MH

Question 1

What is bipolar disorder?

Answer 1

chronic mental health disorder characterised by periods of mania/hypomania alongside episodes of depression

Question 2

What are the two types of bipolar disorder?

Answer 2

type I disorder: mania and depression (most common)

type II disorder: hypomania and depression

Question 3

What is mania?

Answer 3

there is severe functional impairment or psychotic symptoms for 7 days or more

Question 4

What is hypomania?

Answer 4

describes decreased or increased function for 4 days or more

Question 5

Treatment of bipolar?

Answer 5

Psychological interventions

Mood stabiliser - lithium. Valproate is an alternative

Management of mania/hypomania - stopping antidepressant if take one, antipsychotic therapy (e.g., olanzapine or haloperidol)

Management of depression - talking therapies, fluoxetine is antidepressant of choice

Question 6

Co-morbidities associated with bipolar?

Answer 6

2-3 times increased risk of diabetes, cardiovascular disease and COPD

Question 7

Primary care referral of bipolar?

Answer 7

if symptoms suggest hypomania then NICE recommend routine referral to the community mental health team (CMHT)

if there are features of mania or severe depression then an urgent referral to the CMHT should be made

Question 8

When to use ECT in bipolar patient?

Answer 8

1st line Tx if severe/ life threatening manic episode.

Question 9

What is lithium toxicity?

Answer 9

Lithium has narrow therapeutic range (0.4-1.0 mol/L) and a long plasma half-life being excreted primarily from the kidneys

Lithium toxicity generally occurs following concentration >1.5 mol/L

Question 10

What can precipitate lithium toxicity?

Answer 10

dehydration
renal failure
drugs - diuretics (esp thiazides), ACEi/ARBs, NSAIDs and metronidazole

Question 11

Features of lithium toxicity?

Answer 11

coarse tremor (a fine tremor is seen in therapeutic levels)
hyperreflexia
acute confusion
polyuria
seizure
coma

Question 12

Management of lithium toxicity?

Answer 12

mild-moderate toxicity may respond to volume resuscitation with normal saline

haemodialysis may be needed in severe toxicity

sodium bicarbonate is sometimes used but there is limited evidence to support this. By increasing the alkalinity of the urine it promotes lithium excretion

Question 13

What is schizophrenia?

Answer 13

Is the most common psychotic disorder. Requires symptoms to be present most of the time for 1 month of more.

Question 14

ICD-10 for schizophrenia

Answer 14

The diagnostic criteria for schizophrenia (using the International Classification of Diseases-10 [ICD-10] criteria) require the following symptoms to be present most of the time for 1 month or more:
One or more of the following features:
Hallucinatory voices giving a running commentary on the person’s behaviour, or discussing the person among themselves, or other types of hallucinatory voices coming from some part of the body.
Thought echo, thought insertion or withdrawal, and thought broadcasting.
Delusions of control, influence, or passivity, clearly referred to body or limb movements or specific thoughts, actions, or sensations.
Persistent delusions of other kinds that are culturally inappropriate and completely impossible, such as religious or political identity, or superhuman powers and abilities (for example being able to control the weather, or being in communication with aliens from another world).

Or any two of the following criteria:
Persistent hallucinations in any form, when accompanied by fleeting or half-formed delusions without clear affective content, or by persistent over-valued ideas (similar to preoccupations), or when occurring every day for weeks or months on end.
Breaks or interpolations in the train of thought, resulting in incoherence or irrelevant speech, or neologisms (invented words).
Catatonic behaviour, such as excitement, posturing, or waxy flexibility; negativism; mutism; and stupor.
Negative symptoms, such as marked apathy, reduced speech, and blunting or incongruity of emotional responses, usually resulting in social withdrawal and lowering of social performance; it must be clear that these are not due to depression or to antipsychotic medication.
A significant and consistent change in the overall quality of some aspects of personal behaviour, manifest as loss of interest, aimlessness, idleness, a self-absorbed attitude, and social withdrawal.

Question 15

Risk factors for schizophrenia?

Answer 15

Family history is strongest
Black Caribbean ethnicity
Migration
Urban environment
Cannabis use

Question 16

First rank Sx of schizophrenia

Answer 16

Auditory hallucinations - third person discussing pt., thought echo, voices common on pt’s behaviour

Thought disorder - insertion, withdraw, broadcasting

Passivity phenomena - bodily sensations controlled by external influence, actions/impulses/feelings imposed on individual

Delusional perceptions - normal object perceived, then sudden intense delusional insight into the objects meaning for the pt. (e.g., traffic light is green therefore I am the King)

Question 17

Epidemiology of Schizophrenia

Answer 17

Peak early 20s

M>F

Question 18

Pathophysiology of schizophrenia?

Answer 18

Pos Sx: XS dopamine in mesolimbic tracts

Neg Sx: ↓dopamine in mesocoritcal tracts.

Question 19

Catatonic Sx of schizophrenia?

Answer 19

psychomotor disturbance, stupor (immobile, mute, unresponsive, but eyes open + follow people), excitement (periods of extreme + purposeless motor activity), posturing (assume + maintain bizarre positions), rigidity (rigid posture against efforts to be moved), waxy flexibility (minimal resistance to being placed in odd positions, which are maintained for lengthy periods), automatic obedience to any instructions.

Question 20

Seven subtypes of schizophrenia?

Answer 20

Paranoid schizophrenia - most common, delusions + hallucinations
Catatonic schizophrenia - psychomotor disturbance
Postschizophrenic depression
Simple schizophrenia
Hebephrenic schizophrenia - age 15-25, delusions/hallucinations not prominent, disorganised/chaotic mood, shallow/inappropriate affect
Undifferentiated schizophrenia
Residual schizophrenia - prominent neg Sx that remain after delusions + hallucinations subside

Question 21

Features of Schizophrenia?

Answer 21

Prodromal: socially withdrawn, blunted affect, loss of interest.
Active: severe pos/neg Sx
Residual: cog Sx, periods of remission, eccentric behav, emotional blunting, illogical thinking or social withdrawal.

Question 22

Positive Sx in schizophrenia

Answer 22

New feature, no physiological counterpart
Delusions: fixed false beliefs even if opposing evidence Control (something outside controlling), reference (insig remarks directed at them, news speaking to them)
Hallucinations: perceptions w/o sensory stimuli. Auditory 3rd person/ voices comment on behav. Visual. Tactile.
Disorganised speech: word salad (disconnected, nonsensical)
Disorganised behav: bizarre, no purpose, eg multiple layers on hot day. Catatonic eg resistant movement/ unresponsive
Thought insertion, withdrawal broadcast
Disorganised thoughts
Neologisms

Question 23

Negative Sx of schizophrenia

Answer 23

Flatt affect
Alogia: poverty of speech, lack content 
Avolition: ↓motivation 
Apathy, anhedonia 
↓in self care, social withdrawal

Question 24

Management of schizophrenia

Answer 24

CBT, family therapy
Psychodynamic therapy 
Typical antipsychotics
Atypical antipsychotics - first line 
Pay close attention to CVD risk factor modification due to high rates of CVD in schizophrenic patients - due to antipsychotic medication and high smoking rates

Question 25

MOA of typical antipsychotics

Answer 25

block post synaptic D2 receptors. | Chlorpromazine, haloperidol

Question 26

MOA of atypical antipsychotics

Answer 26

block D1 >D2. Fewer extrapyramidal SE. risperidone, olanzapine (weight gain, DM), clozapine (agranulocytosis), quetiapine, aripiprazole, amisulpride

Question 27

Use of clozapine in schizophrenia

Answer 27

Clozapine should be introduced if schizophrenia is not controlled despite the sequential use of two or more antipsychotic drugs (one of which should be a second-generation antipsychotic drug), each for at least 6–8 weeks. Atypical antipsychotic Can cause agranulocytosis Can reduce seizure threshold, cause constipation, myocarditis (baseline ECG taken before starting treatment), hyper salivation Use only if resistant to others Adjust dose if start/stop smoking during Tx Need FBC monitoring during treatment

Question 28

Side effects of typical antipsychotics?

Answer 28

Extrapyramidal side-effects -dystonia (sustained muscle contraction torticollis, oculogyric crisis, Tx > procylidine), akathisia (restlessness), Parkinsonism, tardive dyskinesia (later onset, chewing, outing of jaw) bradykinesia. Hyperprolactinaemia - galactorrhoea, amenorrhoea, gyncaecomastia, hypogonadism, sexual dysfunction, ^ OP - due to inhibition of the dopaminergic tuberoinfundibular pathway antimuscarinic: dry mouth, blurred vision, urinary retention, constipation sedation, weight gain impaired glucose tolerance neuroleptic malignant syndrome: pyrexia, muscle stiffness reduced seizure threshold (greater with atypicals) prolonged QT interval (particularly haloperidol)

Question 29

Risks of using antipsychotics in elderly patients

Answer 29

^ risk of stroke | ^ risk of VTE

Question 30

Side effects of atypical antipsychotics?

Answer 30

Metabolic: - weight gain - clozapine - agranulocytosis - hyperprolactinaemia - olanzapine - higher risk of dyslipiademia and obesity

Question 31

Factors associated with poor prognosis of schizophrenia?

Answer 31

``` strong family history gradual onset low IQ prodromal phase of social withdrawal lack of obvious precipitant ```

Question 32

Monitoring required for use of antipsychotics?

Answer 32

FBC, U+E, LFT: initiation, annually, clozapine wkly. Lipids, weight: initiation, at 3 mnths, annually. Fasting blood glucose, PRL: initiation, 6 mnths, annually BP: baseline, freq during dose titration. ECG: initiation CV risk assessment: annually

Question 33

What is delusional disorder?

Answer 33

Persistent delusions, 1+ over 1 mnth not meeting other criteria for schizophrenia. Hallucinations may occur Affects day-to-day functioning

Question 34

Treatment of delusional disorder

Answer 34

Antipsychotics | Antidepressants

Question 35

What is schizoaffective disorder?

Answer 35

Sx of schizophrenia + mood disorder: Pos: delusions, disorganised speech/ behav hallucinations Neg: flat affect, alogia, avolition Mood Sx: depression, suicide ideation, manic eps A disorder in which the individual suffers from both symptoms that qualify as schizophrenia and symptoms that qualify as a mood disorder (e.g., depression or bipolar disorder) for a substantial portion (but not all) of the active period of the illness; for the remainder of the active period (+2 wks) of the illness, the individual suffers from delusions or hallucinations in the absence of prominent mood symptoms.

Question 36

Treatment of schizoaffective disorder?

Answer 36

``` Antidepressants Antipsychotics Dialectic behav therapy Mentalisation therapy Transference focused therapy ```

Question 37

What is schizoprehniform disorder?

Answer 37

Fragmented patterns of thinking (1-6 mnth) - lasting less than 6 months Similar to active phase of schizophrenia minus prodromal phase. Features: Pos: delusions, hallucinations, disorganised speech, disorganised behav Neg: flat affect, alogia, avolition Cog Sx: difficulties with memory/ learning.

Question 38

What can cause psychosis?

Answer 38

``` Schizophrenia Depression: psychotic depression, more common in elderly pts. Puerperal psychosis Brief psychotic disorder: Sx <1 mnth. Neurological: PD, HD CS, cannabis, phencyclidine ```

Question 39

Sx of psychosis

Answer 39

Hallucinations Delusions Alogia: little info by speech Tangentiality: answers diverge from topic Clanging Word salad: linking real words incoherently > nonsensical content

Question 40

ICD-10 for depression

Answer 40

``` 2+ core Sx for 2+ wks Mild: 2 core + 2 other Mod: 2 core + 3 other Severe: 3 typical + 4 other. Scoring: HADS, BDI, Zung self-rating. PHQ-9: <4 none, 10-14 mod, 15-19 mod severe 20-27 severe. ```

Question 41

What is depression?

Answer 41

Depression is characterised by persistent low mood and/or loss of pleasure in most activities and a range of associated emotional, cognitive, physical, and behavioural symptoms.

Question 42

Epidemiology of depression?

Answer 42

Depressive disorders are very common and are among the leading causes of disability worldwide. In people aged 18-44 years, depression is the leading cause of disability and premature death. F>M

Question 43

Risk factors for depression?

Answer 43

Chronic comorbidities (such as diabetes mellitus, chronic obstructive pulmonary disease, cardiovascular disease and especially people with chronic pain syndromes). Medicines (for example, corticosteroids). Female gender. Older age. Recent childbirth. Psychosocial issues such as divorce, unemployment, poverty, homelessness. Personal history of depression. Genetic and family factors — a family history of depressive illness. Adverse childhood experiences (for example, poor parent-child relationship, physical or sexual abuse). Personality factors (for example, neuroticism,autonomic hyperarousal, lability, neg biases, anxiety, obsession, low self esteem). A past head injury, including hypopituitarism following trauma.

