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Year 3 Sem 1 COPY COPY > PA30324 4. Clinical Therapeutics > Flashcards

PA30324 4. Clinical Therapeutics Flashcards

1
Q

What is the impact of persisting pain?

A
  • Sleep problems
  • Loss of fitness
  • Money worries
  • Medication side-effects
  • Feeling low
  • Stress, fear, anger, shame
  • Grief and Loss
  • Relationship worries
  • Loss of employment
  • Social isolation
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2
Q

Why does the WHO analgesic ladder not work?

A
  • It wasn’t designed for all types of pain
  • Acute and Chronic pain should be treated holistically
  • Medicines are limited in effectiveness particularly in chronic pain
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3
Q

Name some common drugs for pain

A
  • Paracetamol
  • NSAIDS
  • Anti-depressants
  • Gabapentinoids
  • Opioids
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4
Q

What are the possible causes of depression?

A
  • Psychological distress such as adverse life events
  • Genetic/hereditary factors
  • Biochemical
  • Concurrent chronic illness
  • Medication
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5
Q

What the medication-related causes of depression?

A
  • Corticosteroids
  • Oral contraceptives
  • H2 receptor antagonists
  • Calcium channel blockers
  • Retinoic acid derivatives
  • Interferon & Ribivarin preparations
  • Methyldopa
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6
Q

What are the treatment goals of depression?

A
  • Increase remission rates
  • Prevent relapse
  • Restore physical functioning
  • Restore social functioning
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7
Q

Describe the 4 stepped-care model of Depression

A

Step 1

  • All known and suspected presentation of depression
  • Assessment, support, psycho-education, active monitoring and referral for further assessment and interventions

Step 2

  • Persistent subthreshold depressive symptoms; mild to moderate depression
  • Low-intensity psychosocial interventions, psychological interventions, medication and referral for further assessment and interventions

Step 3

  • Persistent subthreshold depressive symptoms or mild to moderate depression with inadequate response to initial interventions; moderate and severe depression
  • Medication, high-intensity psychological interventions, combined treatments, collaborative care2, and referral for further assessment and interventions

Step 4

  • Severe and complex1 depression; risk ot life; severe self-neglect
  • Medication, high-intensity psychological interventions, electroconvlsive therapy, crisis service, combined treatments, multiprofessional and inpatient care
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8
Q

What are the NICE general principles of care for depression?

A

Depression and anxiety
- In comorbid depression and anxiety, treat the depression as a priority

Patient preference
- Consider patient preference and the experience and outcome of previous treatment when deciding on treatment

Information
- Give patients and carers appropriate information on the nature, course and treatment of depression, including the use and likely side effects of medication

Consent
- Ensure that a patient can give meaningful and properly informed consent, especially when heo r she has a more severe depression

Management of care
- Where management is shared between primary and secondary care, establish a clear agreement between all professionals on the responsibility for monitoring and treatment

Assessment
- Consider the psychological, social and physical characteristics of the patient and the quality of interpersonal relationships

RIsk
- Always ask the patients with depression directly about suicidal ideas and intent, and advise patients and carers to be vigilant for changes in mood, negativity and hopelessness, and suicidal intent, particulary during high risk periods such as during initaiton of and changes to medication and increased personal stress

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9
Q

Describe treatment options for Mild depressive disorder

A

Social interventions

  • watchful waiting
  • educate
  • sleep and anxiety management
  • exercise
  • guided self-help
  • support groups
Psychological interventions (HF)
- CBT (Cognitive behaviour therapy)

Pharmacological interventions
- the risk-benefit ratio is generally poor for the use of antidepressants in the treatment of mild depression but they may be appropriate in some cases

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10
Q

Describe treatment options for Moderate to Severe depression

A

Social interventions

  • watchful waiting
  • educate
  • sleep and anxiety management
  • exercise
  • guided self-help
  • support groups

Psychological interventions

  • CBT (Cognitive Behaviour Therapy)
  • Problem solving
  • Interpersonal therapy

Pharmacological interventions

Electroconvulsive therapy

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11
Q

Describe response and effects of Antidepressants

A

Response rate

  • 50~70%
  • There is a large placebo response

Time to effect

  • Effects are not instant
  • May start to see significant changes after 2 weeks but 4 to 6 weeks for full effect

