Mental Health Conditions Flashcards

1
Q

What is depression

A

A Mental state characterised by persistent low mood, loss of interest and enjoyment in everyday activities, neurovegetative disturbance, and reduced energy, causing varying levels of social and occupational dysfunction

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2
Q

How common is depression

A

Affects 5-10% of patients in the primary care setting

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3
Q

Who is affected by depression

A

Common in people of all ages and may be classified depending on duration, severity and number of symptoms, and the degree of functional impairment

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4
Q

What causes depression

A

With or without a known genetic component, stressful life events, personality and sex may play role in risk of depression resulting

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5
Q

What are the risk factors for depression

A
Age >65
Postnatal status
PMH or FH of depression or suicide
Corticosteroids
Interferon
Propanolol
Oral contraceptives
Chronic comorbidities
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6
Q

How does depression present

A
Persistent low mood
Loss of interest and enjoyment
Sleep and appetite changes
Guilt or self-criticism
Poor concentration
Reduced energy
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7
Q

What signs may a person with depression show

A
Weight change
Libido change
Sleep disturbance
Psychomotor problems
Low energy
Excessive guilt
Poor concentration
Suicidal ideation
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8
Q

What are the differentials in suspected depression

A
Adjustment disorder with depressed mood
Substance/medication or medical illness associated a
Other depressive disorders
Bipolar disorder
Premenstrual dysphoric disorder
Grief reaction
Dementia
Anxiety disorders
Alcohol abuse
Anorexia nervosa
Hypothyroidism
Medicine adverse effects
Cushing's disease
Vit B12 deficiency 
Obstructive sleep apnoea
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9
Q

How is suspected depression investigated

A
1st line:
Clinical diagnosis
Metabolic panel
FBC
Thyroid function tests
Patient health questionnaires 2 and 9
Edinburgh postnatal depression scale
Geriatric depression scale
Cornell scale for depression in dementia

Investigations to consider:
24hour free cortisol
Vit B12
Folic acid

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10
Q

What are important discussions to have with patients with depression

A

Although you may often feel that nothing can help you, effective treatments are available.
Medicines and psychotherapy are the most common treatments
There are many different types of antidepressant meds
They may take several weeks before they become effective and should be taken for many months to prevent recurrent symptoms
Talk therapy allows the patient to explore and change thoughts, attitudes and relationship problems associated with depression
Mild or moderate depression can be treated with therapy alone but sever depression requires both therapy and medication
Warn of problems from abrupt discontinuation of antidepressants
Warn that when initially start taking med, pt may have more energy and therefore may be at greater risk to follow through with suicidal ideations and so must be under regular review especially at beginning of med treatment.
Suicidal risk management is critical

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11
Q

What is suicidal risk management in depressed patients

A

Suicidal risk management is critical, especially as the risk may increase early in treatment.
Routinely asking patients about suicidal ideation and reducing access to lethal menas can reduce risk of suicide. Close telephone follow up by a trained psychiatrist may help reduce the risk of death by suicide after a previous suicide attempt

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12
Q

How is depression treated

A

Goal is to eradicate symptoms of depression, improve daily functioning and quality of life, improve workplace functioning, reduce suicidality, minimise treatment adverse effects and prevent relapse.

Treatment options:

  • antidepressants
  • other pharmacotherapies
  • psychotherapies
  • supportive interventions
  • electroconvulsive therapy (ECT)

Antidepressant options:

  • selective serotonin reuptake inhibitors (SSRIs) (citalopram, fluoxetine, sertraline)
  • serotonin-noradrenaline reuptake inhibitors (SNRIs) (venlafaxine, desvenlafaxine, duloxetine)
  • dopamine reuptake inhibitor (bupropion)
  • mirtazapine (a 5-HT2 receptor antagonist)

Therapy options:

  • CBT
  • Interpersonal psychotherapy (IPT)
  • Problem solving therapy (PST)
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13
Q

What are the risks and benefits of treatment for depression

A

Choice of drug should be based on patient preference, tolerability and past evidence of effectiveness in the patient
Although the net result of antidepressant response is a significant reduction in suicidal ideation, there is evidence of increasedsuicidal behaviour in the first weeks of treatment, particularly in teens and young adults and in those on relatively high starting doses
Follow up pt after 1 to 2 weeks and then monthly for next 12 weeks
Patients are likely to begin to show a response within the first 1 to 2 weeks of treatment, however successful to the point of remission of all symptoms may take 6 to 8 weeks.
Caution required when switching from one antidepressant to another due to the risk of drug interactions, serotonin syndrome, withdrawal symptoms or relapse

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14
Q

What is anxiety

A

Common condition defined as chronic, excessive worry for at least 6 months that causes distress or impairment.

