Mental Health

Question 1

Affect vs Mood

Answer 1

• Affect - now, where your at, objective
• Mood - more, so longer tone of mood.

Mood (Affective Disorders): Modo is best described in terms of a continuum rangin from severe depression to severe mania with normal and stable mood in the middle. These are divided into unipolar and bipolar affective disorders.

Question 2

What are mood (affective) disorders

Answer 2

Mood is best described in terms of a cont

Question 3

Unipolar affective disorders and the aetiology

Answer 3

Depressive episodes alone, but commonly recurrent.

Aetiology: multifactorial and composed of mixture of genetic and environmental factors

• Genetic: polygenic but no firm linkage (1st degree relative, monozygotic twins).
• Biochemical:
• Monoamines: depletion of NTs. Also suggested serotonin NT system downregulated.
  
  • Hypothalamo-pituitary-adrenal axis: exogenous steroids. Acute stress associated with rise in glucocorticoids. Severe depressive episodes linked with hypercortisolaemia
  • Brain derived neurotrophic factor: studies show this is reduced in stress and in lower in depressive illness. This normally promotes cell growth etc.
  • Neuroimaging changes: fMRI and PET revealed abnormalities in major depression in the brain. Non specific but regions with emotional and cognitive abnormalities.
  • Sleep: reduced time between onset of sleep and REM sleep and reduced slow wave sleep in depressive illness
  • Childhood traumas and personality
  • Social factors
  • Integrated model aetiology: stress predisposed -> changes in stress hormones…

Question 4

Bipolar affective disorder diagnosis, facts, mania symptoms

Answer 4

Bouts of depression and mania

ICD-10 F31 = Disorder characterised by 2+ episodes in which patients mood and activity levels are significantly disturbed, this disturbance consisting on some occasions of an elevation of mood and increased energy and activity and on others of a lowering of mood and decreased energy and activity.

• Bipolar I - 1+ manic or mixed episodes
• Bipolar II – depressive episode with at least one episode of hypomania (abnormal but no hospitalisation).
• Bipolar III – depressive episodes with hypomania only when taking antidepressant.

More common at younger age groups, 18th highest health condition in number of years lived with disability, 25-56% of those with it will attempt suicide at least nce and 50% recurrence within 12m of an episode. 2/100 lifetime prevalence.

Mania: Elevated mood, increased energy, feelings of well being, inflated self esteem (grandiosity), over-optimism, increased sociability, overfamiliarity, increased libido, decreased need for sleep, irritability, concelt and boolish behaviour, impairment of conc+attention, pressur eof speec, flight of idease, disinhibition, reckless behaviours (financial, seual, physical risk, self neglect), disruption ot normal levels ufnctioning, +/- delisions or hallucinations.

Question 6

OCD- Obsessive compulsive disorder: def, aetiology, management

Answer 6

ICD-10 = recurrent obsessional thoughts or compulsive acts, almost invariable distressing and patient often tries, unsuccessful to resist them.

• Clinical = functional and considerabel stress, ruminations and rituals
• Aetiology
  
  • 5-7% first degree studies.
  • Bio model - dysfunction in orbito-striatal area and dorsolateral prefrontal cortex, combined with abnormalities in serotonergic (underactive) and glutaminergic (overactive) neurotransmission.
  • Cognitive behavioural model – occasional intrusive thoughts develop into obsession causing greater anxiety and anxiety motivates suppression of these thoughts and ritual behaviours developed to reduce anxiety further.
• Management:
  
  • Psychological - CBT focusing on exposure and response prevention. Confront anxiety provokign stimulus to habituate the stimulus and reduce anxiety.
  • Physical. TCAs, SSRIs, deep brains timulation (of basal ganlia creating functional lesion), psychosurgery (for severe and non-responding - sterotacti techniques like subcaudate tractomy and cingulotomy with small radioactive implants to induce lesions in cingulate area or ventromedial quadrant of frontal lobe.
• Prognosis - 2/3 cases improve within year. prognosis worse when personality obsessional or anakastic and OCD is primary and severe

Question 7

How to Approach a disturbed or violent patient

Answer 7

Primary aims are the control of dangerous behaviour and establishment of a provisional diagnosis. 4 strategies may be needed: reassurance + explanation, medication, physical restrain and monitoring.

• Normally a reflection of underlying disorder and can portray suffering and fear.
• Verbal de-escalation: try defuse the situation by talking to them and it may be simple to correct
• Medication: Use oral first where possible Start with short acting benzodiazepine unless they are elderly or delirious. Give medications sequentially than together. Eg, Lorazepam, Haloperidol, promethazine, Haloperidol or Olanzapine
• Physical restraint: Use only to maintains safety and to administer IM medications. Should eb performed by adequately trained psychiatric nurses and security staff. In UK Drs are trained. Very dangerous especially for those on psychotropic med.
• Monitoring: Where medications are used, monitor BP, pulse, RR, O2 saturation dictated by level of ongoing agitation and consciousness.

Question 8

Types of drinkers in alcohol abuse

Answer 8

• Problem drinker – causes/experiences physical/ psychological an/or social harm because of drinking alcohol. Many are not physically addicted
• Heavey drinkers – drink significantly more in terms of quantity and/or frequency than is safe in the long term.
• Binge drinkers – excessive drinking in short bouts, usually 2-48h long, separated by often lengthily periods of absence and their overall months or weekly intake may be quite modest.
• Alcohol dependence – physical dependence on or addiction to alcohol. ‘alcohol dependence syndrome’.

Question 9

Blood alcohol levels and effect on your body

Answer 9

Amount of alcohol in units that contain about 8g of absolute alcohol and raise blood alcohol concentration by about 15-20mg/dl, the amount metabolised in 1hour.

• 20-99 blood alcohol conc (mg/dL) = impaired coordination, euphoria
• 100-99 = ataxia, poor judgement, labile mood
• 200-299 = marked ataxia and slurred speech, poor judgement, labile mood, nausea & vomiting
• 300-399 = stage 1 anaesthesia, memory lapse, labile mood
• 400+ = respiratory failue, coma, death

Question 10

Problems assoicated with alcohol abuse

Answer 10

• Psychological problems: Depression, anxiety, memory problems, delirium rtemens, attempted suicide, suicide, pathological jealousy
• Social: Domestic violence, marital and sexual difficulties, child abuse, employment problems, financial difficulties, accidents at home/road/work, delinquency and crime and homelessness

Question 11

Guidelines for alcohol and diagnostic markers

Answer 11

• Up to 21units week men, 14units women (No long-term health risk)
• 21-35 for men and 14-24 for women (Unlikely long-term damage if drinking spread)
• 36+ men, 24+ women (damage to health increasingly likely)
• 50+ men, 35+ women (definitive health hazard)
• Diagnostic markers: Elevated y-GT and MCV. Blood or breath alcohol tests also useful.