Actual evidence for effect

  • Effective in moderate to severe depression WITH supporting cognitive based treatments
  • None really in children, some in adolescence
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12
Q

Describe how a particular choice of antidepressant is used

A

First choice

  • Safety
  • Effectiveness
  • Tolerability
  • Cost

Effect needed

  • Cant sleep/older = mirtazepine
  • Mood altering = SSRI

First choice
- SSRI

Previous response to an agent

Older or medical illness
- use one with less anticholinergic & CV side effects

Suicidal risk
- avoid TCA’s

Insomniac
- sedative SE, but warn about drowsiness and driving risks

High alcohol use
- Citalopram or sertraline

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13
Q

What is SSRI?

A
  • First choice antidepressant
  • All have similar side effect profile
    : GI, sexual dysfunction
  • May increase anxiety and/or suicide ideation initially
  • Different duration of actions
  • Safer in overdose than TCA
  • Many have once daily regimens
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14
Q

What are the SSRI serotonergic side effects?

A

Gastrointestinal
- nausea, diarrhoea, decreased/increased apperite

Sexual dysfunction
- e.g delayed ejaculation

Insomnia & Agitation

More rarely bruising and bleeding

More rearely hyponatraemia

  • WIthdrawal symptoms
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15
Q

What is Serotonin Syndrome?

A
  • a predictable reaction when two or more agents increasing levels of serotonin are co-prescribed
  • onset is usualy rapid, often occuring within minutes to hours of elevated serotonin levels
  • encompasses a wide range of clinical findings

Clinical symptms

  • Cognitive: headache, agitation, hypomania, mental confusion, hallucinations, coma
  • Autonomic: shivering, sweating, hyperthermia, vasoconstriction, tachycardia
  • Somatic: myoclonus, hyperreflexia, tremor
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16
Q

How is Serotonin syndrome treated?

A

Treating hyperactive bowel sounds, elevated BP and hyperthermia, overeactive reflexes and clonus grater in lower limbs than upper limbs, mental changes, increased heart rate and blood pressure

  • Stop interacting agents
  • Serotonin antagonist cyproheptadine can be used
  • Support organ function
  • Managing tempeartre
  • Agitation and muscle twitching use benzodiazepines
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17
Q

Describe the TCA antidepressants

A
  • Generally more side effects than SSRIs
  • Postural hypotension, sedation, anticholinergic effects, glaucoma, constipation, hangover effects
  • More toxic in overdose
  • Cardiac toxicity
  • Seizures
  • More complicated dosing
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18
Q

What do patients need to know about antidepressants?

A
  • Symptoms may get worse in first week to 10 days, including increased anxiety & suicide ideation (SSRI)
  • Once well treatment continued for at least 6 months to prevent relapse as depression often reoccurs
  • The chance of staying well are improved by antidepressants
  • Greater than 2 major depressive episodes consider long-term prophylaxis at full therapeutic dose
  • Some people may need treatment for several years
  • Antidepressants are not addictive
  • Antidepressants should not be stopped or changed suddenly
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19
Q

Describe treatment resistant depression

A
  • One third of people will not respond to their first antidepressant
  • About 20% of people never respond to antidepressants and may seek ECT or augmented combinations
  • Try switching to another agent, same class or different if adverse effects
  • Can augment with another medication e.g lithium, sodium valproate or olanapine
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20
Q

Whata re the possible causes of Mania?

A
  • L-dopa
  • Corticosteroids
  • Stimulant misuse
  • Multiple sclerosis
  • Thyroid disease
  • Brain lesion in the limbic area
  • Excess exercise
  • Unopposed antidepressants
  • Life stresses
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21
Q

What are the Pharmacists’ roles in managing mental illness?

A

Community/Generalist

  • monitoring treatments
  • promoting good MH lifestyle advice
  • recognising signs & symptoms
  • appropriate referral; advanced prescriptions
  • MUR, weight managemnt, smoking cessation, CVD risk prevention, diabetes awareness
  • awareness of non-pharmacological therapies
  • awareness of support groups

Specialist roles

  • TDM clinics for lithium
  • Prescribing roles
  • Closely linked to addiction pharmacist’s role
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22
Q

What are the medication options for bipolar disease?

