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
What is alcohol withdrawal syndrome
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
26
How common is alcohol dependence
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
27
Who is mostly affected by alcohol dependence
M>F Lifetime prevalence: -males 10% -females 4%
28
What causes alcohol dependence
``` Multifactorial aetiology 50% of the risk of developing alcohol use disorder is gentically determined Association with psychiatric disorders: -Affective disorders -Anxiety disorders -PTSD -Schizophrenia ```
29
What is the clinical course for patients with alcohol dependence
Characterised by phases of repeated intoxication, withdrawal and abstinence Progresses from impulsivity to compulsivity
30
What are the risk factors for alcohol dependence
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
31
How does alcohol dependence present
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
32
What signs may a patient with alcohol dependence have on examination
``` 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
33
What are the differentials in suspected alcohol dependence
Other substance misuse (especially sedatives) | Psychiatric disorders
34
How is a patient with suspected alcohol dependence investigated
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 ```
35
How is alcohol dependence treated
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
36
What are the potential complications in alcohol dependence
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)
37
What is the prognosis in those with alcohol dependence
Relapse is common particularly in first 12 months after treatment initiation
38
What is self harm
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)
39
How common is self harm
Very Especially in young people ~10% of young people self harm
40
Who is affected by self harm
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
What causes self harm
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
What are the risk factors for self harm
``` 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
How does self harm present
``` Withdrawn Stressed Feeling hopeless Thoughts of self-harm and suicidal ideation Marks on skin Self-inflicted injuries: -burning -cutting -ingesting toxic substances ```
44
What other conditions may present similarly to self harm
Suicide attempt
45
How would an individual with suspected self harm by investigated
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
What is the management plan for those who self harm
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
What are the complications of self harm
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
What is the prognosis after self harm diagnosis
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
What is somatisation
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
How common is somatisation
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
Who is affected by somatisation
F>M | High prevalence amoung paediatric patients
52
What causes somatisation
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
What are the risk factors for somatisation
``` History of sexual or physical abuse History or unstable childhood Female Alexithymia (inability to identify and describe one's own emotions) Neuroticism ```
54
How does somatisation present
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
What are the differentials in suspected somatisation
``` Bipolar disorder Schizoaffective disorder Panic disorder Anxiety Schizophrenia Factitious disorder Malingering Health anxiety disorder Body dysmorphia ```
56
How should a patient with suspected somatisation be investigated
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
How would somatisation be explained to the patient
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
How is a patient with somatisation managed
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
What are the potential complications of somatisation
Depression Anxiety Suicidal ideation Poor doctor-patient relationship
60
What is the prognosis for those with somatisation
-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
What is delirium
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
What are the types of delirium
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
How common is delirium
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
Who is affected by delirium
Elderly Patients with multiple co-morbidities Those with a predisposing factor
65
What causes delirium
(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
What are the risk factors for delirium
``` >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
How does delirium present
``` 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
What are the differentials for suspected delirium
``` Dementia Depression Anxiety Epilepsy Primary mental illness Thyroid disease Charles Bonnet syndrome ```
69
How is a patient with delirium investigated
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
How is a patient with delirium treated
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
What are the potential complications of delirium
- 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
What is the prognosis for those with delirium
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
What is dementia
A neurodegenerative syndrome with progressive decline in several cognitive domains. Initial presentation is usually of memory loss over months or years.
74
What is early onset dementia
That which develops under age of 65 years
75
What is mild cognitive impairment
Impairment which does not fulfil the diagnostic criteria for dementia
76
What is Alzheimer's disease
- 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
What is vascular dementia
- ~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
What is Lewy body dementia
- 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
What is fronto-temporal dementia
- 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
How common is dementia
~800,000 people with dementia in the UK
81
Who does dementia affect
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
What causes Alzheimer disease
- 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
What causes vascular dementia
Final common end point of multiple vascular pathologies - - infarction - - leukoaraiosis - - haemorrhage - - AD comorbidity
84
What causes levy body dementia
- 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
What causes fronto-temporal dementia
- 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
What are the risk factors for dementia
``` 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
How does Alzheimers present
``` (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
How does vascular dementia present
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
How does levy body dementia present
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
How does fronto-temporal dementia present
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
What are the differentials for suspected dementia
``` Delirium Depression Bipolar Cerebrovascular events Intracranial tumours ```
92
How would a patient with dementia be investigated
``` 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
What is the diagnostic criteria for all types of dementia
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
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What is the management for patients with dementia
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
What is the pharmacology treatment for dementia
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.
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What are potential complications of dementia
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
What is the prognosis for those with dementia
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