Diagnostic markers: Elevated y-GT and MCV. Blood or breath alcohol tests also useful.

Question 12

What is Alcohol dependance syndrome and the symptoms and diagnosis

Answer 12

Pattern of repeated self-administration that causes tolerance, withdrawal and compulsive taking. Usually develops after 10years ofheavy drinking (3-4women).

Symptoms: inability to limit or avoid getting drunk, spending lots time drinking, missing meals, memory lapses, restless without it, organising day around it, trembling after drinking, morning retching + vomiting, sweating excessively at night, withdrawal fits, morning drinking, increased tolerance and hallucinations.

Diagnostic (any 3): tremor/outstretch hands/tongue/eyelids, sweating, nausea/retching/vomiting, tahcycardia/hypertension, anxiety, psychomotor agitation, headache, insomnia, malaise or weakness, transient hallucinations or illusions and grand mal convulsions.

Question 13

Delerium tremens in relation to alcohol withdrawal

Answer 13

most serious withdrawal state 1-3days after alcohol cessation. Patients disorientated and agitated, have marked tremor and visual hallucinations. They also sweat, tachycardiac, tachypnoeic, pyrexial. Complications are dehydration, infection hepatic disease or Wernicke-Korsakoff syndrome.

Question 14

What is the aetiology of alcohol dependence

Answer 14

• Genetic factors – serotonin transported gene, dopamine2-receptor allele A1, alcohol dehydrogenase subtypes + monoamine oxidase B activity (not specific).
• Environmental factors – childhood maltreatments, history parental alcohol dependence or substance misuse.
• Biochemical – abnormalities in alcohol dehydrogenase NT substances + brain amino acids (eg GABA) but no conclusive evidence
• Psychiatric illness – uncommon but treatable. Some depressed (and those with anxiety) drink excessively to try raise mood
• Excess consumption in society - determined by prince, licensing laws, availability societal norms etc.

Question 15

Management of alcohol dependence and prognosis

Answer 15

Psychological:

• identify early: education on safe drinking, recommendation to cut down + simple support
• Motivation enhancement (therapy), feedback, education about A/Es and agreed goals. Pre-contemplation, contemplation, determination, action + maintenance.
• CBT + 12-step facilitation. Addictive drinking, self-help group therapy also helps long term maintenance. Family. Marital therapy might help too and Al-Anon.

Drug treatments:

• Alcohol; withdrawal + DTs: (no DTs can be outpatient). But generally admit, correct electrolytes + dehydration, parenteral thiamine, prophylactic phenytoin or carbamazepine if previous history of withdrawal fits. Give either diazepam or chlordiazepoxide orally. Additional benzodiazepine when symptoms/signs not controlled (but not for those still using)
• Prevention of alcohol dependence: Naltrexone (opioid antagonist), reduces risk relapse. Acamprosate acts on receptors (eg GABA, NA, serotonin) and some evidence it reduces drinking freq. neither particularly help maintain abstinence. Disulfiram react with alcohol to cause unpleasant acetaldehyde in toxification + histamine release. Orla thiamine can prevent Wernicke-Korsakoff syndrome in heavy drinkers.

Prognosis: research suggests 30-50% alcohol-dependent drinkers are abstinent or drinking vert much less up to 2years after traditional intervention.

Question 16

Differential diagnosis of anxiety disorders

Answer 16

• Psychiatric disorder – depressive illness, OCD, pre-senile dementia, alcohol dependence, drug dependence, benzodiazepine withdrawal.
• Endocrine disorders – hyperthyroidism, hypoglycaemia, phaeochromocytoma.

Question 17

What is generalised anxiety disorders

Answer 17

ICD-10 = anxiety generslised and perisstent but not restricted to, or even strongly predominating in, any environmental cirucmstanes

Clinical signs - Worried looking, tense posture, restless behaviour, pale + sweaty skin, nec + chest intermittent flushing, takes time to sleep and wakes intermittently with worry dreams. Also associated with hyperventilation and can breathe rapid and shallowly or sign deeply, especially when discussing stresses in their life.

Question 18

Mixed anxiety and depressive disorder

Answer 18

ICD-10 = when symptoms anxiety and depression both present but neither clearly predominant and doesn’t justify separate diagnosis.

Most common mood disorder in primary care, equal elements of anxiety and depression

Question 19

Phobic (Anxiety) Disorders

Answer 19

Intense fear triggered by a stimulus, or group of stimuli, that are predictable and normally cause no particular concern to others. This leads to avoidance of the stimulus. The patient knows that the fear is irrational but can’t control it.

Aetiology: May be caused by classical condition, in which a response (fear and avoidance) becomes conditioned to a previously benign stimulus, often after an initiating emotional shock. In children, phobias can arise through imagined threats. Women have twice the prevalence of phobias than men and phobias aggregate in families.\

• Agoraphobia – fear of market place so being away from home, with travelling, walking down road and supermarkets. Often associated with claustrophobia (fear of enclosed spaces).
• Social Phobia – fear of avoidance of social situations: crowds, strangers, parties etc and public speaking would be their worst nightmare
• Simple phobias – most commonly aracnophobia (spiders), particularly women.

Question 20

Management of Anxiety Disorders

Answer 20

• Pyshcological Management - for brief episodes discussing with doctor precipants is enough
  
  • Relaxation tehcniques (Mild/mod)
  • Anxiety management - verbal cues, mental imagery to link with symptoms, distraction
  • Biofeedback - showign patients they arent relaxed when cant see it as used to it . Include electrical reisstance of skin of palm, HR, muscle electromyography or breathing patten
  • Behaviour techniques - change behaviour + symptoms. Graded exposure
  • CBT - panic disorder/ GAD, identify mental ues that may provoke.
• Drug treatments - gradual cessation of anxiogenic rec drugs liek caffeine n alcohol too
  
  • Benzodiazepines - agonists of GABA but get sedation and mem problems and tolerance
  • SSRIs - smaller doses than for depression
  • Antipsychotics - severe or refractory cases
  • Beta-blockers - reduce peripheral symptoms like palps and tremors, tachycardia

Question 21

Acute stress reactions and ajdustment disorder

Answer 21

Types anxiety

• Acute stress reactions: severe but usually subsides in few days. Usually initial state of feeling ‘dazed’ or numb with inability to comprehend situation.
• Adjustment disorder: can follow acute stress and more prolonged (up to 6m) emotion reaction etc.