A
  • Mood stabilisers taken long term: lithium, anti-epileptic agents
  • Antipsychotics as needed
  • Hypnotics as needed
  • Antidepressants as needed but with care
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23
Q

What are the non-pharmalogical interventions for BIpolar disease?

A
  • Exercise (but not too much)
  • Enough sleep
  • Advanced directives
  • Diary
  • CBT
  • high intensity psychological therpay
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24
Q

Define personality disorder

A

DSM V
- The essential features of a personality disorder are impairments in personality (self and interpersonal) functioning and the presence of pathological personality traits

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25
Q

What are the 3 different types of personality disorder under DSM V?

A

Cluster A ( odd/eccentric )
- Paranoid
: Distrusting and suspicious interpretation of the motives of others
- Shizoid
: Social detachment and restricted emotional expression
- Schizotypal
: Social discomfort, cognitive

Cluster B ( dramatic/erratic )
- Antisocial
: Disregard for and violation of the rights of others
- Borderline
: Unstable relationships, self-image and affects and impulsivity
- Histrionic
: Excessive emotionality and attention seeking
- Narcissistic
: Grandiosity, need for admiration, lack of empathy

Cluster C ( anxious/fearful )
- Avoidant
: Socially inhibited feelings of inadequacy, hypersensitivity to negative evaluation
- Dependent
: submissive behaviour, need to be taken care of
- Obsessive-compulsive
: Preoccupation with orderliness, perfectionism and control

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26
Q

What are the factors associated with development of personality disorder?

A

Adverse childhood experiences

  • Trauma
  • Abuse
  • Invalidating environment
  • Complex attachment history
  • Social factors including modelling

Emotional aptitude/sensitivity
- Genetics

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27
Q

Describe Schema model and personality patterns

A
  1. Early experience results in formation of a number of maladaptive schemas
  2. Specific, schema-relevant triggers encountered in adult envrionment
  3. Schema activation
  4. Current circumstances processed and experienced similarly to earlier experience (e.g child trauma)
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28
Q

Describe the following talking therapoes that are currently used

  1. Psychodynamic therapies
  2. CBT (Cognitive Behaviour Therapy)
  3. Purely behavioural techniques/behavioural therapy
  4. Humanistic therapies
A
  1. Psychodynamic therapy
    - draws from psychonalaysis and the unconscious
    - less structured than CBT, no homework
    - key idea is that we unconsciously reenact patterns of relationships from our childhood
    - these reenactments are experienced in the patient’s relationship with the therapist and their current relationships
    - They are driven by unconscious feelings which we have ‘defenses against’
    - Psychodynamic therapy focuses on talking openly to bring these feelings into conscious awareness and change them
  2. CBT (Cognitive Behavioural Therapy)
    - Time limited (usually 6-20 sessions)
    - Strucured
    - Face-to-Face therapist
    - FOcused on cognitions (thoughts and behaviours)
    - In the ‘here and now’
    - Suitable for a range of common conditions
    - Homework tasks
  3. Purely behavioural techniques/ behavioural therapy
    - Sometimes in CBT the focus is on changing behaviour to directly influence behaviour
  4. Humanistic therapies
    - Marslow’s hierarchy of needs
    - aim to promote self-actualisation
    - similar to psychodynamic therapies that they are relatively unstructured
    - session number variable
    - less of a focus on mental health vs mental illness
    - goal is to facilitate the person in fulfilling their full potential
29
Q

Give examples of talking therapies signposting

A
  • IAPT
  • Counselling databases
  • BPS British Psychological Society
  • UKCP UK Council for Psychotherapy
  • BABCP
  • BACP
30
Q

What do the following talking therapies focus on?

  1. Psychodynamic therapies
  2. CBT
  3. Behavioural therapies
  4. Humanistic therapies
A
  1. Psychonamic therapies consider relationships and unconscious drives
  2. CBT considers the relationship between thoughts, feelings and behaviours
  3. Behavioural therapies attempt to change behaviours
  4. Humanistic therapies focus on personal growth and development
31
Q

What is the prevalence of Schizophrenia in UK?

A

population ~64.6 million (2014)

- 342,380 out of 64.6 million

32
Q

What are the symptoms of Schizophrenia?

