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Specialties > Psychiatry Pt. 2 > Flashcards

Psychiatry Pt. 2 Flashcards

1
Q

What is suicide?

A
  • Any act that deliberately brings about own’s death
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2
Q

What is self harm?

A
  • Any act intentionally causing physical injury to the body, but not resulting in death
  • Although some of these may represent attempted suicide, many have little or no suicidal intent and may have very clear alternative reasons for their actions.
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3
Q

What are some methods of self harm?

A
  • Self-cutting
  • Burning
  • Poisoning (overdose)
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4
Q

What age groups are at a higher risk of suicide?

A
  • It is the second most common cause of death in men aged 15-24 years after RTA
  • Men are 3-4 x more likely to die by suicide in the UK than women (because they tend to use more violent methods (e.g. hanging, shooting))
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5
Q

What are social causes of suicide?

A
  • Life events and stress
    • This can be recent life events (e.g. bereavement)
    • Childhood adversity can increase risk of suicide later on
  • Social class
    • Social classes I and V are at highest risk of suicide
  • Social Isolation
    • More common if isolated, divorced, widowed, single, unemployed or living alone
  • Occupation
    • Higher rates in vets, pharmacists, dentists, farmers and doctors
    • Likely to be due to increased access to lethal means (e.g. drugs/firearms)
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6
Q

What are mental health causes of suicide?

A
  • NOTE: 9/10 people who die by suicide have a major mental illness at the time of death
  • Previous suicide attempt
    • Lifetime risk 10-15%
    • Previous suicide attempt is the strongest predictor of eventual suicide
  • Previous self-harm
    • Lifetime risk 3-5%
    • Up to 60% of people who commit suicide have self-harmed
  • Depression
    • Lifetime risk 15%
    • Up to 80% of people who die by suicide are depressed
    • Depressed patients with the following factors are at particularly high risk of suicide:
    • Older
    • Single
    • Have previously self-harmed
    • Experience recurrent suicidal thoughts
    • Suffer insomnia
    • Weight changes
    • Feel extremely hopeless, worthless or guilty
  • Schizophrenia
    • Lifetime risk 10%
    • Suicide risk is particularly high in young ambitious patients with insight into the severity of their diagnosis
  • Substance misuse
    • Alcohol dependence carries lifetime risk of suicide of 3-4%
  • Personality disorder
    • Up to 50% of people who die by suicide have a personality disorder
  • Other factor
    • Physical health problems (chronic, painful and terminal illness)
    • Family history
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7
Q

What are some suicide prevention strategies?

A
  • Limited pack sizes of paracetamol
  • Installing barriers at suicide hotspots and providing a free telephone service (e.g. Samaritans)
  • Catalytic converters in cars
  • NOTE: charity for family of suicide victims: survivors of bereavement by suicide (SOBS)
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8
Q

What is the difference between self-harm and attempted suicide?

A
  • Self-cutting is the most common form

- Self-harm is often performed to release tension that builds up as emotions build and patients feel a sense of pressure

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9
Q

What are the reasons for self-harm?

A
  • Avoiding more dangerous self-harm or suicide
  • Self-punishment
  • Suicide attempt
  • Substituting psychological distress with physical pain
  • Overcoming numbness
  • To change intolerable situations (often relationship issues)
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10
Q

Which age groups is self harm more likely with?

A
  • Children and adolescents
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11
Q

What is self harm associated with?

A
  • Affective disorder and personality disorder
  • Patients who had a traumatic or abusive childhood may find it difficult to reflect and think through emotional experiences, meaning that they can only be dealt with through action
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12
Q

What is the physical treatment for self-harm?

A
  • Overdoses
    • Activated charcoal (decreases intestinal absorption of some substances (e.g. antidepressants))
    • Antidotes (e.g. N-acetylcysteine for paracetamol overdose)
  • Lacerations
    • Superficial cuts: sutures or Steristrips
    • Plastic surgery for deep cuts
    • Adequate analgesia should be given
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13
Q

What is the risk assessment for self-harm/suicide?

A
  • Thoughts about hurting themselves again
  • Thoughts of hurting others
  • Thoughts of being hurt by others
  • Specific features of increased risk:
    • Careful planning
    • Final acts in anticipation of death (e.g. writing wills)
    • Isolation at the time of the act
    • Precautions taken to prevent discovery (e.g. locking doors)
    • Writing a suicide note
    • Definite intent to die
    • Believing the method to be lethal (even if it wasn’t)
    • Violent method (e.g. shooting, hanging, jumping in front of a train)
    • Ongoing wish to die/regret that the attempt failed
  • If the patient is insistent on leaving you need to ASSESS THEIR CAPACITY
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14
Q

What are immediate interventions for self-harm/suicide?

A
  • If at high risk of suicide and lacking capacity, they need to be admitted to a psychiatric ward for their own safety
  • Patients at lower risk may be managed at home (depending on home circumstance (e.g. if they have a supportive family))
  • A plan should be made to deal with future suicidal ideation or thoughts of self-harm
    • Who they will tell
    • How they will get help (e.g. coming straight to hospital)
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15
Q

What are follow-up interventions for self-harm/suicide?

A
  • Follow-up within 1 week of the self-harm or discharge from the inpatient ward
  • This could be:
    • Community mental health team
    • Outpatient clinic
    • GP
    • Counsellor
  • Underlying disorders (e.g. depression) should be treated
    • SSRIs are safest for depression but prescriptions should be short and reviewed regularly to prevent stockpiling for overdose
  • Psychological therapies
    • CBT-based therapies (e.g. dialectical behaviour therapy)
    • Mentalisation-based treatment
    • Transference-focused psychotherapy
  • IMPORTANT: 30% of suicides occur within 3 months of discharge from psychiatric wards
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16
Q

What are coping strategies for self-ham/attempted suicide?

A
  • Distraction techniques
  • Mood-raising activities (e.g. exercise, writing)
  • Strategies to decrease or avoid self-harming
    • Put tablets and sharp objects away
    • Avoid self-harm triggering images (e.g. photos online)
    • Stay in public places or with supportive people when tempted to self-harm
    • Call a friend or support line
    • Avoid drugs and alcohol
    • Squeeze ice cubes
    • Snap a rubber band around their wrist
    • Bite into something strongly flavoured (e.g. lemon)
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17
Q

What are the categories of substance misuse?

A
  • Intoxication
  • Harmful use
  • Dependency
  • Withdrawal
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18
Q

What is intoxication?

A
  • A transient state of emotional and behavioural change following drug use. It is dose-dependent and time-limited
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19
Q

What is harmful use?

A
  • A pattern of use likely to cause physical or psychological damage
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20
Q

What is dependency?

A
  • A cluster of physiological, behavioural and cognitive symptoms in which the use of a substance takes on a much higher priority than other behaviours that once had greater value
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21
Q

What is withdrawal?

A
  • A transient state occurring while re-adjusting to lower levels of the drug in the body
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22
Q

What are the theories of dependence?

A
  • The theories of dependence are a combination of classical conditioning (cravings become cues which trigger drug-seeking behaviour) and operant conditioning (a drug providing pleasure will be used again)
  • There is also a social learning theory - we learn by copying the behaviours of others (peer pressure)
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23
Q

What is the neurobiological model of substance misuse?

A
  • All drugs of abuse affect the dopaminergic (reward) pathway
  • This starts in the ventral tegmental area and projects to the prefrontal cortex and limbic system
    • Prefrontal cortex - role in motivation and planning
    • Dopamine release in the nucleus accumbens causes a sensation of pleasure (reward)
  • Cocaine and amphetamines block dopamine reuptake, thereby increasing synaptic dopamine levels and causing a pleasurable sensation
  • Alcohol and opiates also increase dopamine levels
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24
Q

What are the features of dependency?

A
  • Tolerance: larger doses required to gain the same effect as previously.
    • E.g. an opiate-addict may easily inject enough heroin to kill a non-addict
  • Compulsion: strong desire to use the substance.
    • E.g. craving a cigarette
  • Withdrawal: physiological withdrawal state when the substance is stopped/decreased, demonstrated by:
    • Characteristic withdrawal syndrome for the substance
      • E.g. alcohol withdrawal fits
    • Substance use to prevent or relieve withdrawal symptoms
      • E.g. early morning drinking
  • Problems controlling use: difficulties controlling starting, stopping or amounts used.
    • E.g. it becomes hard to say no
  • Continued Use Despite Harm: despite clear problems caused by the substance, the person can’t stop using
    • E.g. injecting heroin despite developing an abscess
  • Salience (Primacy): obtaining and using the substance becomes so important that other interests are neglected.
    • E.g. not eating because the money is needed for cocaine
  • Reinstatement after Abstinence: tendency to return to the previous pattern and level of use after a period of abstinence.
    • E.g. someone who stops smoking for a year may return quickly to their previous 20/day habit
  • Narrowing of the Repertoire: loss of variation in use of the substance.
    • E.g. only having exactly 12 pints of snakebite every day at the same time
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25
Q

What is the aetiology of alcohol misuse?