Question 44

Core Sx of depression

Answer 44

Depressed mood: most of day, lack responsiveness to circumstances. Anhedonia: ↓pleasure Fatigue/ low energy

Question 45

Other Sx of depression

Answer 45

``` Weight/appetite change Low self confidence Disturbed sleep: insomnia, early morning waking or hyposomnia Poor concentration or indevisiveness Suicidal thoughts/acts Thoughts of death Agitation or slowing of movement Guilt/self-blame Loss of libido Feeling worthlessness Loss emotional reactivity ``` Psychotic Sx Delusions: poverty, inadequacy, guilt, responsibility for world events, nihilistic Auditory: defamatory or accusatory voices, cries for help, screaming Olfactory: rotting food, faeces, decomposing flesh Visual: tormentors, demons, devil, dead bodies Catatonic, psychomotor retardation. Cortards synd: believes they are dead, stops eating/ drinking.

Question 46

Screening for depression?

Answer 46

PHQ-2 During last mnth have you been bothered by feeling down, depressed or hopeless? During last mnth have you been bothered by having little interest or pleasure in doing things? HAD - hospital anxiety and depression scale

Question 47

Management of Persistent subthreshold depressive symptoms or mild to moderate depression

Answer 47

General measures sleep hygiene active monitoring for people who do want an intervention Drug Tx - do not use routinely, but consider for people with: a past history of moderate or severe depression or initial presentation of subthreshold depressive symptoms that have been present for a long period (typically at least 2 years) or subthreshold depressive symptoms or mild depression that persist(s) after other interventions if a patient has a chronic physical health problem and mild depression complicates the care of the physical health problem Low-intensity psychosocial interventions: - individual guided self-help based on CBT principles - computerised CBT - structured group physical activity programme - group based CBT

Question 48

Management of unresponsive, moderate and severe depression

Answer 48

Antidepressant - SSRI first line High-intensity psychological interventions: - individual CBT - interpersonal therapy (IPT) - behavioural activation - behavioural couples therapy - counselling - short term psychodynamic psychotherapy If chronic physical health problems: - group based CBT - individual CBT

Question 49

Adverse effects of antidepressants

Answer 49

Suicidal thoughts and suicide attempts — all antidepressants have been associated with an increase in suicidal thoughts and suicide attempts in adolescents and young adults, and people with a history of suicidal behaviour. Anxiety, agitation, or insomnia — if these are problematic, consider short-term (usually less than 2 weeks) concomitant treatment with a benzodiazepine Hyponatraemia — this can occur with all antidepressants, although the highest risk is with selective serotonin reuptake inhibitors (SSRIs). Consider hyponatraemia if the person develops dizziness, drowsiness, confusion, nausea, muscle cramps, or seizures. Sexual dysfunction — sexual dysfunction is a common symptom of depression, all antidepressants can cause sexual dysfunction Persistent, severe, or distressing adverse effects may be managed by: dose reduction and re-titration, switching antidepressants Mild and transient adverse effects - e.g., nausea from SSRIs can be managed by reassurance, and dose-reduction if necessary

Question 50

Pharmacology of SSRIs

Answer 50

GI sx, ↑risk of GI bleed, ↓Na Citalopram prolongs QT Tx for at least 6 mnths after remission. Interactions: NSAIDs, warfarin, heparin, aspirin, triptans. MOAi (↑risk of serotonin syndrome) When stopping, gradually ↓ over 4 wks. Discontinuation Sx: mood change, restlessness difficulty sleeping, unsteady, sweating, GI sx (pain, D/V cramping), paraesthesia Fluoxetine in children

Question 51

Pharmacology of TCAs

Answer 51

amitriptyline, imipramine, clomipramine SFX - drowsiness, dry mouth, blurred vision, constipation, urinary retention, lengthening of QT interval. Interactions - adrenergic neurone blockers (clonidine, guanethidine)

Question 52

Pharmacology of Mirtazapine

Answer 52

Noradenergic and specific serotonergic antidepressant (NaSSA) - antagonise adrenergic receptors and block 5-HT2/3 receptors SFx - dry mouth, increased appetite and weight gain, headaches, feeling sleepy, N+V, diarrhoea, constipation rare - pancreatitis, hyponatraemia, blood dyscarias Interactions - AEDs (reduce seizure threshold), chlorpromazine, MAOIs, rifampicin

Question 53

Pharmacology of MAOIs

Answer 53

isocarboxazid, phenelzine, selegilline monoamine oxidase is involved in removing the neurotransmitters norepinephrine, serotonin and dopamine from the brain. MAOIs prevent this SFx - drowsiness, dry mouth, N+D, constipation, headache, insomnia

Question 54

Side effects of ECT

Answer 54

loss of STM, retrograde, headache, temp confusion, loss of LTM, personality changes, loss of skill.

Question 55

What is premenstrual dysphoric disorder?

Answer 55

Mood changes during menstrual cycle Only ovulatory cycles, not prior to puberty, during pregnancy or after menopause ``` Features: Affective lability, irritability Anger, anxiety/ angst, stress, mood swings ↓concentration, fatigue Weight loss/gain Inability to sleep/ oversleeping Feeling overwhelmed Bloating/ breast pain ```

Question 56

Diagnosis of premenstrual dysphoric disorder?

Answer 56

Mood changes <1 wk before menses, >5 Sx resolving within 1wk post menses Sx affect day to day life

Question 57

Management of premenstrual dysphoric disorder?

Answer 57

Mild: advice on sleep, exercise, smoking, diet, sunlight, regular, freq (2-3 hrly), small, balanced meals, rich in complex carbs Mod: new gen COCP eg Yasmin Severe: SSRIs, continuously or just in luteal phase

Question 58

What is seasonal affective disorder

Answer 58

describes depression which occurs predominately around the winter months. SAD should be treated the same way as depression, therefore as per the NICE guidelines for mild depression, you would begin with psychological therapies and follow up with the patient in 2 weeks to ensure that there has been no deterioration. Following this an SSRI can be given if needed. In seasonal affective disorder, you should not give the patient sleeping tablets as this can make the symptoms worse. Finally, the evidence for light therapy is limited and as such it is not routinely recommended.

Question 59

What alternative causes and medications can cause anxiety?

Answer 59

- hyperthyroidism, cardiac disease and medication-induced anxiety - salbutamol, theophylline, corticosteroids, antidepressants and caffeine

Question 60

What is GAD?

Answer 60

Anxiety generalised, persistent + not restricted to any circumstances.

Question 61

Who is most likely to suffer from GAD?

Answer 61

F>M, 45-59, martial/ sexual disturbance, stressful life event unemployment

Question 62

Symptoms of GAD?

Answer 62

>6 months, >4 Sx persistent nervousness, trembling, muscle tension, sweating, lightheadedness, palpitations, dizziness, and epigastric discomfort. Persistent fear/ distress, panic, worry, on edge, apprehension about everyday events + problems Palpitations, accelerated HR, sweating, pounding heart, trembling shaking, dry mouth. Difficulty breathing, feeling of choking, CP, nausea or abdo pain Dizzy, unsteady, faint, light headed, derealisation, depersonalisation, fear of losing control, going crazy or passing out, fear of dying. Hot flashes, cold chills, numbness or tingling sensations. Muscle tension, aches/pains, restless, inability to relax, feeling keyed up, on edge, sensation of lump in throat, difficult swallowing Exaggerated startle response Difficulty concentrating or mind going blank, difficulty sleeping Irritability ↓libido, erection failure, painful/ irregular/absent menstruation. Unhelpful behavs: pacing room wringing hands, sighing, attempts at coping (caffeine, smoking, alcohol, illegal/ prescribed drugs), avoiding fear provoking situations, safety behavs (eg only going out with friend in agoraphobia), asking for reassurance (visiting GP)

Question 63

What is GAD-2 screening?

Answer 63

over last 2 wks have you been bothered by feeling nervous, anxious or on edge? Not being able to stop or control worry. 0 = not at all, 1 = several days. 2 = more than ½ days. 3 = nearly every day. Anxiety if person answers 2/3 to 1 or both. With GAD-7 - Add up to poss of 21. 5 mild, 10 mod, 15 severe.

Question 64

Management of GAD?

Answer 64

step 1: education about GAD + active monitoring step 2: low-intensity psychological interventions (individual non-facilitated self-help or individual guided self-help or psychoeducational groups) step 3: high-intensity psychological interventions (cognitive behavioural therapy or applied relaxation) or drug treatment. See drug treatment below for more information step 4: highly specialist input e.g. Multi agency teams

Question 65

Drug treatment of GAD

Answer 65

NICE suggest sertraline should be considered the first-line SSRI if sertraline is ineffective, offer an alternative SSRI or a serotonin–noradrenaline reuptake inhibitor (SNRI) examples of SNRIs include duloxetine and venlafaxine If the person cannot tolerate SSRIs or SNRIs, consider offering pregabalin BDZ for somatic Sx CV Sx - atenolol patients under the age of 30 years NICE recommend you warn patients of the increased risk of suicidal thinking and self-harm. Weekly follow-up is recommended for the first month

Question 66

What is panic disorder?

Answer 66

Recurrent spont panic attacks, sudden intense fear, reach peak 10 mins, don’t last longer 20-30 mins.

Question 67

Risk factors for Panic Disorder

Answer 67

F>M, 15-24 + 45-54 widowed, divorced, city, limited education, early parental loss, abuse. Genes: ADOR2A, CCK, COMT

Question 68

Symptoms of panic disorder

Answer 68

Tachypnoea, HTN Autonomic arousal: palpitations, pounding heart, ↑HR, sweating, trembling, shaking, dry mouth Difficulty breathing, feeling of choking, CP, nausea, abdo distress Feeling dizzy, unsteady, faint, light headed, Derealisation or depersonalisation Fear of losing control, going crazy, passing out Fear of dying Hot flushes, cold chills Numbness or tingling sensation

Question 69

Diagnosis of panic disorder

Answer 69

>4 Sx, not restricted to any particular situation, unpredictable. Behav change to avoid further attacks.

Question 70

Management of panic disorder

Answer 70

step 1: recognition and diagnosis step 2: treatment in primary care - see below step 3: review and consideration of alternative treatments step 4: review and referral to specialist mental health services step 5: care in specialist mental health services Treatment in primary care: NICE recommend either cognitive behavioural therapy or drug treatment SSRIs are first-line. (can initially ^ panic Sx, beneficial effect takes up to 12 weeks) If contraindicated or no response after 12 weeks then TCA > imipramine or clomipramine should be offered

Question 71

What is agoraphobia

Answer 71

Fear, avoidance of places where escape difficult, e.g., crowds, public places, travelling alone/ away from home. Bimodal peak: 15-35 + older

Question 72

Diagnosis of agoraphobia

Answer 72

>6mnths 2+ Sx in feared situations, 1+ occasions. 1 Sx must be autonomic. Recognises fear excessive

Question 73

Treatment of agoraphobia

Answer 73

SSRIs, SNRIs, TCA BDZ: ST use only CBT, systematic desensitisation, exposure, relaxation training, anxiety management. Teach about bodily responses associated with anxiety/ education about panic attacks.

Question 74

What is pathophysiology behind phobias?

Answer 74

Genetic, anxiety, mood, substance use disorder. Psychoanalytical: unconscious conflict repressed + displaced into phobic Sx Learning theory: conditioned fear response to traumatic situation, learned avoidance. Observational eg relatives fears. Preparedness > evolutionarily adaptive. Acquired by classical conditioning, maintained by operant via avoidance (neg reinforcement of no anxiety)

Question 75

Sx of phobias

Answer 75

>6mnths, fear restricted to situation/ contemplation of situation. Response to phobic stimulis: ↑HR, dizziness, trembling, anxiety Excessive thinking about/ avoidance of phobic stimulus cause distress

Question 76

Treatment of phobias

Answer 76

Exposure therapy, relaxation + graded exposure. Flooding Cog: education + anxiety management, coping skills/ strategies, cog restructuring SSRIs, BDZ may be used in severe cases to allow pt to engage in exposure, may ↓ efficacy of behav therapy by inhibiting anxiety during exposure. BB: for sympathetic arousal

Question 77

Sx of separation anxiety

Answer 77

``` Distress at thought of separation Nausea, headache, nightmares Clingy, distressed upon separation Fear separation permanent Reluctance to leave home because of fear of separation, reluctance to be alone. ``` Adult >6mnths Children lasts >4wks

Question 78

Treatment of separation anxiety

Answer 78

SSRIs BDZ CBT: gradually exposing child to separation, challenging unhelpful beliefs.

Question 79

Sx of social anxiety/phobia

Answer 79

Blushing, fear of vomiting + urgency/ fear of micturition or defecation in feared situation Trembling, derealisation, dry mouth perspiration, XS fear of humiliation or others noticing how anxious they are, desire for escape/ avoidance Incapacitating anxiety, restricted to particular social situations XS thinking about/ avoidance of social situations/ circumstances Fear of scrutiny, low self-esteem + fear of criticism, self-critical, perfectionist Suicidal thoughts

Question 80

Diagnosis of social anxiety

Answer 80

>6 mnths Avoidance of social situations Mini SPIN: >6. Fear of embarrassment causes me to avoid doing things/ speaking to people. I avoid activities in which I am centre of attention. Being embarrassed or looking stupid are amongst worst fears. 0 = not at all, 1 = a little bit, 2 = somewhat, 3 = very much, 4 = extremely

Question 81

Treatment of social anxiety

Answer 81

1st: CBT, relaxation training anxiety management, social skill training, integrated exposure methods (modelling + graded exposure) 2nd self help book 3rd: meds, escitalopram or sertraline, then paroxetine, fluvoxamine or venlafaxine then phenelzine or moclobemide. BB Interpersonal therapy

Question 82

What is OCD?

Answer 82

Obsessive-compulsive disorder (OCD) is characterised by the presence of either obsessions or compulsions, but commonly both. The symptoms can cause significant functional impairment and/ or distress. 20y/o, M=F. 5HT dysreg. Cell mediated AI factors eg against BG, Sydenham Chorea PANDAS Associations: depression, schizophrenia, tourette’s, anorexia nervosa

Question 83

Symptoms of OCD

Answer 83

Obsessions: recurrent, intrusive, unpleasant thoughts Compulsions: repeated, ritualistic behavs, often to alleviate anxiety from obsessions. Resisting causes mounting anxiety. Don’t result in completion of useful tasks. Remembers performing act but has to satisfy lingering doubts Originate in mind of pt, not imposed by outside influence, acknowledged as excessive or unnecessary. Pt tries to resist but fails. Trichotillomania, nail biting, pyromania, pathological gambling, kleptomania, skin picking, Tourette's, hypochondriasis, dysmorphobia, pathological jealousy

Question 84

Diagnosis of OCD

Answer 84

Most days for at least 2 wks Yale-Brown OC scale - how much of day? interfere with social or work/school functioning? distress? prevented from compulsions? how much effort to resist? how much control? how long is drive to perform compulsions?

