces alcohol and prevents withdraw symptoms e.g. seizure and delirium tremens
-Thiamine (vitamin B1) - prophylaxis against Wernicke's encephalopathy

691

When would someone have inpatient alcohol detox rather than outpatient?

History of withdrawal fits, comorbid medical/psych problems, lacks someone at home to support or observe them

692

How do you prevent relapse in alcohol misuse?

1) PSYCHOLOGICAL: CBT, identify causes of use and find ways to prevent relapse, group therapy to share experiences and solutions

2) MEDICAL: acamprosate (anti-craving), disulfiram (mimics the 'flush reaction' so drinking is very unpleasant)

693

What are the features of alcohol intoxication?

-Relaxation and euphoria
-Irritability, aggression
-Weepy, morose
-Disinhibited
-Slurred speech
-Ataxic gait
-Increasing sedation, confusion, even coma
-Impulsivity and poor judgement

694

What are the features of alcohol withdrawal?

-Headache
-Nausea, vomiting and retching
-Tremor
-Sweating
-Insomnia
-Anxiety, agitation, tachycardia, hypotension
-Seizures - alcohol is a CNS depressant which stimulates the GABA inhibitory pathway so neural pathways become hyper-excitable when stopping
-Delirium tremens and even death

695

What are the physical complications of alcohol misuse?

-LIVER: alcoholic hepatitis, liver cirrhosis (ascites + hepatic encephalopathy)
-GI: pancreatitis, oesophageal varices, gastritis, peptic ulceration
-NEURO: peripheral neuropathy, seizures + dementia
-CANCERS: bowel, breast, oesophageal, and liver
-HEAD INJURIES/ACCIDENTS: while intoxicated - increased risk of subdural haematoma
-FOETAL ALCOHOL SYNDROME

696

What are the psychological complications of alcohol misuse?

-Depression, anxiety, self harm + suicide
-Amnesia
-Cognitive impairment (alcoholic dementia or Korsakoff's syndrome)
-Alcoholic hallucinosis (often persecutory/derogatory)
-Morbid jealousy (overvalued idea/delusion that a partner is unfaithful)

697

What are the social complications of alcohol misuse?

-Unemployment/work problems
-Domestic violence/separation/divorce
-Law breaking
-Children are at increased risk of neglect, abuse, and conduct disorder

698

What are the etiological factors in Alzheimer's disease?

-Age
-F>M
-Genetics (esp familial early)
-Vascular risk factors
-Low IQ/poor educational level
-Head injury

699

Which genes are implicated in familial early-onset AD?

Usually due to rare autosomal dominant mutations causing increased beta-amyloid:
-Presenilin 1 gene (chr14)
-Presenilin 2 gene (chr1)
-Beta amyloid precursor protein (APP) gene (chr21)

700

Which genes are implicated in late onset AD?

Apolipoprotein E4 allele (chr19)

701

What are the 4 main pathological factors in Alzheimer's disease?

-Atrophy due to neuronal loss (hippocampus first, temporal and parietal lobes later)
-Plaque formation
-Intracellular neurofibrillary tangles (made of abnormal/hyperphosphorylated tau protein)
-Cholinergic loss

702

What is the clinical presentation of Alzheimer's disease?

-Amnesia (recent memories lost first, disorientation early)
-Aphasia (word finding problems)
-Agnosia (recognition problems)
-Apraxia (inability to carry out skilled tasks despite normal motor function

703

What is amnesic syndrome?

Characterised by profound anterograde memory loss - inability to lay down new memories from the time of bran damage onwards. Can be some retrograde loss but other brain functions are relatively intact

704

What is the pathology in amnesic syndrome?

Damage affects the limbic structures dealing with explicit memory (hippocampus, mammillary bodies, parts of the thalamus and surrounding cortex)

705

What are the causes of amnesic syndrome?

Hypoxia
Encephalitis
Carbon monoxide poisoning

706

What is Korsakoff's syndrome?