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15
Q

What is the lifetime prevalence of anxiety

A

7.8%

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16
Q

Who is most affected by anxiety

A

More common in high income countries than in lower income countries
Usually starts in adulthood and persists over time
Increased risk during pregnancy and post-natally
Often occurs along with or precedes other mental health disorders.

Patients with chronic physical health conditions, including cardiovascular disease, cancer, respiratory disease, diabetes and PCOS.

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17
Q

What causes anxiety

A

No single cause but an increase in minor life stressors, the prescence of physical or emotional trauma and genetic factors all seem to contribute

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18
Q

What are the risk factors for anxiety

A

Family history of anxiety
Physical or emotional stress
History of physical, sexual or emotional trauma
Other anxiety disorders such as panic disorder, social phobia or specific phobias may co-occur
Chronic physical health condition
Female sex

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19
Q

How does anxiety present

A

At least three key symptoms out of a possible six are required to make a diagnosis:

  • restlessness or nervousness
  • easily fatigued
  • poor concentration
  • irritability
  • muscle tension
  • sleep disturbance

Other diagnostic factors:

  • headache
  • sweating
  • dizziness
  • GI symptoms
  • Muscle aches
  • tachycardia
  • SOB
  • Trembling
  • Exaggerated startle response
  • Chest pain (uncommon)
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20
Q

What are the differentials in suspected anxiety

A
Panic disorder
Social phobia
OCD
PTSD
Somatoform disorders
Depression
Substance or drug induced anxiety disorder
CNS depressant withdrawal
Situational anxiety (non-pathological)
Adjustment disorder
Cardiac disease
Pulmonary conditions
Hyperthyroidism
Infections
Peptic ulcer disease
Crohn's disease
IBS
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21
Q

How is suspected anxiety investigated

A

Clinical diagnosis

Consider:

  • thyroid function tests
  • urine drug screen
  • 24 hour urine for vanillymandelic and metanephrines
  • Pulmonary function tests
  • ECG
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22
Q

What are important discussions to have with a patient diagnosed with anxiety

A

Involve the pt and their significant others in choice of treatment.
If accompanied by depression (especially with suicidal thoughts), or if drug or alcohol abuse is present, advise pt that they should seek medical help for symptoms that cause significant distress or impairment in functioning

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23
Q

How is anxiety treated

A

The main goals are to improve symptoms of anxiety and to reduce or eliminate disability

Pharmacotherapy and psychotherapy are reasonable treatments and are bothe considered first line options or may be used together.

Non-drug therapies:

  • Cognitive behavioural therapy (CBT) and cognitive therapy (CT) both help people respond differently to worry habits
  • Mindfulness or meditation
  • Applied relaxation
  • Sleep hygeine counselling
  • Exercise interventions
  • Self help books
  • IPT

Pharmacotherapy:

  • SSRI
  • SNRI
  • other antidepressant (eg mirtazapine, busiprone)
  • TCA
  • Second generation antipsychoitic
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24
Q

What is alcohol dependence

A

A common psychoatric disorder that is multifactorial in aetiology, chronic in nature and is associated with a wide variety of medical and psychiatric sequlae.
Features include:
-Increased tolerance
-Withdrawal
-Impaired control of drinking behaviour
-Continued alcohol use despite adverse consequences

Problematic alcohol use is classified in the DSM-5 as alcohol use disorder, with severity specified as mild, moderate or severe, depending on the number of diagnostic criteria that has been met

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25
Q

What is alcohol withdrawal syndrome

A

Can follow sudden cessation or reduction in alcohol consumption

Combination of physical and emotional symptoms:

  • tremors
  • anxiety
  • nausea
  • vomiting
  • headache
  • an increased heart rate
  • sweating
  • irritability
  • confusion
  • insomnia
  • nightmares
  • high blood pressure