Question 22

Normal Grief VS Pathologila grief

Answer 22

• Expressed openly. Shock -> disbelief -> emotional phase (anger, guilt, sadness) and then acceptance and resolution. May take up to a year
• Pathological (abnormal) grief: excessive/ prolonged grief to even absent grieving with abnormal denial of bereavement.

Question 23

PTSD

Answer 23

Post-traumatic stress disorder: Protracted response to stressful event or situation of exceptionally threatening nature, likely to cause pervasive distress. Get flashbacks, insomnia, emotional blunting, anxiety, avoidance, emotional detachment and hypervigilance. Trauma focused CBT good and eye movement desensitisation and reprocessing good. Also SSRIs and venlafaxine.

Question 24

Features of Anxiety Disorders

Answer 24

• Pyshcological - spectrum of feelings from mild unease to terror, anticipatory anxiety, situational or exposure based anxity, may be free floating or generalised, may be experienced as apanic attack, specific to stimuli, fear of dying/loosing control/madness, derealisation o depersonalisation, reptitive intrusive thoughs or images (obsessions), may need to do compulsions.
• Somatic features - Muscular tension, sweting, trembling, palpitations, chest pain or abdo pain, choking sensations or difficulty breathing, dizziness or feeling faint.
• Functional impairment

Question 25

Facts an figures of anxiety

Answer 25

• ¼ will experience anxiety disorder at some point in their lives
• Most commonly adults between 35-55
• In any given week 8/100 people have mixed anxiety/depression in the UK
• In 2020, 37% of population reported high anxiety levels
• Incidence of anxiety in over 75s in 2020 was twice as high as 16-24s, previously always lower

Question 26

WHat is depression and the facts and figures (unipoalr) n dprognosis

Answer 26

Depressive disorders or ‘episodes; are classified by ICD-10 as mild, moderate or severe, with or without somatic symptoms. Severe depressive episodes are divided according to presence or absence of psychotic symptoms.

Facts and Figures for Unipolar depression:

• Incidence 4.4% in UK
• Leading cause of disability and premature death in those 18-44
• 1 in 5 adults, experienced some form of depression from January to March 2021 in UK- double that pre-COVID (increased 1 in 3 for those in financial difficulty.
• 43% women age 16-29 experienced symptoms of depression, 26% if men same age
• 39% of disabled adults compared to 13% none disabled.

Prognosis in Depression: Most recovered by 6m in primary care and 12m in secondary care. ¼ of those attending hospital will; have reoccurrence within 1year, ¾ reoccurrence within10years

Question 27

Features of Depression and screening

Answer 27

• Psycho/behavioural: Low mood, loss of interest + employment, reduced energy/lack motivation, poor conc, low self esteem/confidence, ideas of guilt, feelings worthlessness, pessimistic view of future, hopelessness, thoughts of self harm or suicide, irritability, indecisiveness, increased worries or anxieties, social iso, disruption to normal funcitoning, +/- psychotic symptoms (nihilistic delusions), _/- stupor- mue and unrepsonsive but conscious
• Physiological - Disturbed sleep (initial insomnia, early mornign waking), poor appetitie, motor retardation, constipation, heightened experience of pain, loss libido, menstrual cycle changes.

Screening:

• During the last month, have you often been bothered by feeling down, depressed or hopeless?
• During the last month, have you often been bothered by having little interest or pleasure in doing things?
• If one yes the assess further.

More frequent in those with: Physical diseases, social stres,s interpersonal dififuclties and lack f social support.

Question 28

Dysthymia

Answer 28

Mild to mdoerate depressive illness that lasts intemrittently for 2or + years with tiredness, low modd, lack of pleasure, low self-esteem and feleigns of discouragement. Mood relapses and remits.

Question 29

Seasonal affective disorder

Answer 29

recurrent episodes of depressive illness during winter months in northern hemisphere. Hypersomnia, increased appetite, weight gain, profound fatigue. Higher prevalence to also have bipolar. Evidence of bright light therapy in morning or early evening or SSRIs.

Question 30

Puerperal affective disorders:

Answer 30

• Maternity blues – brie episodes of emotional lability, irritability and tearfulness 2-3days postpartum and spontaneously resolve.
• Postpartum psychosis – usually within 2weeks after delivery Classical psychosis features and disorientation and confusion.
• Non-psychotic postnatal depressive disorders – 1st postpartum year especially within 3m. RFs are 1st preg, poor relationship with partner, ambivalence, emotional personality traits.

Question 31

DDx of depressive illnesses and invetsiagtions

Answer 31

DDx of depressive illness:

• Psychiatric – alcohol misuses, amfetamine misuse & withdrawal, borderline personality disorder, dementia, delirium, schizophrenia, normal and pathological grief.
• Organic (secondary) affective illness – cushing syndrome, thyroid disease, hyperparathyroidisim, corticosteroid treatment, brain tumour.

Investigations of Depressive Disorders:

• History (exclude DDx) which guides…
• FBC, U&Es, serum creatinine, eGFR, liver biochemistry, serum calcium, ESR/CRP, thyroid function tests
• Other: serum cortisol, antinuclear antibody, CXR, EEG or brain scan

Question 32

Management of depressive disorders

Answer 32

• Physical: cessation of drugs, regular exercise, antidepressants (acute increase in monamine activity through prveention or reuptake o enzymes of degredation) , adjunctive drugs, ECT
  
  • Recurrent episode (maintenance treatment), refractory depressive illness (switching classes or other agents), psychotic depression (antidepressant and antipsychotic or ECT) and depressive episodes in bipolar affective disorder (quetiapine or other mood stabilisers with SSRI)
  • Uncommon: transcranial magnetic stimualtion, psychosurgery occaisonal for severe intractabel depressive illness and everythign else failed, vagal nerve and deep brain stimualtion.
• Psychological: education and reg follow up, CBT (identify neg thoughts and link to logic), other indicated psychotherapies. interpersonal therapy (problem solving to find solutions), couple and family therapy.
• Social: financial, employment housing, young children, groups, OT, social workers, educational programs.

Question 34

*Antidepressants

Answer 34

• SSRIS-selective serotonin reuptake inhibitors (of monomaine serotonin 5-HT within synapse)
  
  • Less serious A/Es thn TCA (no weight gain), but can get nausea, vom, diarrhea, dry mouth, erectile dysf, loss libido, serotonin syndrome (2+drugs that icnrease serotonin to it and cause confusion, tremor, agitation, diarrhea, tachyc, prolonged QTc onterval).
  • If stopped suddently - discontinuation syndrome with shivering, anxiety, dizziness, ehadache, nausea etc.
• TCA - Tricyclic anti-D: Potentil aciton of monoamines, noraderenale and serotonin by inhibiting their reuptake into nerve terminals.
  