A common type of amnesic syndrome caused by thiamine (B1) deficiency, usually secondary to alcohol abuse. The main problem is anterograde amnesia despite intact 'short term'/'working' memory - information is lost once it's no longer actively being used.

707

What are the features of Wernicke's encephalopathy?

Acute confusion, ataxia and ophthalmoplegia

708

What are the features of Korsakoff's syndrome?

-Anterograde amnesia
-Confabulating
-Intact procedural memory (basal ganglia, cortex and cerebellum intact)

709

How should Korsakoff's syndrome be managed?

Prompt parenteral thiamine; may prevent further damage but nothing can reverse the amnesic syndrome once the damage has been done

710

List the AMTS questions

1) Age
2) Time to nearest hour
3) Address (for recall at the end of the test: 42 West Street and get them to repeat it)
4) Year
5) Name of this place
6) Identification of 2 people e.g. doctor, nurse
7) Date of birth
8) Year of WW1
9) Name of present monarch
10) Count backwards 20 to 1
11) Address recall correct

Score out of 10

711

What are the features of anankastic personality disorder?

REPORT + 3 of DETAILED:
Doubtful
Excessive detail
Tasks not completed
Adheres to rules
Inflexible
Likes own way
Excludes pleasure + relationships
Dominated by intrusive thoughts

712

What are the differentials of anankastic personality disorder?

OCD, autistic spectrum disorder

713

What are the differentials for anorexia nervosa?

-Medical causes of weight loss: hyperthyroidism, malignancy, GI disease, Addison's, chronic infections, inflammatory conditions, AIDS
-Depression
-Bulimia nervosa
-Eating disorder not otherwise specified (atypical presentations)
-Body dysmorphic disorder
-Psychosis

714

What investigations should you do in anorexia nervosa?

-Height, weight, BMI
-Squat test
-BLOODS: ESR, TFTs, FBC, U+E, phosphate, albumin, LFT, creatine kinase, glucose
-ECG (bradycardia, arrhythmia, and a prolonged QT interval)
-Other tests as indicated e.g. DEXA scan for low bone density

715

How is anorexia nervosa managed?

-Engagement
-Psychoeducation
-Treat comorbid psychiatric illness
-Nutritional management and weight restoration: agree a realistic weekly gain target (usually 0.5-1kg per week, and establish a target weight and eating plan)
-Psychotherapies
-Medical treatment if physical complications, rapid weight loss or BMI

716

Which psychotherapies can help with anorexia nervosa?

-Motivational interviewing
-Family therapy
-Interpersonal therapy
-Cognitive behavioural therapy

717

What are the indications for inpatient treatment in anorexia nervosa?

-BMI

718

What are the 4 main diagnostic points in anorexia nervosa?

-BMI

719

What are the general physical complications of anorexia nervosa?

-Lethargy and cold intolerance
-Pancytopenia if severe (bone marrow hypoplasia)
-Milder cases may have anaemia, leucopenia or thrombocytopenia
-Infections from decreased immunity

720

What are the cardiovascular complications of anorexia nervosa?

-Over 80% have cardiovascular problems risking sudden death
-Bradycardia
-Hypotension
-Postural drop
-Arrhythmias (usually secondary to hypokalaemia)
-Mitral valve dysfunction
-Cardiac failure

721

What are the GI complications of anorexia nervosa?

-Constipation
-Abdominal pain
-Ulcers
-Oesophageal tears
-Gastric rupture due to vomiting
-Delated gastric emptying makes patients feel bloated after eating small amounts
-Nutritional hepatitis occurs in 1/3 of patients - low serum protein, raised bilirubin, lactate dehydrogenase, + alkaline phosphatase

722

What are the reproductive complications of anorexia nervosa?

-Amenorrhoea
-Infertility (due to atrophy of ovaries or testes)
-Usually a loss of libido
-Males may notice loss of morning erections

723

What are the musculoskeletal complications of anorexia nervosa?

-Osteoporosis leads to fractures
-Proximal myopathy is often severe

724

What are the neurological complications of anorexia nervosa?