A
  • Some genetic element
  • Lower rates of alcohol dependence amongst East Asians due to high prevalence of a less effective variant of aldehyde dehydrogenase
  • Occupation: more common in publicans, journalists, doctors, armed forces and entertainment industry
  • Social Background: difficult childhood, parental separation, poor educational achievement, juvenile delinquency
  • Psychiatric Illness: personality disorders, mania, depression and anxiety disorders (especially social phobia)
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26
Q

What is the clinical presentation of alcohol misuse?

A
  • Intoxication
    • Relaxation and euphoria
    • At higher level may make people irritable, aggressive, weepy, morose and disinhibited
    • Impulsivity and poor judgment can make people take risks and behave irresponsibly
  • Withdrawal
    • Headache
    • Nausea, retching and vomiting
    • Tremor
    • Sweating
    • Insomnia (may take weeks to regain normal sleep pattern)
    • Anxiety, agitation
    • CND depressant (stimulates GABA)
    • Tachycardia
    • Delirium Tremens (MEDICAL EMERGENCY)
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27
Q

What is Delirium Tremens?

A
  • Happens around 48 hours into abstinence
  • Duration: 3-4 days
  • Confusion
  • Hallucinations (especially visual e.g. formication)
  • Affective changes (extreme fear and hilarity may alternate)
  • Gross tremor (especially hands)
  • Autonomic disturbance (sweating, tachycardia, hypertension, fever)
  • Delusions
  • 5% mortality
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28
Q

What is the management of Delirium Tremens?

A
  • Reducing benzodiazepine (chlordiazepoxide) regime and parenteral thiamine (pabrinex)
  • Manage potentially fatal dehydration and electrolyte abnormalities
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29
Q

What are the physical complications of alcohol misuse?

A
  • Liver: alcoholic hepatitis, cirrhosis
  • GI: pancreatitis, oesophageal varices, PUD
  • Neurological: peripheral neuropathy, seizures, dementia
  • Cancers: bowel, breast, oesophageal and liver
  • CVS: hypertension, cardiomyopathy
  • Head injuries/accidents
  • Foetal alcohol syndrome
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30
Q

What are the psychological complications of alcohol misuse?

A
  • Depression, anxiety, self-harm and suicide
  • Amnesia
  • Cognitive impairment (alcoholic dementia, Korsakoff syndrome)
  • Alcoholic hallucinosis (experience of auditory hallucinations in clear consciousness while drinking alcohol (often persecutory/derogatory))
  • Morbid jealousy (overvalued idea or delusion that the partner is unfaithful)
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31
Q

What is Wernicke-Korsakoff Syndrome?

A
  • Wernicke’s Encephalopathy
    • Caused by acute thiamine deficiency
      • TRIAD:
        • Confusion
        • Ataxia
        • Ophthalmoplegia
  • MEDICAL EMERGENCY
  • Korsakoff Psychosis
    • Irreversible anterograde amnesia
    • Patient can register new events but cannot recall them within a few minutes
    • Patients may confabulate to fill the gaps in their memory
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32
Q

What are the social complications of alcohol misuse?

A
  • Unemployment, poor attendance and performance at work, domestic violence, separation and divorce
  • DRINK DRIVING - always ask alcoholics about this
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33
Q

What are the differential diagnoses of substance misuse?

A
  • Organic: consider physical causes for certain symptoms (e.g. ataxia, confusion)
    • Be aware of risk of head injury and subdural haematoma from falls
  • Psychiatric Illness: may be primary or comorbid problem
    • Depression/mania
    • Functional psychosis
    • Anxiety disorder
    • Personality disorder
    • IMPORTANT: the chronological relationship between psychiatric issues and substance misuse can help you identify which is the primary problem
      • Which problem came first?
      • Do psychiatric symptoms fit with known symptoms of that substance?
      • Have psychiatric symptoms continued whilst abstinent?
        Is there a family history of psychiatric illness?
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34
Q

What are investigations for alcohol misuse?

A
  • FBC
    • Macrocytic anaemia due to B12 deficiency in alcoholism
  • LFTs
    • GGT rises with recent heavy alcohol use
    • Raised ALT and AST suggests hepatocellular damage
  • Other investigations based on presentation (e.g. ECG, urine drug screen, hepatitis if IVDU)
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35
Q

What is the management for alcohol misuse?

A
  • Assessment and preparation
  • Detoxification
  • Relapse prevention
  • Rehabilitation
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36
Q

What is assessment and preparation?

A
  • Motivation to change
    • Stages of Change Model:
      • Pre-contemplation
      • Contemplation
      • Preparation
      • Action
      • Maintenance
      • Relapse
    • It is important to identify the type of support needed, for example:
      • Short term: reduce alcohol consumption
      • Medium term: undergo detox
      • Long term: attend college
  • Motivational Interviewing
    • Form of counselling which aims to empower the person to change
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37
Q

What is detoxification for alcohol misuse?

A
  • Allows metabolism and excretion of the substance whilst minimising discomfort
  • May be planned (after a period of preparation) or unplanned (after emergency admission)
    • Long-acting Benzodiazepines (e.g. chlordiazepoxide)
      • Replace alcohol and prevent withdrawal symptoms
      • Gradually withdrawn and stopped
    • Thiamine (Vitamin B1)
      • Prophylaxis against Wernicke’s encephalopathy
      • Best given IV or IM
  • Community (home) detox is used for uncomplicated dependency using a fixed-dosage reducing regime of benzodiazepines over 5-7 days
  • Inpatient detox is used if there is a history of withdrawal fits, comorbid medical or psychiatric illness or if the patient lacks support at home
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38
Q

How does relapse prevention work?

A
  • Psychological
    • CBT
    • Problem-solving therapies
    • Group therapy (alcoholic anonymous)
  • Medical
    • Acamprosate (anti-craving drug)
    • Disulfiram (antabuse)
      • Mimics the flush reaction to alcohol thereby making alcohol consumption unpleasant
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39
Q

How does rehabilitation work for substance misuse?

A
  • May be residential or day programme
  • Residential programmes allow a break for people who have become submerged in the drinking community
  • May be skills-based courses to help find employment
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40
Q

What is a Urine Drug Screen?

A
  • A test which shows drugs detected and duration of time detectable
    • Amphetamine: 2 days
    • Heroin: 2 days
    • Cocaine: 5-7 days
    • Methadone: 7 days
    • Cannabis: up to 1 month
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41
Q

What are examples of opiates?

A
  • Heroin
  • Morphine
  • Pethidine
  • Codeine
  • Dihydrocodeine
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42
Q

What is the heroin route of administration?

A
  • Initially smoked (chasing)
  • As tolerance builds, people progress to IV infection
  • May inject SC (skin popping) or IM once venous access becomes difficult
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43
Q

What are the complications of IV drug use?

A
  • Local: abscess, cellulitis, DVT, emboli

- Systemic: septicaemia, infective endocarditis, blood-borne infections, increased risk of overdose

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44
Q

What is the clinical presentation of opiate misuse?

A
  • Intoxication
    • IV heroin produces an intense rush or buzz
    • Euphoria, warmth and wellbeing
    • Sedation and analgesia
    • Vomiting and dizziness
    • Bradycardia and respiratory depression (can die from aspiration)
    • Pinpoint pupils
    • NOTE: non-IV users may experience milder effects (e.g. constipation, anorexia, decreased libido)
    • ANTIDOTE: naloxone
      • WARNING: after giving naloxone, patients may be plunged into withdrawal
  • Withdrawal
    • Starts: 6 hours after injection
    • Peak: 36-48 hours
    • Dysphoria
    • Nausea
    • Insomnia
    • Agitation
    • ‘The runs’ - diarrhoea, vomiting, lacrimation, rhinorrhoea
    • Feverish
    • Abdominal cramps
    • Aching joints and muscles
    • Yawning irresistibly
    • Dilated pupils
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45
Q

What is the management of opiate misuse?