Question 85

Management of OCD

Answer 85

If functional impairment is mild low-intensity psychological treatments: cognitive behavioural therapy (CBT) including exposure and response prevention (ERP) If this is insufficient or can’t engage in psychological therapy, then offer choice of either a course of an SSRI or more intensive CBT (including ERP) If moderate functional impairment offer a choice of either a course of an SSRI (any SSRI for OCD but fluoxetine specifically for body dysmorphic disorder) or more intensive CBT (including ERP) If severe functional impairment offer combined treatment with an SSRI and CBT (including ERP) if treatment with SSRI is effective then continue for at least 12 months to prevent relapse and allow time for improvement

Question 86

What is ERP?

Answer 86

ERP is a psychological method which involves exposing a patient to an anxiety provoking situation (e.g. for someone with OCD, having dirty hands) and then stopping them engaging in their usual safety behaviour (e.g. washing their hands). This helps them confront their anxiety and the habituation leads to the eventual extinction of the response

Question 87

Poor prognostic indicators of OCD

Answer 87

given in to compulsions, longer duration, early onset, M, tics, bizarre compulsions, hoarding, symmetry, comorbid depression, delusional beliefs, over-values ideas + PD

Question 88

Good prognostic indicators of OCD

Answer 88

good premorbid social + occupational adjustment, a precipitating event, episodic symptoms, less avoidance.

Question 89

What is body dysmorphic disorder?

Answer 89

Obsessive belief appearance is flawed. Can cause compulsive behavs eg XS grooming Genetic, 5HT Tx = CBT, SSRI

Question 90

Sx of physical and sexual abuse?

Answer 90

``` Bruising, cuts, sores, burns or rashes Broken bones, damage to organs FTT Anxiety, depression, PTSD, aggression, fear towards sexual activity, suicide. STIs, UTIs ```

Question 91

What is acute stress disorder?

Answer 91

defined as an acute stress reaction that occurs in the first 4 weeks after a person has been exposed to a traumatic event

Question 92

Features of acute stress disorder

Answer 92

intrusive thoughts e.g. flashbacks, nightmares dissociation e.g. 'being in a daze', time slowing negative mood avoidance arousal e.g. hypervigilance, sleep disturbance

Question 93

Management of acute stress disorder

Answer 93

trauma-focused cognitive-behavioural therapy (CBT) is usually used first-line benzodiazepines sometimes used for acute symptoms e.g. agitation, sleep disturbance should only be used with caution due to addictive potential and concerns that they may be detrimental to adaptation

Question 94

When does acute stress reaction occur?

Answer 94

Onset: immediate or within mins Duration: 0-72hrs Partial/complete amnesia of event

Question 95

Sx of acute stress reaction

Answer 95

Initial daze with constriction of field of consciousness + narrowing of attention, inability to comprehend stimuli + disorientation Followed by further withdrawal from surrounding situation or by agitation + over activity Autonomic anxiety signs Low mood, irritability, poor sleep + concentration, wanting to be alone Recurrent dreams or flashbacks, avoidance of anything that will trigger memory. Reckless or aggressive self destructive behav Feeling numb + detached

Question 96

What is adjustment disorder

Answer 96

Within 1 mnth of psycho-social stressor, lasts <6mnths Feeling depressed/ anxiety or worry. Feeling inability to cope, plan ahead or continue in current situation. Some degree of disability in performance of daily routine Children: regressive phenomena, return to bed-wetting, babyish speech or thumb sucking.

Question 97

What is PTSD?

Answer 97

Severe psychological disturbance following traumatic event. T1: uncomplicated, single traumatic event. T2: complex. Multiple/ prolonged trauma. Impulsivity, aggression, sexual acting out, substance misuse, EDs. Amnesia, dissociation. Slower + difficult to engage + treat.

Question 98

Risk factors for PTSD

Answer 98

F>M, ↓education, SES. ↓ self-esteem/ neurotic trats. FH/ PMH of MH, prev traumatic events, trauma severity, peri traumatic dissociation

Question 99

Protective factors for PTSD

Answer 99

M, white, high IQ, SES, chance to view dead body.

Question 100

Sx of PTSD

Answer 100

re-experiencing: flashbacks, nightmares, repetitive and distressing intrusive images avoidance: avoiding people, situations or circumstances resembling or associated with the event hyperarousal: hypervigilance for threat, exaggerated startle response, sleep problems, irritability and difficulty concentrating emotional numbing - lack of ability to experience feelings, feeling detached depression, drug/alcohol misuse, anger, unexplained physical Sx Children less likely to show distress often play to express memories

Question 101

Diagnosis of PTSD

Answer 101

Sx within 6 mnths of traumatic event or present for at least 1 mnt

Question 102

Management of PTSD

Answer 102

Trauma focused CBT + EMDR: education about PTSD, self-monitoring of Sx, anxiety management, breathing techniques, imaginal reliving. Use voluntary multi-saccadic eye movements to ↓ anxiety associated with disturbing thoughts + help process emotions associated with trauma. SSRIs, venlafaxine. Severe cases > risperidone Exposure therapy: describe trauma as if in situations, 1st person, present tense. All sensory modalities. Sleep disturbance: mirtazapine/zopiclone / levomepromazine/ prazosin Debriefing: manage immediate psychological distress, prevent PTSD Watchful waiting for Sx lasting <4wks.

Question 103

What are medically unexplained symptoms?

Answer 103

Extended periods of physical Sx w/o evidence of organic cause

Question 104

Risk factors/ causes of MUS?

Answer 104

F>M Genetics, cultural + family attitudes, stressful LE, insecure attachment, childhood neglect + abuse. Cog overinterpreting physical Sx as disease, central pain mechanism.

Question 105

Maintaining factors of MUS?

Answer 105

unnecessary investigations + opinions, untreated anxiety or depression, 2° gains.

Question 106

Features of MUS?

Answer 106

Pain, changes over time, unable to give clear + precise description Worry/anxiety Fibromyalgia, IBS, dyspepsia Dizzy, tinnitus, headache, pelvic pain, lower back pain Clear psychosocial stressors. Pts understanding of illness tend to inform their Sx. Can show unusual characteristics, don’t fit with known disease models + excessive in comparison to pathology Pt attends freq with diff Sx Overly anxious about meaning of Sx

Question 107

Diagnosis of MUS?

Answer 107

>1 Sx, distress in other areas of life, lasts > 6mnths | Rule out organic cause

Question 108

What is hypochondriasis?

Answer 108

pts believe have specific illness eg cancer rather than presenting with inexplicable Sx.

Question 109

What is somatisation?

Answer 109

multiple, recurrent + freq changing Sx for 2+yrs, no organic cause. Pt refuses to accept reassurance or neg test results

Question 110

What is conversion disorder?

Answer 110

unconscious converting of psychological stressor into physical illness. Loss of motor/ sensory function

Question 111

What is factitious/Munchausen's disorder?

Answer 111

deliberate production of Sx to relieve medical Tx

Question 112

What is malingering?

Answer 112

feigning Sx to obtain external reward.

Question 113

Management of MUS?

Answer 113

``` Treat psychiatric comorbid illnesses’: anxiety /depression Full history + exam. Explain + reassure. Avoid over-investigation, unnecessary referrals. Encourage normal function SSRIs CBT Graded exercise ```

Question 114

What is chronic fatigue syndrome?

Answer 114

Sx of: Extreme fatigue, exhausted by mild exertion. Alternating pattern of activity + debilitating fatigue or complete exercise avoidance. Chronic insomnia, hypersomnia, unrefreshing sleep, loss of memory, ↓concentration or orthostatic intolerance. Muscle/joint pain Word finding difficulties Freq headache, sore throat, tender, LN w/o enlargement General malaise, flu like Sx Dizziness, nausea, palpitations May follow viral infection, can arise spontaneously F>M, 30-50, past psychiatric Hx EBV,

Question 115

Diagnosis of CFS?

Answer 115

>6mnths of disabling fatigue Tiredness screen. Physical or mental exertion makes Sx worse DePaul Sx Q: 54 items, freq + severity scores combined for overall indicator of each Sx.

Question 116

Treatment of CFS?

Answer 116

``` Graded exercise Pacing of activity, realistic goals. CBT improves fatigue + physical functioning Low dose antidepressants/ amitriptyline Referral to pain clinic ```

Question 117

What is somatoform autonomic dysfunction?

Answer 117

Da Costas syndrome - a psychiatric disorder in which the patient experiences chest pain which may mimic angina gastric neurosis - applied here to those conditions of dyspepsia or indigestion, the symptoms of which were found to have a predominantly psychological basis. CFS

Question 118

Diagnosis of somatoform autonomic dysfunction?

Answer 118

1+ of: nonspecific/ changing nature, CP, dyspnoea or hyperventilation, XS tiredness on mild exertion. Hiccup, ↑ freq of micturition or dysuria, bloating, distended, heavy 2+ of: palpitations, sweating, dry mouth, flushing or blushing, tremor, fear + distress about possibility of physical disorder, epigastric discomfort ‘butterflies’ or churning in stomach

Question 119

What is Persistent somatoform pain disorder

Answer 119

Persistent, severe + distressing pain for 6+ mnths, continuous on most days, can’t be explained by physiological process or organic Sx.

Question 120

What is dissociative disorder?

Answer 120

dissociation is a process of 'separating off' certain memories from normal consciousness in contrast to conversion disorder involves psychiatric symptoms e.g. Amnesia, fugue, stupor dissociative identity disorder (DID) is the new term for multiple personality disorder as is the most severe form of dissociative disorder La Belle indifference: lack of concern about disability + prospects of recover. Dissociative stupor: absence of voluntary movement/ responsiveness to stimuli. Normal muscle tone, static posture, + breathing. ``` Conversion = physical Mental = dissociation ```

Question 121

Sx of depersonalisation/ derealisation disorder?

Answer 121

feel detached from body/ mind/ feeling world not real. Emotional/physical numbness, weak sense of self, deadpan speech, altered sense of time, brain fog/ light-headedness, prone to rumination, anxiety.

Question 122

Sx of dissociative amnesia?

Answer 122

memory loss, usually centred on traumatic event, unable to recall significant info about self eg childhood home.

Question 123

Sx of dissociative fugue?

Answer 123

confused about identity, starts sudden travel/ wandering. Partial/complete amnesia for journey.

Question 124

Sx of dissociative convulsions?

Answer 124

absence of tongue biting, bruising + incontinence

Question 125

Sx of dissociative identity disorder?

Answer 125

only 1 evident at a time, each has own memories, preferences/ behav patterns. Overt (aware of identity shifts, struggles to manage), covert (unaware).

Question 126

Management of dissociative disorders

Answer 126

Memory aids | SSRIs

Question 127

Pathophysiology of substance use disorders?

Answer 127

Classical conditioning: cravings conditioned to cues Operant conditioning: repetitive behav have predictable outcomes. Pos reinforcement: drugs provide pleasure. Neg reinforcement: use again to avoid withdrawal or to avoid painful consciousness Social learning theory: learn from others, peer pressure Neurobiological: drugs affect dopaminergic reward pathway Acute intoxication: follows administration of substance disturbance in level of consciousness, cognition, perception, affect/behav.

Question 128

Sx of substance use disorders?

Answer 128

Dependence: inability to feel normal without using. Use of substance takes higher priority than other behavs. Addiction: compulsive use to, achieve reward stimuli despite neg effects Tolerance: receptors become less sensitive or neurons have fewer receptors. Must consume more of substance to feel desired effect. Stopping use causes withdrawal: body predictively counters consumption, no consumption = nothing to counter, must consume more to avoid discomfort. Withdrawal: anxiety, depression, irritability, fatigue, tremors, palpitations, clammy skin, dilated pupils, headache, vomiting, seizures

Question 129

Diagnosis of substance use disorders?

Answer 129

``` 3+ of for 12 mnths: Consuming more than intended Strong desire/ compulsion to take substance. Inability to cut down Use takes up lot of time Cravings Use affects responsibilities Using in spite of social problems caused Use replaces important activities Use in phsycially dangerous situation Using even if worsens problem Tolerance Withdrawal ```

Question 130

Predisposing factors for alcohol use disorder?

Answer 130

Genetics Occupation: stressful work + socially sanctioned drinking eg entertainment industry Difficult childhood, parental separation MH: mania, depression, social phobias, anxiety Alcohol stimulates nucleus accumbens ↑dopamine + potentiates effects at 5HT3 receptors. MAO, NMDA + GABA receptors also implicated Psychodynamic: intoxication to gain disinhibition allowing expression of aggression, maternal overprotection, childhood sexual abuse. Behav: drinking conditioned response to range of circumstances, modelling. Euphoriant effect, important reinforcer.

Question 131

Sx of acute alcohol intoxication

Answer 131

severe confusion stupor, relaxation, euphoria, irritable, aggressive, weepy, disinhibition. Impulsivity + poor judgement, slurred speech, ataxic gait, sedation, coma, lapses of consciousness, vomiting, seizures, resp depression. Dry mouth, red eyes.