  • A/E - weight gain, antimuscarinic (tremor, contipation…), CV (QT prolongation, arrhythmias etc), convulsant activity, weight gain, sedation, mania.
  • Txic in overdose so not for those suicidal without monitoring.
• Serotonergic and noradrenergic anti-D:
  
  • Dual-acting agents (serotonin and NA reuptake inhibitors SNRIs): Venlafaxine (blocks serotonin and NA reuptake and at high doses affects dopamine transmission. Less sedation and fewer muscarinic effects. s/e= nausea, monitor for hypertension. Duloxetine similar.
  • Tetracyclics: Trazodone – serotonin antagonist and reuptake inhibitor used in anxiety and depressive disorders also insomnia. S/E= dizziness and postural hypotension and monitor BP
  • Mirtazapine: 5-HT2 and 5-HT3 receptor antagonist and potent a2-adrenergic blocker. Increases NA and selective serotonin transmission (NSSA). Can aid sleep and rarely causes sexual A/Es. Can be sedating in low dose and can cause weight gain. Uncommonly can cause agranulocytosis.
  • Noradrenaline reuptake inhibitors (NRIs): Reboxetine – good for antidepressant but also for panic disorder and attention deficit disorder. Can cause insomnia and antimuscarinic A/Es.
• Monomaine oxidase inhibitors:Irreversibly inhibit the intracellular enzymes monoamine oxidase A and B, leading to an increase of NA, dopamine and 5-HT in the brain. Rarely used as S/Es and can produce dangerous hypertensive reaction with foods with tyramine (cheese, red wines…) or dopamine (broad beans.) Also interact with drugs like pethidine and can cause liver damage sometimes.
• Reversible inhibitors of monoamine oxidase A: (RIMA) – moclobemide. Fewer A/Es than MAOIs and constitute low risk in overdose. Careful with foods with lots of tyramine
• Selective irreversible inhibitors of monoamine oxidase B: Selegiline – at higher doses looses specificity and inhibits MAO-A. More for Parkinson’s than depression as prolongs activity of levodopa.
• Melatonin receptor agonist and serotonin receptor antagonist: Agomelatine – agonist at melatonin MT1 and MT2 receptors. Weak antagonist at 5-H2c receptors. Does not affect uptake of serotonin, NA or dopamine.
• Antidepressant augmentation: If 2 trials have failed, add second concomitant drug like lithiu

Question 35

Classic monoamine hypothesis of depression

Answer 35

If the normal amount of monoamine NT activity becomes reduced depleted or dysfunctional for some reason, depression may ensue.

Question 36

**Antidepressants

Answer 36

• TCA: Block serotonin and NA reuptake, increasing noradrenergic and serotoninergic Neurotransmission. Eg amitriptyline
  
  • Amitryptyline, Lofepramine, Clomipramine, Dosulepin, Trazodone
  • Sedating, antimuscarinic effects, toxic in overdoses, quicker onset than SSRIs
  • Dosulepin highly cardiotoxic/fatal in overdose. Do not use as Lofepramine safest.
• SSRIs : blocks serotonin re-uptake, increasing serotonergic neurotransmission. Eg, cirtraline
  
  • Fluoextine, Sertraline, Citalopram Escitalopram, Paroxetine
  • May increase agitation/anxiety, sexual dysfunction, increased risk of GI bleeds, less sedating, safer in CHD and overdose
  • Es/citalopram cause QT prolongation.
  • WIthdraal syndrome with paroxetine
• SNRI (Serotonin/NA reuptake inhibitor) : Blok serotonin, NA and possibly dopamine reuptake, increasing serotonergic and noradrenergic Neurotransmission.
  
  • Venlafaxine, Duloxetine
  • Raise BP at higher doses, sexual dysfunction, toxic in overdose, non-sedating
  • Venlafaxine – SSRI action only up to 150mg/day, high risk of withdrawal effects
• NaSSa= (Noradrenaline and specific serotonergic antidepressant): Block re-synaptic a2-adrenoreceptors increasing NA and serotonergic neurotransmission. Eg, aptazapine
  
  • Mirtrazapine
  • Weight gain, sedation, safer in overdose
  • More sedating at lower doses
• MAOI ( mono-amine oxidase inhibitor) : Block enzymatic breakdown of NA, serotonin and dopamine and tyramine increasing neurotransmission. Eg Phenelzine.
  
  • Phenelzine, Tranylcypromine
  • Interaction with foods
  • Specialist use only
• Other: Agomelatine, vortioxetine. Both licensed of major depression only and can cause liver toxicity. Nice approved.

Be aware:

• All Ads are associated with risk of increased suicidal thoughts and ideation during first few weeks treatment
• Risk of hyponatremia due to inappropriate secretion of ADH – particularly in elderly with SSRIs

Question 37

Other indications for use of antidepressants

Answer 37

• Anxiety disorders: (SSRIs, venlafaxine)
• OCD (SSRIS, clomipramine)
• Panic disorder (SSRIs)
• Eating disorders (fluoxetine)
• Neuropathic pain (TCAs)
• Migraine prophylaxis (amitriptyline)
• Nocturnal enuresis (imipramine)

Question 38

*Antipsychotics

Answer 38

Based on major pathway (dopamine) ones in the brain. There are 4 (nigrostriatal, mesolimbic, neocortical and tuberoinfundibular pathways)

• Increase in dopamine causes positive symptoms of schizophrenia eg, mania.
• Deficit in dopamine causes negative and cognitive symptoms of schizoprohrenia eg, apathy, amotivation

First generation: Act predominantly by blocking dopamine D2 receptors. Not selective for any of the 4 dopamine pathways in the brain so cause a range of side effects eg, epse, elevated prolactin

• Oral = chlorpromazine, haloperidol. Trofluoperazine, sulpridie, pimozide
• Depot = Haloperidol, fliphenazine, flupentixol, zuclopenthixol

Second generation: Atypical ones, act on a range of receptors, including Serotonin receptors. More idstinct clinical profiles and side effects.

• Oral = amisulpride, aripriprazole, clozapine, olanzapine, quietapine, risperidone
• Depot = Risperidone, olanzapine, aripiprazole and laiperidone.

Clozapine = most effective antipsychotic but S/Es = Hypersalivation, hyperthermia, tachycardia, constipation, seizures, myocarditis, agranulocytosis.

• Mandatory blood monitoring for neutropenia and agranulocytosis (CPMS). Patients, prescribers, and pharmacies must be registered. Weekly for 18weeks, fortnightly for 34 weeks then 4-weekly. RAG system. Other drugs associated with agranulocytosis- chlorpromazine, aripiprazole, fluphenazine, haloperidol, olanzapine.
• Fatalities form bowel impaction.