A
  • Harm reduction
    • Pragmatic approach involving assessing and minimising risk rather than insisting on abstinence
    • Information should be provided on improving safety of drug use
    • Examples:
      • Needle exchanges for IV drug users
      • Vaccination and testing for blood-borne viruses for sex-workers and IVDU
  • Substitute prescribing
    • Deliberate prescribing of drugs in a controlled manner
    • Methadone (liquid) and buprenorphine (sublingual tablet) are oral preparations that replace injectable opiates
      • NOTE: methadone is a full agonist of opiate receptors and buprenorphine is a partial agonist
    • They are initially taken in a supervised environment and the doses are gradually titrated down until the patient does not experience any withdrawal symptoms
    • Detox can be helped with medications to help manage symptoms (e.g. anti-diarrhoeals, anti-emetics, pain killers)
    • Some people may remain on methadone maintenance because they deteriorate with detoxification
    • Naltrexone (opiate antagonist) may be given after detoxification to prevent relapse as it blocks the euphoric effects of opiates
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46
Q

What is the psychoactive compound in cannabis? Which receptors does it act on?
What are synonyms and symptoms of cannabis/cannabis use?

A
  • Psychoactive compound: delta-9 tetrahydrocannabinol (THC)
  • Acts on cannabinoid receptors in the brain
  • Synonyms: blow, dope, draw, ganja, hemp, marijuana, pot, wacky-backy
    • Grass/weed: made from dried cannabis leaves
    • Hash/hashish: squidgy, brown-black lump made from resin and flowers
    • Skunk and sinsemilla: particularly STRONG
  • Can cause perceptual distortion, the munchies, nausea and vomiting (greening)
  • Early heavy use is going to precipitate psychosis
  • Lethargy and poor motivation are features of chronic heavy use
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47
Q

What are stimulants?

A
  • Potentiate the effects of neurotransmitters, increasing energy, alertness and euphoria and decreases need for sleep
  • Increase confidence and impulsivity (risky behaviour)
  • Crash is experienced after the substance wears off
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48
Q

What are the side-effects of stimulants?

A
  • arrhythmia, hypertension, stroke, anxiety, panic and drug-induced psychosis
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49
Q

What is the management of stimulants?

A
  • Harm reduction is the mainstay of treatment

- Short-term benzodiazepines may be offered to help withdrawal anxiety

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50
Q

Describe cocaine

A
  • Usually snorted
  • May cause formication
  • Powerful vasoconstrictor
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51
Q

Describe crack cocaine

A
  • Concentrated smokeable form of cocaine
  • Produces almost immediate and extremely intense high
  • Smoking crack lasts about 5-10 mins
  • The on-off effect makes crack highly addictive
  • Speedballing is the use of crack with heroin
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52
Q

Describe amphetamine and khat

A
  • Amphetamine
    • White powder of tablets
    • Can be dissolved or injected
  • Khat
    • Mild stimulant
    • It comes as chewable leaves that can cause florid psychosis
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53
Q

Describe ecstasy

A
  • Ecstasy causes serotonin reuptake inhibition and release
  • Usually taken as a tablet
  • Users become very chatty, dance relentlessly and show bruxism (tooth-grinding)
  • Side-effects: nausea, vomiting and sweating
  • Death is associated with hyperthermia and dehydration
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54
Q

Describe hallucinogens

A
  • Cause visual illusions and hallucinations
  • Synaesthesia may occur (experience of a sensation in another modality (e.g. hearing a smell))
  • Some people become acutely anxious
  • Behavioural toxicity is the accidental harm that occurs when people act on drug-induced beliefs (e.g. being able to fly)
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55
Q

Describe LSD

A
  • Affects dopamine and serotonin transmitter systems
  • Usually impregnated in tabs (e.g. paper with pictures on them)
  • Trips could last up to 12 hours
  • Bad risks
  • Other risks include anxiety, depression and psychosis
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56
Q

Describe phenylcyclidine

A
  • Becoming increasingly popular
  • Can be snorted or added to a joint
  • Associated with violent outbursts and ongoing psychosis
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57
Q

Describe ketamine

A
  • Powerful veterinary anaesthetic

- The anaesthetic effect has led to self-harm

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58
Q

Describe magic mushrooms

A
  • Eaten or drunk

- Risk of eating poisonous mushrooms

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59
Q

Describe sedatives

A
  • Benzodiazepines have a sedative effect
  • Enhances GABA transmission
  • Usually swallowed as tablets
  • Similar to alcohol (calm and mild)
  • Slurred speech, ataxia and stupor at higher doses
  • Withdrawal effects are similar to alcohol
  • Overdose is treated with flumenazil
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60
Q

What is the prognosis of substance misuse?

A
  • Drug and alcohol disorders tend to follow a relapsing/remitting course
  • People relapse several times before eventually becoming abstinent
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61
Q

What is dementia?

A
  • Acquired, chronic and progressive cognitive impairment sufficient to impair activities of daily living
  • Effect of dementia on ADLs is an important part of the assessment
  • Problems should have been present in clear consciousness for at least 6 months
  • 20% of people > 80 years have dementia
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62
Q

What are the causes of low MMSE?

A
  • Dementia
  • Delirium
  • Most psychiatric illnesses (e.g. depression, anxiety, psychosis)
  • Learning disability
  • Sensory impairment
  • Language barrier
  • Feeling unwell, tired or irritable
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63
Q

What are ADLs?

A
  • Financial management
  • Using the toilet
  • Washing
  • Dressing
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64
Q

What are the most common types of dementia?

A
  • Alzheimer’s disease is the MOST COMMON type (2/3 of cases)
  • 2nd most common: vascular dementia
  • 3rd most common: dementia with Lewy bodies
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65
Q

What are the clinical features of dementia?

A
  • Often begins with forgetfulness, mainly for recent events
  • Mild day-to-day mistakes (e.g. muddling up appointments)
  • Anxiety or depression may occur early whilst insight is intact
  • Forgetfulness worsens over time
  • New information becomes harder to retain
  • Disorientation develops
  • Patients may confuse day and night, become lost easily or fail to recognise family and friends
  • Patients will become less independent and need more help with ADLs
  • Wandering, sleep disturbance, delusions/hallucinations, shouting, inappropriate behaviour and aggression can occur
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66
Q

What are the risk factors of Alzheimer’s disease?

A
  • Age
  • Genetics (presenilin 1, presenilin 2, beta-amyloid precursor protein, apolipoprotein E4)
  • Vascular risk factors
  • Low IQ
  • Head injury
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67
Q

What is the pathology of Alzheimer’s disease?

A
  • Atrophy due to neuronal loss (hippocampus is affected early)
  • Plaque formation - APP is abnormally cleaved into beta-amyloid which aggregates in insoluble clumps
  • Intracellular neurofibriliary tangles made up of hyperphosphorylated tau proteins kill neurones
  • Cholinergic loss (cholinergic pathways are most affected)
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68
Q

What is the clinical presentation of Alzheimer’s disease?

A

4 A’s

  • Amnesia: recent memories are lost first, disorientation occurs early
  • Aphasia: word-finding problems occur, speech can become muddled
  • Agnosia: recognise problems (e.g. faces)
  • Apraxia: inability to carry out skilled tasks despite normal motor function (e.g. dressing)
  • Personality may erode
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69
Q

What is vascular dementia?

A
  • Caused by infarcts due to thromboemboli or atherosclerosis
  • Risk factors are the same as for stroke
  • CT will show multiple lucencies
70
Q

What is the clinical presentation of vascular dementia?

A
  • Stepwise progression
  • Each step is a sudden deterioration
  • Several tiny infarcts may cause a smoother, more subtle degeneration
  • Symptoms are dependent on site of infarct
71
Q

What is dementia with lewy bodies (DLB)?

A
  • Lewy bodies are eosinophilic intracytoplasmic neuronal structures consisting of alpha-synuclein and ubiquitin
  • In DLB they are seen in the cyngulate gyrus and neocortex
  • In Parkinson’s disease, Lewy bodies are found in the brainstem
72
Q

What is clinical presentation of DLB?

A
  • Fluctuating confusion with marked variation in levels of alertness
  • Vivid visual hallucinations (often people or animals)
  • Spontaneous parkinsonian sings (may present late)
  • DLB can resemble delirium due to fluctuating cognition and hallucinations
  • Do NOT prescribe antipsychotics (e.g. haloperidol)
  • Extreme antipsychotic sensitivity in DLB can result in DEATH
73
Q

What are the differential diagnoses of dementia?

A
  • Delirium
  • Reversible dementias
  • Pseudodementia
74
Q

What is delirium?

A
  • Presents suddenly with altered or clouded consciousness
  • Losing touch with surroundings
  • Poor attention
  • Presentation usually fluctuates
  • May be evidence of underlying physical problems
  • Symptoms resolve once underlying cause is treated
75
Q

What are reversible dementias?

A
  • Presents with cognitive impairment that may resolve if treated
  • Brain: subdural haematoma, SOL, normal pressure hydrocephalus
  • Endocrine: hypothyroidism, hyperparathyroidism, Addison’s disease, Cushing’s syndrome
  • Vitamin deficiency: B12, folate, thiamine, niacin
76
Q

What is pseudodementia?