Question 132

Sx of alcohol withdrawal

Answer 132

symptoms start at 6-12 hours: tremor, sweating, tachycardia, anxiety peak incidence of seizures at 36 hours peak incidence of delirium tremens is at 48-72 hours: coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia

Question 133

Management of alcohol withdrawal

Answer 133

patients with a history of complex withdrawals from alcohol (i.e. delirium tremens, seizures, blackouts) should be admitted to hospital for monitoring until withdrawals stabilised first-line: long-acting benzodiazepines e.g. chlordiazepoxide or diazepam. Lorazepam may be preferable in patients with hepatic failure. Typically given as part of a reducing dose protocol carbamazepine also effective in treatment of alcohol withdrawal

Question 134

Mechanism of alcohol withdrawal

Answer 134

chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)

Question 135

What is Wernicke encephalopathy

Answer 135

Acute thiamine (B1) def Confusion, ataxia, ophthalmoplegia Confusion, altered GCS, peripheral sensory neuropathy Progress to KS if untreated

Question 136

What is Korsakoff's syndrome

Answer 136

Irreversible anterograde amnesia + retrograde amnesia. | Register new events, can’t recall within a few mins, may confabulate.

Question 137

What is alcoholic ketoacidosis

Answer 137

Often alcoholics don’t eat regularly + may vomit leading to starvation After alcohol binge body can start to break down body fat producing ketones Metabolic acidosis Elevated anion gap Elevated ketones Normal/ low glucose Infusion of saline + thiamine.

Question 138

Complications of alcohol use

Answer 138

Dilated CM, arrhythmias, HTN, stroke. Liver damage. Pancreatitis, varices, gastritis, ulceration, MW tears, DM, Barrett’s Cancer Peripheral neuropathy, optic atrophy, blindness Macrocytic anaemia, thrombocytopenia, Zieve’s synd FAS, depression, anxiety, self-harm, suicide. Alcoholic dementia Central pontine myelinolysis Cerebellum damage. Social problems.

Question 139

Diagnosis of alcohol use disorder

Answer 139

FBC, LFTs, ^ GGT and transaminases CAGE C - felt should cut down? A - annoyed by people criticising drinking? G - ever felt guilty about drinking? E - eye opener - have you ever had a drink first thing in the morning to steady nerves/get rid of hangover +2 significant AUDIT-C 5+ indicates ↑ or higher risk drinking.

Question 140

Management of alcohol use disorder

Answer 140

Motivational interviewing, CBT, AA. Buspirone: 5HT1A agonist Naltrexone: opioid antagonist, ↓cravings, relapses + consumption. ↓reinforcing actions of alcohol. Acamprosate: enhance GABA. ↓cravings, weak antagonist of NMDA receptors. Disulphiram: prevents breakdown of acetaldehyde, if alcohol drunk lead to facial flushing, headaches, palpitation, N+V. can cause fulminant hepatitis. Only after trial of naltrexone or acamprosate. CI ischaemic heart disease + psychosis. ``` Stages of change model Pre-contemplation Contemplation Preparation Action Maintenance Relapse ```

Question 141

Management of alcohol withdrawal

Answer 141

long-acting benzodiazepines e.g. chlordiazepoxide or diazepam. Lorazepam may be preferable in patients with hepatic failure. Typically given as part of a reducing dose protocol

Question 142

Management of alcohol withdrawal

Answer 142

Reducing BDZ regime | Parenteral thiamine

Question 143

Management of Wernicke's encephalopathy

Answer 143

parenteral thiamine pabrinex. prevent KS

Question 144

Summary of cannabis use disorder

Answer 144

Continued use causes tolerance Upon withdrawal: cravings, irritability, anxiety, difficulty sleeping, restlessness Acute intoxication: drowsiness, euphoria + relaxation, anxiety + panic, N/V, coordination affected, HTN, ↑HR, RR, tremors, slurred speech, acute psychosis, agitation, urinary retention, distorted perception, hunger pangs (sweet foods), effects depend on mood, blood shot eyes, dry mouth. Motivational Treatment

Question 145

Summary of cocaine use disorder

Answer 145

Formication: insects crawling on/ below skin. Cocaine blocks uptake of dopamine, noradrenaline + serotonin Complications = Coronary a spasm > MI/ infarction. Hyperthermia, seizures, stroke, HTN, arrhythmias, brain haem, overdose, perf nasal septum (vasoconstriction + ischemic necrosis), aortic dissection Ischaemic colitis: abdo pain/ rectal bleeding. Acute: ↑confidence, impulsivity, euphoria, energy + alertness. Impair judgement, CP, dyspnoea, epistaxis, mydriasis, blurred vision, restless, severe agitation. Hypertonia, hyperreflexia. Tachy/bradycardia. Agitation, psychosis, hallucinations Withdrawal: depression, anxiety, fatigue, ↓concentration, cravings, tiredness, lethargy, dysphoria, ↑ appetite, XS sleeping, vivid dreaming suicidal ideation, N/V, hallucinations QRS widening + QT prolongation Metabolic acidosis Rhabdomyolysis

Question 146

Tx of cocaine use disorder

Answer 146

Modafinil: ↓craving Psychotherapy: motivational interviewing, peer support Cocaine overdose: keep person safe, protect airway give sedative (diazepam,, lorazepam), cool body (cool compress, fan) Acute: BDZ, CP (BDZ + GTN). HTN (BDZ + Na nitroprusside) Use of BB controversial

Question 147

Summary of opioid use disorder

Answer 147

Complications: disease from shared needles, overdose (cardiac, resp depression), abscess, cellulitis, DVT, sepsis, IE, hep B+C, HIV, syphilis. Depressants Sx: Acute: CNS/ resp depression, pin point pupils, aspiration of vomit in overdose, constipation, anorexia + ↓ libido. Bradycardia. Slurred speech. ↓LOC, rhinorrhoea, watering eyes Withdrawal: begins around 6hrs after injection, peak 36-48hrs. extremely unpleasant, rarely life threatening. D/V, lacrimation + rhinorrhoea. Feverish, abdo cramps, aching joints, muscles. Shivering, tremors, yawning. ↑HR + BP, piloerection cause goose-flesh, pupils dilate. Needle track marks.

Question 148

Management of opioid use disorder

Answer 148

Harm reduction > sterile needles via needle exchange, vaccination, testing for blood borne viruses. Detox often takes 12 wks outpt, 28 days inpt. Drug dependence clinics, some GPs Methadone or buprenorphine first-line compliance monitored using urinalysis Naloxone: IV or IM for overdose, opiate antagonist. Immediate withdrawal. Naltrexone: opiate antagonist, blocks receptors + euphoric effects of opiates. Prevent relapse. Methadone: opioid for maintenance. Full agonist at opiate receptors, longer ½ life than heroin. Buprenorphine: sublingual partial agonist at mu receptor, blocking euphoric effect of heroin whilst preventing withdrawal Sx. Methadone + buprenorphine initially taken supervised, dose titrated until pt doesn’t experience withdrawal.

Question 149

Summary of tobacco dependence

Answer 149

Nicotine ½ life, 1-2hrs, smoke every 2hrs for steady state Sx: Tar-stained fingers Acute intoxication: abdo pain, pallor, headache, sweating, ataxia, HTN, ↑HR, tremors, fasciculations, seizures, resp failure, bradycardia Withdrawal: cravings, irritability, anxiety, anger, poor concentration, restless, impatient, ↑appetite + weight gain, insomnia. Management in pregnancy: Pregnancy: CBT, structured self help, motivational interviewing. NRT.

Question 150

Pharmacology of treatment for tobacco dependence

Answer 150

NRT: patches + another form eg gum, lozenge, spray. If high dependence. Single forms inadequate in past. SE: N/V, flu like Sx, headaches. Bupropion: noradrenaline + dopamine reuptake inhib. Nicotinic antagonist. 1-2 wks before target stop date. Seizures. CI in epilepsy, pregnancy + BF. Having an ED is relative CI. Varenicline: nicotine receptor partial agonist. 1 wk before target stop date. 12 wk duration. Monitored, only continued if not smoking. SE: nausea, headache, insomnia, abnormal dreams. CI in pregnancy + BF.

Question 151

Summary of LSD use

Answer 151

Tabs Ingestion can cause trips of up to 12 hrs Bad trip: panic, self aggression, suicidal/ homicidal ideation, hallucinations, mydriasis, HTN, tachycardia, flushing, sweating Pyrexia, hyperreflexia, paresthesia Variable subjective experiences, impaired judgement > injury, amplification of mood, agitation, withdrawn, psychosis. Nausea, dry mouth, tremors, drowsiness palpitations Complications: resp arrest, coma, hyperthermia, autonomic dysfunction, bleeding disorders. Supportive reassurance in calm, stress free environment, if ineffective BDZ

Question 152

Summary of ketamine use

Answer 152

Prevents brains awareness of pain Can severely harm themselves whilst hallucinating eg pulling out own teeth

Question 153

Summary of BDZ use

Answer 153

Complications: resp depression, coma, hypotension Can lead to tolerance/ dependence Feelings of calm + mild euphoria Hallucinations, slurred speech Paradoxical agitation Nystagmus, ataxia Withdrawal: may occur up to 3 wks after stopping. Insomnia, irritability, anxiety, tremor, loss of appetite, tinnitus, perspiration, perceptual disturbance, seizures. Management Activated charcoal Flumazenil: ↑ risk of seizure Supportive care

Question 154

Summary of ecstasy/MDMA use

Answer 154

Stimulant/hallucinogen ``` Empathy + closeness to others Chatty, dance relentlessly Bruxism (tooth grinding) N/V, sweating Agitation, anxiety, confusion, ataxia ``` Complications: Death due to hyperthermia + dehydration Rhabdomyolysis Tx: Supportive Dantrolene for hyperthermia if simple measures fail.

Question 155

Causes of serotonin syndrome

Answer 155

``` monoamine oxidase inhibitors SSRIs St John's Wort, often taken over the counter for depression, can interact with SSRIs to cause serotonin syndrome ecstasy amphetamines ```

Question 156

Features of serotonin syndrome

Answer 156

``` Neuromuscular excitation: clonus hyperreflexia, myoclonus, rigidity ANS excitement: hyperthermia, sweating Confusion Fast onset Dilated pupils ```

Question 157

Management of serotonin syndrome

Answer 157

supportive including IV fluids benzodiazepines more severe cases are managed using serotonin antagonists such as cyproheptadine and chlorpromazine

Question 158

What are personality disorders?

Answer 158

a series of maladaptive personality traits that interfere with normal function in life. It is thought that around 1 in 20 people have a personality disorder. They are typically categorised as belonging to one of three clusters: - A = odd or eccentric (paranoid, schizoid, schizotypal) - B = dramatic, emotional or erratic (antisocial, EUPD, histrionic, narcissistic) C = anxious and fearful (obsessive-compulsive, avoidant, dependent)

Question 159

Summary of paranoid personality disorder

Answer 159

Hypersensitivity and an unforgiving attitude when insulted Unwarranted tendency to questions the loyalty of friends Reluctance to confide in others Preoccupation with conspirational beliefs and hidden meaning Unwarranted tendency to perceive attacks on their character Need 4+ of: XS sensitivity to setbacks + rebuffs Bear grudges / unforgiving Suspicious, distort experience, misconstruing neutral/ friendly actions as hostile/ contemptuous Self-righteous Possessive/jealous of partner suspicion of sexual fidelity Self-importance Conspiratorial explanations of events/ hidden meaning Tx: Psychotherapy: improving social understanding, can be challenging due to trust issues CBT

Question 160

Summary of schizoid personality disorder

Answer 160

Overlap with neg Sx of schizophrenia schizoiD = distant Anhedonia ``` Indifference to praise and criticism Preference for solitary activities Lack of interest in sexual interactions Lack of desire for companionship Emotional coldness Few interests Few friends or confidants other than family ``` 4+ of Few activities pleasurable Emotional coldness, detachment, flat affect Limited capacity to affect feelings for others Indifferent to praise/ criticism Little interest in sex Solitary activities XS preoccupation with fantasy + introspection Doesn’t desire/ have any close friends Insensitivity to social norms/ if not followed, unintentional Tx: Psychotherapy: improve social understanding CBT Antidepressants