A

Delusion

  • False belief/opinion maintained despite contradiction by reality or rational argument and not explained by culture or religious concepts
  • Persecutory delusions, reference, control, thought insertion and/or withdrawal, special powers, special role/mission

Insight
- Experiences not due to illness but action of others

Speech

  • Blunting
  • Neologisms
  • Disordered and rambling
  • Paucity

Movement

  • Posturing
  • Waxy flexibility
  • Stereotypes and mannerisms
  • Dyskinesias

Mood

  • Flatness
  • Incongruity

Other

  • Avoliton
  • Anergia
  • Social withdrawal
  • Poor self care
  • Socially unconventional behaviour
33
Q

What are the characteristics of the following types of Schizophrenia?

  • F 20.0 Paranoid
  • F 20.1 Hebephrenic
  • F 20.2 Catationic
A

F 20.0 Paranoid

  • Delusions or hallucinations prominent
  • Affective symptoms do not dominate

F 20.1 Hebephrenic

  • Flat/shallow affect or incongruous affect
  • Non-goal directed behaviour or thought disorder affecting speech
  • Delusions or hallucinations do not dominate
F20.2 Catatonic
- One of more, for > 2 weeks of
\: stupor or mutism
\: excitement
\: posturing
\: negativism
\: rigidity
\: waxy flexibility (maintenance of imposed position)
34
Q

Statistics about Physical health and Mental Health

A
  • People with poor mental health are likely to experience 3 times more physical health problems than the general population
  • Those with a mental health illness are more likely to have a poor diet, smoke and have lower exercise levels
  • Mental health patients can die up to 20 years earlier than the general population
35
Q

What are the statistical consequences of Schizophrenia?

A
  • People with mental health problems more likely to suffer poor health for other reasons
  • Mortality 2.5 x average population
  • 1/4 people with Schizophrenia experience another physical complaint
  • Completed suicide 4-13%
  • Type II diabetes 2-4 x higher with schizophrenia
  • Primary treatment modality is pharmacotherapy
36
Q

What do the following Dopamine pathways induce?

  • Mesolimbic pathway
  • Mesocortical pathway
  • Nigrostriatal pathway
  • Tuberoinfundibular pathway
A

Mesolimbic pathway
- positive symptoms

Mesocortical pathway
- negative & cognitive symptoms

Nigrostriatal pathway
- neurological effects & EPSE

Tuberoinfundibular pathway
- prolactin release

37
Q

How is dopamine level related to Schizophrenia?

A

Dopamine

  • positive symptoms due to increased activity at mesolimbic pand nigrostriatal DA pathways
  • negative symptoms due to decreased activity at mesocortical DA pathway
  • increased DA can lead to hallucinations
  • D2 is thought to be associated with schizophrenia
38
Q

How is Serotonin (5-HT) level related to Schizophrenia

A
  • 5-HT.2a blockade can stimulate DA in mesocorticol pathway without increasing activity in mesolimbic
  • decreased 5-HT.2a in frontal cortex in Schizophrenia
  • LSD is a 5-HT2 agonist
39
Q

How is Glutamate level related to Schizophrenia?

A
  • Antagonists of NMDA glutamate receptors can induce schiz-like psychosis
  • DA-ergic dysfunction secondary to problems with glutamatergic neurones
  • Decreased activation at NMDA receptor on cortical interneurones leads to increased activation of mesolimbic (+ symptoms) and decreased activation of mesocortical (- symptoms) DA pathways
  • Decreased activation at NMDA receptors in ventral hippocampus leads to increased activation of mesolimbic DA pathway
40
Q

How are GABA and Acetylcholine levels related to Schizophrenia?