A
  • Memory problems in severe depression
  • Low mood precedes cognitive problems
  • May lack motivation to answer questions (e.g. ‘I don’t know’)
77
Q

What are the investigations for dementia?

A
  • Physical examination and basic observations
  • Blood tests
    • FBC (infection/anaemia)
    • U&Es (dehydration/renal failure/hyponatraemia)
    • Glucose
    • TFTs (hypothyroidism)
    • LFTs (may suggest alcohol abuse)
    • B12 and folate
    • Calcium levels
    • VDRL (neurosyphilis)
  • MMSE
  • Collateral history
  • Septic screen: MSU, CXR, blood cultures, wound swabs, sputum/stool samples (dependant on symptoms)
  • CT or MRI head if:
    • Unusual presentation/neurological signs
    • First onset of psychotic symptoms later in life
    • Planning to start anti-dementia medication
78
Q

What is the management of dementia?

A
  • Focuses on quality of life and preservation of independence and dignity
  • Adaptations for Patients
  • Social support
  • Support Carers
  • Optimise Physical Health
  • Psychological therapies
  • Psychotropic medications
79
Q

What kind of adaptations are needed for patients with dementia?

A
  • Always carry ID, address and contact number in case they get lost

Dossett boxes/blister packs to aid medication compliance

Change gas to electricity

Reality orientation (visible clocks, calendars)

Environmental modifications (e.g. patterned carpets can predispose to hallucinations)

Assistive technology (e.g. door mat buzzers)

80
Q

What social support is recommended for dementia patients?

A
  • Personal care, meal preparation and medication prompting
  • Day centres provide enjoyable daytime activities and social contact
  • Day hospitals enable daily psychiatric care for more complex patients
81
Q

How can support carers be involved with dementia patients?

A
  • Emotional support
  • Educate about dementia
  • Train to manage common problems
  • Provide respite care
82
Q

How can you optimise physical health for dementia patients?

A
  • Treat sensory impairment (hearing aids, glasses)
  • Exclude superimposed delirium
  • Treat underlying risk factors
  • Review all medication
83
Q

What psychological therapies are used for dementia patients?

A
  • Behavioural approaches
    • Identify and modify underlying triggers for difficult/risky behaviours (e.g. wandering may be due to disorientation, boredom or anxiety)
  • Reminiscence Therapy
    • Talking about the old days enhances a sense of belonging and reinforced identity
  • Validation Therapy
    • Reassure and validate the emotion behind what is said
  • Multisensory Therapy
    • As dementia advances and speech is lost, it may be easier to respond to touch, music etc.
  • Cognitive Stimulation Therapy
    • Memory training and re-learning
84
Q

What psychotropic medications can dementia patients use?

A
  • Start doses low and increase slowly with any medication used
  • Older people are very sensitive to drug side-effects
  • Treat comorbid psychiatric illness (e.g. depression)
  • Acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine)
    • Can cause symptomatic relief
    • Has no effect on the progression of dementia
  • Behavioural disturbance may require sedatives as a last-resort (e.g. trazodone, sodium valproate, haloperidol)
85
Q

What is the prognosis of dementia?

A
  • 2/3 of people with dementia live in their own home or with a carer
  • People should be supported to stay in their homes for as long as possible
  • Placement in a nursing home may be required
86
Q

What are medically unexplained symptoms (MUS)?

A
  • Physical complaints without evidence of an underlying organic cause
  • Aka functional, psychosomatic, somatised and somatoform
  • Contributing factors include childhood experiences (e.g. parental illness) and cultural/family attitudes
  • Symptoms may be precipitated by stressful life events
87
Q

What are the theories of MUS?

A
  • Somatisation
    • Unconscious expression of psychological distress through physical symptoms
    • E.g. anger as abdominal pain
  • Psychiatric illness
    • Depression and anxiety symptoms can be psychological (e.g. sadness/fear) and physical (e.g. muscle aches, constipation, palpitations)
  • Cognitive models
    • An individual’s interpretation of normal physiology can create anxiety and perpetuate MUS (e.g. someone concerned about palpitations may misinterpret normal physiological experiences (e.g. rapid heart rate whilst anxious) as a feature of a heart attack)
    • Selective attention to the problem would lead to acute awareness of palpitations
    • Behaviours such as repeated checking (e.g. pulse) and constantly seeking reassurance will maintain anxiety long term
    • Reassurance will REINFORCE these behaviours
88
Q

What is the clinical presentation of MUS?

A
  • Rheumatology - fibromyalgia
  • Gastroenterology - IBS, non-ulcer dyspepsia
  • Otolaryngology - dizziness, tinnitus
  • Cardiology - non-cardiac chest pain, palpitations
  • Military Medicine - Gulf War syndrome
  • Pain clinics - headache, pelvic pain, lower back pain
  • There may be very clear psychological stressors
89
Q

What is the differential diagnosis of MUS?

A
  • Organic: rule out any physical cause
    • Don’t be too cynical about multiple and changing symptoms because this could be caused by a multisystem physical illness (e.g. sarcoidosis, TB)
  • Psychiatric illness
    • Anxiety and Depression: can cause and exacerbate symptoms (e.g. depression lowers pain threshold)
    • Hypochondriasis: extreme form of health anxiety where patients believe they have a specific illness (e.g. cancer) rather than presenting with inexplicable symptoms
    • Schizophrenia, persistent delusional disorder: hypochondriacal delusions and somatic hallucinations may occur
  • Deliberate Production of Symptoms (RARE)
    • Factitious Disorder: deliberate production of symptoms to receive medical treatment (e.g. PUO, haematuria, skin lesions)
      • Extreme cases are called Munchausen’s Syndrome
    • Malingering: feigning symptoms to obtain external reward (e.g. escape military service, get money or drugs)
90
Q

What is the management of MUS?

A
  • Therapeutic Assessment
    • Full history and physical examination
  • Explain and Reassure
    • Many patients will benefit from being reassured that their symptoms are not serious, are common and familiar
    • Reattribution Model
      • Ensure they feel understood
      • Broaden the agenda from a physical AND psychological cause
      • Make a link between symptoms and psychological factors
    • Avoidance of over-investigation, unnecessary specialist referrals or physical medications
      • These reinforce physical illness beliefs
      • May increase anxiety
      • Ensure reasonable investigation
    • Emotional Support
      • Encourage patients to discuss emotional difficulties
      • Support them in dealing with stress
    • Encourage Normal Function
      • Patients may avoid normal activities because they think it will exacerbate problems
    • Antidepressants
      • May be useful even without depression (e.g. tension headache, IBS)
    • Treat comorbid illness
      • Particularly anxiety or depression
    • CBT
    • Graded Exercise
      • Helpful in CFS and fibromyalgia
91
Q

What is Chronic Fatigue Syndrome?

A
  • Aka myalgic encephalomyelitis
  • May follow viral infection (e.g. glandular fever)
  • Can arise spontaneously
  • Extreme fatigue is the main complaint
  • Patients will become exhausted by mild exertion
  • Other symptoms include aches and pains
  • Strong evidence for graded exercise (scheduled and gradually increasing activity)
  • Patients need realistic goals and should not do more activity than planned
  • CBT improves fatigue and physical functioning
92
Q

What is the Somatisation Disorder?

A
  • Rare, disabling and chronic
  • 10 x more common in women
  • Multiple medically unexplained symptoms affecting any system in the body
  • Symptoms are difficult to treat
93
Q

What is the prognosis for MUS?

A
  • Shorter duration with milder symptoms have a better prognosis
  • Chronic presentations fluctuate and stress can cause exacerbations
94
Q

What is Conversion (Dissociative) disorder?

A
  • An internal conflict is unconsciously converted into neurological symptoms
  • Presentations are acute, specific and often DRAMATIC following sudden stress or conflict
  • Examples:
    • Paralysis
    • Blindness
    • Aphonia (inability to produce speech)
    • Seizures
    • Psychogenic amnesia (loss of ALL somatic memories including own identity)
    • Multiple personality disorder (rare and controversial)
    • Fugue (patients lose their memory entirely and wander away from home)
    • Stupor
  • Exclude organic causes
  • Encourage a return to normal activities and avoid reinforcing symptoms of disability (e.g. providing a wheelchair)
  • Patients should be supported to address triggering stressors rather than focusing on physical manifestations
  • Better outcome than MUS
  • La belle indifference - a relative lack of concern despite obviously worrying symptoms (may be seen in conversion disorder)
95
Q

What are the main eating disorders and what are their epidemiology?