Can be serious so assessed by the Clinical Institute Withdrawal Assessment for Alcohol

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26
Q

How common is alcohol dependence

A

Alcohol is one of the most widely used psychoactive substances
8 million people currently meet diagnostic criteria for alcohol-use disorders in the US
In primary care settings the prevalence is around 20-36%
Significant global mortality burden (3.2% of global deaths)
More than 24% of English population consume alcohol in a harmful way

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27
Q

Who is mostly affected by alcohol dependence

A

M>F
Lifetime prevalence:
-males 10%
-females 4%

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28
Q

What causes alcohol dependence

A
Multifactorial aetiology
50% of the risk of developing alcohol use disorder is gentically determined 
Association with psychiatric disorders:
-Affective disorders
-Anxiety disorders
-PTSD
-Schizophrenia
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29
Q

What is the clinical course for patients with alcohol dependence

A

Characterised by phases of repeated intoxication, withdrawal and abstinence
Progresses from impulsivity to compulsivity

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30
Q

What are the risk factors for alcohol dependence

A

Family history of alcoholism
Pre-morbid antisocial behaviour
High trait anxiety level
Lack of facial flushing on exposure to alcohol
Low responsivity to the effects of alcohol

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31
Q

How does alcohol dependence present

A

Increased tolerance
Denial (be sure to question relatives)
Overwhelming desire for alochol
Out of control drinking
An increasing consumption of alcohol
Social, economic, legal, psychological problems
Nausea, vomiting, abdo pain, haematemesis
Muscle cramps, pain, tendernessm altered sensory perception
Nicotine dependence comorbidity

Withdrawal:

  • Increased autonomic activity
  • Agitation
  • Nervousness
  • Generalised seizures
  • Delirium
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32
Q

What signs may a patient with alcohol dependence have on examination

A
Increased/decreased liver size jaundice, ascites
Hypertension
Tachycardia
Impaired nutritional status
Alterations in normal dental hygeine
Depressions
Sweating/ clammy skin
Hand tremors
Anxiety
Insomnia
Dilated pupils
Irritability
Fatigue

Withdrawal:

  • tachycardia
  • hypotensive
  • tremor
  • confusion
  • fits
  • hallucinations
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33
Q

What are the differentials in suspected alcohol dependence

A

Other substance misuse (especially sedatives)

Psychiatric disorders

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34
Q

How is a patient with suspected alcohol dependence investigated

A

Diagnosed when, over a 12 month period, the patient’s drinking has caused clinically significant impairment or distress, as determined by the presence of at least 2 or more diagnostic criteria

CAGE
Cut down on drinking?
Annoyed by being criticised for drinking
Guilt over drinking
Ever had a drink first thing in morning to steady nerves or get rid of a hangover

Dignosis interview:
-DSM 5 or ICD 10 criteria to make diagnosis
-Alcohol Use Disorders Identification Test
Severity of Alcohol Dependence Questionnaire

Bloods:
-Increased YGT
-Increased ALT
-Increase MCV
-AST:ALT>2
-Decreased urea
-Decreased platelets
Ultasound imaging of fatty liver/ cirrhosis
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35
Q

How is alcohol dependence treated

A

Detoxification and supportive medical care
-diazepam
-lorazepam
-Oxazepam
-Thiamine
Frequent reassurancem, low-stimulation environment, hydration, vitamin infusion (especially thiamine supplementation or infusion for the prevention/ treatment of Wekicke’s encephalopathy)

Inpatient speciality treatment recommended in the following patients:
-previous episode of significant alcohol withdrawal complications
-concurrent moderate-to-severe medical conditions
-concurrent moderate-to-severe psychiatric conditions
-highly adverse life circumstances
If intensive monitoring not required then outpatient treatment recommended

In mild alcohol dependence:

  • physician advise and brief interventions
  • Pharmacotherapy to prevent relapse and support abstinence:
    • Naltrexone
    • Acamprosate
    • Disulfiram
    • Nalmefene

Prevention:

  • family intervention
  • internet based interventions
  • routine screening in primary care
  • Alcoholic Anonymous support groups
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36
Q