-Peripheral neuropathy
-Delirium
-Convulsions or even coma

725

What are the signs of anorexia nervosa?

-Lanugo hair
-Swollen parotid and submandibular glands after bingeing
-Hypercarotinaemia
-Peripheral oedema
-Dry skin, brittle hair/nails
-Tender abdomen
-If vomiting:
---Russell's sign (cuts/callouses on knuckles)
---Erosion of dental enamel
---Caries

726

What are some examples of SSRIs?

Fluoxetine
Sertraline
Paroxetine
Fluvoxamine
Citalopram
Escitalopram

727

What are the common side effects of SSRIs?

Nausea and vomiting
Appetite + weight change
Blurred vision
Anxiety + agitation
Insomnia, tremor, dizziness, sweating
Headache

728

What are some examples of SNRIs?

Venlafaxine
Duloxetine

729

What are some common side effects of SNRIs?

Constipation
Hypertension
Raised cholesterol
Plus as SSRIs:
Nausea and vomiting
Appetite + weight change
Blurred vision
Anxiety + agitation
Insomnia, tremor, dizziness, sweating
Headache

730

What are some examples of NASSAs? (noradrenergic and specific serotonin antidepressants)

Mirtazapine

731

What are the common side effects of NASSAs?

Sedation
Increased appetite + weight
Oedema

732

What are some examples of NARIs? (noradrenaline reuptake inhibitor antidepressants)

Reboxetine

733

What are the common side effects of NARIs?

Dry mouth
Constipation
Excessive sweating
Urinary problems
Tachycardia
Insomnia

734

What are some examples of TCAs?

Amitriptyline
Clomipramine
Imipramine
Lofepramine
Dosulepin

735

What are the common side effects of TCAs?

Tachycardia, arrhythmias
Dry mouth
Blurred vision
Constipation
Urinary retention
Postural hypotension
Sedation
Nausea, weight gain

736

What are some examples of MAOIs?

Phenelzine
Tranylcypromine

737

What are the common side effects of MAOIs?

Hypertensive crisis (cheese reaction)
Postural hypotension, dizziness
Drowsiness, insomnia
Headache
Blurred vision
Nausea + vomiting
Constipation

738

What are some examples of reversible inhibitors of monoamine oxidase A (RIMAs)?

Moclobemide

739

What are the common side effects of RIMAs?

Agitation/anxiety
Sleep disturbance
Nausea
Hypertension

740

What is trazodone?

A 5-HT reuptake blockade and 5-HT2 antagonist

741

What are the common side effects of trazodone?

Sedation
Dizziness, postural hypotension
Tachycardia
Nausea
Constipation, diarrhoea
Tremor

742

What are the common side effects of St John's Wort?

Photosensitivity
Anxiety, dizziness
Gastrointestinal symptoms
Fatigue
Headache

743

What are the classes of antidepressants?

-Selective serotonin reuptake inhibitors (SSRIs)
-Serotonin + noradrenaline reuptake inhibitors (SNRIs)
-Noradrenergic and specific serotonin antidepressant (NASSAs)
-Noradrenaline reuptake inhibitor antidepressants (NARIs)
-Tricyclic antidepressants (TCAs)
-Monoamine oxidase inhibitors (MAOIs)
-Reversible inhibitors of monoamine oxidase a (RIMAs)
-Trazodone
-St John's Wort

744

What are the 6 categories of antidepressant discontinuation symptoms?

-Affective e.g. irritability
-Gastrointestinal e.g. nausea
-Neuromotor e.g. ataxia
-Vasomotor e.g. diaphoresis
-Neurosensory e.g. paraesthesia
-Other neurological e.g. increased dreaming

745

What do antipsychotics do?

Block DA receptors - D2. They also block noradrenergic and cholinergic receptors.

746

What determines the clinical response with antipsychotics?

DA receptor binding - clinical response usually achieved with 60% D2 receptor occupancy

747

At what D2 receptor occupancy will patients get EPSEs with antipsychotics?

Greater than 80%

748

What do antipsychotics reduce?