For antipsychotics:

• Baseline ECG recommended and continued monitoring especially at dose changes. U&Es, FBC, lipid profile, Glucose, or Hba1c, TFTs, LFTs, prolactin, CK, weight, BP
• Clozapine is subject to mandatory blood monitoring is only available from specialist prescribers/ registered pharmacies.

Question 39

Antimuscarinics

Answer 39

• For antipsychotic-induced parkinsonism/EPSEs: Procyclidine, trihexyphenidyl, orphenadrine
• For hypersalivation – hyoscine hydrobromide – patches or sublingual tablets.

Question 40

Modo stabilisers

Answer 40

Drugs for bipolar and mania. Depression is recurrent episodes of low and bipolar is both low and high episodes outside of normal range.

• Acute phase – benzodiazepines (lorazepam short term), antipsychotics
• Long term – carbamazepine, valproate, lamotrigine, lithium

Lithium:

• Most effect long term
• Narrow therapeutic index – need to be prescribed by brand name
• Close monitoring: lithium levels (target 0.6-0.8 mmol/l) – weekly until stable then every 3m and take sample 12hours after last dose
• eGFR/U&Es, TFTs, weight, calcium- baseline then every 6m
• Signs of toxicity (>1mmol/l) – loss appetite, nausea, diarrhoea, muscle weakness/twitching, drowsiness, coarse tremor, ataxia
• Levels 0.6 mmol/l: check timing of sample and adjust dosage if correct and recurrent
• Interactions – NSAIDs, thiazide diuretics, ACE inhibitors.

Question 41

Hypnotics

Answer 41

• Benzodiazepines: Temazepam (short acting) = act on receptors associated with GABA an inhibitory transmitter. High potential for dependency
• Z drugs: Zaleplon, zolpidem zopiclone.
• Others = Promethazine (antihistamine), melatonin ((pineal hormone)

Question 42

Anxiolytics short term (as cbt/SSRIs long term)

Answer 42

• Benzodiazepines: Diazepam (long acting), lorazepam (short acting), chlordiazepoxide (alcohol detox, oxazepam for liver impairment)
• Others: Buspirone (low pot for dependency), pregabalin (antiepileptic licensed for GAD and neuropathic pain) and barbiturates which are no longer recommended.

Question 43

Dementia mendications

Answer 43

• Mild to moderate Alzheimer’s: Acetylcholinesterase inhibitors – donepezil (1st line) and rivastigmine/Galantamine (2nd line).
• Severe – or if AChei not tolerated then memantine (glutamine receptor antagonist)
• Behavioural and psychological symptoms: AChEis, memantine, antipsychotics, antidepressants, benzodiazepines

Question 44

Mmeory drugs

Answer 44

• Acetylcholinesterase inhibitors: prevents Ache from breaking down Ach. Licensed for midl to moderate Alzheimer’s.
• S/E = loss appetitie, nausea, vomiting, diarrhoea, dizzy, bradycardia, insomnia.

Question 45

Memantine

Answer 45

• NMDA.
• Blocks glutamate which causes cell damage.
• S/E = constipation, hypertension, dyspnoea, dizziness and best effects in BPDS.

Question 46

Psychiatry drugs and substance dpeendence

Answer 46

Question 47

WHta is used for rapid tranquilisation

Answer 47

NICE (NG10) and Trust recommendations

• Promethazine IM and/or
• Lorazepam IM and/or
• Haloperidol IM
• Others: Zuclopentixol acetate IM (accuphase)
• Rapid tranquilisation is used only with detained patients who present as a risk to themselves and/or others, who are refusing oral medications and for whom other de-escalation techniques have been unsuccessful.
• They are a last resort to ensure safety and require regular monitoring and full documentation.
• For all psychotropic medications, but mainly rapid tranquilisation, smaller doses should be given from older patients. BNF has specific guidance.

Question 48

CNS Stimulants and ADHD meds

Answer 48

• Methylphenidate, atomoxetine, dexamfetamine/lisdexamfetamine, guanfacine
• For ADHD causing severs impairment of learning and/or functioning
• In combo with psychological interventions
• Potential for misuse or diversion
• Can affect growth and physical development – monitoring of height and weight required
• CV effects so monitor pulse and BP.

Question 49

Electroconvulsive therapy (ect)

Answer 49

• In severe, life-threatening depressive illness, particularly when psychotic symptoms present/
• Under GA with passage of electric current across two electrodes applied to anterior temporal areas of the scalp to induce a seizure. The motoric seizure is less significant than its electrophysiological evidence. Normally 2x a week for 3-6weeks.
• Controversial but free of serious A/Es. Post-ictal confusion and headache not uncommon, and transient and short term retrograde amnesia and temporary defect in new learning can occur during weeks of treatment only.

Question 50

Why is the Mental health Law/Act used, and what are the laws.

Answer 50

Involuntary detention or commitment: admitting or keeping a patient in hospital against their will. Done in compliance with the MH legislation.

Laws for detention in general:

1. Individual detained must be suffering form defined mental disorder
2. Detention is for purpose of observation + refiement of diagnosis and/or to actively treat the disorder
3. Attempts to tret the individual on an outpatient basis have failed
4. The offer of a voluntary admission to hospital has been refused or impractical
5. Treatment in hospital is necessary: will benefit outcome of illness, protect patient and others from harm.

MH act: Legal framework for detailing and treating patients with psychiatric illness. Used when patients are unwilling or lack capacity to consent.

Mental health Act:

• Mental disorder of a nature or degree which makes it appropriate for them to receive treatment in hospital
• Risk to self or others
• Appropriate treatment must be available.

Exceptions in isolation (With no other additional mental disorder at risk): Dependence on drug or alcohol or learning disabilities

Question 51

Police sections

Answer 51

– common: Used by police if mental illness suspected and person needs immediate care or control for the interests of that person or protection of others.

136: Public place by the police- to take person from public place to place of safety which can be house or hospital. No warrant need and can be kept on this for 24hours which may be extended for additional 12 hours

135: Private address by police, allows police access to a private address without permission – including necessary property damage. Requires warrant from magistrate’s court. Also used to take patient to place of safety. Can be kept for 24hours which can be extended by 12hours.