A

GABA

  • Primary inhibitory neurontransmitter in brain
  • decreased synthesis in Schizophrenia
  • decreased GABA-ergic neurone density
  • Altered expression of GABA.a receptors

Acetylcholine

  • acts at muscarinic and nicotinic receptors
  • involved in modulating DA and glutamate
  • implicated in memory, attention, sensory gating, processing&raquo_space; cognitive impairements in schizophrenia
41
Q

Describe the 1st generation (typical) and 2nd generation (Atypical) antipsychotic agents

A

Antipsychotic effects due to antagonism of D2 receptors in temporal cortex

EPSEs caused by antagonism of D2 in basal ganglia

T Cortex (antipsychotic): TA and AA = high blockade
B Ganglia (EPSE): TA = high blockade / AA = low blockade

Cannot block more than 100% so,
- increasing antagonist dose (drug dose or number of drugs) cause EPSE without improved antipsychotic action

1st generation (typical) antipsychotics

  • Primarily aimed at blocking dopamine D2 receptors
  • Side effects most commonly linked including EPSE, anticholinergic effects, sedation…

2nd generation (atypical) antipsychotics 8

  • still block D2 but to lesser extend, more involvement of other receptors
  • side effects most commonly linked including metabolic syndrome, sedation
42
Q

What are the common side effects of Clozapine and the managements for them?

A

Sedation
- give smaller dose in the mornings or single night-time dose

Hypersalivation
- wrap a towel around the pillow

Constipation
- ensure adequate fluid, dietary fibre and exercise

Sore throat and Feverish illness
- important to check their white blood cell count

Seizure
- anticonvulsant

Diabetes, impared glucose tolerance and metabolic syndrome
- encouraged to have regular checks of their physical health

Weight gain
- dietary advice and exercise management is essential

43
Q

Define Dementia and describe its prevalence in UK

A
  • a syndrome consisting of progressive impairement in two or more areas of cognition
    : memory, language, visuopatial, perceptual ability, thinking, problem-solving, personality
  • In 2015, 850,000 people living with dementia
  • > 40,000 people with early-onset dementia (before 65)
  • Total pop prevalnce in over 65s is 7.1% (2013)
44
Q

What are the signs and symptoms of Alzheimer’s disease in early, mid and late stages?

A

Early stage

  • forgetting recent events, difficulty following or recalling conversations
  • misplace items
  • impaired judgement
  • decrease in flexibility, less willing to try new things
  • mood: anxious, irritable, depressed

Mid stage

  • increasing confusion and disorientation
  • behaviour: obsessive, compulsive and/or repetitive
  • difficulty with spatial tasks
  • dysphasia (using wrong words)
  • mood: blunted emotions, sudden mood changes

Late stage

  • Fragmented and incoherent thoughts and language
  • Double incontinence
  • Dysphagia: swallowing and eating problems
  • Weight loss, often severe
  • Mood: unresponsive to stimuli
45
Q

What are the causes and prevalence of VD (Vascular Dementia)?

A
  • Interruption of the brain’s blood supply
  • Ischaemia leads to neuronal cell death and loss of function
  • Risk factors
    : family history, hypertension, male sex, history of strokes/TIAs, diabetes, smoking, AF
  • affects around 150,000 (UK)
  • Preventable: statins, aspirin
46
Q

What are the signs and symptoms of Vascular Dementia?

A
  • Usually a sudden onset and step-wise progression (unlike AD)
  • Focal neurological signs & symptoms
    : Agnosia, Dysarthria, Dizziness and balance problems
  • Relative preservation of personality
  • Difficulty with planning and understanding
  • Feeling disoriented and confused
47
Q

What are the causes and prevalence of Lewy Body Dementia (LBD)?

A
  • Lewy Bodies are circular aggregates of protein that form inside brain cells. Can be identified with histology
  • First identified by Fritz Lewy in 1910
  • Dopaminergic and acetylcholinergic neurotransmission affected by Lewy bodies in the cortex
48
Q

What are the signs and symptoms of Lewy Body Dementia (LBD)?

A

Three core features of LBD

1) Fluctuating concentration and attention
2) Spontaneous Parkinson’s-like motor symptoms
3) Recurring visual hallucinations

  • Progressive but shifting course
  • Memory impairment is less pronounced than other dementias , especially in early stage
  • Other psychotic symptoms are common
49
Q

What are the causes of Frontotemporal dementia (FTD)?

A
  • Genetic factors play a big part in the cause
    : mutations in DNA binding protein 43, MAPT, GRN and C9ORF72 are major known genetic causes
  • The frontal and temporal lobes of the brain shrink
  • The affected parts of the brain can contain microscopic tau filled structures
  • Uncertain risk factors for FTD
50
Q

What are the signs and symptoms of Frontotemporal Dementia (FTD)?