A
  • Tends to affect perfectionist, high-achieving young women with low self-esteem
  • Main Disorders:
    • Anorexia nervosa (AN)
    • Bulimia nervosa (BN)
    • Binge eating disorder (BED) is BN without the purging
  • Mainly affects women (90%)
  • BN is more common than AN
  • Usually starts aged 16-22 years
  • Often comorbid with other mental health disorders
96
Q

What is the aetiology of eating disorders?

A
  • Genetic component
  • Perfectionist and low self-esteem are risk factors
  • A theory for AN includes the idea that successful weight loss enhances the patient’s sense of achievement, autonomy and perfectionism
    • When life feels uncontrollable, AN comforts by providing the ability to control something (i.e. weight)
    • It may also be a way of avoiding separation from family or becoming an independent sexual being (maintains dependency)
  • Sociocultural
    • Pressures to be thin and promotion of dieting are important influences
    • High-risk groups (models, athletes, dancers)
  • Personal History
    • People with BN often have a history of obesity
    • Up to 50% of people with BN have previously suffered from AN
    • Child abuse
  • Family History
    • Parental overprotection and family enmeshment (over-involved relationships with poor boundaries making it difficult for members to feel independent)
97
Q

What is the clinical presentation of anorexia nervosa?

A
  • BMI < 17.5 (or weight 15% less than expected)
  • DELIBERATE WEIGHT LOSS
    • People with AN go to extra-ordinary extents to lose weight and become extremely emaciated
    • They restrict calorie intake by avoiding fattening foods (e.g. chocolate)
    • May use laxatives, vomiting and excessive exercise
    • Appetite suppressants, thyroxine, diuretics and stimulants may be used
    • Diabetics may skip insulin
  • DISTORTED BODY IMAGE
    • Preoccupied with body shape and a dread of weight gain
    • Overvalued ideas that they are fat despite being very thin
  • ENDOCRINE DYSFUNCTION
    • Hypothalamo-pituitary-gonadal axis is affected leading to amenorrhoea (women) and impotence (men)
    • Loss of libido
    • If occurring before puberty, may cause delay or arrest of menarche and breast development
98
Q

What are examination findings for anorexia nervosa secondary to malnutrition?

A
  • General appearance: Dry skin, brittle hair/nails, fine downy (lanugo) hair, anaemia, oedema
  • Cardiovascular: bradycardia, low BP, postural drop. peripheral oedema,
  • Gastrointestinal: tender abdomen
  • Musculoskeletal: muscle wasting (general and proximal myopathy), short stature (early onset AN), previous or current fractures
  • Metabolic: hypercholesterolaemia, hypercarotenaemia (yellow skin tinge especially soles and palms)
  • Neurological: peripheral neuropathy
99
Q

What are examination findings for anorexia nervosa secondary to binge/vomit/purge?

A
  • General appearance: Russell’s sign (calluses or cuts on the knuckles from self-induced vomiting), swollen salivary glands (puffy face), oedema
  • Cardiovascular: arrhythmias
  • Gastrointestinal: tender abdomen, erosion of dental enamel, caries
  • Metabolic: hypercholesterolaemia, hypercarotenaemia
  • Neurological: peripheral neuropathy
100
Q

What are the physical complications of anorexia nervosa?

A
  • General
    • Lethargy and cold intolerance
    • Pancytopaenia in severe anorexia
    • Infections resulting from reduced immunity
  • Cardiovascular
    • Over 80% experience cardiac complications and risk sudden death
    • Problems include bradycardia, hypotension, arrhythmia (due to hypokalaemia), mitral valve dysfunction and cardiac failure
  • GI
    • Constipation
    • Abdominal pain
    • Ulcers
    • Oesophageal tears
    • Gastric rupture due to vomiting
    • Nutritional hepatitis (low serum protein, raised bilirubin, LDH and ALP)
  • Reproductive
    • Amenorrhoea is a diagnostic criterion in women
    • Infertility (atrophy of ovaries and testes)
    • Loss of libido
    • Loss of morning erections in men
  • Musculoskeletal
    • Osteoporosis (leading to fractures and proximal myopathy)
  • Neurological
    • Peripheral neuropathy
  • Other
    • Lanugo hair (attempt to keep the body warm)
    • Swollen salivary glands after bingeing
101
Q

What are the differential diagnoses of AN?

A
  • Medical causes of weight loss
    • Hyperthyroidism, malignancy, GI disease, Addison’s disease, chronic infection, inflammatory conditions, AIDS
  • Depression
    • Seen in severe depression
    • Would NOT be denied unlike in AN
  • Bulimia Nervosa
    • Bingeing and vomiting can occur in AN
    • BN should be diagnosed if bingeing and vomiting is the predominant behaviour and the patient is NOT underweight
  • Eating Disorders Not Otherwise Specified (EDNOS)
    • Term used for atypical presentations
  • Body Dysmorphic Disorder (BDD)
    • Characterised by body image distortion (e.g. nose is misshapen)
    • Deliberate weight loss is unusual in BDD
  • Psychosis
    • Self-starvation may occur if food is believed to be poisoned
102
Q

What are the investigations for eating disorders?

A
  • Height, weight and BMI
  • Squat test
    • Ask the patient to squat down and rise without using their arms
    • Tests proximal myopathy
  • Essential blood tests
    • ESR, TFTs (excludes more organic causes e.g. hyperthyroidism, chronic inflammatory disease)
    • FBC, U&E, phosphate, albumin, LFT, creatine kinase, glucose
    • Evaluates nutritional state and risk
  • ECG
    • Bradycardia, arrhythmias and prolonged QT interval
  • Other tests as indicated
    • DEXA
  • (Pay close attention to ECG and electrolyte levels for eating disorders)
103
Q

What is the management of anorexia nervosa?

A
  • Engagement
  • Psycho-education
    • Advice on nutrition and health
  • Treat comorbid psychiatric illness
    • Depression, OCD and substance misuse are common
  • Nutritional management and weight restoration
    • Realistic weekly weight gain target (usually 0.5-1 kg/week)
    • Set eating plan
  • Psychotherapies
  • Medical treatment
    • Particularly important if there are physical complications, rapid weight loss or BMI < 13.5
  • Inpatient treatment
    • May be necessary if:
      • BMI < 13 or extremely rapid weight loss
      • Serious physical complications
      • High suicide risk
    • Mental Health Act may be needed to enable compulsory feeding
104
Q

What is the clinical presentation of bulimia nervosa?

A
  • BINGE EATING
    • Repeated bouts of overeating is a hallmark of BN
    • Patients experience irresistible cravings for food and lose control, eating enormous amounts of food that’s often considered forbidden (e.g. sweets, high calorie, high fat)
    • Example: 15 chicken selects and 3 large fries
    • There is often a sense of desperate urgency and compulsion
    • Often triggered by distress
  • PURGING
    • Binges cause feelings of shame and guilt leading to measures to undo the damage (e.g. vomiting, using laxatives or diuretics)
    • Between binges there may be episodes of fasting or excessive exercise
  • BODY IMAGE DISTORTION
    • Patients feel fat and are pre-occupied by shape and weight
    • Often hate their body
  • BMI > 17.5
    • Patients usually have a normal or slightly increased weight
    • Periods are usually present
  • Patients are usually very secretive about their binging or purging behaviour
  • Symptoms may arise secondary to vomiting/purging (e.g. arrhythmia (hypokalaemia) and convulsions (hyponatraemia))
105
Q

What is the management of bulimia nervosa?

A
  • Treat medical complications
  • SSRIs (Fluoxetine)
    • Reduce binging and purging by enhancing impulse control
  • Treat comorbid psychiatric illness
    • Depression, self-harm and substance misuse are common
  • CBT
    • Helpful to control symptoms
106
Q

What is the prognosis for eating disorders?

A
  • At 10 years after diagnosis of AN:
    • 50% have no eating disorder
    • 10% have died
    • 40% have ongoing problems and crossover to BN is common
  • At 10 years after diagnosis of BN:
    • 70% have no eating disorder
    • 1% have died
107
Q

What are the markers in high-risk patients with nutritional decompensation?

A
  • BMI < 13
  • Weight loss > 1 kg/week
  • Purpuric rash
  • Cold peripheries
  • Core body temperature < 34.5 degrees
  • Hypotension (< 80/50 mm Hg)
  • Bradycardia (< 40 bpm) with prolonged QT interval on ECG
  • Inability to stand from squatting without using arms for leverage
  • Electrolyte imbalance (K+ < 2.5, Na+ < 130, phosphate < 0.5)
108
Q

What is refeeding syndrome?

A
  • Complication of establishing adequate food intake
  • Characterised by electrolyte imbalance (low phosphate, potassium and magnesium)
  • Caused by sudden intracellular movement of electrolytes due to switch from fat to carbohydrate metabolism and associated increased secretion of insulin
109
Q

What is the classification of sexual dysfunction?