Question 52

Sections under mental health act

Answer 52

• S2: Approved mental health practitioner AMHP(usually social worker) + 2 doctors. One doctor must have seen patient within 14days, one doctor must be section 12 approved. Admission from assessment and possibly treatment. Then doctors can’t determine treatment, type mental disorder and impact. Can be kept in hospital 28days and can’t be renewed. Treatment can be given against will but only mental health treatment unless MH disorder causes physical one like re feeding.
• Section 3: Admission for treatment, carried out like section2 but patient can be kept in hospital for 6m and this may be renewed. Patient may be treated without their consent for 3months, after this it requires approval by a second onion appointed doctor (SOAD) who will tell you what you can give them.
• Section 4: Emergency one, like section 2 but only when one doctor available at short notice. They should know the patient or be section 12 approved and this is very rare and should be avoided where possible. Must meet the criteria for other sections in addition to: Greater level of urgency needed to admit to hospital and finding another doctor would cause ‘undesirable delay’. Application can be made by approved mental health professional (AMHP) or nearest relative. Detention lasts for up to 72hours and not renewable but if second medical recommendation by hospital managers within this time can be converted to section 2.
• Section 5(4): Used to detain patient already in hospital. Trained mental health or LD nurses if no doctor available and only in psychiatric hospital. Can hold for up to 6hours to get doctor and cant be renewed.
• Section 5(2): Used to detain patient in hospital. This is doctors holding power F2 and above (fully registered Drs). This lasts for 72hours and can’t be renewed or extended. Written report must be submitted to hospital managers. If previous on 5(4) then 72hours from 5(4) started. Have to be admitted to a ward to 5(2) them so if in A&E and worried about someone then call police to try 136 them.
• Section 17: Temporary leave so patients can go home or somewhere for a bit. For observation. Used as stepping stone towards recovery and discharge.
• Section 117: (Aftercare)Patients detained entitled to help in community after discharge. This may include healthcare, social care and supported accommodation (financially supported).

CTO: Community Treatment Order: Where medication concordance a problem. Usually for those who have been treated before and then relapsed back into hospital. Legal power which means supervised treatment in community and if don’t meet conditions then may result in readmission to hospital. Clinician could then hold for 72hours in hospital till decide what to do. Full MHA assessment not required I CTO is converted back to section 3. May be challenged by patients/Nearest relative (legally defined) if they believe it is inappropriate.

Question 53

What is mental capscity and when to assess it

Answer 53

Mental capacity = ability to make decisions about all aspects of one’s life, including but not exclusively to healthcare.

• Every adult has right to make own decisions and assume to have capacity unless they don’t
• People must be supported as much as possible to make their own decisions before anyone concludes they cant
• People have the right to make what others might regard as unwise or eccentric decisions
• Anything done for on behalf of a person who lacks mental capacity must be done in their best interests with the least restrictive of their basic rights and freedoms.

When should it be assessed:

• Any assessment of a persons capacity must be ‘decision-specific’
• Must be about that decision at that particular time
• If someone can’t make complex decisions this does not mean they cant make simple ones
• Decisions about capacity must not be based on a persons age, appearance, condition or behaviour.

Question 54

how to assess mental capacity

Answer 54

1. Functional tests of capacity: to be able to make a decision about if they have mental capacity to make a particular decision, it must be first established whether there is an impairment of or disturbance in, the functioning of their mind or brain
2. Are they able to make a decisions: if there is then does the impairment/disturbance make them unable to make particular decision. They will be unable to make the decision, if, after all appropriate help and support to make the decision has been provided, he or she cannot:

• Understand information relevant to that decision
• Retain that information (for as long as needed to make decision)
• Use or weigh that info as part of process of making decision
• Communicate their decision.

If no capacity, then DOLS them. – deprivation of liberty safeguards.

If someone agrees to come into hospital but lacks capacity then it isn’t valid. As for consent need: free of coercion have capacity and it be informed consent.

Question 55

Risk assessing patients - what risks to think about

Answer 55

• Risk to self: Eg, suicide, self-neglect…Alcoholism
• Risk to others: Abuse to others
• Risk by others:
• Other:

Question 56

What is Panic disorder

Answer 56

Panic Disorder: ICD-10 = recurrent attacks of severe anxiety which are not restricted to any aprticular situation or set of circumstances and are unpredictable.

• Repeated, sudden attacks of overwhelming anxiety, accompanied by severe physical symptoms, usually related to both hyperventilation and sympathetic NS overactivity (palpitations, tremor, restlessness + sweating).
• These people often have catastrophic illness beliefs during the panic attack. Fear of stroke eg, linked to dizziness and headache.
• More common in first degree relatives of affected patients (same with GAD). This is linked to SNS overactivity, increased muscle tension and hyperventilation.
• Anxiety is the emotional response to threat of loss, whereas depression is response to loss itself.

Question 57

What is schizophrenia, aetiology and clinical festures

Answer 57

Schizophrenia: ICD-10 F20 = Characterized by fundamental and characteristic distortions of thinking and perception and affects that are inappropriate or blunged.

• Aetiology: No single cause identified. Schizophrenia likely to be due to neurodevelopment disconnection caused by an interaction of genetic and multiple environmental factors that affects brain and development. Daily cannabis use is a likely risk factor. Heritability of 60%.
• Clinical: Peak age early 20s. Diagnostic symptoms are auditory hallucinations, thought withdrwal, primary delusions, delusional perception, somatic passivitiy and feleings (feels thoughts etc controlled by others). Also behaviourl distrubances, secondayr delusions, hallucinations, blunting of mood.
  
  • Positive schizophrenia = acute onset, prominent delusions + hallucinations, normal brain structure, biochemical disorder involving dopaminergic transmission, a good response to neuroleptics and good outcome.
  • Negative schizophrenia = slow, insidious onset, relative absence of acute symptoms, apathy, social withdrawal, lack of motivation, underlying brain structure abnormalities and poor neuroleptic response.
  • Motor abnormlaities - catatonic behaviours (eg, negativism, posturing, mutism, waxy flexibility)
  • Emtional + social behaviour abn = apathy, blunting of emotional responses, social withdrawal, poor conc. Disruption to normal levels of functioning
• Chronic schizophrenia = long duration and by the the ‘negative’ symptoms of underactvitiy, lack of drivem, social withdrawal and emotional emptiness,

Question 58

Dirsorder of thoughts in Schizophrenia

Answer 58

• Disorder of Posession of thought: Thoucht echo, though insertion, thought withdrawl, though broadcasting.
• Disodrer of Form or Process of Thinking: Loosening of associations (derailment, thoughts arent logical process), circumstantiality, concreatness, incoherence, flight of ideas, neologisms (call it a word that isnt a word and doesnt make sense)
• Disorder of content of thought: Delusions (unsuual bizarre beliefs in many different forms- persecutory, grandiose-imppressive + imposing, external control/influence)
• Disorder of perceptions: Hallucinations - often 3rd perosna uditory but any sensory modality (perception of sitmulus in absence of stimulus)

Question 59

DDx diagnosis of schizophrenia and facts/figures

Answer 59

DDx Schizophrenia:

Distinguish from: Organic mental disorders (eg, partial complex epilepsy), modo (affective) disorders (mania), drug psychoses and personality disorders. In older patients any acute or chronic brain syndromes can present like schizophrenia but altered consciousness or memory problems don’t occur in schizophrenia and visual hallucinatiosn unusual.