What are the potential complications in alcohol dependence

A

Liver cirrhosis
Mallory-Weiss syndrome
Alcoholic liver disease
Dilated cardiomyopathy- arrythmias, stroke
Oral and oesophageal cancer
Pancreatitis
Vitamin deficiencies (Wernicke-Korsakoff syndrome- vision changes, ataxia, impaired memory)

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37
Q

What is the prognosis in those with alcohol dependence

A

Relapse is common particularly in first 12 months after treatment initiation

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38
Q

What is self harm

A

Self-inflicted injury that is not associated with an implicit or explicit intent to die

Self-harm is a broad term which may involve:

  • self-injury
  • cutting
  • burning
  • overdose
  • ligature
  • physical relief of emotional distress by converting emotional suffering to physical

Deliberate self-harm is not an attempt at suicide in the vast majority of cases.

Usually an attempt to maintain control in very stressful situations or emotional pressures (e.g. bullying, abuse, academic pressure or work pressure)

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39
Q

How common is self harm

A

Very
Especially in young people
~10% of young people self harm

40
Q

Who is affected by self harm

A

Around one in every four 16-24 year old women which is more than twice the rate for men in the same age group.

Around one in every 20 men and one in every 12 women have attempted suicide at some point with highest rates in women aged 16-24 and men aged 25-34 years

41
Q

What causes self harm

A

Psychiatric disorder:

  • Depression
  • Borderline personality disorder
  • Bipolar disorder
  • Schizophrenia
  • Drug misuse
  • Alcohol abuse

Social problems:

  • Child abuse
  • Relationship problems with partners, friends and family
  • Being unemployed, or work difficulties
42
Q

What are the risk factors for self harm

A
Mental health diagnosis
Age
Substance misuse
Living with disability
Socioeconomic disadvantage
Chronic health problems
LGBTQ+ community
Bereaved by suicide
Involvement in the criminal justice system
Repetition of self-harm is associated with long-standing psychosocial vulnerabilities

Risk factors: not always present and a person can have some/all of above and never self harm

43
Q

How does self harm present

A
Withdrawn
Stressed
Feeling hopeless
Thoughts of self-harm and suicidal ideation
Marks on skin
Self-inflicted injuries:
-burning
-cutting
-ingesting toxic substances
44
Q

What other conditions may present similarly to self harm

A

Suicide attempt

45
Q

How would an individual with suspected self harm by investigated

A

When an individual presents in primary care following an episode of self-harm healthcare professionals should urgently establish the likely physical risk and the person’s emotional and mental state
Evaluation of social, psychosocial, motivational factors of self-harm

Current suicidal intent and hopelessness

  • thoughts of ending life
  • plan of how this would be done
  • access to the supplies needed to carry out this plan
  • started to put affairs in order (writing a will, writing a note to loved ones)

Full mental health/social needs assessment:

  • PHQ-9
  • GAD-7
46
Q

What is the management plan for those who self harm

A

Putting support in place:

  • develop trust with patient
  • treat psychiatric illness
  • assessment by local MH services
  • risk management plan
  • assessing risk
  • 3 to 12 sessions of psychological intervention for reducing self-harm
  • support group

Treatment of underlying MH condition (e.g. depression, anxiety)

Overdose treatment:

  • Activated charcoal reduces absorption of the drug
  • Should be used with caution for drowsy or comatose patients due to risk of aspiration or reduced GI motility
  • N-acetyle Cysteine used in paracetamol overdose

Preventative strategies:

  • protective support - alcohol drug avoidance, healthy sleep, parental support
  • prescribing medication in least dose if risk of self-poisoning
  • self help links and leaflets

Referral:

  • Psych team
  • Self refferal information (e.g. support groups, MIND charity, Crisis team details)
  • A and E if extensive self-harm
47
Q

What are the complications of self harm

A

Suicide/death
-increased risk by between 50 and 100 fold compared to rest of population

Physical health and life expectancy severely compromised

Acute liver failure in paracetamol overdose

Permanent scarring of skin

Damge to tendons and nerves caused by self cutting and other injuries

48
Q

What is the prognosis after self harm diagnosis

A

High risk of repetition of self harm and suicide due to long standing psychosocial vulnerabilities
Some people will use the harm as a coping strategy and so it will resolve when the problems are resolved