A
  • Primary: normal function was never obtained

- Secondary: loss of function

110
Q

Describe libido and its treatment?

A
  • More common in women
  • Normally idiopathic
  • May be linked to childhood sexual abuse
  • New onset may be related to:
    • Physical illness
    • Medication
    • Relationship problems
    • Childbirth
  • Identify the underlying cause
111
Q

What is the treatment of libido?

A
  • Treatment is mainly psychological
  • Communication is encouraged
  • Sensate Focus Therapy
    1) Intercourse is banned
    2) Non-genital caressing (focus on pleasure and relaxation)
    3) Genital touching to achieve arousal and subsequent orgasm
    4) In time, intercourse occurs naturally
  • Timetabling Sex
    • Helps partners with different libidos reach a compromise
112
Q

Describe hypersexuality and its treatment

A
  • Usually affects men
  • Important to exclude:
    • Mania
    • Substance misuse
    • Organic brain disorders (e.g. frontal lobe syndrome)
  • Treatment
    • CBT-based treatments
113
Q

What are causes of erectile dysfunction?

A
  • Organic
    • Diabetes
    • Arteriosclerosis
    • Neurological (e.g. autonomic neuropathy)
    • Pituitary failure
    • Medication (antidepressants, antipsychotics, antihypertensives, beta-blockers and diuretics)
    • Substance misuse
  • Psychological
    • Depression
    • Performance anxiety
114
Q

What are investigations for erectile dysfunction?

A
  • Physical examination including genitals (usually normal)
  • Blood tests
    • Testosterone and sex hormone (may see low testosterone/hyperprolactinaemia)
    • Glucose (diabetes)
    • LFTs/GGT (alcohol misuse)
115
Q

What is the management for erectile dysfunction?

A
  • Modifiable Risk Factors
    • Stop smoking, exercise, reduce weight and alcohol
    • Treat diabetes, hypertension etc.
    • Review medication (e.g. mirtazapine is associated with placebo-level sexual dysfunction whereas SSRIs have a much higher rate)
  • Psychological Approaches
  • Physical Treatments
    • Phosphodiesterase-5 inhibitors (e.g. sildenafil (viagra))
    • Intracavernosal prostaglandin self-injections before intercourse
    • Vacuum pumps
      • Plastic dome and pump placed over the penis creating a vacuum to produce an erection
      • This is maintained by slipping a tight ring around the base of the penis
116
Q

What are different types of orgasm problems?

A
  • Anorgasmia
  • Premature ejaculation
  • Delayed ejaculation
117
Q

What is anorgasmia and its treatment?

A
  • Many women need direct clitoral stimulation to reach orgasm
  • Sex education may resolve anorgasmia if women or their partners are unaware of this
  • TREATMENT: self-exploration, masturbation and sensate focus therapy
118
Q

What is premature ejaculation and its treatment?

A
  • Very common in younger men
  • Improves with practice
  • Squeezing the glans postpones orgasm
  • SSRIs can help
119
Q

What is delayed ejaculation and its treatment?

A
  • Delayed or absent male orgasm
  • Can be physical (e.g. SSRIs) or psychological (e.g. fear of conception)
  • TREATMENT: psychotherapy, advice on varying sexual techniques and medication review
120
Q

What are paraphilias?

A
  • Disorders of sexual preference
  • Occur almost exclusively in men
  • Only require treatment if they cause harm or distress
  • Fetishism: sexual arousal and gratification relies on an object rather than a person (e.g. leather, rubber)
  • Paedophilia
  • Sadism: inflicting pain causes arousal
  • Masochism: humiliation or suffering cause arousal
  • Patients should avoid activities that reinforce the paraphilia (e.g. pornography)
  • Anti-androgens may be useful in dangerous situations (e.g. paedophiles who feel that they may be overwhelmed by sexual urges)
121
Q

What are disorders of gender identity and treatment options?

A
  • Transsexual people believe that their gender does NOT correspond to their body
  • They want to live and be accepted as a member of the other sex
  • More common in biological males
  • Hormone therapy
  • Gender reassignment surgery
  • NOTE: patient must demonstrate the ability to live successfully in their desired gender before surgery can be considered
122
Q

What is the prognosis for psychosexual disorders?

A
  • Low libido and paraphilias tend to show little improvement
123
Q

What is learning disability?

A
  • A developmental condition characterised by global impairment of intelligence and significant difficulties in socially adaptive functioning
  • More common in males (3:2)
  • Prevalence is rising, partly due to increased survival of very premature babies
124
Q

What are the causes of learning disability?

A
  • Antenatal
    • Genetic (e.g. PKU)
    • Foetal alcohol syndrome
    • Drugs
    • Medications
    • Smoking
    • Infection (e.g. rubella)
  • Perinatal
    • Neonatal hypoxia
    • Birth trauma
    • Hypoglycaemia
    • Prematurity
  • Postnatal
    • Social deprivation
    • Malnutrition
    • Lead
    • Infections (e.g. meningitis)
    • Head injury
125
Q

What is the clinical presentation of learning difficulty?

A
  • Usually presents in childhood
  • Abilities can be:
    • Delayed
    • Reduced
    • Absent
  • Domains affected:
    • Language
    • Schooling
    • Motor ability
    • Independent living
    • Employment
    • Social ability
  • Behavioural difficulties may arise due to a combination of communication problems, psychiatric or physical illness, epilepsy or suboptimal support for individual needs
    • Behavioural phenotypes - commonly recognised behaviours in particular syndrome (e.g. self-harm in Lesch-Nyhan syndrome)
126
Q

What is Mild Learning Disability?

A
  • Language is usually good (development may be delayed)
  • Problems may go undiagnosed
  • Individuals struggle through school
  • May be labelled as having behavioural problems
  • May live and work independently with appropriate support
127
Q

What is Moderate Learning Disability?

A
  • Language and cognitive abilities are less developed
  • Reduced self-care abilities and limited motor skills may need support
  • May need long-term accommodation with their family or in a staff-supported group home
  • Simple practical work should be achievable in supported settings
128
Q

What is Severe Learning Disability?

A
  • Marked impairment of motor function
  • Little/no speech during early childhood (may develop during school years)
  • Simple tasks can be performed without assistance
  • Likely to require their family home or 24-hour staffed home
129
Q

What is Profound Learning Disability?

A
  • Severely limited language, communication, self-care and mobility
  • Significant associated medical problems
  • Usually require higher levels of support
130
Q

What are issues with learning disability?

A
  • Often have increased physical morbidity and mortality
  • Respiratory infections are a leading cause of death
  • Many have comorbid mental health problems and autism-spectrum disorders
  • Increased risk of mood and anxiety disorders and schizophrenia
  • Diagnostic overshadowing - attributing everything to the learning disability (e.g. changes in behaviour and mental state are dismissed as being part of the learning disability)
131
Q

What are differential diagnoses for learning disability?

A
  • Autism spectrum disorder
    • People with Asperger’s syndrome (autism with normal intelligence) may have social deficits, communication problems and difficulties living independently
  • Epilepsy
    • Causes transient cognitive impairment
  • Adult brain injury or progressive neurological conditions
    • Learning disabilities occur while the brain is still developing
    • With patients presenting late, decide whether the impaired intellect was present before any adult illness
  • Psychiatric
    • Severe and enduring mental illness (e.g. schizophrenia) can lead to chronic cognitive impairment and reduced social functioning
  • Educational Disadvantage/Neglect
    • Lacking opportunity to learn must be distinguished from learning disability
132
Q

What are investigations for learning disabilities?

A
  • IQ testing
    • Is there a global impairment?
  • Functional assessment of skills, strength and weaknesses
  • Detailed developmental history from parents
    • Include details about pregnancy, birth language and motor skills development, schooling, emotional development, relationships
    • School reports may be useful
  • Exclude reversible disturbances (FBC, U&E, LFT, TFT, bone profile)
  • Investigations for associated physical illness (e.g. EEG for epilepsy)
  • Genetic testing if appropriate
133
Q

What is the management of Learning Disabilities?

A
  • Prevention
    • Education (e.g. risks of alcohol during pregnancy)
    • Improved antenatal/perinatal care
    • Genetic counselling
    • Early detection and treatment of reversible causes (e.g. excluding phenylalanine in babies with PKU
  • Treat physical comorbidity
  • Treat psychiatric comorbidity
    • Mental health problems can be difficult to diagnose because of cognitive, language and communication difficulties
    • Patients may be particularly sensitive to medications so slower dose titration and careful monitoring maybe required
  • Educational support
    • Statement of special Educational Needs allow appropriate support
    • This may be in mainstream or specialised schools
    • The aim is to maximise the child’s potential
  • Psychological Therapy
    • May include counselling, group therapy and modified CBT
    • Behavioural therapy - helps improve unhelpful behaviour patterns
    • ABC approach
      • Antecedants
      • Behaviour
      • Consequences
    • Management involves:
      • Avoiding antecedents
      • Reinforcing positive behaviours
      • Preventing reinforcement of negative behaviours (e.g. using distraction techniques)
      • Helping people understand the consequences of their actions
  • Other support
    • Support network is needed to provide specific help with daily living, housing, employment and finances
    • Assess carers’ needs
134
Q

What is the prognosis of learning disabilities?