A
  • Tends to present earlier than other dementias (45-65 yrs)
  • Personality and behaviour changes
    : loss of empathy, disinhibition, apathy, excessive risk taking, alterations in food preference
  • Language features
    : limited phrases, slow and hesitant speech, aparaxia, impaired sentence comprehension, impaired object knowledge, word/sentence repetition
51
Q

How is dementia diagnosed?

A
  • NICE (JUNE 2018) recommend that an initial assessment takes place in a non-specialist setting
  • Ideally a person who knows the patient well will also be present. Cognitive, behavioural and psychological symptoms are assessed.
  • If dementia is still suspected then a physical examination is conducted, cognitive testing is undertaken and appropriate blood and urine tests are performed to rule out other, reversible, causes of cognitive decline
52
Q

What are the Cognitive testing instruments recommended by NICE?

A
  • 10-point cognitive screener (10-CS)
  • 6-item cognitive impairment test (6CIT)
  • 6-item screener
  • Memory Impairment Screen (MIS)
  • Mini-Cog
  • Test Your Memory (TYM)
53
Q

What are the other causes of cognitive decline other than dementia ?
Hint: DEMENTIAS

A 
D - Drugs/medication
E - Emotional problems, ears, eyes
M - Metabolic
E - Endocrine
N - Nutritional deficiency
T - Tumour
I - Infection
A - Anaemia or Alcohol
S - Systemic disease
54
Q

Describe differential diagnosis of Alzheimer’s Dementia, Vascular Dementia, Lewy Body Dementia

A

Alzheimer’s Dementia

  • Insidious onset
  • Progressive decline

Vascular Dementia

  • Stepwise progression
  • History of stroke
  • History of cardiovascular disease
  • Preserved insight

Lewy Body Dementia

  • Impaired attention & visuospatial skills
  • Preservation recent memory
  • Persistent visual hallucinations
  • Spontaneous parkinsonism
  • Increased sensitivity to antipsychotics
55
Q

What are the pharmacological treatments for Dementia?

A 
Cholinesterase inhibitors (ChEI) 
- work by augmenting cholinergic pathway

NMDA receptor antagonists
- work by decreasing pathological calcium influx and ultimately cell death

Monoclonal antibodies

  • work by reducing amyloid plaque build up in the brain
  • in clinical trials

Secretase inhibitors
- in clinical trials

Initiation of pharmacological treatments for dementia should be initiated and supervised by a specialist

56
Q

Describe the efficacy and adverse effects of Cholinesterases inhibitors (ChEIs)

A
  • No response with one dose not mean all
  • Linear dose pharmacokinetics
  • Improve cognitive function

Adverse effects

  • Cholinergic especially GI (nausea, vomitting, diaarhoea)
  • Leg cramps, excess mucous production
  • Bradycardia
57
Q

Describe the use of Donepezil

A

General

  • Licensed for mild to moderate dementia in Alzheimer’s disease
  • Greater selectivity acetylcholinesterase
  • Once daily dosing
  • Low side effects profile

Pharmacokinetics

  • Peak concentration 3 to 4 hours
  • t1/2 = 70 hours
  • Linear PK
  • Food does not affect absorption
  • 93 to 96% protein bound
  • metabolised in liver by CYP450
  • Renal excretion
58
Q

Describe the use of Rivastigmine

A

General

  • licensed for AD and mild to moderate dementia in Parkinson’s disease
  • Greater selectivity acetylcholinesterase
  • Twice daily dosing, also available as a patch
  • low side effect profile, especially when patch is used
  • Monitoring: patient’s body weight should be monitored whilst being treated

Pharmacokinetics

  • t1/2 = approx 2 hours
  • inhibition lasts 10 hours
  • inactive metabolites
  • renal excretion
  • no hepatic metabolism
  • little protein binding
59
Q

Describe the use of Galantamine

A

General

  • Licensed for mild to moderately severe dementia in Alzheimer’s disease
  • Enhances response of nicotinic receptors to Ach
  • t1/2 = approx 7-8 hours
  • starting dose is 8mg/day titrating to max 24mg/day
  • Twice daily dosing liquid or once daily MR capsule
  • low side effect profile
60
Q

Why would long term efficacy of drugs for dementia decline?