49
Q

What is somatisation

A

Somatic syndrome and related disorders are those with prominant physcial symptoms associated with significant distress and impairment of function that are not linked to any physical/mental disorder.
Multiple physical symptoms present for at least two years
Patient refuses to accept reassurance or negative test results
Individuals are not faking the symptoms, they are real but cannot be explained
Previously thought to result from psychological stress that is unconsciously expressed somatically
Can affect any organ system

50
Q

How common is somatisation

A

10-15% od primary care patients have multiple unexplained symptoms that are present for more than 2 years
The prevalence of somatic symptom disorder is not known but may be around 5-7%

51
Q

Who is affected by somatisation

A

F>M

High prevalence amoung paediatric patients

52
Q

What causes somatisation

A

Chronic and/or acute stress or conflict in combination with either:

  • emotional processing deficits
  • avoidance tendancies
  • social, cultural or family taboo against emotional expression
53
Q

What are the risk factors for somatisation

A
History of sexual or physical abuse
History or unstable childhood
Female
Alexithymia (inability to identify and describe one's own emotions)
Neuroticism
54
Q

How does somatisation present

A

Incredibly varied symptoms:

  • Pain
  • GI problems
  • Sexual symptoms
  • Inconsistent paralysis
  • Gait disorders
  • Bizarre movements
  • Generalised seizure-like motor movements without loss of awareness
  • Unusual neurological deficits

Location, kind and severity of symptoms can change over time with the only exception to this being the symptom of pain

Social history:

  • Recent life stressors
  • Remote life stressors

Cognitive symptoms:

  • Forgetful
  • Unable to multitask
  • Short term memory loss
  • Persistent worrying about symptoms
  • Thoughts of death
  • Tendancy to suppress and aboid emotions
  • Rumination (deep thoughts)

Hoover’s sign:
-Involentary extension of the psuedoparalysed leg when the unaffected leg is flexing against restance can indicate functional psychogenic aetiologies

Speach disturbances:

  • Aphonia
  • dysphonia
  • Stuttering
  • Foreign accent syndrome
  • All can indicate functional psychogenic aetiologies

Distractable symptoms:
-Disappear if attention drawn elsewhere in consultation

Inconsisten examination findings:
-e.g patient claiming to be blind but avoiding obstacles when walking

55
Q

What are the differentials in suspected somatisation

A
Bipolar disorder
Schizoaffective disorder
Panic disorder
Anxiety
Schizophrenia
Factitious disorder
Malingering
Health anxiety disorder
Body dysmorphia
56
Q

How should a patient with suspected somatisation be investigated

A

At initial presentation, should have lab testing to rule out potential medical or neurological conditions

Continuous EEG monitoring for pattern recognition in non-epileptic seizures

Comprehensive neuropsychological testing

Standardised personality testing

Focused symptoms inventories

DSM-5 criteria:

  • > 1 symptom of altered voluntary motor or sensory function
  • Symptom cannot be accredited to medical or psychiatric disorder
57
Q

How would somatisation be explained to the patient

A

Do not have a life threatening illness but a condition which has no cure and so the goal of treatment is to control the symptoms

Do not say that it is to take away symptoms or relieve illness as then may substitue with another symptom

58
Q

How is a patient with somatisation managed

A

Management plan:

  • Full sympathetic history
  • Exclude disease but avoid unnecessary referral for investigation
  • Seek specific treatable psychiatric syndromes
  • Demonstrate to pt that they are believed
  • Give positive explanation for symptoms, including but not overemphasising psychological factors
  • Encourage return to normal functioning
Treatments:
-CBT
-Physio
-Hypnosis
-Biofeedback training
-Benzodiazepine
-Treat comorbid psychiatric disorders
-Antidepressants
-Atypical antipsychotic
-Electroconvulsive therapy
-Exploration of psychosocial stressors:
(BATHE)
B-ackground
A-ffect
T-roubles
H-andle
E-mpathy
59
Q

What are the potential complications of somatisation

A

Depression
Anxiety
Suicidal ideation
Poor doctor-patient relationship

60
Q

What is the prognosis for those with somatisation

A

-50 to 90% short term resolution of symptoms but 25% then relapse or develop new symptoms over time

Favourable prognostic factors:

  • Acute onset of symptoms
  • Precipitation by a well-defined stressful event
  • Good premorbid health
  • Absence of psychiatric or neurological comorbidities