A
  • Lifelong condition
  • Life expectancy is reduced because of comorbid physical illness and unmet health needs
  • IMPORTANT: people with learning disabilities are very vulnerable to neglect, abuse and exploitation
    • This may be compounded by communication difficulties
    • Behavioural change may be their way of communicating distress
135
Q

Describe Baby Blues

A
  • Distressing but NORMAL
  • Experienced by 50-75% of mothers a few days after birth
  • Lasts a few days
  • Patients feel weepy, irritable and muddled
  • They may complain that their mood feels all over the place (labile)
  • May experience trouble sleeping
  • TREATMENT
    • Explanation and reassurance
    • Occasionally, this may progress to postnatal depression
136
Q

Describe postnatal depression

A
  • 1 in 10 mothers will suffer from PND in the year after birth
  • Risk Factors
    • Personal or family history of PND or depression
    • Younger maternal age
    • Recent life events
    • Marital discord
    • Poor social support
  • Similar presentation to normal depression
  • Fatigue, irritability and anxiety may be particularly prominent
  • Depressive cognitions tend to relate to the baby (e.g. guilt or feeling of failure as a mother)
    • IMPORTANT: low energy, concentration and sleep are normal in mothers with newborns, so it is important to focus on cognitive symptoms to establish a diagnosis of PND
  • Recurrent intrusive thoughts about harming the baby can occur as distressing obsessions
137
Q

What is the management of postnatal depression?

A
  • Same as depression but take care with drugs used in breastfeeding mothers
    • Antidepressants can be secreted in breast milk
    • Low-dose amitriptyline is probably safe
    • Lithium should be avoided if possible
    • Seek specialist advice
  • Hospital admission should be considered if depression is severe with suicidal or infanticidal ideation
    • Mother and Baby Unit (MBU)is the optimal setting under these circumstances
    • Separation should be avoided if possible
  • Most women respond well to treatment within a month
  • Early and effective treatment of PND is important because it can affect the baby’s attachment and have lasting effects on development and personality
138
Q

What is Puerperal Psychosis?

A
  • Occurs in 1 in every 500/1000 births
  • Usually occurs 2 weeks after childbirth
  • Risk Factors
    • Personal or family history of puerperal psychosis or BPAD
    • Puerperal infection
    • Obstetric complications
  • Usually rapid onset
  • Often starts with insomnia, restlessness and perplexity (inability to understand something)
  • Later, psychotic symptoms will emerge
  • Psychotic symptoms tend to follow one of THREE patterns:
    • Delirium
    • Affective (like psychotic depression or mania)
    • Schizophreniform (like schizophrenia)
  • Symptoms can fluctuate dramatically and rapidly
  • Exclude underlying delirium or substance misuse (intoxication or withdrawal)
139
Q

What is the management of puerperal psychosis?

A
  • Depending on the presentation, antipsychotics, antidepressants or lithium may be needed
  • Benzodiazepines may be needed for agitation
  • In severe cases, ECT may be life-saving (women tend to respond well)
  • Admission is usually required, preferably to a mother and baby unit
  • Most patients recover within 6-12 weeks
  • IMPORTANT: suicide is the leading cause of maternal death in the UK
    • Risk to the baby can be through neglect or violence
    • Watch out for depressive delusions (e.g. the baby is evil, possessed or abnormal)
140
Q

What are organic psychiatric disorders?

A
  • Those caused directly by a demonstrable physical problem (e.g. brain tumour, hypothyroidism)
141
Q

What are functional illnesses?

A
  • Conditions traditionally viewed as having NO organic basis (e.g. schizophrenia)
142
Q

What is delirium?

A
  • Acute and transient global brain dysfunction with clouding of consciousness (acute confusional state)
  • Patient is not fully aware of their environment
  • Very COMMON especially in the elderly
  • It is a manifestation of a physical problem so always search for an underlying cause
143
Q

What are risk factors for delirium?

A
  • Old age
  • Pre-existing physical or mental illness (especially dementia)
  • Substance misuse
  • Polypharmacy
  • Malnutrition
144
Q

What are causes for delirium?

A
  • Trauma (e.g. head injury)
  • Hypoxia (cardiovascular, respiratory)
  • Infection (e.g. intracranial infection or systemic (septicaemia))
  • Metabolic (e.g. liver failure, renal failure, electrolyte imbalance)
  • Endocrine (e.g. hypoglycaemia)
  • Nutritional (e.g. Wernicke’s encephalopathy)
  • CNS pathology (e.g. raised intracranial pressure)
  • Drugs and alcohol (e.g. intoxication, withdrawal)
  • Medication (e.g. anticholinergics, opiates)
145
Q

What is the clinical presentation of delirium?

A
  • Onset is sudden (hours to days) and symptoms fluctuate often worsening in the evening/night
  • Patient is usually disorientated with poor attention and short-term memory
  • Mood changes may be prominent (may be mistaken for depression or mania)
  • Illusions and hallucinations are common (usually visual)
  • Transient muddled delusions may present
  • Sleep is often disturbed (insomnia and reversal of the sleep-wake cycle)
146
Q

What is an example of a typical delirium mental state examination?

A
  • Appearance and behaviour
    • Agitated 82 year-old woman in a hospital gown. Plucking at cubicle curtains. Fearful expression. Hitting out with her stick. Smells of urine.
  • Speech
    • Screaming, incoherent mumbling
  • Mood
    • Subjective: refused to comment
    • Objective: frightened, irritable, suspicious
  • Thought
    • Persecutory delusions (e.g. ‘they’re experimenting on me’)
  • Perception
    • Visual hallucinations (insects on her bed)
    • Illusions (misinterpreting curtains as ghosts)
  • Cognition
    • Unable to engage in MMSE
    • Disorientated in time, place and person
    • Poor attention and concentration
    • Unable to retain simple facts
  • Insight
    • Refusing all interventions
    • Does not believe she is ill
147
Q

What are behavioural changes in delirium?

A
  • Hyperactivity
    • Agitation and aggression
    • E.g. wandering into other patients’ beds
  • Hypoactivity
    • Lethargy, stupor, drowsiness and withdrawal
    • More difficult to spot
    • Quiet delirium (silently laying in bed)
148
Q

What investigations are done for delirium?

A
  • Physical examination
  • Collateral history (what is the baseline?)
  • Check the drug chart
  • Essential
    • FBC
    • U&Es
    • Glucose
    • Calcium
    • MSU
    • Oxygen saturation
    • ECG
    • CXR
    • Septic screen
  • Consider: LFTs, blood cultures, CT head, CSF, EEG
149
Q

What is the management of delirium?

A
  • Treat the cause
    • Manage aggravating factors (e.g. pain, dehydration, constipation)
    • Stop unnecessary medications
  • Behavioural management
    • Frequent reorientation (e.g. clocks, calendars, verbal reminders)
    • Good lighting (gloomy conditions increase risk of hallucinations/illusions)
    • Address sensory problems (e.g. hearing aids, glasses)
    • Avoid over- or understimulation (side-room if the main ward is disruptive)
    • Minimise change
      • Don’t keep moving the patient
      • One staff member to engage the patient each shift
      • Establish a routine (regular toileting and sleep hygiene)
    • Remove things that can be thrown or tripped over
    • Silence unnecessary noises (e.g. bleeping alarms)
    • Allow safe or supervised wandering
  • Medication
    • Small night-time dose of benzodiazepines could promote sleep
    • If short-term sedation is needed, low-dose typical antipsychotics (e.g. haloperidol) or benzodiazepines can be used
  • Consider referral
    • Geriatrics
    • Psychiatry
150
Q

How can you prevent delirium?

A
  • Good sleep hygiene without medication
  • Minimal moves around hospital
  • Encouraging mobility
  • Proactive management (minimise dehydration, pain, constipation, urinary retention and sensory problems)
151
Q

What is the prognosis of delirium?

A
  • Associated with
    • Increased mortality
    • Longer admissions
    • Higher readmissions rates
    • Subsequent nursing home placement
  • May take days to weeks to resolve
  • Some patients do NOT return to pre-morbid levels
152
Q

What is frontotemporal lobar degeneration?