Question 161

Summary of schizotypal personality disorder

Answer 161

``` Ideas of reference (differ from delusions in that some insight is retained) Odd beliefs and magical thinking Unusual perceptual disturbances Paranoid ideation and suspiciousness Odd, eccentric behaviour Lack of close friends other than family members Inappropriate affect Odd speech without being incoherent ``` Tx: CBT Family therapy

Question 162

Summary of antisocial personality disorder

Answer 162

Failure to conform to social norms with respect to lawful behaviours as indicated by repeatedly performing acts that are grounds for arrest; More common in men; Deception, as indicated by repeatedly lying, use of aliases, or conning others for personal profit or pleasure; Impulsiveness or failure to plan ahead; Irritability and aggressiveness, as indicated by repeated physical fights or assaults; Reckless disregard for the safety of self or others; Consistent irresponsibility, as indicated by repeated failure to sustain consistent work behaviour or honour financial obligations; Lack of remorse, as indicated by being indifferent to or rationalizing having hurt, mistreated, or stolen from another Substance abuse disorders, overrepresented in prison Genetic, M>F, environmental >18, conduct disorder since <15 3+ of Doesn’t conform to norma, law, rules, obligations Callous unconcern for others Can’t maintain enduring relationships, though no difficulty establishing Low tolerance to frustration/ aggression/ violence Incapacity for guilt/ profit from punishment Blame others, or offer plausible rationalisation for behave. Tx: Behav not modifiable by adverse experience incl punishment Self help groups CBT

Question 163

Summary of EUPD

Answer 163

Efforts to avoid real or imagined abandonment Unstable interpersonal relationships which alternate between idealization and devaluation Unstable self image Impulsivity in potentially self damaging area (e.g. Spending, sex, substance abuse) Recurrent suicidal behaviour Affective instability Chronic feelings of emptiness Difficulty controlling temper Quasi psychotic thoughts Impulsive, 3+ of: Act unexpectedly, w/o thinking of consequences (don’t plan ahead) Quarrelsome behav + conflict esp when impulsive acts thwarted or criticised. Outburst of anger/ violence, can’t control Difficulty maintaining any course that offers no immediate reward Unstable + capricious mood Borderline 3+ of impulsive and 2+ of: Frantic avoidance/ fear of abandonment Unstable, intense relationships, sour over time. Disturbances in + uncertainty about self image, aims, preferences Self-destructive impulsivity Suicide/ self harm Feeling empty Anger management issues Transient paranoid thinking. Splitting: extreme perspectives completely good or bad. Tx: Antipsychotics Antidepressants Cog analytic therapy: look at way person thinks, feels, acts, events, relationships. Psychodynamic: way we see world develops through relationships in infancy/ childhood. DBT: mindfulness, distress tolerance, interpersonal effectiveness (how to ask for things + say no to people while maintaining self respect + relationships), emotional regulation

Question 164

Summary of histrionic personality disorder?

Answer 164

Inappropriate sexual seductiveness Need to be the centre of attention Rapidly shifting and shallow expression of emotions Suggestibility Physical appearance used for attention seeking purposes Impressionistic speech lacking detail Self dramatization Relationships considered to be more intimate than they are 4+ of Self dramatization, theatricality, exaggerated expression of emotion Suggestible, easily influenced Shallow, labile affect Seeking excitement, appreciation by other + being centre of attention Inappropriate seductiveness Over concern with physical attractiveness. Relationships, believed > actual intimacy. Lots of acquaintances few deep relationships. Speech, impressionistic + vague Egocentric, self-indulgence, lack of consideration for others Prone to picking fights. Tx: Psychoanalytic therapy

Question 165

Summary of narcissistic personality disorder?

Answer 165

Grandiose sense of self importance - requires attention Preoccupation with fantasies of unlimited success, power, or beauty Sense of entitlement Taking advantage of others to achieve own needs Lack of empathy Excessive need for admiration Chronic envy Arrogant and haughty attitude Tx: Lithium, SSRIs Psychoanalytic therapy Group therapy

Question 166

Summary of avoidant personality disorder

Answer 166

Avoidance of occupational activities which involve significant interpersonal contact due to fears of criticism, or rejection. Unwillingness to be involved unless certain of being liked Preoccupied with ideas that they are being criticised or rejected in social situations Restraint in intimate relationships due to the fear of being ridiculed Reluctance to take personal risks due to fears of embarrassment Views self as inept and inferior to others Social isolation accompanied by a craving for social contact 4+ of Persistent + pervasive feelings of tension + apprehension Belief 1 is socially inept, unappealing or inf to others XS preoccupation with being criticised/ rejected i Unwillingness to be involved with people unless certain of being liked. Restrictions in lifestyle due to need for physical security. Avoidance of social/ occupational activities that involve interpersonal contact because of fear of criticism, disapproval or rejectio Tx: BB SSRIs Psychotherapy, group therapy, assertiveness training

Question 167

Summary of obsessive compulsive personality disorder

Answer 167

Is occupied with details, rules, lists, order, organization, or agenda to the point that the key part of the activity is gone Demonstrates perfectionism that hampers with completing tasks Is extremely dedicated to work and efficiency to the elimination of spare time activities Is meticulous, scrupulous, and rigid about etiquettes of morality, ethics, or values Is not capable of disposing worn out or insignificant things even when they have no sentimental meaning Is unwilling to pass on tasks or work with others except if they surrender to exactly their way of doing things Takes on a stingy spending style towards self and others; and shows stiffness and stubbornness Ego-dystonic: anxiety, repetition of ritualistic actions, wishes they could stop Ego-syntonic: happy with how they are, don’t want to change 4+ of Preoccupation with details, rules, lists, order, schedule XS doubt + caution Perfectionism, interferes with task completion Conscientiousness + scrupulousness Preoccupation with productivity to exclusion of pleasure + relationships Rigidity, stubborn XS pedantry + adherence of social conventions Unreasonable insistence that others submit to their way of doing things, reluctance to allow others to do things. ``` Tx: SSRIs BDZ CBT Group therapy ```

Question 168

Summary of dependent personality disorder

Answer 168

Difficulty making everyday decisions without excessive reassurance from others Need for others to assume responsibility for major areas of their life Difficulty in expressing disagreement with others due to fears of losing support Lack of initiative Unrealistic fears of being left to care for themselves Urgent search for another relationship as a source of care and support when a close relationship ends Extensive efforts to obtain support from others Unrealistic feelings that they cannot care for themselves 4+ of Encourage others to make most of important decisions Subordinating needs to those of others on who they depend undue compliance with their wishes. Unwilling to make even reasonable demands on people they depend on Uncomfortable or helpless when alone because of fears of inability to care for self. Preoccupation with fears of being left to care for self Limited capacity to make everyday decisions w/o advice + reassurance. ``` Tx: SSRIs BDZ Psychotherapy Assertiveness training Insight orientated ```

Question 169

Causes/risk factors for ADHD

Answer 169

2%, M>F Causes: genes/ environment, ↓ dopamine/ norepinephrine, frontal lobe abnormalities Most children are diagnosed between the ages of 3 and 7; Prevalence is twice that of autism

Question 170

Sx of ADHD

Answer 170

Inattentive Careless mistakes, fails to pay close attention to detail Struggles to stay focuses, sustain attention in tasks or play Doesn’t appear to listen Doesn’t follow instructions Poor organisational skills Avoids mentally engaging tasks/ moves from 1 activity to another without completion Loses things, forgetful Easily distracted ``` Hyperactive Fidgets/ squirms Struggles to stay seated Struggles to keep quiet/ still Likes to keep moving/ on the go Talks before others finished/ interrupts, talks excessively Doesn’t like waiting, blurts answer before question finished Trouble waiting turn Runs, jumps, climbing, wandering ```

Question 171

Diagnosis of ADHD

Answer 171

>6 mnths <12 y/o, should be present by age 6/7 2+ settings 6+ of features. 5+ if >17. Connor’s rating scales: completed by child, parents + teacher to rate ADHD behavs Achenbach child behave checklist Edelbrock child attention problems rating scale Barley DuPaul ADHD rating scale Tests of attention + persistence: paired association learning test, continuous performance test. Classroom obs by clinician Drugs used are cardiotoxic so perform baseline ECG

Question 172

Management of ADHD

Answer 172

ten-week 'watch and wait' period should follow to observe whether symptoms change or resolve. If they persist then referral to secondary care is required > offers tailored plan of action drug therapy is last resort for those >5 mild/moderate - parents attending education and training programmes CBT, behavioural therapy, family therapy, appropriate school placement failure to respond or severe: - Methylphenidate is first line in children and should initially be given on a six-week trial basis. It is a CNS stimulant which primarily acts as a dopamine/norepinephrine reuptake inhibitor. Side-effects include abdominal pain, nausea and dyspepsia. In children, weight and height should be monitored every 6 months - If there is inadequate response, switch to lisdexamfetamine; - Dexamfetamine should be started in those who have benefited from lisdexamfetamine, but who can't tolerate its side effects. - 3rd line - guanfacine in kids (α adrenergic receptor agonist), atomoxetine in adults (inhibition of presynaptic norepinephrine reuptake) Drugs can cause appetite suppression/ insomnia. Drug holidays > weekends/ holidays, limit growth retardation. Only given to children >5.

Question 173

Causes/RFs for autism

Answer 173

M>F (3/4:1) Causes: genes, environment, obstetric complications, maternal rubella, tuberos sclerosis, down’s, fragile X, 50% of children with ASD have intellectual disability

Question 174

Sx of Autism

Answer 174

6 Sx, 2+ from 1, 1+ from 2 + 3 1) Social interaction Failure to use eye contact, gestures expressions, to reg social interaction Failure to develop peer relationships that involve mutual sharing of interests, activities, emotions Lack spont seeking to share enjoyment, interests or achievements with others. Play alone 2) Abnormalities in communication Delay/ total lack of development of spoken language, not accompanied by attempt to compensate through gestures/ mime. Failure to initiate/ sustain conversational interchange where there is responsiveness to communication of another. Stereotypes + repetitive use of language or idiosyncratic use of words/ phrases. Lack of varied make-believe play or social imitative play 3) Restricted, repetitive, stereotypes patterns of behav, interests Preoccupation with 1+ stereotyped + restricted pattern of interest, that is abnormal in content or focus or 1+ interest abnormal in intensity Compulsive adherence to specific, non-functional routines or rituals Stereotyped + repetitive motor mannerisms, finger flapping or twisting or complex whole body movements Preoccupations with part of non function elements of play materials eg odour, feel. also have higher head circumference to brain volume ratio ADHD and epilepsy also commonly seen

Question 175

Diagnosis of Autism

Answer 175

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

Question 176

What is Autism Spectrum Disorder

Answer 176

a neurodevelopmental condition characterized by qualitative impairment in social interaction and communication as well as repetitive stereotyped behaviour, interests, and activities.

Question 177

Management of Autism

Answer 177

Non-Pharmacological Therapy: Early educational and behavioural interventions: Applied behavioural analysis (ABA). ASD preschool program. Treatment and Education of Autistic and Communication related handicapped CHildren (TEACCH)/Structured Teaching method. Early Start Denver Model (ESDM). Joint Attention Symbolic Play Engagement and Regulation (JASPER). Social-communication - play based strategies, carers + teachers to increases attention, engagement + reciprocal communication in child. Support + advice National autistic society Speech + language therapy Treat comorbid problems eg epilepsy SSRIs ↓ repetitive stereotyped behav, anxiety + aggression Antipsychotics: ↓aggression, self injury Methylphenidate for ADHD

Question 178

What is conduct disorder?

Answer 178

a type of behavior disorder. It's when a child has antisocial behavior. He or she may disregard basic social standards and rules.

Question 179

Risk factors for conduct disorder

Answer 179

urban upbringing, deprivation, parental criminality, inconsistent + harsh parenting, maternal depression, FH of substance misuse. Social CD - peer group also share in antisocial behav. Unsocialised CD - rejected by other children, isolated/ hostile

Question 180

Features of conduct disorder

Answer 180

Persistent, aggressive/ harmful behav. Cruelty to people/animals. Freq/severe temper tantrums Argues with adults, defies rules Deliberately annoys people Blames others for mistakes/ behav Touchy/ easily annoyed, angry, resentful, spiteful, vindictive Lies or breaks promises to obtain goods/ favours, or avoid obligations Initiates fights Has used a weapon Despite parental prohibition often stays out after dark Delib sets fire with risk or intention of causing serious damage Steals objects of non-trivial value without confronting victim either within home or outside Commits crimes Forces another into sexual activity Bullies Breaks into someone’s house, building, car

Question 181

Management of conduct disorder

Answer 181

Focused on therapy not meds CBT, social skills training, anger management Family therapy Educational support Parental management training: reward good behav, deal constructively with neg behav

Question 182

What is a learning disability

Answer 182

Global impairment of intelligence, sig difficulties in socially adaptive functioning

Question 183

Causes of learning disability?

Answer 183

Antenatal: genes (PKU), FAS, drugs, smoking, rubella. Perinatal: neonatal hypoxia, birth trauma, hypoglycaemia, prematurity Postnatal: social deprivation, malnutrition, lead, meningitis, head injury

Question 184

Complications of learning disability's?

Answer 184

epilepsy, less freq health screening + preventative interventions (resp infection leading cause of death but flu vaccine levels lower than gen pop), diagnostic overshadowing, schizophrenia, depression. H pylori, CHD, hypothyroidism.

Question 185

Features of learning disability's?

Answer 185

Mild: IQ 50-69, mental age 9-12. Language reasonably good, development may be delayed. With support, can be independent, maintain good social relationships. Often undiagnosed + struggle. Mod: 35-49, mental age 6-9. Lang + cog abilities less developed, receptive better than expressive. ↓ self-care, limited motor skills. May need LT accommodation with family or in staff supported home. Severe: IQ 20-34, mental age 3-6. Marked impairment in motor function, little/ no speech, simple tasks can be performed with assistance. 50% have epilepsy. Family home or 24hr staffed home. Profound: IQ <20. Severely limited communication, self care, mobility, sig medical problems, high levels of support.

Question 186

Diagnosis of learning disability

Answer 186

Start before adulthood IQ testing Functional assessment of skills

Question 187

Management of learning disability

Answer 187

``` Modified approach to education Supported access to mainstream services Treat physical/ psychiatric comorbidity d CBT Carers ```

Question 188

What is Tourette's?

Answer 188

a condition that causes a person to make involuntary sounds and movements called tics

Question 189

What is Tourette's?

Answer 189

a condition that causes a person to make involuntary sounds and movements called tics Causes/RFs - Genes, dopamine + serotonin. FH, M>F, environment

Question 190

What are Tics?

Answer 190

rapid, repeated, involuntary movements/ vocalisations Simple: short, particular body part, blinking, throat clearing Complex: multiple simultaneous tics, self-hitting, swearing

Question 191

Features of tics?

Answer 191

Motor: repeat movement of others (echopraxia), obscene gestures (copropraxia) Vocal: repeating words/ phrases (echolalia), blurt out inappropriate lang (coprolalia) Tics recede when concentrating or doing something else. Voluntarily supressed with internal tension relieved by expression

Question 192

Diagnosis of Tourette's?

Answer 192

2+ motor tics, 1+ vocal tics, several times a day, nearly every day. 1+ yr from 1st tic, no tic free period of >3mnths Start <18

Question 193

Management of Tourette's?

Answer 193

Severe: topiramate Botox injections ↓ appearance of facial tics CBT, DBS Habit reversal training Reassurance + stress management Clonidine, guanfacine, methylphenidate. Antipsychotics.