Patients with many somatic symptoms, anxiety or depression, and old age or marked impairment are more likely to have persistent symptoms

61
Q

What is delirium

A

Sometimes called acute confusional state
An acute, fluctuating syndrome of inattention, impaired level of consciousness and disturbed cognition
Usually develops over hours to days and behavioural disturbance, personality changes and psychotic features may occur

62
Q

What are the types of delirium

A

Hyperactive delirium:
Can present as inappropriate behaviour, hallucinations, agitations, restlessness and wandering

Hypoactive delirium:
Can present with lethargy and reduced concentration and appetite and quiet and withdrawn

Mixed delirium:
Can present with signs and symptoms of both types

63
Q

How common is delirium

A

Prevalence if delirium in primary care is thought to be between 1-2%
0.4% of the general population
25% of older adults (>65)
50% of older people in hospital
3-45% of patients in palliative care are estimated to be affected by delirium

64
Q

Who is affected by delirium

A

Elderly
Patients with multiple co-morbidities
Those with a predisposing factor

65
Q

What causes delirium

A

(PINCH ME)

P:

  • pain
  • palliative
  • post-surgical

I:

  • infection
  • isolation

N:

  • nutrition
  • night pattern (sleep cycle)
  • noise (too loud/quiet/disturbing)

C:

  • constipation
  • continence (new changes)

H:

  • hydration status
  • hyper or hypo metabolic/endocrine conditions
  • hallucinations

M:

  • medication
  • mobility (changes/falls)

E:

  • environment (over or under stimulated)
  • emotional (stressors)
66
Q

What are the risk factors for delirium

A
>65
Cognitive impairment (e.g. dementia)
Frailty
Multiple co-morbidities (e.g. stroke or heart failure)
Hip fracture
Psychological agitation
Fanctional impairment
Iatrogenic events (e.g. bladder catheterisation, polypharmacy or surgery)
History of alcohol excess
Sensory impairment (visual or hearing loss)
Poor nutrition
Lack of stimulation
Terminal phase of illness
67
Q

How does delirium present

A
8 signs of delirium:
D-isordered thinking
E-uphoric
L-anguage impaired
I-llusions/delusions/hallucinations
R-eversal of sleep/awake cycle
I-nattention
U-naware/disorientated
M-emory deficits
68
Q

What are the differentials for suspected delirium

A
Dementia
Depression
Anxiety
Epilepsy
Primary mental illness
Thyroid disease
Charles Bonnet syndrome
69
Q

How is a patient with delirium investigated

A

Look for a cause:

  • Septic screen
  • Urinalysis
  • Sputum culture
  • Full blood count
  • Folate and B12
  • U and Es
  • HbA1c
  • Calcium
  • LFTs
  • Inflammatory markers
  • Drug levels
  • TFTs
  • Chest Xray
  • Electrocardiogram
  • AMTS or MMSE
70
Q

How is a patient with delirium treated

A

As well as identifying and treating the underlying cause, aim to:

  • Reorientate the patient
  • Encourage communication with family
  • Monitor fluid levels
  • Mobilise and encourage physical activity
  • Practice sleep hygeine
  • Avoid or remove catheters, IV canulae, monitoring leads etc due to risk of infection and may be pulled out
  • Watch out for infection and physical discomfort
  • Review medications
  • Regularly review patient
71
Q

What are the potential complications of delirium

A
  • Delirium may persist beyond the duration of the original illness by several weeks in the elderly
  • Increased mortality
  • Increased length of stay in hospital
  • Nosocomial infection
  • Increased incidence of dementia
  • Falls
  • Pressure sores
  • Continence problems
  • Malnutrition
  • Functional impairment
  • Distress for the patient, their family and/or carers
72
Q

What is the prognosis for those with delirium

A

Delirium has a fluctuating course and recovery can be rapid or take weeks to months

Factors associated with a poorer prognosis include:

  • pre-existing dementia or cognitive impairment
  • hypoxic illness such as severe pneumonia
  • visual impairment
73
Q

What is dementia

A

A neurodegenerative syndrome with progressive decline in several cognitive domains.
Initial presentation is usually of memory loss over months or years.