A
  • Asymmetrical frontal and/or anterior temporal lobe atrophy
  • Most are sporadic
  • Some are autosomal dominant
153
Q

What are the three types of frontotemporal lobar degeneration?

A
  • Frontotemporal Dementia
    • Causes frontal lobe syndrome with prominent disinhibition and social/personality changes
  • Semantic Dementia
    • Progressive loss of understanding of verbal and visual meaning
  • Progressive Non-Fluent Aphasia
    • Begins with naming difficulties progressing to mutism
  • Usually death within 5-10 years
154
Q

What is Huntington’s Disease?

A
  • Autosomal dominant
  • Caused by CAG trinucleotide repeat in the Huntingtin gene on chromosome 4
  • Onset usually in early middle ages
  • More CAG repeats leads to earlier more severe presentations
  • Lengthening of CAG repeats occurs with each inheritance so onset is younger in subsequent generations (anticipation)
  • Deposits of abnormal Huntingtin protein causes atrophy of the basal ganglia and thalamus as well as some cortical lobe loss (particularly frontal lobe)
  • CT/MRI may show caudate nucleus atrophy and EEG may be flat
155
Q

What are the clinical features of Huntington’s Disease?

A
  • Personality and behavioural changes (sometimes aggression)
  • Depression, irritability and euphoria are common
  • Chorea affects limbs, trunk, face and speech muscles
  • Wide-based lurching gait
  • No cure
  • Death within 15 years
156
Q

What is HIV dementia?

A
  • Due to direct effect of the virus on the brain
  • Incidence has reduced due to HAART
  • Early apathy and withdrawal progresses to subcortical dementia
  • Neurological features: ataxia, tremor, seizures, myoclonus
  • MRI may show atrophy and diffuse white matter changes
157
Q

What is Normal Pressure Hydrocephalus?

A
  • Rare but potentially reversible cause of dementia
  • CSF absorption is impaired with normal communication between ventricles (i.e. not obstructed)
  • CSF accumulates in the ventricles (hydrocephalus) but the CSF pressure remains fairly normal as CSF production adjusts to compensate
  • Distortion of periventricular white matter tracts leads to a TRIAD:
    • Dementia (subcortical)
    • Unsteady gait
    • Urinary incontinence
  • A ventriculo-atrial shunt may allow CSF drainage from the brain ventricles into the heart
158
Q

What are Prion diseases?

A
  • Aka transmissible spongiform encephalopathies
  • Cause rapidly progressive neurological and psychiatric symptoms
  • Most common is sporadic CJD
  • Other types include:
    • Variant CJD
    • Iatrogenic CJD
    • Kuru
    • Familial prion diseases
  • Normal prion protein changes into an insoluble form which appears to act as a template for further transformation of normal to abnormal prion
  • Accumulation of abnormal prion proteins leads to spongiform and amyloid changes
  • No treatment
159
Q

What is Amnesic Syndrome?

A
  • Characterised by profound anterograde memory loss - an inability to lay down new memories from the time of brain damage onwards
  • Other brain functions are relatively intact
  • Damage tends to affect limbic structures dealing with memory (e.g. hippocampus, mamillary bodies)
  • Korsakoff Syndrome is the most common type of amnesic syndrome
    • Caused by thiamine (B1) deficiency
    • Usually secondary to alcohol abuse
  • Some patients confabulate to try and make sense of confusing memory gaps
  • Procedural memory (how to do things) is intact
  • Prompt parenteral thiamine can prevent further damage in Korsakoff syndrome but nothing reverses the amnesic syndrome
160
Q

What is Transient Global Amnesia?

A
  • Acute global memory loss , lasting from 1-24 hours
  • May be due to transient ischaemia of memory structures
  • Sometimes precipitated by physical or emotional stress
  • Patients usually > 50 years
  • Anterograde memory is particularly affected
  • Patients are often bewildered: ‘Where am I!?’
  • Patient does NOT forget their identity
  • Consciousness and cognition re normal
  • NO signs of neurological disease
  • Exclude intoxication, head injury, stroke and epilepsy
  • Good prognosis
161
Q

What is Frontal Lobe Syndrome?

A
  • The frontal lobe is responsible for controlling basic impulses
  • Anything that damages this area (e.g. head injury, dementia or stroke) can cause frontal lobe syndrome
  • Executive Dysfunction
    • Poor judgment
    • Poor reasoning and problem-solving
    • Poor planning and decision-making
  • Social Behaviour and Personality Change
    • Loss of social awareness: irresponsible/disinhibited, inappropriate behaviour
    • Impulsivity
    • Euphoric or fatuous mood, lability
    • Repetitive or compulsive behaviour
  • Apathy
    • Lack of motivation and initiative
    • Decline in self-care
  • MRI may be useful
  • Occupational therapy and neuropsychological testing will give insight into the functional impairment
  • Management is usually rehabilitation and supporting the family
162
Q

Describe head injuries

A
  • Open: skull is penetrated causing local cerebral damage
  • Closed: no penetration but brain damage is caused by acceleration/deceleration and shearing forces
  • Severity is based on GCS, duration of coma and duration of post-traumatic amnesia (PTA)
163
Q

What is Post Traumatic Amnesia?

A
  • Lasts from the time of injury until recovery of normal memory. The longer it lasts, the greater the risk of complications
164
Q

What is Retrograde Amnesia?

A
  • Retrograde Amnesia: memory loss before the injury. NOT a good predictor of outcome
  • Longer-term cognitive impairments are more likely to be focal in open head injuries and global in closed head injuries
  • Previous personality traits may be exaggerated
  • Depression and anxiety occur in up to 50%
165
Q

What is Post-concussional syndrome?

A
  • Condition which may follow head injury with loss of consciousness
  • Mood (e.g. depression, anxiety, irritability)
  • Cognitive (e.g. poor concentration and memory)
  • Somatic (e.g. headache, dizziness, fatigue, insomnia, noise sensitivity)
166
Q

What is the management of head injuries?

A
  • Specialist head injury services offer rehabilitation and family support
167
Q

What is Parkinson’s Disease?

A
  • Idiopathic movement disorder caused by degeneration of dopaminergic neurones in the substantia nigra
  • TRIAD of extrapyramidal symptoms:
    • Tremor (pill-rolling)
    • Rigidity (stiffness)
    • Bradykinesia
  • Other features: stooped posture, shuffling gait, hypomimic face, recurrent falls, constipation, urinary problems, sleep disturbance
  • Depression is present in 45% of PD patients
    • Treatment is the same as for primary depression
  • Dementia in Parkinson’s Disease (occurs in 80% of cases)
    • Slowness of though (bradyphrenia) is a common early symptom
    • Lewy Body Dementia should be distinguished from PD dementia
      • In PD Dementia, the PD comes first
      • In LDB, the dementia comes first
    • Can be treated with acetylcholinesterase inhibitors
168
Q

What are secondary forms of parkinsonism?

A
  • Drug-induced (e.g. antipsychotics)
  • Multiple cerebral infarcts
  • Repeated head injury (e.g. punch drunk syndrome/chronic traumatic encephalopathy)
  • Parkinson plus syndromes (e.g. PSP, corticobasal degeneration, multiple system atrophy)
169
Q

Describe psychotic symptoms and parkinson’s disease

A
  • Affect 40% of patients
  • Strongest predictor of nursing home placement
  • Visual hallucinations are common
  • Symptoms may result from the use of dopaminergic anti-Parkinson’s drugs
  • Management is focused on striking a balance between too little dopamine and too much dopamine
    • Dopaminergic drugs can be slowly withdrawn or atypical antipsychotics can be cautiously trialled
    • WARNING: both approaches may worsen parkinsonism
170
Q

What is Multiple Sclerosis?

A
  • Characterised by episodes of inflammation and demyelination occurring at different sites, and at different times, within the white matter tracts of the CNS
  • The disease may be relapsing-remitting and then become progressive
    • It is rarely progressive from the start
  • Depression is present in up to 50% of MS patients
    • This may be linked to the medications used (e.g. steroids)
    • Treatment is for primary depression
  • Cognitive impairment is present in up to 60% in the late stages of MS
171
Q

Describe Stroke

A
  • 30% mortality within 1 year
  • Type of cognitive deficit depends on the area of the brain affected
  • Depression
    • Affects up to 1/3 of stroke patients and impairs rehabilitation
    • Treat as for primary depression
172
Q

What is Epilepsy?

A
  • DEFINITION: tendency to recurrent, unprovoked seizures
    • There need to have been 2 or more seizures and unprovoked by an immediate identifiable cause
  • Cognitive impairment, psychotic symptoms and learning disabilities are common in epilepsy
  • Depression is present in 50% of patients and suicide rates are 4 x higher than the general population

Specialties (14 decks)

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