-Hallucinations
-Delusions
-Psychomotor excitement

749

What are the categories of antipsychotics?

Typical (1st generation)
Atypical (2nd generation)

750

What are the features of typical antipsychotics?

Increased risk of acute EPSEs, hyperprolactinaemia, tardive dyskinesia

751

What are the features of atypical antipsychotics?

Less risk of EPSEs, hyperprolactinaemia and tar dive dyskinesia. However, they do have metabolic side effects.

752

What are some typical antipsychotics?

Haloperidol, chlorpromazine

753

What are some atypical antipsychotics?

Clozapine, olanzapine, risperidone

754

What are some typical antipsychotic depots?

Clopixol, depixol

755

What are some atypical antipsychotic depots?

Risperdal consta, panliperidone

756

What are the side effects of antipsychotics?

-ANTIDOPAMINERGIC: acute dystonia, akathisia, parkinsonian effects, tardive dyskinesia
-ANTIADRENERGIC EFFECTS
-ANTICHOLINERGIC EFFECTS
-OTHER: arrhythmias, weight gain, amenorrhoea, galactorrhea
-NEUROLEPTIC MALIGNANT SYNDROME

757

What are the psychological symptoms of anxiety?

Fears/worries
Poor concentration
Irritability
Feelings of unreality (depersonalisation/derealisation)
Insomnia: difficulties falling asleep
Night terrors

758

What are the motor symptoms of anxiety?

Restlessness, fidgeting
Feeling 'on edge', unable to relax

759

What are the neuromuscular symptoms of anxiety?

Trembling/tremor
Tension headache (tight band)
Muscle aches (especially neck and back)
Feeling dizzy, light headed, or unsteady
Tinnitus

760

What are the GI symptoms of anxiety?

Dry mouth
Difficulty swallowing/lump in throat
Nausea
Indigestion/stomach pains
'Butterflies' (abdominal churning)
Flatulence
Frequent/loose motions

761

What are the cardiovascular symptoms of anxiety?

Chest discomfort
Palpitations, feeling the heart pound or 'miss beats'

762

What are the respiratory symptoms of anxiety?

Difficulty inhaling
Tight, constricted chest

763

What are the genitourinary symptoms of anxiety?

Urinary frequency
Erectile dysfunction
Amenorrhoea

764

What kind of life experiences predispose to anxiety?

Childhood adversity predisposes; life events can trigger it especially if experienced as threatening

765

What is the neurochemical theory of anxiety?

Central NTs serotonin, noradrenaline and GABA are dysregulated. Drugs that target these combat anxiety symptoms

766

Which NT do SSRIs target?

Serotonin

767

Which NT do TCAs target?

Noradrenaline

768

Which NT do benzodiazepines target?

GABA

769

What are the behavioural and cognitive theories of anxiety?

Classical conditioning
Negative reinforcement
Cognitive theories - worrying thoughts are repeated in an automatic way which both induces and maintains the anxiety response
Attachment theory - quality of attachment between children and their parents affects their confidence as adults; insecurely attached children become anxious adults

770

What investigations should you do in someone with anxiety?

-Rule out organic causes if appropriate
-Rating scales e.g. Beck Anxiety Inventory, Hospital Anxiety + Depression Scale
-Social and occupational assessments (effect on QoL)
-Collateral history

771

What is the initial help you can offer someone with anxiety?

Advice and reassurance
Basic counselling to address worries
Problem solving approach
Self help materials
Relaxation techniques
Breathing exercises

772

How does CBT help in anxiety?

Explore likelihood and impact of anticipated catastrophe. Predictions are discussed and behavioural experiments set up to test them. These increase confidence and ability to cope, and over time more adaptive coping mechanisms replace the unhelpful behaviours that maintained anxiety.

773

How does exposure therapy work in anxiety?

Desensitisation - stay in the situation long enough for habituation to occur in order to challenge thoughts. Repeated attempts at the same task cause the anxiety to decrease more quickly each time.

774

What medication can you offer someone with anxiety?