74
Q

What is early onset dementia

A

That which develops under age of 65 years

75
Q

What is mild cognitive impairment

A

Impairment which does not fulfil the diagnostic criteria for dementia

76
Q

What is Alzheimer’s disease

A
  • 50-75% of dementia cases
  • Atrophy of the cerebral cortex and formation of amyloid plaques and neurofibrillary tangles and acetylcholine production in affected neurones is reduced
  • Post-mortem studies show that AD and VD often co-exist
77
Q

What is vascular dementia

A
  • ~25% of dementia cases
  • Cumulative effect of many small strokes
  • Stepwise deterioration is characteristic (but often hard to recognise)
  • Look for evidence of arteriopathy (↑BP, History of stroke, focal signs, CNS signs)
  • Do not use acetylcholinesterase inhibitors memantine in these patients
78
Q

What is Lewy body dementia

A
  • 15-25% of dementia cases
  • Fluctuating cognitive impairment, detailed visual hallucinations, and Parkinsonism
  • Histology is characterised by Lewy bodies in the brainstem and neocortex
  • Avoid using antipsychotics in Lewy body dementia due to high risk of neuroleptic malignant syndrome
79
Q

What is fronto-temporal dementia

A
  • Frontal and temporal atrophy with loss of >70% of spindal neurons
  • Patients display executive impairment, behavioural/personality change, disinhibition, hyperorality, stereotypes behaviour, emotional concern
  • Episodic memory and spatial orientation are preserved until the later stages
80
Q

How common is dementia

A

~800,000 people with dementia in the UK

81
Q

Who does dementia affect

A

Prevalence increases with age with 20% of people over 80 y/o are known to have dementia yet probably only half of cases are diagnosed
People with Trisomy 21 are at increased risk
Overall prevalence is similar in men and women

82
Q

What causes Alzheimer disease

A
  • Formation of beta amyloid plaques and neurofibrillary tangles
  • Neuronal loss is selective - the hippocampus, amygdala, temporal neocortex and subcortical neuclei
  • 95% of AD patients show evidence of vascular dementia too
  • Cerebral atrophy (medial temporal lobe), senile plaques, amyloid deposition, neuro-fibrillary tangles, acetyle choline levels reduced
83
Q

What causes vascular dementia

A

Final common end point of multiple vascular pathologies

    • infarction
    • leukoaraiosis
    • haemorrhage
    • AD comorbidity
84
Q

What causes levy body dementia

A
  • Most cases are sporadic but some familial clusters have been reported
  • Toxic protein aggregation
  • Abnormal phosphorylation
  • Molecular mechanisms of nitriation, inflammation, oxidative stress and lysosomal dysfunction
85
Q

What causes fronto-temporal dementia

A
  • Focal neurodegeneration of the frontal temporal lobes of the brain
  • Genetics:
    • Autosomal dominant transmission
    • Microtubule-associated proetien tau gene
    • Progranulin gene
  • Other causes
    • Alcohol/drug abuse
    • Repeated head trauma
    • Pellagra
    • Whipple’s disease
    • Huntington’s
    • CJD
    • Parkinson’s
    • HIV
86
Q

What are the risk factors for dementia

A
1st degree relative with AD
Obesity/ increased weight circumference
Down's syndrome
Homozygosity for apolipoprotein E E4 allele
PECALM, CL1 and CL2 variants
Vascular risk factors (↑BP, diabetes dyslipidaemia, ↑homocysteine, AF)
↓physical/cognitive activity
Depression
Loneliness
Smoking
Alcohol misuse
Recreational drug use
Stroke
87
Q

How does Alzheimers present

A
(5 A’s of Alzheimer’s)
Amnesia 
Aphasia 
Agnosia 
Apraxia 
Associated Behaviours 
Memory loss 
Disorientation 
Nominal Dysphasia
Misplacing items/getting loss 
Apathy 
Decline in activities of daily living and instrumental activities of daily living 
Personality change 
Mood changes 
-depressed
-apathetic
-irritability. 
Poor abstract thinking 
-complex tasks requiring organisation and planning become difficult 
Constructional dyspraxia 
-parietal lobe deficits may lead to difficulties completing the clock-drawing test
88
Q