A

As the disease progresses, the amount of Ach produced will be less than at pre-treatment and individual patient performance will decline, eventually to a stage where the agent will seem to have little clinical effect

61
Q

Describe some potential pharmacist inputs regarding Dementia

A
  • Recognition of possible symptoms of dementia especially when responding to symptoms and refer as appropriate
  • Early access to: information, treatment, care and support networks
  • Reversible causes can be eliminated or treated
  • Make the most of remaining abilities
  • Explain to family and friends: plan for the future
  • Easier to determine subtype at early stages and treat accordingly
62
Q

Describe Medicine Management issues with Dementia and why is it important to deal with them well?

A

Counselling

  • expectation of patient and carer
  • limitations of treatment
  • negotiation of endpoint
  • side effects and what to do

Concomitant Medication

  • check for anticholinergic load e.g oxybutynin, antidepressants, antipsychotics
  • Check for adverse CNS effects

Progression

  • swallowing difficulties
  • behaviour
  • dietary intake and fluid

Social care & support

  • care&patient counseling, support stimulation
  • day hospital services
  • social worker assessment

Compliance issues / MUR

  • large number of medicines
  • appropriate titration
  • interactions and side effects

Prolonged stress leads to poorer health outcomes for both carer and PWD and then insitutionalisation

Better quality of life for people if better adherence to their medicines

Carers more supported in coping with supervisory medicines role

63
Q

Define Delirium

A

Acute confusional State
- is a common neuropsychiatric condition that presents in medical and surgical settings and is known by various names including organic brain syndrome, intensive care psychosis and acute confusional state

64
Q

Describe the three clinical subtypes of Delirium

A

Hyperactive
- Heightened arousal, restlessness, agitation, aggression

Hypoactive
- Sleepiness, lack of interest in daily activities, quiet and withdrawn

Mixed
- Move between 2 subtypes

Generally present as being restless and oversensitive to stimuli with many psychotic symptoms or lethargic and quiet with few psychotic symptoms

Emotional disturbances such as anxiety, fear, depression, irritability, anger, euphoria and apathy may also be present

65
Q

How is Delirium assessed?

A
  1. History of presenting symptoms
    - when were symptoms first noticed, what were they and what seemed to trigger them
    - medical and medication history
    - history of falls, potential precipitants such as alcohol or substance misuse
  2. Physical examination
    - exclude underlying medical condition e.g urinary tract or respiratory infection, constipation
  3. Assessment of consciousness and cognitive function
    - Abbreviated mental test score (AMTS)
    - Confirm using Confusion assessment method (CAM)
66
Q

What are the risk factors for Delirium?

A
  • increasing age: blood brain barrier breakdown
  • anxiety/depression
  • sensory over/under-stimulation/impairment
  • substance/alcohol misuse
  • brain damage of any kind
  • co-morbidity e.g infection
  • Dehydration
  • General frailty
  • social isolation
  • medication
  • cholinergic deficit
67
Q

What are the medicines commonly implicated in Delirium?

A
  • Benzodiazepines
  • TCAs
  • Antiparkinsonian agents
  • Analgesics
  • Steroids
  • Antihypertensives
  • Anti-arrhythmatic agents
  • Anti-psychotics
  • Anti-histamines
  • Antibiotics
  • Anticonvulsants
68
Q

How is Delirium treated? And also the pharmacological treatment option?

A
  • Treat the physical condition or underlying cause
  • Review medication
  • Manage substance withdrawal
  • Address underlying abnormality such as infection, electrolyte imbalance, dehydration or constipation
  • Relieve patient distress and prevent behaviour that may result in injury to themselves or others
  • Non-pharmacological methods should be used first line

Pharmacological

  • If a person is a risk to themselves or others and verbal/non-verbal de-escalation techniques are ineffective
  • Consider giving short term antipsychotics (usually 1 week or less)
69
Q

Define Learning Disability (LD) and its prevalence

A
  • a significantly reduced ability to understand new or complex information, to learn new skills (impaired intelligence)
  • with a reduced ability to cope independently (impaired social functioning)
  • which started before adulthood, with a lasting effect on development
  • 1.5 million people in UK have a learning disability
  • This includes 905,000 adults aged 18+

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