SSRIs (therapeutic dose generally higher than in depression and response takes longer)
TCAs
Buspirone (serotonin partial agonist - not popular due to delayed action and dysphoric side effects)
Benzodiazepines - useful as a short term treatment; tolerance and dependency develop quickly
Beta blockers for adrenergic symptoms

775

What are some side effects of benzodiazepines?

Amnesia
Ataxia
Respiratory depression - especially in the elderly and those with pre-existing respiratory disease

776

How long should you take benzodiazepines for in anxiety?

Only 2-4 weeks

777

What are the features of anxious (avoidant) PD?

REPORT + 3 of AFRAID:
Avoids social contact
Fears rejection/criticism
Restricted lifestyle
Apprehensive
Inferiority
Doesn't get involved unless sure of acceptance

778

What are the differentials for anxious (avoidant) PD?

Social phobia
Autistic spectrum disorder
Schizophrenia
Depression

779

What is the definition of erectile dysfunction?

Erections that are insufficiently hard to allow penetration

780

What are some organic causes of erectile dysfunction?

Diabetes
Arteriosclerosis
Neurological e.g. autonomic neuropathy
Pituitary failure
Medication: antidepressants, antipsychotics, beta blockers, diuretics
Substance misuse

781

What are some psychological causes of erectile dysfunction?

Depression
Performance anxiety

782

What makes a physical cause of erectile dysfunction more likely?

Older
Gradual onset
No erections at all
Risk factors e.g. smoking, hypertension
History of a physical illness

783

What investigations should you do in erectile dysfunction?

Physical examination including genitals (usually normal but reassures patients
Bloods:
-Testosterone + sex hormones (low tesosterone/hyperprolactinaemia)
-Glucose (diabetes)
-LFTs/gamma GT (alcohol misuse)

784

How should you manage erectile dysfunction?

-Improve modifiable risk factors/general physical health
-Psychological approaches e.g. sensate focus therapy
-Physical treatments:
---Phosphodiesterase-5 inhibitors e.g. sildenofil (Viagra)
---Intracavernosal prostaglandin self infections prior to intercourse
---Vacuum pump

785

What is a failure of genital response?

A lack of lubrication which causes pain on vaginal penetration

786

What are the causes of failure of genital response?

Psychological, or secondary to physical problems such as infection or menopausal atrophic vaginitis

787

What are the treatments for failure of genital response?

Psychological approaches
Lubricating gels
Hormone replacement therapy

788

How much more common is Asperger's in men than in women?

8:1

789

What are the features of Asperger's syndrome?

Poor social skills
Restricted interests
Normal language and IQ
Tendency to literal interpretation of language
Difficulty in reading social cues

790

How can you manage Asperger's syndrome?

Advice
Support
Routine
Social skills training

791

How common is autism?

1:1000 children, with as many again being on the spectrum

792

How much more common in men than in women is autism?

4:1

793

What are the risk factors for autism?

Obstetric complications
Perinatal infection e.g. rubella
Genetic disorders e.g. tuberose sclerosis, Down syndrome, fragile X

794

What are the features of autoism

-RECIPROCAL SOCIAL INTERACTION - not interested in people, can't 'read' others, attachments are poor without mutuality or warmth
-COMMUNICATION ABNORMALITIES - expressive speech and comprehension are delayed and minimal, few/no gestures, classically 'I' and 'me' confused with you/he/she
-RESTRICTED BEHAVIOURS AND ROUTINES - small changes can cause intense tantrums
-75% have a learning disability
-25% have seizures
-Overactive behaviour is common

795

What are the differentials in autism?

Deafness
Asperger's,
Specific language disorder
Learning disability
Rare disorders e.g. childhood schizophrenia, Rett's syndrome, neglect

796

What investigations should you do in autism?

Hearing tests
Speech and language assessment
Neuropsychological testing: assess IQ and confirm diagnosis

797

How can you manage autism?