Question 194

What is anorexia nervosa

Answer 194

a serious mental illness where people are of low weight due to limiting how much they eat and drink 10% mortality

Question 195

Types of anorexia nervosa

Answer 195

Atypical: AN Sx w/o LBW Restricting AN: loses weight by highly restricted food intake/ XS exercise. Hasn’t binged/ purged over last 3mnths Binge/purge AN: repeated binge/purge over last 3mnth

Question 196

Risk factors for anorexia nervosa?

Answer 196

F, western society, 16-22, FH, sexual abuse, dieting in fam occupational/ recreational pressure to be slim, criticism about weight or eating, parental overprotection, family enmeshment, perfectionism, high achiever, low self-esteem, obsessional traits, anxiety, BPD severe life stress.

Question 197

Predictors of poor outcomes for anorexia nervosa?

Answer 197

late age of onset, ill for several yrs at presentation (>6), disturbed relationship between family, premorbid obesity, very low body weight on admission, bulimic behav, M>F

Question 198

Symptoms of anorexia nervosa?

Answer 198

Fear of weight gain: restrictive food behav, purging, XS exercise, weight checks, food rituals. Distorted body image, influence of BW on self-evaluation, denial of seriousness of LBW. Fatigue, weak bones, dry/scaly skin, vit def, hair falls out, muscle low Easy bleeding/ bruising, poor CR Fainting, cold intolerance Preoccupation with food, people may cook elaborate meals for fam Laguno hair: body’s attempt to keep warm following fat loss. Enlarged salivary glands Pancytopenia, infections CVD: sudden death, bradycardia, hypotension, arrhythmias, mitral valve dysfunction, HF Constipation, abdo pain, ulcers, tears, vomiting, delayed gastric emptying > bloating, SMA syndrome Amenorrhoea, infertility, ↓libido AKI, CKD, renal calculi Osteoporosis, #, proximal myopathy Peripheral neuropathy, convulsions Suicide

Question 199

Diagnosis of anorexia nervosa

Answer 199

↓Cr, K, Na, Mg, Ca, Cl, Hb, WBCC, plt, urea, albumin, glucose, TFT/T3, FSH, LH, oestrogen, progesterone, ↑CK, GH, cortisol, cholesterol, amylase. β-carotene Nutritional hepatitis: ↓protein, ↑BR, LDH, ALP Sit up test: lay flat, ask to sit up without using hands Squat: ask person to squat + stand up without using hands. BMI: mild >17, mod 16-17, severe 15-16, extreme <15. Severe + needs urgent referral: rapid WL, >-0.5kg per wk, BMI <14, HR<40, BP <90/70, postural drop >10, unable to perform squat test, cold periph, <35°C, prolonged QT, T wave changes, purpuric rash.

Question 200

Management of anorexia nervosa?

Answer 200

For adults with anorexia nervosa, NICE recommend we consider one of: individual eating-disorder-focused cognitive behavioural therapy (CBT-ED) Maudsley Anorexia Nervosa Treatment for Adults (MANTRA) specialist supportive clinical management (SSCM). In children and young people, NICE recommend 'anorexia focused family therapy' as the first-line treatment. The second-line treatment is cognitive behavioural therapy. Careful weight gain 0.5-1kg per week motivational interviewing Feeding against will - MHA or children's act

Question 201

What is refeeding syndrome?

Answer 201

describes the metabolic abnormalities which occur on feeding a person following a period of starvation. It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism. The metabolic consequences include: hypophosphataemia hypokalaemia hypomagnesaemia: may predispose to torsades de pointes abnormal fluid balance can occur 4 days – 2wks after commencing feeding. These abnormalities can lead to organ failure.

Question 202

Who is at risk of refeeding syndrome?

Answer 202

Patients are considered high-risk if one or more of the following: BMI < 16 kg/m2 unintentional weight loss >15% over 3-6 months little nutritional intake > 10 days hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high) If two or more of the following: BMI < 18.5 kg/m2 unintentional weight loss > 10% over 3-6 months little nutritional intake > 5 days history of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids

Question 203

Management of refeeding syndrome?

Answer 203

NICE recommend that if a patient hasn't eaten for > 5 days, aim to re-feed at no more than 50% of requirements for the first 2 days.

Question 204

Pathophysiology of refeeding syndrome

Answer 204

Insulin secretion resumes, due to ↑blood sugar, ↑glycogen, fat, protein synthesis, requires P, Mg, K which are already depleted, stores rapidly used up, cells take electrolytes from serum.

Question 205

Features of refeeding syndrome

Answer 205

Peripheral oedema, arrhythmias, HF, convulsions, coma. ↓P, K, Mg (TdP), abnormal fluid balance.

Question 206

What is bulimia nervosa

Answer 206

People with bulimia are caught in a cycle of eating large quantities of food (called bingeing), and then trying to compensate for that overeating by vomiting, taking laxatives or diuretics, fasting, or exercising excessively (called purging).

Question 207

Risk factors for bulimia nervosa

Answer 207

arental/ childhood obesity FH dieting/ ED, severe life stress, abuse, MH disorder, substance abuse, parental high expectations, low care, over protection, criticism of eating habits + weight. Pressure to be thin eg occupation. Perfectionism, low self-esteem, obsessional traits, anxiety, BPD, 50% prev suffered AN.

Question 208

Features of bulimia nervosa

Answer 208

Repeated binge eating, compensatory behavs to prevent weight gain, belief body weight/ appearance crucial for self-worth Binge: loss of control Compensatory behav: vomiting, laxatives, diuretics, enemas, intense exercise, thyroxine or amphetamines, fasting/ restricting intake, diabulimia. Binge causes guilt/shame. Vomiting: enamel erosion, parotid gland swelling, bad breath, Russel’s sign (calloused knuckles > repeated abrasion against tetth in vomiting), stomach tearing, ↑HR. Bloating, fullness, lethargy, reflux, heartburn, sore throat Complications: DM, suicidal ideation, death, convulsions (↓Na), haematemesis, arrhythmias, renal impairment.

Question 209

Diagnosis of bulimia nervosa

Answer 209

``` ↓Cl, K, Na Met acidosis Repeated binge eating once a wk for >3mnth Mild: 1-3 compensatory behav/wk Moderate: 4-7 Severe: 8-13 Extreme: >14 ``` SCOFF questionnaire Do you make yourself Sick because you feel uncomfortably full? Do you worry that you have lost Control over how much you eat? Have you lost more than one stone in a 3 month period? Do you believe yourself to be fat when others say you’re too thin? Would you say food dominates your life? 2+ indicate ED.

Question 210

Management of bulimia nervosa

Answer 210

Careful weight gain <18 FT, CBT-ED >18 bulimia focused guided self help > CBT-ED High dose fluoxetine

Question 211

What is binge eating disorder?

Answer 211

People with binge eating disorder eat large quantities of food over a short period of time (called binge eating). Unlike people with bulimia, they don’t usually follow this by getting rid of the food through, for example, vomiting, though sometimes they might fast between binges. Find this distressing w/ loss of control no efforts to compensate for binge eating

Question 212

Features of binge eating disorder

Answer 212

Binges may be planned, purchase of special binge foods 3+ of: eating until uncomfortably full, eating large quantities when not hungry, eating faster than normal, eating alone due to embarrassment

Question 213

Diagnosis of binge eating disorder

Answer 213

2X wkly for 6 mnths

Question 214

Management of binge eating disorder

Answer 214

CBT-BED, evidence based self-help programme, interpersonal psychotherapy SSRI Change neg beliefs about body, identify binge cues, eat regular meals to avoid hunger. Avoid to not lose weight during Tx

Question 215

What is insomnia?

Answer 215

defined as difficulty initiating or maintaining sleep, or early-morning awakening that leads to dissatisfaction with sleep quantity or quality. This is despite adequate time and opportunity for sleep and results in impaired daytime functioning. Can be considered acute or chronic. Acute insomnia is more typically related to a life event and resolves without treatment. Chronic insomnia may be diagnosed if a person has trouble falling asleep or staying asleep at least three nights per week for 3 months or longer.

Question 216

Features of insomnia

Answer 216

ecreased daytime functioning, decreased periods of sleep (delayed sleep onset or awakening in the night) or increased accidents due to poor concentration. Often the partner's rest will also suffer. Nonrestorative sleep Enlarged tonsils/tongue, small jaw, retrognathia, lateral narrowing of oropharynx. important to identify aetiology of the insomnia

Question 217

Risk factors for insomnia

Answer 217

↑cortisol, ↓oestrogen/ progesterone, F>M, widowed, unemployment, increased age, low educational attainment, economic inactivity ``` Other risk factors include: Alcohol and substance abuse Stimulant usage Medications such as corticosteroids Poor sleep hygiene Chronic pain Chronic illness: patients with illnesses such as diabetes, CAD, hypertension, heart failure, BPH and COPD have a higher prevalence of insomnia than the general population. Psychiatric illness: anxiety and depression are highly correlated with insomnia. People with manic episodes or PTSD will also complain of extended periods of sleeplessness. ```

Question 218

Diagnosis of insomnia?

Answer 218

Problem initiating/ maintaining sleep, awakening early morning, can’t return to sleep Presence of risk factors >3 days/wk for >1mnth Sx cause functional impairment/ distress Focus extremely on sleep disorder, worry about neg consequences Not caused by substance/ med use Sx despite having enough time to sleep No underlying/ coexisting psychiatric or medical disorder than explains Sx. Actigraphy (non-invasive method for monitoring motor activity) Polysomnography (not routinely indicated, may be considered in patients with suspected OSA or periodic limb movement disorder, or when insomnia is poorly responsive to conventional treatment) Sleep diary

Question 219

Management of insomnia?

Answer 219

Improve sleep hygiene: regular sleep schedule, exercise (avoid 6hrs before bed), ↓alcohol, smoking, daytime naps + going to sleep hungry, wind down time. Milky drink Use bed only to sleep, remove bright lights, minimise noise, regular time to get up, no more than 1 hr variation. Comfy bed. Try to sleep for 20 mins then stop. Not to drive while sleepy. Relaxation therapy Only use hypnotics if daytime impairment is severe: BDZ: ↓sleep latency + awakenings in sleep. Only ST, high risk of addiction Antidepressants: trazodone, amitriptyline, mirtazapine. Z-drugs: zolpidem, zaleplon, zopiclone. Lowest effective dose for shortest period. Repeat prescriptions not usually given >55: modified release melatonin. Review after 2 weeks, and consider referral to CBT: sleep diary for 5-14 days, calculate total sleep time + efficiency. TST = total time in bed – time spent awake during night. SE = (TST X 100)/ total time spent in bed. 1st wk, spend same number of hrs in bed as average TST, when calculated SE for 5 nights >85% go to bed 15 min earlier, repeat wif remains >85%. Other sedative drugs (antidepressants, antihistamines, choral hydrate, clomethiazole and barbiturates) not recommended

Question 220

What is narcolepsy?

Answer 220

rare long-term brain condition that causes a person to suddenly fall asleep at inappropriate times. Early onset of REM sleep. Low levels of orexin (hypocretin) - protein responsible for controlling appetite and sleep patterns

Question 221

Causes of narcolepsy?

Answer 221

damage to orexin transporting neurons, AI or injury. Genes (HLA-DR2), low histamine levels. Infections. onset - teen years

Question 222

Features of narcolepsy

Answer 222

hypersomnolence - sleep intrudes wakefulness, fall asleep almost instantly cataplexy (sudden loss of muscle tone often triggered by emotion) sleep paralysis vivid hallucinations on going to sleep or waking up sleep brief but refreshing

Question 223

Diagnosis of narcolepsy

Answer 223

Recurrent sleepiness during day, >3X/wk, >3mnths 1+ of: cataplexy, hypocretin def, short REM sleep. Polysomnography Multiple sleep latency EEG

Question 224

Management of narcolepsy

Answer 224

``` SSRIs daytime stimulants (e.g. modafinil) and nighttime sodium oxybate ```

Question 225

What are night terrors?

Answer 225

episodes of screaming, intense fear and flailing while still asleep often paired with sleepwalking parasomnia - an undesired occurrence during sleep

Question 226

Causes/ RFs of night terrors

Answer 226

Past traumatic events, sleep deprivation, genetic, FH. 3-8y/o, discrete eps common, disorder rare RF: stress/fatigue, OSA, nocturnal seizures, fever, drugs e.g. lithium

Question 227

Features of night terrors

Answer 227

Intense fear at night, during deep non-REM sleep. Sharp scream, sits up, unresponsive, when woke, confused, no memory of eps. ↑HR, diaphoresis, RR during eps Difficulty arousing pts

Question 228

Management of night terrors

Answer 228

↓stress, follow night time routine, often resolves spont Education + reassurance Remove dangerous objects from bedroom, ↓risk of self injury Refractory: BDZ

Question 229

What is REM sleep behaviour disorder

Answer 229

is a sleep disorder in which you physically act out vivid, often unpleasant dreams with vocal sounds and sudden, often violent arm and leg movements during REM sleep — sometimes called dream-enacting behavior.

Question 230

Features of REM sleep behaviour disorder

Answer 230

Pt remembers dream. | Physically acting out dreams during sleep. Alert + orientated after waking.

Question 231

Management of REM sleep behaviour disorder

Answer 231

Remove dangerous objects from bedroom to ↓injury BDZ Melatonin receptor agonist

Question 232

What is nightmare disorder?

Answer 232

also known as dream anxiety disorder, is a sleep disorder characterized by frequent nightmares. The nightmares, which often portray the individual in a situation that jeopardizes their life or personal safety, usually occur during the REM stages of sleep.

Question 233

Risk factors for nightmare disorder

Answer 233

PTSD, stress, suddenly withdrawing REM suppressants can cause REM rebound.

Question 234

Features of nightmare disorder

Answer 234

Recurrent frightening dreams during 2nd ½ of sleep cycle (middle of night or early morning). Pt remembers dream, functional impairment or distress

Question 235

Management of nightmare disorder

Answer 235

Reassurance Imagery rehearsal therapy: modifying recurrent nightmare by writing it down, rehearsing new endings, make nightmares less frightening when they occur. Antidepressants if PTSD

Question 236

What is hypersomnia?