Facts + Figures – Psychosis:

· Cannabis use has a 40% increased risk of psychotic illness

· Migration increase risk of psychotic illness 3x

· Parent with schizophrenia increases risk to child by 7.5x

· In 2014, 0.5% of people >!6yrs had a diagnosis of psychotic disorder

· 80% show some response to treatment in the first year

· 20% will have no further episode within 5years

· About 15% have treatment resistant psychosis two years after acute episode

Question 60

Management Schizophrenia + prognosis

Answer 60

Drug + social mixed is optimal.

• Antipsychotic (neuroleptic) drugs: block D1 and D2 groups of dopamine receptors, mostly useful in acute, positive symptoms. S/Es (motor, autonomic, antimuscarinic, metabolic) = acute dystonia, parkinsonism, akathisia, tardive dyskinesia, hypotension, failure ejaculation, dry mouth, urinary retention, constipation, blurred vision, weight gain, lots others like seizures, amenhorria… Watch for neurleptic malignant syndrome (tachy, pallor, fluctuating consciousness). Balance pregnancy not treating risk vs potential teratogenicity.
  
  • 1st gen antipsychotics typical: phenothiazines (chlorpromazine, trifluoperazine, fluphenazine decanoate) and Butryreophenomes (haloperidol- likely dystonia and s/e)
• Atypical Antipsychotics or serotonin dopamine antagonists: 2nd gen antipsychotics. Block D2 receptors less than D1 so fewer A/Es.
  
  • Risperidone: benzisoxazole derivative with compined dopamine D2 receptor and 5-HT2A- receptor blocking properties.
  • Olanzapine: has affinity for 5-HT2, D1, D2, D4 and muscarinic receptor sites. Weight gain problem
  • Clozapine – intractable schizophrenia and fail to respond to 2 conventional antipsychotic drugs.
• Psychological management – reassurance, support, good doctor patient relationship, Psychotherapy of intensive or exploratory kind contraindicated.
• Social management – attention being paid to patients’ environment and social functioning. Family education can help so not too much emotion expressed.

Prognosis: Variable with 15-25% people recover completely and about 70% relapses and may have moderate negative symptoms and about 20% remain seriously disabled.

Question 61

Psychological Treatments in psychiatry

Answer 61

Psychotherapy = ‘talking treatments’.

Types:

• Psychodynamic psychotherapy – regular time to think and talk about feelings. Discuss what is happening right now, what has happened and how the pats affect the now. They will help you make connections between past and present to show not all driven by thoughts the unconscious feelings from the past affect the present.
• CBT – combines challenging how you behave and what you believe and think.
• Family and marital therapy
• Cognitive analytical therapy (CAT) – used techniques and understanding from cognitive and psychodynamic approaches and commonly involves letters and diagrams in developing an understanding of your problems. They help you describe problems, looks at ways of coping and think of ways changing your ways of coping so you feel better
• Interpersonal therapy – for depression but used with others. Aims to help you understand how your problems may be connected to the way your relationship works. Then helps you find out how to strengthen your relationships and find better ways of coping.
• Mentalisation-based therapy and Dialectic behaviour therapy – mostly aimed at helping people with borderline personality disorder and is a mix of individual and group session
• Counselling – often in primary care short and aims you to be clearer about your problems and come up with your own answers. Tends not to aim to help you change as a person.
• Group therapy
• Therapeutic communities

Question 62

Risk assessment of a patient

Answer 62

The risk the patient poses to themselves and what they pose to others.

Main causes of disturbed behaviour: Drug in toxification (esp. alcohol), delirium, acute psychosis and personality disorder.

Question 63

Drugs of Misuse

Chornic misuses of drugs is mutlifactorial: availability drugs, vulnerbale perosnality, social pressures

Answer 63

• Inhaled substances – eg sniff solvents like glue. Tolerance develops weeks/months. Characterised by euphoria, excitement, floating sensation, dizziness, slurred speech and ataxia and acute intoxication can cause amnesia and visual hallucinations. Nitric oxide (laughing gas) is also common.
• Amfetamines + related – temporary stimulant + euphoriant effects followed by fatigue + depression. Can also produce paranoid psychosis. Ecstasy (MDMA) is amfetamine derivate with brief duration 4-6h and can give you malignant hyperpyrexia and dehydration leading to acute renal and liver failure.
• Cocaine – CNS stimulant. Prolonged use high doses can produce irritability, restlessness, paranoid ideation and sometimes convulsions. Persistent sniffinfgof the drug can case perforation of nasal septum. Overdoses cause death through MI, cerebrovascular disease, hyperthermia and arrhythmias.
• Hallucinogenic drugs – like LSD and mescaline produce distortions and intensifications of sensory perception and frank hallucinations in acute in toxification. Psychosis is long term complication.
• Cannabis – when smoked exaggerates pre-existing mood and has specific analgesic properties. An amotivational syndrome with apathy and memory problems have been reported in chronic daily use. It can also cause psychosis in right circumstances.
• Tranquilisers – barbiturates and benzodiazepines can cause dependence.
• Opiates – morphine, heroin, codeine, methadone, pethidine and fentanyl. Psychological effect are calm, euphoric mood and flattening of emotional response. Opiate withdrawal syndrome consists of a constellation of signs and symptoms that reaches peak intensity 2/3rd day after ad subside 7days. 12-16h after – yawn, rhinorrhea, pupillary dilation, sweating, restlessness etc and 24-72h is muscular twitches aches/pains, abdominal cramps, vomiting, diarrhoea, hypertension, insomnia, anorexia, profuse sweating, agitation.

Question 64

Management chronic misuse

Answer 64

Psychiatrist or drug misuse clinic if inpatient. It’s about helping them to live without drugs or regularise and control use to prevent secondary ill health. If they can tmanage abstinence they may be managed with oral methadone. In the uK only spcialised licensed Drs can prescribe heroin and cocaine for maintenance treatment of addiction. Overdose should be treated immediately with naloxone.

Question 65

Drug induced Psychosis

Answer 65

Reported with amfetamine and derivates and with cocaine and hallucinogens. More so chronic misuses.