Support and advice for family
Behaviour therapy: reinforce positive behaviours
Speech and language therapy
Special education
Treat comorbid problems e.g. epilepsy
Antipsychotics or mood stabilisers

798

What is the prognosis for autism?

1-2% gain full independence; the rest need lifelong support and care

799

What are the good prognostic indicators in autism?

IQ >70
Having some useful language

800

What are some examples of barbiturates?

Chloral
Paraldehyde
Meprobamate

801

What reduced the prescribing of benzodiazepines?

Addiction and withdrawal problems

802

What is the mode of action of benzodiazepines?

Act via GABA receptors. GABA is the principal inhibitory neurotransmitter and benzodiazepines enhance the effect of GABA
No effect in the absence of GABA or if the FABA receptor is blocked. Diazepam is a full agonist at the receptor

803

What are the 3 main effects of diazepam?

Sedative
Anxiolytic
Anticonvulsant

804

What clinical uses are there for benzodiazepines?

Short term use in moderate-severe anxiety disorder
Generalised anxiety disorder
Alcohol detox
Acute behavioural disturbance

805

How long can you use a benzodiazepine for and why?

4 weeks; tolerance, dependence, and withdrawal symptoms

806

What are the 4 normal stages of grief?

Numbness
Pining
Depression
Recovery

807

What symptoms can someone have while they are grieving?

May see/hear the dead person
Immense anger, guilt, anxiety or sadness
Can feel overwhelmed but sudden 'pangs' of grief

808

How can you manage grief?

Listen, explain and normalise their experiences; don't medicalise by giving antidepressants

809

What is an abnormal grief response?

Where the grief is:
Extremely intense, reaching the level for depression/disabling the person
Prolonged (>6 months) without relief
Delayed with no sign of an emotional response

810

When should you worry about grief?

When it's not moving forward aka when it has got 'stuck'

811

What are the uses of beta blockers in anxiety?

To relieve palpitations and tremor

812

What are the contraindications for beta blockers?

Asthma/bronchospasm/COPD
Heart failure or heart block
Systolic BP below 90mmHg
Low pulse rate

813

What are the features of bulimia nervosa?

Binge eating
Purging
Body image distortion (feeling fat, preoccupied with weight)
BMI >17.5

814

What are the physical symptoms of bulimia nervosa?

Arrhythmias (hypokalaemia)
Convulsions (hyponatraemia)

815

What investigation should you pay particular attention to in bulimia?

ECG and electrolytes

816

How should you manage bulimia nervosa?

-Treat medical complications
-SSRIs (fluoxetine); can reduce bingeing and purging through enhancing impulse control
-Treat comorbid psychiatric illness
-CBT

817

What are the questions in the CAGE questionnaire?

Have you ever felt that you should Cut down on your drinking?Have people ever Annoye you by criticising your drinking?
Have you ever felt Guilty about your drinking
Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover? (Eye opener/Early morning drink)

818

What is the psychoactive compound in cannabis?

delta-9-tetrahydrocannabinol (THC)

819

What are the effects of cannabis?

Depends on expectation and original mood state, which tends to be enhanced by the drug:
-Relaxation and euphoria
-Paranoia, anxiety, panic
-Perceptual distortion: time slows down, aesthetic appreciation enhanced
-Hunger pangs common
-Nausea and vomiting especially with alcohol
-Coordination affected
-Injected conjunctivae, tachycardia and dry mouth
-Restlessness and irritability

820

What are the risks with cannabis use?

Early heavy use particularly can precipitate psychosis leading to psychosis in those vulnerable.
Lethargy and poor motivation are recognised features of chronic heavy use.
Smoking aggravates asthma and risks lung disease + cancer

821

What are the features of separation anxiety disorder?

Clingy and distressed on separation from parents, often fearing that it will be permanent
Exploration of FH may reveal a threatened or unmourned loss

822

How can separation anxiety disorder be managed?

Increased periods of separation with reunion

823

What is a typical presentation of school refusal?

Tummy ache just before school but never at weekends/during holidays

824

What are some causes of school refusal?

