MH Flashcards
What is bipolar disorder?
chronic mental health disorder characterised by periods of mania/hypomania alongside episodes of depression
What are the two types of bipolar disorder?
type I disorder: mania and depression (most common)
type II disorder: hypomania and depression
What is mania?
there is severe functional impairment or psychotic symptoms for 7 days or more
What is hypomania?
describes decreased or increased function for 4 days or more
Treatment of bipolar?
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
Co-morbidities associated with bipolar?
2-3 times increased risk of diabetes, cardiovascular disease and COPD
Primary care referral of bipolar?
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
When to use ECT in bipolar patient?
1st line Tx if severe/ life threatening manic episode.
What is lithium toxicity?
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
What can precipitate lithium toxicity?
dehydration
renal failure
drugs - diuretics (esp thiazides), ACEi/ARBs, NSAIDs and metronidazole
Features of lithium toxicity?
coarse tremor (a fine tremor is seen in therapeutic levels) hyperreflexia acute confusion polyuria seizure coma
Management of lithium toxicity?
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
What is schizophrenia?
Is the most common psychotic disorder. Requires symptoms to be present most of the time for 1 month of more.
ICD-10 for schizophrenia
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.
Risk factors for schizophrenia?
Family history is strongest Black Caribbean ethnicity Migration Urban environment Cannabis use
First rank Sx of schizophrenia
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)
Epidemiology of Schizophrenia
Peak early 20s
M>F
Pathophysiology of schizophrenia?
Pos Sx: XS dopamine in mesolimbic tracts
Neg Sx: ↓dopamine in mesocoritcal tracts.
Catatonic Sx of schizophrenia?
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.
Seven subtypes of schizophrenia?
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
Features of Schizophrenia?
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.
Positive Sx in schizophrenia
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
Negative Sx of schizophrenia
Flatt affect Alogia: poverty of speech, lack content Avolition: ↓motivation Apathy, anhedonia ↓in self care, social withdrawal
Management of schizophrenia
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
MOA of typical antipsychotics
block post synaptic D2 receptors.
Chlorpromazine, haloperidol
MOA of atypical antipsychotics
block D1 >D2. Fewer extrapyramidal SE. risperidone, olanzapine (weight gain, DM), clozapine (agranulocytosis), quetiapine, aripiprazole, amisulpride
Use of clozapine in schizophrenia
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
Side effects of typical antipsychotics?
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)
Risks of using antipsychotics in elderly patients
^ risk of stroke
^ risk of VTE
Side effects of atypical antipsychotics?
Metabolic:
- weight gain
- clozapine - agranulocytosis
- hyperprolactinaemia
- olanzapine - higher risk of dyslipiademia and obesity
Factors associated with poor prognosis of schizophrenia?
strong family history gradual onset low IQ prodromal phase of social withdrawal lack of obvious precipitant
Monitoring required for use of antipsychotics?
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
What is delusional disorder?
Persistent delusions, 1+ over 1 mnth not meeting other criteria for schizophrenia.
Hallucinations may occur
Affects day-to-day functioning
Treatment of delusional disorder
Antipsychotics
Antidepressants
What is schizoaffective disorder?
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.
Treatment of schizoaffective disorder?
Antidepressants Antipsychotics Dialectic behav therapy Mentalisation therapy Transference focused therapy
What is schizoprehniform disorder?
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.
What can cause psychosis?
Schizophrenia Depression: psychotic depression, more common in elderly pts. Puerperal psychosis Brief psychotic disorder: Sx <1 mnth. Neurological: PD, HD CS, cannabis, phencyclidine
Sx of psychosis
Hallucinations
Delusions
Alogia: little info by speech
Tangentiality: answers diverge from topic
Clanging
Word salad: linking real words incoherently > nonsensical content
ICD-10 for depression
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.
What is depression?
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.
Epidemiology of depression?
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
Risk factors for depression?
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.
Core Sx of depression
Depressed mood: most of day, lack responsiveness to circumstances.
Anhedonia: ↓pleasure
Fatigue/ low energy
Other Sx of depression
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.
Screening for depression?
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
Management of Persistent subthreshold depressive symptoms or mild to moderate depression
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
Management of unresponsive, moderate and severe depression
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
Adverse effects of antidepressants
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
Pharmacology of SSRIs
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
Pharmacology of TCAs
amitriptyline, imipramine, clomipramine
SFX - drowsiness, dry mouth, blurred vision, constipation, urinary retention, lengthening of QT interval.
Interactions - adrenergic neurone blockers (clonidine, guanethidine)
Pharmacology of Mirtazapine
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
Pharmacology of MAOIs
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
Side effects of ECT
loss of STM, retrograde, headache, temp confusion, loss of LTM, personality changes, loss of skill.
What is premenstrual dysphoric disorder?
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
Diagnosis of premenstrual dysphoric disorder?
Mood changes <1 wk before menses, >5 Sx resolving within 1wk post menses
Sx affect day to day life
Management of premenstrual dysphoric disorder?
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
What is seasonal affective disorder
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.
What alternative causes and medications can cause anxiety?
- hyperthyroidism, cardiac disease and medication-induced anxiety
- salbutamol, theophylline, corticosteroids, antidepressants and caffeine
What is GAD?
Anxiety generalised, persistent + not restricted to any circumstances.
Who is most likely to suffer from GAD?
F>M, 45-59, martial/ sexual disturbance, stressful life event unemployment
Symptoms of GAD?
> 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)
What is GAD-2 screening?
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.
Management of GAD?
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
Drug treatment of GAD
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
What is panic disorder?
Recurrent spont panic attacks, sudden intense fear, reach peak 10 mins, don’t last longer 20-30 mins.