Answer 236

Excessive daytime sleepiness a condition where people fall asleep repeatedly during the day; sometimes in the middle of eating a meal or during a conversation.

Question 237

Causes of hypersomnia

Answer 237

F>M, 15-25, | Cause: genes, head trauma, viral infection, depression, dysthymic disorder with atypical features.

Question 238

Features of hypersomnia

Answer 238

XS sleep, ↓sleep quality Difficulty waking Drowsy when should be alert Sleep talking: REM sleep > pronunciation clear + understandable, in deep sleep mumbled + unintelligible.

Question 239

Diagnosis of hypersomnia

Answer 239

Recurrent period of sleep on same day/ 9hrs sleep that is non restorative/ impaired alertness after awakening Sx on >3 days/wk for >3mnth

Question 240

Management of hypersomnia

Answer 240

Regularly scheduled naps Exercise when becoming sleepy 1st line: modafinil or methyphenidate 3rd: atomoxetine

Question 241

What is restless legs syndrome?

Answer 241

a syndrome of spontaneous, continuous lower limb (B/L) movements that may be associated with paraesthesia. It is extremely common, affecting between 2-10% of the general population. Males and females are equally affected and a family history may be present complications - insomnia

Question 242

Causes of restless leg syndrome

Answer 242

50% of patients with idiopathic RLS ↓iron, dopamine, idiopathic, familial, peripheral Ns, chronic conditions, vit def, periph neuropathy, ESKD, DM (uraemia), CD, RA, IBD, anxiety, depression, PD, SC Dx, MS, TCA SSRIs, SNRIs, neuroleptics, lithium, metoclopramide, MDMA, BB, anti-histamines, pregnancy, obesity.

Question 243

Features of restless legs syndrome

Answer 243

uncontrollable urge to move legs (akathisia). Symptoms initially occur at night but as condition progresses may occur during the day. Symptoms are worse at rest paraesthesias e.g. 'crawling' or 'throbbing' sensations movements during sleep may be noted by the partner - periodic limb movements of sleeps (PLMS)

Question 244

Diagnosis of restless leg syndrome

Answer 244

Clinical diagnosis Bloods - ferritin to exclude iron deficiency anaemia may be appropriate Nerve conduction studies Polysomnogram: quantify periodic limb movement of sleep Needle electromyogram + nerve conduction studies: if polyneuropathy or radiculopathy suspected.

Question 245

Management of restless leg syndrome?

Answer 245

simple measures: walking, stretching, massaging affected limbs treat any iron deficiency dopamine agonists are first-line treatment (e.g. Pramipexole, ropinirole) benzodiazepines gabapentin

Question 246

What is amnesia?

Answer 246

refers to the loss of memories, such as facts, information and experiences

Question 247

Causes of amnesia?

Answer 247

Damage affects limbic structures (hippocampus, mamillary bodies, thalamus) Cortex, BG + cerebellum intact so procedural memory intact Head trauma, infection, neurodegen disease (AD/ dementia), thiamine def (WK synd, ↑demand for thiamine to metabolise alcohol, w/o, cells unable to metabolise glucose to ATP, metabolised as fat as pyruvate, converted to lactate > lactic acidosis, damage mamillary bodies, thalamus, hypothalamus), BDZ, brain tumour, ECT, hypoxia, encephalitis, LT heavy drug use, toxins eg lead, mercury, CO insecticides.

Question 248

Features of amnesia

Answer 248

Acute memory loss, profound anterograde loss, some retrograde Some pts confabulate Disturbances of time sense eg chronological sequences. May have personality change.

Question 249

Diagnosis of amnesia

Answer 249

MRI/CT: brain damage/ abnormalities, | Nutritional def/ inections

Question 250

Management of amnesia

Answer 250

Psychotherapy: occupational + cog therapies to enhance memory Often temporary Mobile phones + digital devices as work arounds to memory loss Parenteral thiamine

Question 251

What is delirium?

Answer 251

is a serious disturbance in mental abilities that results in confused thinking and reduced awareness of the environment start of delirium is usually rapid — within hours or a few days.

Question 252

Causes of delirium

Answer 252

Something physically wrong Trauma (head injury, burns), hypoxia (CV/resp), sepsis, encephalitis, liver/renal failure, electrolyte imbalances, Wernicke’s encephalopathy, ↑ICP (IC pathology), alcohol/ drugs (intoxication/ withdrawal), opiates, anticholinergics. ↑Ca. hypo/hyperglycaemia, dehydration. Change of environment, severe pain

Question 253

Risk factors for delirium

Answer 253

dementia, constipation, pneumonia, UTIs, renal impairment, hip #, post-surgery meds (opiates, BDZ), old age, substance misuse/ polypharmacy, malnutrition, >65

Question 254

Symptoms of delirium

Answer 254

``` ↓attention span, concentration Not fully aware of environment Disorganised/ delayed thinking Clouding of consciousness Disorientated, poor STM ``` Transient muddled delusions: diff to convey experiences. Impoverished, pressured or rambling speech. Sleep disturbed, insomnia/ reversal of sleep wake cycle Hyperactive: agitated/ aggressive, delusions/ hallucinations, wandering climbing in pts beds, pulling out catheters. Hypoactive: sluggish, drowsy, less reactive, withdrawn, lethargy, stupor, easily missed. Rapid shifts from hypoactivity to hyperactivity. ↑reaction time, startle reaction Nocturnal worsening of Sx Disturbing dreams + nightmares may continue as hallucinations or illusions after waking.

Question 255

Diagnosis of delirium

Answer 255

FBC, U+E, glucose, Ca, urinary test, sats, ECG, CXR, septic screen, LFTs, blood cultures, CT, EEG. Abbreviated mental test score: age, DOB, time (within 1 hr), where are we? (exact name of hosp), address, date of WW1, count back from 20, recognise ward staff, recall address. Score 1 for each correct answer, 10 in total. Objective evidence of cerebral/ systemic disease presumed to be responsible for clinical manifestations.

Question 256

Treatment of delirium

Answer 256

Treat underlying cause Haloperidol or olanzapine Small night dose of BDZ Make sure glasses + hearing aids used, encourage daily restraints Freq re-orientations (clocks, calendars) Good lighting: gloomy conditions ↑hallucinations + illusions. Avoid over/ under stimulation: side room, ↓XS noise. Minimise change: don’t keep moving pt, 1 staff member to engage pt shift, regular toileting ↑mortality, longer admission, higher remission. Some never fully recover to premorbid level. Careful reduction of Parkinson med may be helpful.

Question 257

What is mild cognitive impairment?

Answer 257

Set of Sx rather than specific disease Mild problem with 1 of: memory, reasoning, planning or problem solving, attention, language, visual depth perception, judgement May cause people to experience minor problems or need help with more demanding daily tasks (paying bills, managing meds) Decline in mental abilities greater than normal ageing + often caused by underlying illness. 10-15% of MCI progress to dementia

Question 258

What are symptoms of normal grief?

Answer 258

Disbelief, shock, numbness, feelings of unreality Anger, guilt Sadness, tearfulness Preoccupation with deceased Disturbed sleep + appetite. Seeing or hearing voice of deceased. Sx gradually ↓ with acceptance of loss + readjustment <12mnths Intensity of grief greatest for child, then spouse then parent

Question 259

What are symptoms of abnormal grief?

Answer 259

Very intense, prolonged, delayed/ absent, or Sx outside normal range (sometimes said to occur when more than 2 weeks passes before grieving begins) Preoccupation with feelings of worthlessness Thoughts of death Excessive guilt Marked slowing of thoughts/ movements Prolonged period of not being able to function normally (normal grief may take up to and beyond 12m) Halucinatory experiences (other than image/voice of deceased) more likely to occur in women and if the death is sudden and unexpected. Other risk factors include a problematic relationship before death or if the patient has not much social support.

Question 260

Management of grief?

Answer 260

Support groups BDZ of severe autonomic arousal or problematic sleep disturbance Antidepressants may be considered Counselling

Question 261

Model of grief

Answer 261

5 stages: Denial: this may include a feeling of numbness and also pseudohallucinations of the deceased, both auditory and visual. Occasionally people may focus on physical objects that remind them of their loved one or even prepare meals for them Anger: this is commonly directed against other family members and medical professionals Bargaining Depression Acceptance

Question 262

What is suicide and self-harm?

Answer 262

Suicide: any act that delib brings around ones death. Self-harm: physical injury to body, not resulting in death. Self harm may be: response to profound + overwhelming emotional pain. Coping mechanism. Temp relief of intense feelings, M>F, men more violent way

Question 263

What are causes of suicide/self-harm?

Answer 263

life events/stress (bereavements, abuse, neglect domestic violence), social class 1 + 5, social isolation (divorced, single, unemployed, living alone), stressful jobs with access to lethal.

Question 264

Risk factors for suicide/self-harm?

Answer 264

FH, prev suicide attempt, prev SH, depression, schizophrenia, substance misuse, PDs (EUPD), anxiety, recent discharge from psychiatric inpt care. Terminal/ chronic illness. Risk ↑ as depressed person begins to recover, gain motivation + energy.

Question 265

Protective factors against suicide/self-harm?

Answer 265

family support, having children at home, religious belief.

Question 266

Features of suicide/self-harm?

Answer 266

Impulsivity, low frustration tolerance, emotional dysreg (mood swings), binary thinking, cog rigidity problem solving deficits, maladaptive coping style, hopelessness

Question 267

What increases risk of suicide/self-harm?

Answer 267

careful planning, final act in preparation for death, isolation at time of act, precautions taken to prevent discovery, writing suicide note, definite intent to die (not just temp escape), believe method to be lethal, violent method, ongoing wish to die, regret attempt failed.

Question 268

Preventing suicide/self harm?

Answer 268

Prevention: limit pack sizes of paracetamol, install barriers at suicide hotspots, free telephone call to Samaritans, catalytic converters have ↓ suicide rates from inhaling car exhaust fumes. Promotion of good mental well being. Inform pts how to contact you + who to contact if you’re not available. Harm reduction: not sharing aids, learning basic 1st aid, cleaning skin

Question 269

Managing suicide/self harm?

Answer 269

Manage immediate risk, may require admission. Discuss alternative ways of dealing with painful moods/ stations. Distraction techniques, mood raising activities. Call friend/ support line. Avoid drugs/ alcohol. Squeeze ice cubes, snap rubber band around wrist, red food dye on dull side of knife

Question 270

What is dementia?

Answer 270

a term used to describe a group of symptoms affecting memory, thinking and social abilities severely enough to interfere with your daily life

Question 271

What are features of dementia?

Answer 271

Confuse day + night, get lost easily Memory loss: new info Disorientation: 1st time, then place, eventually person Diff handling complex tasks, conc, poor judgement. Visuospatial impairment Mirror sign: no longer recognise own reflection. Sun-downing: confusion worse in evening, ↑illusions in poor light + when tired. Behav: coarsening of social behav, personality/ mood changes, emotional lability, irritability, apathy hallucinations, sexual disinhibition

Question 272

Causes of dementia?

Answer 272

↑age, vascular, LBD, frontotemporal, PD, HD, DM, ethanol, environmental (CO), nutritional, infection, AD, chronic hepatic/renal impairment most common Alzheimers, then vascular, then LBD

Question 273

Diagnose of dementia?

Answer 273

>6mnths, cog impairment suffi enough to impair ADLs. Bloods to exclude reversible causes (e.g., hypothyroidism) > FBC, U+Es, glucose, TFTs, LFTs, Ca level, ESR/CRP, Vit B12, folate VDRL (neurosyphilis) Referred to old-age psychiatrists/memory clinics Montreal Cog assessment (MoCA), mini-mental state exam (MMSE). Mild: memory loss interferes with everyday activities, not incompatible w independent living. Complicated tasks can’t be undertaken. Mod: serious handicap to independent living. Only highly learned/very familiar material retained. New info retained only briefly. Unable to recall basic info about geog Severe: complete inability to retain new info. Only fragments of prev learned info remain. Fail to recognise even close relatives. Neuroimaging in secondary care to exclude other reversible conditions (e.g. Subdural haematoma, normal pressure hydrocephalus) and help provide information on aetiology to guide prognosis and management

Question 274

Management of dementia

Answer 274

Find out if still driving Identify/ modify triggers for difficult/ risky behav eg wandering, may be due to anxiety, boredom, hunger, needing toilet. Regular food or quiet environment Reminiscence therapy: talk about ‘old days’, enhances belonging, reinforces identity Multisensory therapy: as advances, speech lost, easier to respond to touch/ music

Question 275

What is Alzheimer's disease

Answer 275

Abnormal amyloid precursor protein degradation via β secretase. Cut into insoluble fragments > aggregate, β amyloid plaque. Signalling obstruction, neuronal apoptosis, ↑haem risk. Tau protein: pathologically hyperphosphorylated > aggregate, stop supporting microtubules, form neurofibrillary tangles, obstruct signalling, neuron apoptosis. Atrophy: neuron loss, cortex hippocampus affected early, temporal + parietal lobes later Cholinergic loss.

Question 276

Risk factors for Alzheimer's disease

Answer 276

age, F>M, FH, trisomy 21, APP gene (Chr21), presenilin 1 (gene 14) + 2 (Chr 1). ApoEe4, HTN, dyslipidaemia, cerebro vascular disease, altered glucose metabolism, brain trauma, smoking, XS alcohol, low IQ, poor education.

Question 277

Symptoms of Alzheimer's disease

Answer 277

Early: memory impairment, inability to acquire new info. Impaired reasoning, handling complex tasks, concentration/ motivation loss, diff making plans, poor judgement. Impaired visuospatial skills (judging difference, recognising steps), sleep disturbance. Interfere with work Intermediate: apathy, social disengagement, irritability, agitation aggression, wandering, psychosis, dyspraxia/apraxia (inability to carry out skilled tasks), impaired language (word finding deficit), remote memory loss seizure, motor signs (pyramidal signs) Advanced: complete dependence on others, urinary/faecal incontinence, gait disturbance Agnosia: recognition problems eg faces Aphasia: word finding problems

Question 278

Diagnosis of Alzheimer's disease

Answer 278

CT - sulci + ventricles enlarged (occurs in normal ageing, isn’t diagnostic).

Question 279

Management of Alzheimer's disease

Answer 279

No cure Acetylcholinesterase inhib: donepezil, rivastigmine, galantamine. Delay worsening Sx, doesn’t slow/ change overall rate of decline. Mild -mod. Memantine: advanced stages, NMDA antagonist, ↓XS glutamate. 2nd line. Antipsychotics only used for pts at risk of harming themselves or others, or when agitation, hallucinations or delusions are causing them severe distress Donepezil: CI in pts with bradycardia, AE > insomnia.

Question 280

What is Lewy body dementia

Answer 280

50-85y/o, more rapid decline than AD. α-synuclein protein with ubiquitin aggregation in neurons (cortex + substantia nigra) forming Lewy bodies (eosinophilic intracytoplasmic neuronal structures), apoptosis ↓neurons for signalling + ↓Ach + dopamine. Substantia nigra, paralimbic + neocortical areas.

Question 281

Features of Lewy body dementia

Answer 281

progressive cognitive impairment in contrast to Alzheimer's, early impairments in attention and executive function rather than just memory loss cognition may be fluctuating, in contrast to other forms of dementia usually develops before parkinsonism parkinsonism visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)

Question 282

Features of Lewy body dementia

Answer 282

progressive cognitive impairment in contrast to Alzheimer's, early impairments in attention and executive function rather than just memory loss cognition may be fluctuating, in contrast to other forms of dementia usually develops before parkinsonism parkinsonism visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen) Later: motor Sx mimic PD, resting tremor, stiffness, slow movement, ↓facial expression, shuffling gait, rigidity, falls. REM sleep behav disorder: sleep walking/ talking, restlessness, nightmares. ANS: orthostatic hypotension, syncope, urinary incontinence/ retention, constipation, impotence, transient LOC, diff swallowing.

Question 283

Diagnosis of Lewy body dementia?

Answer 283

Usually clinical Single photon emission computed tomography (SPECT) scan: dopamine transporter ligand ioflupane I-123 (DaTSCAN) shows ↓ transporter perfusion MoCA, MMSE Post-autopsy brain biopsy: LB in cortical neurons Can resemble delirium (due to fluctuating cognition with visual hallucinations) but don’t prescribe antipsychotics as extreme antipsychotic (neuroleptic) sensitivity in DLB can result in death.

Question 284

Management of Lewy body dementia?

Answer 284

both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer's. Dopamine analogue - motor Sx, L dopa neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism.

Question 285

What is frontotemportal dementia?

Answer 285

<65. Specific protein cellular inclusions, Tau proteins, TAR DNA binding protein 43, stop neuronal signalling, apoptosis in frontal/temporal lobe. Pick disease: Pick bodies (hyperphosphorylated Tau proteins), silver staining, frontal lobe, gliosis, neurofibrillary tangles, senile plaques.

Question 286

Features of frontotemporal dementia

Answer 286

<65 Insidious onset Relatively preserved memory and visuospatial skills Personality change and social conduct problems Behav: early change in personality, emotions. Frontal lobe. Disinhibition emotional blunting, apathy, hyperorality, sweet tooth, struggling with planning + organising. Stereotypical, repetitive, compulsive behav, impaired judgement 1° progressive aphasia: temporal, lang impairment, emotional disturbance (anxiety), word finding, impaired word comprehension, diff recognising sarcasm. ↓speech fluency, artic problems, phonological (organisation of sounds) + syntactical (sentence structure), grammatical errors. Semantic (loss of understanding of verbal/ visual meaning, diff naming + comprehension). Mutism. Speech fluent but converys no meaning Movement: similar to PD/ ALS, corticobasal synd (arms + legs uncoordinated/stiff). PSP. Later: cog decline, working memory, inability to learn new things, conc loss, visuospatial skills + planning.

Question 287

What is Pick's disease

Answer 287

Type of FTLD characterised by personality change and impaired social conduct. Other common features include hyperorality, disinhibition, increased appetite, and perseveration behaviours. Focal gyral atrophy with a knife-blade appearance is characteristic of Pick's disease. Macroscopic changes seen in Pick's disease include:- Atrophy of the frontal and temporal lobes ``` Microscopic changes include:- Pick bodies - spherical aggregations of tau protein (silver-staining) Gliosis Neurofibrillary tangles Senile plaques ```

Question 288

Diagnosis of frontotemporal dementia

Answer 288

MRI: unilat/bilat temporal atrophy, ventricle enlargement SPECT/perfusion-MRI/ PET: affected lobe hypometabolism, hypoperfusion Pick disease biopsy: pick bodies (round/oval, Tau-pos, neuronal cytoplasmic inclusions. Pick cells (swollen ballooned neurons) MoCA, MMSE Post-autopsy brain biopsy: microvacuolation, neuronal loss, swollen, myelin loss, astrocytic gliosis, abnormal protein inclusions Pick’s disease: focal gyral atrophy with knife-blade appearance Unlike AD: memory better for recent rather than remote events.

Question 289

Management of frontotemporal dementia

Answer 289