Bullying
Fear of failure
Unsympathetic teacher
Families with 'precious' children (death of a sibling, difficulty conceiving)
Vulnerable parents (life threatening illness, agoraphobia)

825

How can you manage school refusal?

Help parents to tackle the problem
Enlist school support to deal with anxiety about performance, bullying, etc

826

What is the prognosis for school refusal?

Rapid return to full attendance has the best prognosis
Failure to do so signals a deeper problem - depression or separation anxiety (in parent or child)

827

How common is childhood depression (in boys and girls)

1-2% of children and 8% of adolescents
Sex ratio equal before puberty but girls outnumber boys after

828

How does childhood depression present?

Similar to adults
Children more likely to complain of somatic problems
Irritability and deteriorating school performance may be reported by teachers

829

How is childhood depression managed?

CBT is first line
Antidepressants only prescribed by specialists in severe cases

830

What is the prognosis of childhood depression?

Generally good; severe episodes are likely to recur

831

What are the child risk factors for childhood MH problems?

Male
Sensory impairment
Physical illness
Developmental delay
'Difficult' temperament - impulsive, intense negative emotions
Genetic factors

832

What are the family risk factors for childhood MH problems?

Family breakdown/conflict
Separation/death and loss
Abuse/neglect
Inconsistent discipline
Hostility
Large family (>4 children)
Parental factors: psychiatric or physical illness, substance misuse, criminality, personality disorder

833

What are the environmental risk factors for childhood MH problems?

Inner city
Overcrowding
Migration
Homelessness
Trauma
Poor social support
Peer criminality

834

What is chronic fatigue syndrome also known as?

Myalgic encophalomyelitis

835

What does chronic fatigue syndrome commonly follow?

Viral infection

836

What are the features of chronic fatigue syndrome?

Extreme fatigue
Exhausted by mild exertion
Alternating pattern of activity and debilitating fatigue, or complete exercise avoidance
Aches and pains

837

How can chronic fatigue syndrome be managed?

Graded exercise
CBT

838

What is clozapine used for?

Treatment resistant schizophrenia

839

How is treatment resistant schizophrenia defined?

Failure to respond to 2 or more antipsychotics, at least one of which is an atypical, each given at therapeutic dose for at least 6 weeks

840

What is the major risk with clozapine?

Potentially fatal - agranulocytosis in 0.7% of patients

841

What monitoring do patients on clozapine need?

Weekly blood tests to detect early signs of neutropenia; occurs in 3% which means it must be stopped, but without problems the tests get reduced to once a month

842

How common is conduct disorder?

10% of 10 year olds; 4x more common in boys

843

What are the risk factors for conduct disorder?

-Urban upbringing
-Deprivation
-Parental criminality
-Harsh and inconsistent parenting
-Maternal depression
-Family history of substance misuse

844

What are the features of conduct disorder?

Persistently antisocial behaviour that isn't just 'rebellious' e.g. cruelty to animals, stealing, fire setting

845

What are the 2 main types of conduct disorder?

Socialised - has a peer group (who often share in the behaviour)
Unsocialised - rejected by other children which makes them isolated and more hostile

846

What are the differentials for conduct disorder?

Oppositional defiant disorder
ADHD
Depression

847

What is oppositional defiant disorder?

A milder form of CD in children

848

How is conduct disorder managed?

Family education
Parent management training
Family therapy
Educational support
Anger management
Treat comorbid problems e.g. ADHD

849

What is the prognosis in conduct disorder?

Up to 50% develop substance misuse problems or disposal personality disorder as adults

850

What is a conversion disorder?

Where an internal conflict is unconsciously 'converted' into neurological symptoms

851

What are the ways in which a conversion disorder might present?

Acute, specific and often dramatic following sudden stress or conflict:
-Paralysis
-Blindness
-Aphonia (inability to produce speech)
-Seizures
-Psychogenic amnesia (loss of all semantic memories including own identity)
-Multiple personality disorder
-Fugue (lose memory entirely and wander away from home)
-Stupor

852

How is conversion disorder managed?