Risk factors for Panic Disorder
F>M, 15-24 + 45-54
widowed, divorced, city, limited education, early parental loss, abuse.
Genes: ADOR2A, CCK, COMT
Symptoms of panic disorder
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
Diagnosis of panic disorder
> 4 Sx, not restricted to any particular situation, unpredictable.
Behav change to avoid further attacks.
Management of panic disorder
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
What is agoraphobia
Fear, avoidance of places where escape difficult, e.g., crowds, public places, travelling alone/ away from home.
Bimodal peak: 15-35 + older
Diagnosis of agoraphobia
> 6mnths
2+ Sx in feared situations, 1+ occasions. 1 Sx must be autonomic.
Recognises fear excessive
Treatment of agoraphobia
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.
What is pathophysiology behind phobias?
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)
Sx of phobias
> 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
Treatment of phobias
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
Sx of separation anxiety
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
Treatment of separation anxiety
SSRIs
BDZ
CBT: gradually exposing child to separation, challenging unhelpful beliefs.
Sx of social anxiety/phobia
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
Diagnosis of social anxiety
> 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
Treatment of social anxiety
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
What is OCD?
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
Symptoms of OCD
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
Diagnosis of OCD
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?
Management of OCD
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
What is ERP?
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
Poor prognostic indicators of OCD
given in to compulsions, longer duration, early onset, M, tics, bizarre compulsions, hoarding, symmetry, comorbid depression, delusional beliefs, over-values ideas + PD
Good prognostic indicators of OCD
good premorbid social + occupational adjustment, a precipitating event, episodic symptoms, less avoidance.
What is body dysmorphic disorder?
Obsessive belief appearance is flawed. Can cause compulsive behavs eg XS grooming
Genetic, 5HT
Tx = CBT, SSRI
Sx of physical and sexual abuse?
Bruising, cuts, sores, burns or rashes Broken bones, damage to organs FTT Anxiety, depression, PTSD, aggression, fear towards sexual activity, suicide. STIs, UTIs
What is acute stress disorder?
defined as an acute stress reaction that occurs in the first 4 weeks after a person has been exposed to a traumatic event
Features of acute stress disorder
intrusive thoughts e.g. flashbacks, nightmares
dissociation e.g. ‘being in a daze’, time slowing
negative mood
avoidance
arousal e.g. hypervigilance, sleep disturbance
Management of acute stress disorder
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
When does acute stress reaction occur?
Onset: immediate or within mins
Duration: 0-72hrs
Partial/complete amnesia of event
Sx of acute stress reaction
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
What is adjustment disorder
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.
What is PTSD?
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.
Risk factors for PTSD
F>M, ↓education, SES. ↓ self-esteem/ neurotic trats. FH/ PMH of MH, prev traumatic events, trauma severity, peri traumatic dissociation
Protective factors for PTSD
M, white, high IQ, SES, chance to view dead body.
Sx of PTSD
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
Diagnosis of PTSD
Sx within 6 mnths of traumatic event or present for at least 1 mnt
Management of PTSD
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.
What are medically unexplained symptoms?
Extended periods of physical Sx w/o evidence of organic cause
Risk factors/ causes of MUS?
F>M
Genetics, cultural + family attitudes, stressful LE, insecure attachment, childhood neglect + abuse. Cog overinterpreting physical Sx as disease, central pain mechanism.
Maintaining factors of MUS?
unnecessary investigations + opinions, untreated anxiety or depression, 2° gains.
Features of MUS?
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
Diagnosis of MUS?
> 1 Sx, distress in other areas of life, lasts > 6mnths
Rule out organic cause
What is hypochondriasis?
pts believe have specific illness eg cancer rather than presenting with inexplicable Sx.
What is somatisation?
multiple, recurrent + freq changing Sx for 2+yrs, no organic cause. Pt refuses to accept reassurance or neg test results
What is conversion disorder?
unconscious converting of psychological stressor into physical illness. Loss of motor/ sensory function
What is factitious/Munchausen’s disorder?
deliberate production of Sx to relieve medical Tx
What is malingering?
feigning Sx to obtain external reward.
Management of MUS?
Treat psychiatric comorbid illnesses’: anxiety /depression Full history + exam. Explain + reassure. Avoid over-investigation, unnecessary referrals. Encourage normal function SSRIs CBT Graded exercise
What is chronic fatigue syndrome?
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,
Diagnosis of CFS?
> 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.
Treatment of CFS?
Graded exercise Pacing of activity, realistic goals. CBT improves fatigue + physical functioning Low dose antidepressants/ amitriptyline Referral to pain clinic
What is somatoform autonomic dysfunction?
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
Diagnosis of somatoform autonomic dysfunction?
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
What is Persistent somatoform pain disorder
Persistent, severe + distressing pain for 6+ mnths, continuous on most days, can’t be explained by physiological process or organic Sx.
What is dissociative disorder?
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
Sx of depersonalisation/ derealisation disorder?
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.
Sx of dissociative amnesia?
memory loss, usually centred on traumatic event, unable to recall significant info about self eg childhood home.
Sx of dissociative fugue?
confused about identity, starts sudden travel/ wandering. Partial/complete amnesia for journey.
Sx of dissociative convulsions?
absence of tongue biting, bruising + incontinence
Sx of dissociative identity disorder?
only 1 evident at a time, each has own memories, preferences/ behav patterns. Overt (aware of identity shifts, struggles to manage), covert (unaware).
Management of dissociative disorders
Memory aids
SSRIs
Pathophysiology of substance use disorders?
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.
Sx of substance use disorders?
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
Diagnosis of substance use disorders?
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
Predisposing factors for alcohol use disorder?
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.
Sx of acute alcohol intoxication
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.
Sx of alcohol withdrawal
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