How does vascular dementia present

A

History of stroke
Difficulty solving problems
Apathy

Vary depending on region of damage:
Frontal- personality change
Parietal- loss of speech
Temporal- difficulty with memory

Symptoms appear suddenly 
Disinhibition
Poor attention
Retrieval memory deficit
Frontal release reflexes (jaw jerk)
Seizures
89
Q

How does levy body dementia present

A

Cognitive fluctuations (cognition, attention, arousal)
Visual hallucination
Motor symptoms (spontaneous parkinsonian features)
Depression
Repeated falls & syncope
Urinary incontinence
Constipations
Hypersomnia (excessive daytime sleepiness)
Hyposmia

Severe antipsychotic sensitivity 
Orthostatic hypotension 
Attention and visuospatial abnormalities (key distinguishing feature from AD) 
Delusions 
REM sleep behavioural disturbance
90
Q

How does fronto-temporal dementia present

A

Poor emotional processing
Coarsening of personality, social behaviour and habits
FHx of FTD
Altered eating habits
Progressive self-neglect and abandonment of work, activities and social contacts
Development of memory impairment, disorientation or apraxias
Progressive loss of language fluency or comprehension
Inattentiveness, puerile preoccupations, economy of effort and impulsive responding
Stealing, practical jokes, unusual sexual advances

91
Q

What are the differentials for suspected dementia

A
Delirium 
Depression 
Bipolar 
Cerebrovascular events 
Intracranial tumours
92
Q

How would a patient with dementia be investigated

A
Look for reversible/organic causes. 
•↑TSH/↓B12/↓folate 
•↓Thiamine (e.g., alcohol) 
•↓Ca2+
•Check MSU, FBC, ESR, U&E, LFT, glucose 

Cognitive / memory assessments
•AMTS
•Mental State Exam
•6 Six-item Cognitive Impairment Test (6CIT)

CT/MRI

Bloods: 
FBC
U&Es and creatinine, glucose
calcium
magnesium
LFTs
TFTs
cardiac enzymes
vitamin B12 levels
syphilis serology
autoantibody screen and PSA
→ ensure no treatable cause missed. 

ECG
Biopsy
Full neuro examination

93
Q

What is the diagnostic criteria for all types of dementia

A

Diagnosis = clear history progressive impairment memory + cognition and personality change – NO CHANGE CONSCIOUSNESS!

Diagnostic criteria for all types dementia:

  • Affect ability function normal activities
  • Represent decline previous level function
  • Not explained by delirium or other major psychiatric disorder
  • Established by history taking patient + formal cognitive assessment
  • Involve impairment of at least 2 of:
    • Ability to remember new info
    • Judgement/handling complex tasks
  • -Visuospatial ability
    • Language function
    • Personality/behaviour
94
Q

What is the management for patients with dementia

A

Screening relatives if genetic cause found. Rehabilitation
Supporting carers
Discussing management with suffers when they have capacity.
Treating problems – e.g. UTI, chest infection, pain etc.
Safety – arrange door catches, fire/electrical safety.
Cognitive behavioural therapy (CBT)
Community care (eg. music therapy, cognitive stimulation programmes, memory loss management etc)
Inform DVLA for driving
Pharmacology treatment

95
Q

What is the pharmacology treatment for dementia

A

AChE inhibitor treatment - Donepezil, Galantamine or Rivastigmine = 1st line

N-methyl-D-aspartate (NMDA) antagonists – Memantine = 2nd line

Antidepressants

  • Avoid tricyclic antidepressants + other anticholinergics → may have an adverse effect on cognition.
  • Avoid antipsychotics unless serious threat to behaviour (e.g., aggression/violence/agitation) as can be dangerous so benefits/risks need to weighed up.
96
Q

What are potential complications of dementia

A

Hospital-acquired infections - eg, Clostridium difficile and methicillin-resistant Staphylococcus aureus (MRSA).
Pressure sores.
Fractures – e.g., femoral or hip fractures from falls.
Residual psychiatric and cognitive impairment.
Some progress to stupor, coma and eventual death

97
Q

What is the prognosis for those with dementia

A

The outlook for most types of dementia is poor – vascular poorer than Alzheimer’s.
Dementia usually continues to worsen over time with the condition usually progressing over years until the person’s death
AD has a mean survival of 7yrs from initial symptom presentation