``` No cure Antidepressants: severe behav Sx Atypical antipsychotics have sig SEs Exercise, speech therapy, supervision Memantine + AChEi not recommended ```

Question 290

What is vascular dementia?

Answer 290

Multiple cerebrovascular events, cortical subcortical infarcts, chronic ischaemia Binswanger: large subcortical white matter area Cerebral a artherosclerosis, carotid a/ heart embolization, chronic HTN, vasculitis, TIA, haem stroke. Progressive, stepwise cog impairment (sudden as infarct occurs). Many tiny infarcts > more subtle deterioration. 2nd most common

Question 291

Risk factors for vascular dementia

Answer 291

RF: smoking, HTN, DM, ↑lipids, hyperhomocyteinemia, M, AF, FHx, hypercholesterolaemia, Hx of stroke/TIA, obesity, CHD Rarely, VD can be inherited as in the case of CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. Prevalence of dementia following a first stroke varies depending on location and size of the infarct, definition of dementia, interval after stroke and age among other variables. Overall, stroke doubles the risk of developing dementia. Incidence increases with age

Question 292

Features of vascular dementia

Answer 292

Several months or several years of a history of a sudden or stepwise deterioration of cognitive function. Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms The difficulty with attention and concentration Seizures Memory disturbance Gait disturbance Speech disturbance Emotional disturbance

Question 293

Diagnosis of vascular dementia

Answer 293

A comprehensive history and physical examination Formal screen for cognitive impairment Medical review to exclude medication cause of cognitive decline Carotid doppler: plaques ECHO: emboli Holter monitor: arrhythmias Focal neurological deficits NINDS-AIREN criteria: cog decline that interferes with ADL, cerebrovascular disease (neurological signs/ brain imaging), onset of dementia within 3mnths of stroke/ abrupt deterioration in cog functions/ fluctuating stepwise progression of cog deficits.

Question 294

Management of vascular dementia

Answer 294

No cure Vascular RF control: antihypertensives, antidiabetics, statins, antiplt agents Memantine/ AChEi: if suspect comorbid, AD, LBD Non-pharmacological management: Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication

Question 295

What is HIV dementia?

Answer 295

occurs when the HIV virus spreads to the brain 10% of HIV pts, prevalence ↑ with ↑survival rates. Behav changes + motor impairment

Question 296

Symptoms of HIV dementia

Answer 296

Early apathy + withdrawal, progress to subcortical dementia with ataxia, tremor, seizures, myoclonus, cog impairment, diff concentrating/ speaking. Depression, mania, psychosis, psychiatric problems

Question 297

Diagnosis of HIV dementia

Answer 297

MRI: cortical + subcortical atrophy, diffuse white matter signal changes

Question 298

What is CJD/Prion disease?

Answer 298

Rare Creutzfeldt-Jacob disease. rapidly progressive neurological condition caused by prion proteins. These proteins induce the formation of amyloid folds resulting in tightly packed beta-pleated sheets resistant to proteases.

Question 299

Features of CJD/Prion disease?

Answer 299

Rapidly progressing, neurological + psychiatric Sx. Dementia, myoclonus Sporadic/ familial. Mean age of onset 65 New variant: 25y/o, anxiety, withdrawal, dysphonia. Survival 13 mnths.

Question 300

Diagnosis of CJD/Prion disease?

Answer 300

Accumulation of abnormal prion > spongiform + amyloid changes in cerebrum, BG + cerebellum EEG: biphasic, high amplitude sharp waves MRI: hyperintense signals in BG + thalamus CSF usually normal

Question 301

What can long-term lithium use result in?

Answer 301

hyperparathyroidism and resultant hypercalcaemia

Question 302

Clozapine and seizure threshold?

Answer 302

Clozapine reduces seizure threshold, making seizures more likely

Question 303

What is delusional parasitises?

Answer 303

Patient with a fixed, false belief (delusion) that they are infested by 'bugs

Question 304

What is Capgras delusion?

Answer 304

psychiatric disorder in which a person believes that a friend or family member has been replaced by an identical imposter. This can occur in schizophrenia, but also may occur in organic diseases such as brain injury and dementia.

Question 305

What is Cotard's delusion?

Answer 305

fixed false belief that a person may hold where they believe that their body or body part is dead or dying. This can occur with severe depression and psychosis.

Question 306

What is Formication?

Answer 306

a type of paraesthesia in which it feels like insects are crawling on the skin.

Question 307

Use of SSRIs in pregnancy?

Answer 307

* BNF says to weigh up benefits and risk when deciding whether to use in pregnancy. * Use during the first trimester gives a small increased risk of congenital heart defects * Use during the third trimester can result in persistent pulmonary hypertension of the newborn * Paroxetine has an increased risk of congenital malformations, particularly in the first trimester

Question 308

Sx of SSRI discontinuation syndrome

Answer 308

Dizziness, electric shock sensations and anxiety

Question 309

Management of mania/hypomania in patients taking antidepressants

Answer 309

Consider stopping the antidepressants

Question 310

When do symptoms/seizures/delirum tremens occur after alcohol withdrawal?

Answer 310

* symptoms: 6-12 hours * seizures: 36 hours * delirium tremens: 72 hours

Question 311

What is catatonia?

Answer 311

Stopping of voluntary movement or staying still in an unusual position

Question 312

Acute stress disorder vs PTSD

Answer 312

Acute stress disorder is defined as an acute stress reaction that occurs in the 4 weeks after a traumatic event, as opposed to PTSD which is diagnosed after 4 weeks

Question 313

What is Hoover's sign

Answer 313

a quick and useful clinical tool to differentiate organic from non-organic leg paresis. In non-organic paresis, pressure is felt under the paretic leg when lifting the non-paretic leg against pressure, this is due to involuntary contralateral hip extension

Question 314

Are pseudo hallucinations a part of the normal grieving process?

Answer 314

Pseudohallucinations can form a part of the normal greiving process

Question 315

What is circumstantiality?

Answer 315

A circle comes back around eventually Circumstantiality can be a sign of anxiety disorders or hypomania.

Question 316

What is tangentiality?

Answer 316

A Tangent goes off forever in another direction

Question 317

What is derailment?

Answer 317

A derailed train goes off the track after a little while and needs to be nudged back on

Question 318

What is conversion disorder?

Answer 318

a psychiatric condition where psychological stress is unconsciously manifested as physical, neurological symptoms

Question 319

Key SFx of TCAs?

Answer 319

Urinary retention

Question 320

What is erotomania?

Answer 320

De Clerambault's syndrome presence of a delusion that a famous is in love with them, with the absence of other psychotic symptoms

Question 321

When to check lithium levels?

Answer 321

Lithium levels are normally measured one week after starting treatment, one week after every dose change, and weekly until the levels are stable. Once levels are stable, levels are usually measured every 3 months. When checking lithium levels, the sample should be taken 12 hours post-dose

Question 322

What is Othello syndrome?

Answer 322

This is a delusion of sexual infidelity on the part of a sexual partner.

Question 323

What is De Fregoli syndrome?

Answer 323

This is the delusion of identifying a familiar person in various people they encounter.

Question 324

What can be used to assess withdrawal severity?

Answer 324

The revised Clinical Institute Withdrawal Assessment for Alcohol (CIWA) scale can be used to assess alcohol withdrawal severity

Question 325

Common features of PTSD

Answer 325

* re-experiencing e.g. flashbacks, nightmares * avoidance e.g. avoiding people or situations * hyperarousal e.g.hypervigilance, sleep problems * Emotional numbing

Question 326

Avoid triptans when also taking...?

Answer 326

SSRIs

Question 327

Sudden onset psychosis following course of corticosteroids?

Answer 327

consider steroid-induced psychosis

Question 328

Features of obsessive-compulsive personality

Answer 328

rigid with respect to morals, ethics and values and often are reluctant to surrender work to others

Question 329

First-line treatment for acute stress disorder

Answer 329

trauma-focused cognitive behavioural therapy.

Question 330

Features of pseudodementia

Answer 330

some cognitive impairment, the key feature present is a global memory loss affecting both short and longer-term memory, over a short history problems with speech and language. lapses or loss of memory reluctance to engage with clinical assessment. recent loss loss of interest in activities social withdrawal difficulty paying attention, regulating emotions, organising or planning general fatigue