Characterised with vivid hallucinates (usually auditory), misidentifications, delusions, psychomotor disturbances and abnormal affect. ICD-10 needs condition to occur within 2weeks and usually within 48hours of drug use, persisting for more than 48h but not more than 6m. Evidence suggests risk is raised in those using cannabis at an early age and on daily basis.

Question 66

SUicide and parasuicide

Answer 66

Suicide increases with Male, older, living alone, immigrant status, recent bereavement, unemployment, FH MH problems, previous MH problems, substance abuse, sever edepression…

Assessment: Concerning if clear cause for attempt, if it was planned, suicide note, taken measures to not be discovered, would they do it again. Explore in all and refer to psychiatrist for depression, psychotic illness, pre-planned, persistent intent, violent method.

Parasuicide = Apparent attempt at suicide, commonly called suicidal gesture here the aim is not death. Eg, sublethal drug overdose or wrist slash. This is a predictor of suicide.

Question 67

Taking an alachol history

Answer 67

1. ​Open consultatin
2. Screening - CAGE questionare. Cut down, annoyed you, bad or guilty feeling, eye opener (dirnk in morning to calm nerves)

• Audit C - how often, units, etc. AUDIT is more detailed.
• FAST - shorter AUDIT for a and e.

1. Details of alcohol intake
2. Assess impact of alcohol
3. Effect on daily living
4. PMH
5. Drug history
6. Social history
7. Psychological assessment
8. Closing ocnsultation

Question 68

Psychiatric exam

Answer 68

• Presenting complaint
• History of presenting complaint
• Past Psychiatric History – If any past episodes think about what, when, who was involved and the outcome.
• Past medical history
• Family medical and Psychiatric History: Genetic component to lots of conditions and risk with completed suicide within the family.
• Person History: Include Early development, childhood behaviour, schooling, occupational, sexual, relationships and marriage, children, forensic (any contact with the police)
• Current social circumstances: employment, financies, houing, relationships, life events.
• Substance use: drugs and alcohol. Think what & how, when & how often, what happens if they stop and associated behaviours.
• Pre-morbid Personality. Include: Character, hobbies/interests, aims&aspirations, relationships, mood, stressors.
• Medication History: Consider past and current medication and compliance. Also think about allergies

Question 69

Define and perform a Mental State Examination (MSE) using recognised headings / terminology

Answer 69

• Appearance and behaviour
• Speech: rate, tone, volume, quality & quantity of info
• Mood: Subjective/objective. Mood is depressed, labile etc and affect is flattened, restricted…
• Thought: content, form and flow
• Perceptions: hallucinations and types.
• Cognitions: orientation to time and date
• Insight: do they think there is a problem and if so what. What do they need?

Question 70

Psychiatric formulation

Answer 70

Question 71

Assessing cognitive function in patient with memory problems - MMSE

Answer 71

MoCA test is good for finding mild cognitive impairment. MMSE better for more serious cognitive problems.

MoCA- can detect short term memory visuospatial abilities, executive functions, attention/ concentration and working memory, language and orientation to time and place. It can uncover cognitive impairment associated with some of the most debilitating is disorder eg Alzheimers, Huntingtons.

MMSE: Mini mental state exam: Commonly used set of questions for screening cognitive function. Provides measures of orientation, registration (immediate memory), short-term memory and language functioning

• 25-30/30 = normal
• 21-24 = mild
• 10-20 = moderate
• <10 = Severe impairment

Question 72

Eating Disorders (EXTRA)

Answer 72

Obesity – Most common. Combo constitutional and social factors.

Anorexia nervosa:

• Onset usually adolescence with previous history of faddish eating. Generally eats little, yet is obsessed by food and exercise is excessive.
• Criteria = body weight>15% below standard or BMI<17.5, self induced weight loos, avoidance fattening foods, vomiting, purging, exercise or appetite suppressants. Distortion of body image, morbid fear of fatness and amenorrhoea in women.
• Consequences = sensitivity to cold, constipation, hypotension, bradycardia. If they binge then hypokalaemia and alkalosis.
• Aetiology = Genetic (siblings), hormonal (reductions in sex hormones and down reg of HPA axis), individual psych factors and family problems. Social and cultural factors.
• Management – outpatient unless severe weight loss and marked C signs and or electrolyte and vitamin disturbances. CBT, interpersonal psychotherapies. Vits and minerals may need replacement.
• Prognosis – fluctuate course, with exacerbations and partial remissions.

Bulimia Nervosa: Episodes of uncontrolled excessive eating which are termed ‘binges’ accompanied by means to lose weight. Preoccupation with food and habitual behaviours to avoid fattening effects of periodic binges. Eg, self induced vomiting or misuses of drugs like laxatives. Individual CBT and SSRIs.

Atypical Eating disorders: Binge eating disorders (discrete episodes significant over eating combined with sense of having no control over eating 3m+).

Question 73

Sexual disorders (extra)

Answer 73

Sexual dysfunctions – affecting sexual desire (low libido), impaired sexual arousal (erectile dysfunction, failure of arousal in women), affecting orgasm (premature ejaculation, retarded ejaculation, orgasmic dysfunction in women)

• In men = repeated inability to achieve normal sexual intercourse
• In women = repeatedly unsatisfactory quality of sexual satisfaction.
• Medical conditions affecting sexual performance – DM, Hyper/Hypothyroidism, Angina, previous MI, cirrhosis, chronic kidney disease, neuropathy, spinal cord lesion, asthma, COPD, depressive illness, substance misuse.
• Drugs affect sexual arousal

Sexual deviations – Variations of sexual object (fetishism, transvestism. Paedophilia, bestiality, necrophilia), variations of sexual act ( exhibitionism, voyeurism, sadism, masochism, frotteurism).

More so unusual forms of behaviour and doctors likely involved when behaviour breaks the law and when there is a question of an associated mental or physical disorder.

Genetic role disorders – (transsexualism) – disturbance in gender identity where patient convinced body is wrong gender. More evidence this is biologically determined.

Question 74

Organic mental disorders

Answer 74

Result from structural pathology, as in dementia or from disturbed central nervous system function as in fever induced delirium

Delirium = (toxic confusional state and acute organic psychosis) is an acute or subacute brain failure in which impairment of attention is accompanied by abnormalities of perception and mood. Develops over short period and fluctuates with disturbance of consciousness and cognition. Extremes of age, damaged brail, dislocation to unfamiliar environment, sleep deprivation, sensory extremes, immobilisation, and visual/hearing impairments predispose. Review drug therapy, nurse, rehydrate. Usually clears within few weeks

Question 75

Personality Disorders:

Answer 75

Enduring patterns of behaviour that manifest as inflexible response to broad range of personal and social situations. Developmental conditions that appear in childhood/ adolescence and continue nto adult life.