-Exclude organic cause
-Reassure that problem will resolve fully and quickly
-Encourage return to normal activities
-Avoid reinforcing symptoms or disability
-Suppor tot address triggering stressors rather than focusing on physical manifestations

853

What is 'la belle indifference'?

Relative lack of concern despite obviously worrying symptoms - seen in conversion disorder

854

Define 'delirium'

Acute and transit state of global brain dysfunction with clouding of consciousness; patient is not fully aware of their environment

855

What are the risk factors for delirium?

Old age
Pre existing physical or mental illness (especially dementia)
Substance misuse
Polypharmacy
Malnutrition

856

What are the causes of delirium?

TRAUMA: head injury, burns
HYPOXIA: cardiovascular/respiratory
INFECTION: intracranial, systemic
METABOLIC: liver failure, renal failure, electrolyte imbalance
ENDOCRINE: hypoglycaemia
NUTRITIONAL: Wernicke's encephalopathy
CNS PATHOLOGY: Raised ICP
DRUGS AND ALCOHOL: intoxication or withdrawal
MEIDCATION: anticholinergics/opiates

857

What are the features of delirium?

Sudden onset
Fluctuates
Disorientated
Poor attention and short term memory
Prominent mood changes
Illusions and hallucinations common (often visual +/- transient muddled delusions)
Disordered thinking and impoverished, pressured or rambling speech
Disturbed sleep (insomnia/cycle reversal)
Behaviour change

858

What are the two patterns of behaviour change in delirium?

Hyperactivity, agitation, aggression OR
Hypoactivity, lethargy, stupor, drowsiness, withdrawal

859

What investigations should you do in delirium?

Physical exam
Collateral history
Check for recently added drugs
Essential: FBC, U+E, glucose, Ca2+, MSU, SaO2, ECG, CXR, septic screen
Consider: LFTs, blood culture, CT head, CSF, EEG

860

How is delirium managed?

Treat the cause and manage aggravating factors e.g. pain, dehydration
Stop unnecessary medications
Behavioural management
Medication: a small nocturnal dose of benzodiazepine or if should term sedation needed, use low dose typical antipsychotics or benzos (beware risk of falls)
Consider referring to old age psych
Prevent it!

861

What are the behavioural management strategies in delirium?

Frequent reorientation
Good lighting
Address sensory problems e.g. hearing aids, spectacles
Avoid over- or under-stimulation
Minimise change
Remove things (throwing/tripping)
Silence unnecessary noises
Allow safe/supervised wandering

862

What is the prognosis in delirium?

Associated with increased mortality, longer admission, higher readmission rate, as well as subsequent using home placement
May take days/weeks or longer to fully resolve
Some never fully recover to premorbid level

863

When does delirium tremens come on?

About 48 hours into abstinence

864

How long does delirium tremens last?

3-4 days

865

What are the symptoms of delirium tremens?

Confusion
Hallucination - especially visual, of animals and people
Affective changes: extreme fear and hilarity may alternate
Gross tremor, especially of hands
Autonomic disturbance: sweating, tachycardia, hypertension, dilated pupils, fever
Delusions

866

What is the mortality rate of delirium tremens?

5% but rises to 30% if complications, e.g. sepsis

867

How is delirium tremens managed?

Urgen medical treatment: reducing benzodiazepine regime and parenteral thiamine
Manage potentially fatal dehydration and electrolyte abnormalities

868

Define 'dementia'

Acquired, chronic, and progressive cognitive impairment, sufficient to impair ADLs

869

How long do symptoms have to be present to make a confident diagnosis of dementia?

At least 6 months

870

What are the 3 most common causes of dementia?

Alzheimers (2/3rds)
Vascular
Lewy body

871

What are the features of dementia?

Forgetfulness
Anxiety/depression
Disorientation
Impoverished thinking and language
Mood and personality changes
Day/night reversal
Hallucinations
Wandering
Inappropriate behaviour including sexual disinhibition
Sleep disturbance
Delusions
Calling out, shouting ,swearing
Aggression